Mitochondria
Mitochondria, Liver
Mitochondria, Muscle
Muscle Proteins
Muscle, Skeletal
Muscle, Smooth
Muscle Fibers, Skeletal
Muscle Development
Muscle Contraction
Mitochondrial Proteins
Muscle Fibers, Fast-Twitch
Muscle Fatigue
Muscle Fibers, Slow-Twitch
Oxidative Phosphorylation
Mitochondrial Swelling
Oxygen Consumption
Myocytes, Smooth Muscle
Mitochondrial Membranes
Intracellular Membranes
Oculomotor Muscles
Neck Muscles
Muscle, Striated
Calcium
Cell Respiration
Muscle Spindles
DNA, Mitochondrial
Adenosine Triphosphate
Papillary Muscles
Muscle Weakness
Electron Transport Complex IV
Uncoupling Agents
Membrane Potential, Mitochondrial
Cytochromes c
Mitochondrial Membrane Transport Proteins
Microscopy, Electron
Abdominal Muscles
Muscle Cells
Quadriceps Muscle
Cells, Cultured
Oxidation-Reduction
Reactive Oxygen Species
Oligomycins
Molecular Sequence Data
Apoptosis
Membrane Potentials
Facial Muscles
Masticatory Muscles
Muscular Atrophy
Intercostal Muscles
Electromyography
Rats, Wistar
Cytochrome c Group
Atractyloside
Biological Transport
Isometric Contraction
Myofibrils
Rats, Sprague-Dawley
Antimycin A
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Cytosol
Satellite Cells, Skeletal Muscle
Energy Metabolism
Pectoralis Muscles
Rabbits
Electron Transport
Amino Acid Sequence
Models, Biological
Mitochondrial ADP, ATP Translocases
Protein Transport
Myocardium
Submitochondrial Particles
Carbonyl Cyanide m-Chlorophenyl Hydrazone
Succinates
Saccharomyces cerevisiae
Adenosine Diphosphate
Oxidative Stress
RNA, Messenger
NAD
Citrate (si)-Synthase
Rats, Inbred Strains
Membrane Proteins
Base Sequence
Carrier Proteins
Psoas Muscles
Permeability
bcl-2-Associated X Protein
Signal Transduction
Electron Transport Complex I
Cattle
Hindlimb
Subcellular Fractions
Temporal Muscle
Ruthenium Red
Succinate Dehydrogenase
Liver
Succinic Acid
Cell Fractionation
Mutation
Caspases
Myosin Heavy Chains
Proto-Oncogene Proteins c-bcl-2
Mitochondrial Proton-Translocating ATPases
Blotting, Western
Mersalyl
Mitochondrial Diseases
Diaphragm
Ion Channels
Aging
Oxygen
Carnitine
Pharyngeal Muscles
Sarcolemma
Voltage-Dependent Anion Channels
Ubiquinone
Electron Transport Complex III
Hydrogen Peroxide
Cardiolipins
Actins
Adenosine Triphosphatases
Hydrogen-Ion Concentration
Biomechanical Phenomena
Dose-Response Relationship, Drug
Cell Nucleus
Myoblasts
Microscopy, Fluorescence
Microscopy, Confocal
Endoplasmic Reticulum
NADH Dehydrogenase
Glucose
Gene Expression Regulation
Phosphorylation
Enzyme Activation
Bongkrekic Acid
Microscopy, Electron, Transmission
Immunohistochemistry
Cytoplasm
Creatine Kinase
Ketoglutaric Acids
Fatty Acids
Mitochondrial Dynamics
Mice, Knockout
Membranes
Guinea Pigs
Proton-Translocating ATPases
Pyruvic Acid
Muscle Cramp
Polarography
Electrophoresis, Polyacrylamide Gel
Potassium
Enzyme Inhibitors
Carnitine O-Palmitoyltransferase
Magnesium
Insulin
Protein Binding
Hexokinase
BH3 Interacting Domain Death Agonist Protein
Calcium Signaling
Organelles
Physical Exertion
Sarcoplasmic Reticulum
Glycolysis
Saccharomyces cerevisiae Proteins
Voltage-Dependent Anion Channel 1
Proteins
Neurospora crassa
Gene Expression
Mice, Inbred mdx
Apoptosis Inducing Factor
Histocytochemistry
Palmitoyl Coenzyme A
Fluorescent Dyes
Valinomycin
Autophagy
Exercise
Digitonin
Expression of uncoupling protein-3 and mitochondrial activity in the transition from hypothyroid to hyperthyroid state in rat skeletal muscle. (1/1585)
We sought a correlation between rat skeletal muscle triiodothyronine (T3)-mediated regulation of uncoupling protein-3 (UCP3) expression and mitochondrial activity. UCP3 mRNA expression increased strongly during the hypothyroid-hyperthyroid transition. The rank order of mitochondrial State 3 and State 4 respiration rates was hypothyroid < euthyroid < hyperthyroid. The State 4 increase may have been due to the increased UCP3 expression, as the proton leak kinetic was stimulated in the hypothyroid-hyperthyroid transition and a good correlation exists between the State 4 and UCP3 mRNA level. As a significant proportion of an organism's resting oxygen consumption is dedicated to opposing the proton leak, skeletal muscle mitochondrial UCP3 may mediate part of T3's effect on energy metabolism. (+info)Reduced cytosolic acidification during exercise suggests defective glycolytic activity in skeletal muscle of patients with Becker muscular dystrophy. An in vivo 31P magnetic resonance spectroscopy study. (2/1585)
Becker muscular dystrophy is an X-linked disorder due to mutations in the dystrophin gene, resulting in reduced size and/or content of dystrophin. The functional role of this subsarcolemma protein and the biochemical mechanisms leading to muscle necrosis in Becker muscular dystrophy are still unknown. In particular, the role of a bioenergetic deficit is still controversial. In this study, we used 31p magnetic resonance spectroscopy (31p-MRS) to investigate skeletal muscle mitochondrial and glycolytic ATP production in vivo in 14 Becker muscular dystrophy patients. Skeletal muscle glycogenolytic ATP production, measured during the first minute of exercise, was similar in patients and controls. On the other hand, during later phases of exercise, skeletal muscle in Becker muscular dystrophy patients was less acidic than in controls, the cytosolic pH at the end of exercise being significantly higher in Becker muscular dystrophy patients. The rate of proton efflux from muscle fibres of Becker muscular dystrophy patients was similar to that of controls, pointing to a deficit in glycolytic lactate production as a cause of higher end-exercise cytosolic pH in patients. The maximum rate of mitochondrial ATP production was similar in muscle of Becker muscular dystrophy patients and controls. The results of this in vivo 31P-MRS study are consistent with reduced glucose availability in dystrophin-deficient muscles. (+info)Subcellular adaptation of the human diaphragm in chronic obstructive pulmonary disease. (3/1585)
Pulmonary hyperinflation impairs the function of the diaphragm in patients with chronic obstructive pulmonary disease (COPD). However, it has been recently demonstrated that the muscle can counterbalance this deleterious effect, remodelling its structure (i.e. changing the proportion of different types of fibres). The aim of this study was to investigate whether the functional impairment present in COPD patients can be associated with structural subcellular changes of the diaphragm. Twenty individuals (60+/-9 yrs, 11 COPD patients and 9 subjects with normal spirometry) undergoing thoracotomy were included. Nutritional status and respiratory function were evaluated prior to surgery. Then, small samples of the costal diaphragm were obtained and processed for electron microscopy analysis. COPD patients showed a mean forced expiratory volume in one second (FEV1) of 60+/-9% predicted, a higher concentration of mitochondria (n(mit)) in their diaphragm than controls (0.62+/-0.16 versus 0.46+/-0.16 mitochondrial transections (mt) x microm(-2), p<0.05). On the other hand, subjects with air trapping (residual volume (RV)/total lung capacity (TLC) >37%) disclosed not only a higher n(mit) (0.63+/-0.17 versus 0.43+/-0.07 mt x microm(-2), p<0.05) but shorter sarcomeres (L(sar)) than subjects without this functional abnormality (2.08+/-0.16 to 2.27+/-0.15 microm, p<0.05). Glycogen stores were similar in COPD and controls. The severity of airways obstruction (i.e. FEV1) was associated with n(mit) (r=-0.555, p=0.01), while the amount of air trapping (i.e. RV/TLC) was found to correlate with both n(mit) (r=0.631, p=0.005) and L(sar) (r=-0.526, p<0.05). Finally, maximal inspiratory pressure (PI,max) inversely correlated with n(mit) (r=-0.547, p=0.01). In conclusion, impairment in lung function occurring in patients with chronic obstructive pulmonary disease is associated with subcellular changes in their diaphragm, namely a shortening in the length of sarcomeres and an increase in the concentration of mitochondria. These changes form a part of muscle remodelling, probably contributing to a better functional muscle behaviour. (+info)Release of Ca2+ from the sarcoplasmic reticulum increases mitochondrial [Ca2+] in rat pulmonary artery smooth muscle cells. (4/1585)
1. The Ca2+-sensitive fluorescent indicator rhod-2 was used to measure mitochondrial [Ca2+] ([Ca2+]m) in single smooth muscle cells from the rat pulmonary artery, while simultaneously monitoring cytosolic [Ca2+] ([Ca2+]i) with fura-2. 2. Application of caffeine produced an increase in [Ca2+]i and also increased [Ca2+]m. The increase in [Ca2+]m occurred after the increase in [Ca2+]i, and remained elevated for a considerable time after [Ca2+]i had returned to resting values. 3. The protonophore carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), which causes the mitochondrial membrane potential to collapse, markedly attenuated the increase in [Ca2+]m following caffeine application and also increased the half-time for recovery of [Ca2+]i to resting values. 4. Activation of purinoceptors with ATP also produced increases in both [Ca2+]i and [Ca2+]m in these smooth muscle cells. In some cells, oscillations in [Ca2+]i were observed during ATP application, which produced corresponding oscillations in [Ca2+]m and membrane currents. 5. This study provides direct evidence that Ca2+ release from the sarcoplasmic reticulum, either through ryanodine or inositol 1,4, 5-trisphosphate (InsP3) receptors, increases both cytosolic and mitochondrial [Ca2+] in smooth muscle cells. These results have potential implications both for the role of mitochondria in Ca2+ regulation in smooth muscle, and for understanding how cellular metabolism is regulated. (+info)Mitochondrial regulation of the cytosolic Ca2+ concentration and the InsP3-sensitive Ca2+ store in guinea-pig colonic smooth muscle. (5/1585)
1. Mitochondrial regulation of the cytosolic Ca2+ concentration ([Ca2+]c) in guinea-pig single colonic myocytes has been examined, using whole-cell recording, flash photolysis of caged InsP3 and microfluorimetry. 2. Depolarization increased [Ca2+]c and triggered contraction. Resting [Ca2+]c was virtually restored some 4 s after the end of depolarization, a time when the muscle had shortened to 50 % of its fully relaxed length. The muscle then slowly relaxed (t = 17 s). 3. The decline in the Ca2+ transient was monophasic but often undershot or overshot resting levels, depending on resting [Ca2+]c. The extent of the overshoot or undershoot increased with increasing peak [Ca2+]c. 4. Carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 5 microM), which dissipates the mitochondrial proton electrochemical gradient and therefore prevents mitochondrial Ca2+ accumulation, slowed Ca2+ removal at high ( > 300 nM) but not at lower [Ca2+]c and abolished [Ca2+]c overshoots. Oligomycin B (5 microM), which prevents mitchondrial ATP production, affected neither the rate of decline nor the magnitude of the overshoot. 5. During depolarization, the global rhod-2 signal (which represents the mitochondrial matrix Ca2+ concentration, [Ca2+]m) rose slowly in a CCCP-sensitive manner during and for about 3 s after depolarization had ended. [Ca2+]m then slowly decreased over tens of seconds. 6. Inhibition of sarcoplasmic reticulum Ca2+ uptake with thapsigargin (100 nM) reduced the undershoot and increased the overshoot. 7. Flash photolysis of caged InsP3 (20 microM) evoked reproducible increases in [Ca2+]c. CCCP (5 microM) reduced the magnitude of the [Ca2+]c transients evoked by flash photolysis of caged InsP3. Oligomycin B (5 microM) did not reduce the inhibition of the InsP3-induced Ca2+ transient by CCCP thus minimizing the possibility that CCCP lowered ATP levels by reversing the mitochondrial ATP synthase and so reducing SR Ca2+ refilling. 8. While CCCP reduced the magnitude of the InsP3-evoked Ca2+ signal, the internal Ca2+ store content, as assessed by the magnitude of ionomycin-evoked Ca2+ release, did not decrease significantly. 9. [Ca2+]c decline in smooth muscle, following depolarization, may involve mitochondrial Ca2+ uptake. Following InsP3-evoked Ca2+ release, mitochondrial uptake of Ca2+ may regulate the local [Ca2+]c near the InsP3 receptor so maintaining the sensitivity of the InsP3 receptor to release Ca2+ from the SR. (+info)Contribution of mitochondrial proton leak to respiration rate in working skeletal muscle and liver and to SMR. (6/1585)
Proton pumping across the mitochondrial inner membrane and proton leak back through the natural proton conductance pathway make up a futile cycle that dissipates redox energy. We measured respiration and average mitochondrial membrane potential in perfused rat hindquarter with maximal tetanic contraction of the left gastrocnemius-soleus-plantaris muscle group, and we estimate that the mitochondrial proton cycle accounted for 34% of the respiration rate of the preparation. Similar measurements in rat hepatocytes given substrates to cause a high rate of gluconeogenesis and ureagenesis showed that the proton cycle accounted for 22% of the respiration rate of these cells. Combining these in vitro values with literature values for the contribution of skeletal muscle and liver to standard metabolic rate (SMR), we calculate that the proton cycle in working muscle and liver may account for 15% of SMR in vivo. Although this value is less than the 20% of SMR we calculated previously using data from resting skeletal muscle and hepatocytes, it is still large, and we conclude that the futile proton cycle is a major contributor to SMR. (+info)Calcium-dependent regulation of cytochrome c gene expression in skeletal muscle cells. Identification of a protein kinase c-dependent pathway. (7/1585)
Mitochondrial biogenesis can occur rapidly in mammalian skeletal muscle subjected to a variety of physiological conditions. However, the intracellular signal(s) involved in regulating this process remain unknown. Using nuclearly encoded cytochrome c, we show that its expression in muscle cells is increased by changes in cytosolic Ca2+ using the ionophore A23187. Treatment of myotubes with A23187 increased cytochrome c mRNA expression up to 1.7-fold. Transfection experiments using promoter-chloramphenicol acetyltransferase constructs revealed that this increase could be transcriptionally mediated since A23187 increased chloramphenicol acetyltransferase activity by 2.5-fold. This increase was not changed by KN62, an inhibitor of Ca2+/calmodulin-dependent kinases II and IV, and it was not modified by overexpression of protein kinase A and cAMP response element-binding protein, demonstrating that the A23187 effect was not mediated through Ca2+/calmodulin-dependent kinase- or protein kinase A-dependent pathways. However, treatment of myotubes with staurosporine or 12-O-tetradecanoylphorbol-13-acetate reduced the effect of A23187 on cytochrome c transactivation by 40-50%. Coexpression of the Ca2+-sensitive protein kinase C isoforms alpha and betaII, but not the Ca2+-insensitive delta isoform, exaggerated the A23187-mediated response. The short-term effect of A23187 was mediated in part by mitogen-activated protein kinase (extracellular signal-regulated kinases 1 and 2) since its activation peaked 2 h after A23187 treatment, and cytochrome c transactivation was reduced by PD98089, a mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor. These results demonstrate the existence of a Ca2+-sensitive, protein kinase C-dependent pathway involved in cytochrome c expression and implicate Ca2+ as a signal in the up-regulation of nuclear genes encoding mitochondrial proteins. (+info)Sub maximal oxygen uptake related to fat free mass and lean leg volume in trained runners. (8/1585)
The sub maximal oxygen uptake (VO2) of 32 trained male middle and long distance runners aged 19.5-36.0 years was determined at five treadmill speeds. There was a significant linear relationship (p less than 0.01) between VO2 at each of the treadmill speeds and Fat-Free Mass (FFM) and Lean Leg Volume (LLV). To explain the relationship other factors are considered, the most important of which may be the mechanical configuration of muscle and mitochondrial function. (+info)There are several causes of muscle weakness, including:
1. Neuromuscular diseases: These are disorders that affect the nerves that control voluntary muscle movement, such as amyotrophic lateral sclerosis (ALS) and polio.
2. Musculoskeletal disorders: These are conditions that affect the muscles, bones, and joints, such as arthritis and fibromyalgia.
3. Metabolic disorders: These are conditions that affect the body's ability to produce energy, such as hypoglycemia and hypothyroidism.
4. Injuries: Muscle weakness can occur due to injuries such as muscle strains and tears.
5. Infections: Certain infections such as botulism and Lyme disease can cause muscle weakness.
6. Nutritional deficiencies: Deficiencies in vitamins and minerals such as vitamin D and B12 can cause muscle weakness.
7. Medications: Certain medications such as steroids and anticonvulsants can cause muscle weakness as a side effect.
The symptoms of muscle weakness can vary depending on the underlying cause, but may include:
1. Fatigue: Feeling tired or weak after performing simple tasks.
2. Lack of strength: Difficulty lifting objects or performing physical activities.
3. Muscle cramps: Spasms or twitches in the muscles.
4. Muscle wasting: Loss of muscle mass and tone.
5. Difficulty speaking or swallowing: In cases where the muscle weakness affects the face, tongue, or throat.
6. Difficulty walking or standing: In cases where the muscle weakness affects the legs or lower back.
7. Droopy facial features: In cases where the muscle weakness affects the facial muscles.
If you are experiencing muscle weakness, it is important to seek medical attention to determine the underlying cause and receive proper treatment. A healthcare professional will perform a physical examination and may order diagnostic tests such as blood tests or imaging studies to help diagnose the cause of the muscle weakness. Treatment will depend on the underlying cause, but may include medication, physical therapy, or lifestyle changes. In some cases, muscle weakness may be a sign of a serious underlying condition that requires prompt medical attention.
There are several types of muscular atrophy, including:
1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.
Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.
1. Muscular dystrophy: A group of genetic disorders characterized by progressive muscle weakness and degeneration.
2. Myopathy: A condition where the muscles become damaged or diseased, leading to muscle weakness and wasting.
3. Fibromyalgia: A chronic condition characterized by widespread pain, fatigue, and muscle stiffness.
4. Rhabdomyolysis: A condition where the muscle tissue is damaged, leading to the release of myoglobin into the bloodstream and potentially causing kidney damage.
5. Polymyositis/dermatomyositis: Inflammatory conditions that affect the muscles and skin.
6. Muscle strain: A common injury caused by overstretching or tearing of muscle fibers.
7. Cervical dystonia: A movement disorder characterized by involuntary contractions of the neck muscles.
8. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue.
9. Oculopharyngeal myopathy: A condition characterized by weakness of the muscles used for swallowing and eye movements.
10. Inclusion body myositis: An inflammatory condition that affects the muscles, leading to progressive muscle weakness and wasting.
These are just a few examples of the many different types of muscular diseases that can affect individuals. Each condition has its unique set of symptoms, causes, and treatment options. It's important for individuals experiencing muscle weakness or wasting to seek medical attention to receive an accurate diagnosis and appropriate care.
Mitochondrial diseases can affect anyone, regardless of age or gender, and they can be caused by mutations in either the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). These mutations can be inherited from one's parents or acquired during embryonic development.
Some of the most common symptoms of mitochondrial diseases include:
1. Muscle weakness and wasting
2. Seizures
3. Cognitive impairment
4. Vision loss
5. Hearing loss
6. Heart problems
7. Neurological disorders
8. Gastrointestinal issues
9. Liver and kidney dysfunction
Some examples of mitochondrial diseases include:
1. MELAS syndrome (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes)
2. Kearns-Sayre syndrome (a rare progressive disorder that affects the nervous system and other organs)
3. Chronic progressive external ophthalmoplegia (CPEO), which is characterized by weakness of the extraocular muscles and vision loss
4. Mitochondrial DNA depletion syndrome, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
5. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
6. Leigh syndrome, which is a rare genetic disorder that affects the brain and spinal cord.
7. LHON (Leber's Hereditary Optic Neuropathy), which is a rare form of vision loss that can lead to blindness in one or both eyes.
8. Mitochondrial DNA mutation, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
9. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
10. Kearns-Sayre syndrome, which is a rare progressive disorder that affects the nervous system and other organs.
It's important to note that this is not an exhaustive list and there are many more mitochondrial diseases and disorders that can affect individuals. Additionally, while these diseases are rare, they can have a significant impact on the quality of life of those affected and their families.
1. Duchenne muscular dystrophy: This is the most common form of muscular dystrophy in children, caused by a defect in the DMD gene that codes for dystrophin protein. It affects boys primarily and can lead to progressive muscle weakness and wasting, as well as cardiac and other complications.
2. Becker muscular dystrophy: This is a milder form of muscular dystrophy than Duchenne, caused by a defect in the DMD gene that codes for dystrophin protein. It primarily affects boys but can also affect girls.
3. Limb-girdle muscular dystrophy: This is a group of disorders characterized by progressive muscle weakness and degeneration, particularly affecting the shoulder and pelvic girdles. There are several types of limb-girdle muscular dystrophy, including type 1A, 1B, 2A, and 2B.
4. Facioscapulohumeral muscular dystrophy: This is a type of muscular dystrophy that affects the muscles of the face, shoulder blades, and upper arms. It can cause progressive muscle weakness, wasting, and fatigue.
5. Myotonic muscular dystrophy: This is the most common form of adult-onset muscular dystrophy, caused by a defect in the DMPK gene that codes for myotonia protein. It can cause progressive muscle stiffness, spasms, and weakness, as well as other complications such as cataracts and type 2 diabetes.
In animals, muscular dystrophy is similar to human forms of the disorder, caused by genetic mutations that affect muscle function and strength. It can be caused by a variety of factors, including genetics, nutrition, and environmental exposures.
Symptoms of muscular dystrophy in animals can include:
1. Progressive muscle weakness and wasting
2. Loss of coordination and balance
3. Difficulty walking or running
4. Muscle cramps and spasms
5. Poor appetite and weight loss
6. Increased breathing rate and difficulty breathing
7. Cardiac problems, such as arrhythmias and heart failure
8. Cognitive decline and seizures
Diagnosis of muscular dystrophy in animals is similar to human patients, involving a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies, and muscle biopsy.
Treatment for muscular dystrophy in animals is limited, but may include:
1. Supportive care, such as antibiotics for respiratory infections and pain management
2. Physical therapy to maintain joint mobility and prevent deformities
3. Nutritional support to ensure adequate nutrition and hydration
4. Medications to manage symptoms such as muscle spasms and seizures
5. Assistive devices, such as wheelchairs or slings, to improve mobility and quality of life
Prevention of muscular dystrophy in animals is not possible at present, but research into the genetic causes and potential treatments for the disease is ongoing. It is important for pet owners to be aware of the signs of muscular dystrophy and seek veterinary care if they suspect their pet may be affected.
Example sentences:
1. The runner experienced a muscle cramp in her leg during the marathon, causing her to slow down and almost drop out.
2. After experiencing frequent muscle cramps, the patient was diagnosed with hypokalemia, a condition characterized by low potassium levels.
3. During pregnancy, muscle cramps are common due to changes in hormone levels and increased pressure on the musculoskeletal system.
4. The elderly man's muscle cramps were caused by a lack of physical activity and dehydration, which can be a challenge for older adults.
5. Proper stretching and warm-up exercises can help prevent muscle cramps in athletes, especially those participating in endurance sports.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
There are several possible causes of muscle rigidity, including:
1. Injury: Muscle rigidity can be a result of direct trauma to the muscle, such as a strain or sprain.
2. Infection: Certain infections, such as Lyme disease or endocarditis, can cause muscle rigidity as a symptom.
3. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, and stroke can all cause muscle rigidity due to damage to the nervous system.
4. Medication side effects: Certain medications, such as steroids and certain antidepressants, can cause muscle rigidity as a side effect.
5. Metabolic disorders: Conditions such as hypocalcemia (low calcium levels) and hyperthyroidism can cause muscle rigidity.
6. Autoimmune disorders: Conditions such as polymyositis and dermatomyositis can cause muscle rigidity due to inflammation of the muscles.
Symptoms of muscle rigidity may include:
* Stiffness or inflexibility in the affected muscles
* Pain or tenderness in the affected area
* Limited range of motion in the affected joints
* Muscle spasms or cramps
* Fatigue or weakness
Treatment for muscle rigidity will depend on the underlying cause. In some cases, medication may be prescribed to relax the muscles and improve mobility. Physical therapy and exercise may also be helpful in improving range of motion and strength. In other cases, treatment may involve addressing the underlying condition or disorder that is causing the muscle rigidity.
There are several types of muscular dystrophies, including:
1. Duchenne muscular dystrophy (DMD): This is the most common form of muscular dystrophy, affecting males primarily. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, wheelchair dependence, and shortened lifespan.
2. Becker muscular dystrophy (BMD): This is a less severe form of muscular dystrophy than DMD, affecting both males and females. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, but with a milder course than DMD.
3. Limb-girdle muscular dystrophy (LGMD): This is a group of disorders that affect the muscles around the shoulders and hips, leading to progressive weakness and degeneration. There are several subtypes of LGMD, each with different symptoms and courses.
4. Facioscapulohumeral muscular dystrophy (FSHD): This is a rare form of muscular dystrophy that affects the muscles of the face, shoulder, and upper arm. It is caused by a mutation in the D4Z4 repeat on chromosome 4.
5. Myotonic dystrophy: This is the most common adult-onset form of muscular dystrophy, affecting both males and females. It is characterized by progressive muscle stiffness, weakness, and wasting, as well as other symptoms such as cataracts, myotonia, and cognitive impairment.
There is currently no cure for muscular dystrophies, but various treatments are available to manage the symptoms and slow the progression of the disease. These include physical therapy, orthotics and assistive devices, medications to manage pain and other symptoms, and in some cases, surgery. Researchers are actively working to develop new treatments and a cure for muscular dystrophies, including gene therapy, stem cell therapy, and small molecule therapies.
It's important to note that muscular dystrophy can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific type of dystrophy. This means that the risk of inheriting the condition depends on the mode of inheritance and the presence of mutations in specific genes.
In summary, muscular dystrophy is a group of genetic disorders characterized by progressive muscle weakness and degeneration. There are several types of muscular dystrophy, each with different symptoms and courses. While there is currently no cure for muscular dystrophy, various treatments are available to manage the symptoms and slow the progression of the disease. Researchers are actively working to develop new treatments and a cure for muscular dystrophy.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are several types of muscle neoplasms, including:
1. Leiomyoma: A benign tumor that develops in the smooth muscle tissue of the uterus. It is the most common type of uterine tumor and is usually found in women over the age of 30.
2. Rhabdomyosarcoma: A rare type of cancerous muscle tumor that can develop in children and young adults. It can occur in any part of the body, but is most commonly found in the head, neck, or genitourinary tract.
3. Liposarcoma: A rare type of cancerous muscle tumor that develops in the fat cells of the soft tissue. It can occur in any part of the body and is more common in older adults.
4. Fibromyxoid tumor: A rare benign tumor that develops in the muscles and connective tissue. It usually affects the arms or legs and can be diagnosed at any age, but is most commonly found in children and young adults.
5. Alveolar soft part sarcoma: A rare type of cancerous muscle tumor that develops in the soft tissue of the body. It is more common in younger adults and can occur anywhere in the body, but is most commonly found in the legs or arms.
The symptoms of muscle neoplasms vary depending on the location and size of the tumor. They may include pain, swelling, redness, and limited mobility in the affected area. Diagnosis is usually made through a combination of imaging tests such as X-rays, CT scans, or MRI, and a biopsy to confirm the presence of cancerous cells.
Treatment for muscle neoplasms depends on the type and location of the tumor, as well as the stage of the disease. Surgery is often the first line of treatment, followed by radiation therapy or chemotherapy if the tumor is malignant. In some cases, observation and monitoring may be recommended if the tumor is benign and not causing any symptoms.
It's important to note that muscle neoplasms are relatively rare, and most muscle masses are benign and non-cancerous. However, it's always best to consult a medical professional if you notice any unusual lumps or bumps on your body to determine the cause and appropriate treatment.
Muscle spasticity can cause a range of symptoms, including:
* Increased muscle tone, leading to stiffness and rigidity
* Spasms or sudden contractions of the affected muscles
* Difficulty moving the affected limbs
* Pain or discomfort in the affected area
* Abnormal postures or movements
There are several potential causes of muscle spasticity, including:
* Neurological disorders such as cerebral palsy, multiple sclerosis, and spinal cord injuries
* Stroke or other brain injuries
* Muscle damage or inflammation
* Infections such as meningitis or encephalitis
* Metabolic disorders such as hypokalemia (low potassium levels) or hyperthyroidism
Treatment options for muscle spasticity include:
* Physical therapy to improve range of motion and strength
* Medications such as baclofen, tizanidine, or dantrolene to reduce muscle spasms
* Injectable medications such as botulinum toxin or phenol to destroy excess nerve fibers
* Surgery to release or sever affected nerve fibers
* Electrical stimulation therapy to improve muscle function and reduce spasticity.
It is important to note that muscle spasticity can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, maintain independence, and engage in social and recreational activities. As such, it is important to seek medical attention if symptoms of muscle spasticity are present to determine the underlying cause and develop an appropriate treatment plan.
The symptoms of DMD typically become apparent in early childhood and progress rapidly. They include:
* Delayed motor development
* Weakness and wasting of muscles, particularly in the legs and pelvis
* Muscle weakness that worsens over time
* Loss of muscle mass and fatigue
* Difficulty walking, running, or standing
* Heart problems, such as cardiomyopathy and arrhythmias
* Respiratory difficulties, such as breathing problems and pneumonia
DMD is diagnosed through a combination of clinical evaluation, muscle biopsy, and genetic testing. Treatment options are limited and focus on managing symptoms and improving quality of life. These may include:
* Physical therapy to maintain muscle strength and function
* Medications to manage pain, spasms, and other symptoms
* Assistive devices, such as braces and wheelchairs, to improve mobility and independence
* Respiratory support, such as ventilation assistance, to manage breathing difficulties
The progression of DMD is highly variable, with some individuals experiencing a more rapid decline in muscle function than others. The average life expectancy for individuals with DMD is approximately 25-30 years, although some may live into their 40s or 50s with appropriate medical care and support.
Duchenne muscular dystrophy is a devastating and debilitating condition that affects thousands of individuals worldwide. While there is currently no cure for the disorder, ongoing research and advancements in gene therapy and other treatments offer hope for improving the lives of those affected by DMD.
1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.
The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.
The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.
Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
There are several types of mitochondrial myopathies, each with different clinical features and inheritance patterns. Some of the most common forms include:
1. Kearns-Sayre syndrome: This is a rare progressive disorder that affects the nervous system, muscles, and other organs. It is characterized by weakness and paralysis, seizures, and vision loss.
2. MELAS syndrome (mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes): This condition is characterized by recurring stroke-like episodes, seizures, muscle weakness, and cognitive decline.
3. MERRF (myoclonic epilepsy with ragged red fibers): This disorder is characterized by myoclonus (muscle jerks), seizures, and progressive muscle weakness.
4. LHON (Leber's hereditary optic neuropathy): This condition affects the optic nerve and can lead to sudden vision loss.
The symptoms of mitochondrial myopathies can vary widely, depending on the specific disorder and the severity of the mutation. They may include muscle weakness, muscle cramps, muscle wasting, seizures, vision loss, and cognitive decline.
There is no cure for mitochondrial myopathies, but various treatments can help manage the symptoms. These may include physical therapy, medications to control seizures or muscle spasms, and nutritional supplements to support energy production. In some cases, a lung or heart-lung transplant may be necessary.
The diagnosis of a mitochondrial myopathy is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include blood tests to measure the levels of certain enzymes and other molecules in the body, as well as muscle biopsy to examine the muscle tissue under a microscope. Genetic testing can help identify the specific mutation responsible for the condition.
The prognosis for mitochondrial myopathies varies depending on the specific disorder and the severity of the symptoms. Some forms of the disease are slowly progressive, while others may be more rapidly debilitating. In general, the earlier the diagnosis and treatment, the better the outcome.
There is currently no cure for mitochondrial myopathies, but research is ongoing to develop new treatments and therapies. In addition, there are several organizations and support groups that provide information and resources for individuals with these conditions and their families.
1. Muscular dystrophy: A group of genetic disorders that cause progressive muscle weakness and degeneration.
2. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
3. Spinal muscular atrophy: A genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement.
4. Peripheral neuropathy: A condition that causes damage to the peripheral nerves, leading to weakness, numbness, and pain in the hands and feet.
5. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, causing muscle weakness and fatigue.
6. Neuropathy: A term used to describe damage to the nerves, which can cause a range of symptoms including numbness, tingling, and pain in the hands and feet.
7. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the peripheral nerves, leading to muscle weakness and wasting.
8. Guillain-Barré syndrome: An autoimmune disorder that causes inflammation and damage to the nerves, leading to muscle weakness and paralysis.
9. Botulism: A bacterial infection that can cause muscle weakness and paralysis by blocking the release of the neurotransmitter acetylcholine.
10. Myotonia congenita: A genetic disorder that affects the nerve-muscle connection, causing muscle stiffness and rigidity.
These are just a few examples of neuromuscular diseases, and there are many more conditions that can cause muscle weakness and fatigue. It's important to see a doctor if you experience persistent or severe symptoms to receive an accurate diagnosis and appropriate treatment.
Muscle mass is an important component of overall body strength, and as people age, their muscles naturally begin to atrophy due to a combination of hormonal changes and disuse. This leads to a decrease in the amount of protein available for other bodily functions, which can further exacerbate the decline in physical functioning.
Sarcopenia can be caused by various factors such as inactivity, malnutrition, chronic diseases like diabetes and heart disease, and genetics. It is a major risk factor for falls, disability, and cognitive decline in the elderly population.
There is no single test to diagnose sarcopenia, but healthcare professionals use a combination of physical examination, medical history, and laboratory tests to assess muscle mass and function. Treatment options include resistance training exercises, nutritional supplements, and medications such as selective estrogen receptor modulators (SERMs) and growth hormone-releasing peptides.
In conclusion, sarcopenia is a progressive condition that affects the muscles in older adults, leading to a loss of strength and physical functioning. It can be caused by various factors, and healthcare professionals use a combination of physical examination and laboratory tests to diagnose and treat it.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
There are several factors that can contribute to the development of insulin resistance, including:
1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.
There are several ways to diagnose insulin resistance, including:
1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.
There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:
1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.
Medications that may be used to treat insulin resistance include:
1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.
It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.
Examples of atrophic muscular disorders include:
1. Muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength, leading to muscle wasting and weakness.
2. Myotonia congenita: An autosomal dominant disorder characterized by muscle stiffness and spasms, particularly in the neck, shoulder, and limb muscles.
3. Inclusion body myositis: An inflammatory muscle disease that leads to progressive muscle weakness and wasting, with deposits of abnormal protein called inclusion bodies in the muscle fibers.
4. Limb-girdle muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength in the arms and legs, leading to muscle wasting and weakness.
5. Facioscapulohumeral muscular dystrophy: An inherited disorder characterized by progressive weakness of the facial, shoulder, and upper arm muscles, with a loss of motor neurons in the spinal cord.
The symptoms of atrophic muscular disorders can vary depending on the specific disorder and its severity, but may include:
1. Muscle weakness and wasting
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Fatigue and decreased endurance
5. Loss of motor neurons in the spinal cord
6. Cognitive impairment
7. Developmental delays
8. Vision loss
9. Hearing loss
10. Skeletal deformities
Atrophic muscular disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and muscle biopsy. Treatment is focused on managing the symptoms and slowing the progression of the disease, and may include:
1. Physical therapy to maintain muscle strength and function
2. Medications to manage pain and spasms
3. Assistive devices such as braces and walkers
4. Respiratory support in advanced cases
5. Gene therapy is an area of ongoing research, but it is not yet widely available for the treatment of atrophic muscular disorders.
It is important to note that atrophic muscular disorders are a group of rare and complex conditions, and each type has its own unique set of symptoms and characteristics. If you suspect that you or someone you know may be experiencing symptoms of an atrophic muscular disorder, it is important to consult with a healthcare professional for proper evaluation and diagnosis.
There are several potential causes of muscle hypertonia, including:
1. Neurological disorders such as cerebral palsy, Parkinson's disease, or multiple sclerosis
2. Musculoskeletal injuries or inflammation
3. Infections such as Lyme disease or viral infections
4. Metabolic disorders such as hypokalemia (low potassium levels) or hyperthyroidism
5. Adverse reactions to certain medications
6. Emotional stress or anxiety
Symptoms of muscle hypertonia can vary depending on the severity and location of the condition, but may include:
1. Stiffness and rigidity of the affected muscles
2. Pain or tenderness in the muscles
3. Limited range of motion in the affected joints
4. Fatigue or weakness in the affected limbs
5. Difficulty with movement and balance
6. Muscle spasms or cramping
Treatment for muscle hypertonia typically involves a combination of physical therapy, medication, and lifestyle modifications. Physical therapy may include stretching and strengthening exercises to improve range of motion and reduce stiffness, as well as techniques such as heat or cold therapy to relax the muscles. Medications such as muscle relaxants or anti-inflammatory drugs may be prescribed to reduce muscle spasms and inflammation. Lifestyle modifications such as regular exercise, proper nutrition, and stress management techniques can also help to reduce symptoms of muscle hypertonia. In severe cases, surgery may be necessary to release or lengthen the affected muscles.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.
Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.
Hypotonia is a state of decreased muscle tone, which can be caused by various conditions, such as injury, disease, or disorders that affect the nervous system. It is characterized by a decrease in muscle stiffness and an increase in joint range of motion. Muscle hypotonia can result in difficulty with movement, coordination, and balance.
There are several types of muscle hypotonia, including:
1. Central hypotonia: This type is caused by dysfunction in the central nervous system and results in a decrease in muscle tone throughout the body.
2. Peripheral hypotonia: This type is caused by dysfunction in the peripheral nervous system and results in a selective decrease in muscle tone in specific muscle groups.
3. Mixed hypotonia: This type combines central and peripheral hypotonia.
Muscle hypotonia can be associated with a variety of symptoms, such as fatigue, weakness, poor coordination, and difficulty with speech and swallowing. Treatment options vary depending on the underlying cause of the condition and may include physical therapy, medication, and lifestyle modifications.
Muscle hypotonia is a common condition that can affect people of all ages, from children to adults. Early diagnosis and treatment are important to help manage symptoms and improve quality of life. If you suspect you or your child may have muscle hypotonia, consult with a healthcare professional for proper evaluation and treatment.
The exact cause of cachexia is not fully understood, but it is thought to be related to a combination of factors such as inflammation, hormonal imbalances, and changes in metabolism. Treatment for cachexia often focuses on addressing the underlying cause of the wasting, such as managing cancer or HIV/AIDS, as well as providing nutritional support and addressing any related complications.
In the medical field, cachexia is a serious condition that requires careful management to improve quality of life and outcomes for patients. It is important for healthcare providers to be aware of the signs and symptoms of cachexia and to provide appropriate treatment and support to affected individuals.
Some common examples of neurodegenerative diseases include:
1. Alzheimer's disease: A progressive loss of cognitive function, memory, and thinking skills that is the most common form of dementia.
2. Parkinson's disease: A disorder that affects movement, balance, and coordination, causing tremors, rigidity, and difficulty with walking.
3. Huntington's disease: An inherited condition that causes progressive loss of cognitive, motor, and psychiatric functions.
4. Amyotrophic lateral sclerosis (ALS): A disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, paralysis, and eventually death.
5. Prion diseases: A group of rare and fatal disorders caused by misfolded proteins in the brain, leading to neurodegeneration and death.
6. Creutzfeldt-Jakob disease: A rare, degenerative, and fatal brain disorder caused by an abnormal form of a protein called a prion.
7. Frontotemporal dementia: A group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.
Neurodegenerative diseases can be caused by a variety of factors, including genetics, age, lifestyle, and environmental factors. They are typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment options for neurodegenerative diseases vary depending on the specific condition and its underlying causes, but may include medications, therapy, and lifestyle changes.
Preventing or slowing the progression of neurodegenerative diseases is a major focus of current research, with various potential therapeutic strategies being explored, such as:
1. Stem cell therapies: Using stem cells to replace damaged neurons and restore brain function.
2. Gene therapies: Replacing or editing genes that are linked to neurodegenerative diseases.
3. Small molecule therapies: Developing small molecules that can slow or prevent the progression of neurodegenerative diseases.
4. Immunotherapies: Harnessing the immune system to combat neurodegenerative diseases.
5. Lifestyle interventions: Promoting healthy lifestyle choices, such as regular exercise and a balanced diet, to reduce the risk of developing neurodegenerative diseases.
In conclusion, neurodegenerative diseases are a complex and diverse group of disorders that can have a profound impact on individuals and society. While there is currently no cure for these conditions, research is providing new insights into their causes and potential treatments. By continuing to invest in research and developing innovative therapeutic strategies, we can work towards improving the lives of those affected by neurodegenerative diseases and ultimately finding a cure.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.
Symptoms of malignant hyperthermia can include:
* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure
If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.
Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.
Telocyte
Striated muscle tissue
Skeletal muscle
Glycerol phosphate shuttle
Mitochondrion
HK2
Muscle contraction
Monocarboxylate transporter 1
Exertional rhabdomyolysis
Tricarboxylate transport protein, mitochondrial
Cav1.2
Michael Roden
Staining
David A. Hood
Plectin
NMNAT3
Twinkle (protein)
Norbormide
Thoracic diaphragm
MT-TE
Limb body wall complex
Myopathy, X-linked, with excessive autophagy
Choline
Ophiocordyceps unilateralis
Sodium fluoroacetate
Cardiac physiology
SOD1
Uncoupling protein
Phosphotungstic acid-haematoxylin stain
Pyruvate dehydrogenase complex
Metabolism
Tetratricopeptide repeat protein 39B
Mitochondrial DNA
Systemic primary carnitine deficiency
Meldonium
Heart-type fatty acid binding protein
ENDOG
Physiological effects in space
Alpha-Ketoisocaproic acid
Index of biochemistry articles
DNA damage theory of aging
Beta-Hydroxybutyric acid
Immunosenescence
Trichrome staining
Heme
Albert von Kölliker
Plácido Navas Lloret
Mitochondrial myopathy
Obesity and fertility
Substrate-level phosphorylation
Aldolase A
Pearson syndrome
Malonyl-CoA decarboxylase
Diacylglycerol O-acyltransferase 2
BCS1L
Estrogen receptor beta
Lipid signaling
Spongy degeneration of the central nervous system
Muscle Mitochondria May Form Energy Power Grid | National Institutes of Health (NIH)
ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and...
Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. |...
Disuse-associated loss of the protease LONP1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass...
Skeletal muscle insulin resistance: role of mitochondria and other ROS sources.
Dietary nitrate accelerates postexercise muscle metabolic recovery and O2 delivery in hypoxia
Category A - Anatomy
Qigong Institute
ERα36, a Variant of Estrogen Receptor α, is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and...
ERα36, a Variant of Estrogen Receptor α, is Predominantly Localized in Mitochondria of Human Uterine Smooth Muscle and...
Parkinson's disease: MedlinePlus Genetics
talks.cam : Sackler Lecture Theatre (Level 7) Wellcome Trust/MRC Building, Addenbrooke's Site
Muscle weakness seen in alcoholism linked to mitochondrial repair issues | National Institute on Alcohol Abuse and Alcoholism ...
NIOSHTIC-2 Search Results - Full View
Skeletal Muscle Pathology: Overview, Neurogenic Changes in Muscle Biopsy, Muscle Biopsy in Myopathy
Becn1 beclin 1, autophagy related [Mus musculus (house mouse)] - Gene - NCBI
Muscle Meals 2 Go - Healthy lifestyle
Publication Detail
Muscle Energetics | NHLBI, NIH
Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise? - PubMed
Phosphine | Medical Management Guidelines | Toxic Substance Portal | ATSDR
McMaster researchers find missing genes may separate coach potato from active cousin
Seminar Series
Exercise can make cells healthier, promoting longer life, study finds
Biomarkers Search
Definition of Aerobic Fitness | livestrong
Carnitine-acylcarnitine translocase deficiency: MedlinePlus Genetics
How four cups of coffee might protect the heart
Metabolism5
- Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. (oregonstate.edu)
- It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates. (oregonstate.edu)
- In this review we have summarized the effects of NO on glycolysis, fatty acid metabolism, the TCA cycle, and oxidative phosphorylation with reference to skeletal muscle. (cdc.gov)
- Mitochondrial fatty acid oxidation represents an important energy source for muscle metabolism particularly during physical exercise. (nih.gov)
- Mitochondria are microscopic organelles that function as energy factories for aerobic metabolism. (livestrong.com)
Autophagy4
- Mechanistically, aberrant accumulation of mitochondrial-retained protein in muscle upon loss of LONP1 induces the activation of autophagy-lysosome degradation program of muscle loss. (nature.com)
- Overexpressing a mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC), a known protein degraded by LONP1, in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. (nature.com)
- 4. Denervation-induced mitochondrial dysfunction and autophagy in skeletal muscle of apoptosis-deficient animals. (nih.gov)
- 19. Time-dependent changes in autophagy, mitophagy and lysosomes in skeletal muscle during denervation-induced disuse. (nih.gov)
LIVER10
- 11. Increased production of reactive oxygen species by rat liver mitochondria after chronic ethanol treatment. (nih.gov)
- 12. The redox state of free nicotinamide-adenine dinucleotide in the cytoplasm and mitochondria of rat liver. (nih.gov)
- 15. An electron-transport system associated with the outer membrane of liver mitochondria. (nih.gov)
- 16. [Intermembrane electron transport in the dynamics of high-amplitude swelling of rat liver mitochondria]. (nih.gov)
- People with CACT deficiency also usually have excess ammonia in the blood (hyperammonemia), an enlarged liver (hepatomegaly), and a weakened heart muscle (cardiomyopathy). (nih.gov)
- Fatty acids and long-chain acylcarnitines (fatty acids still attached to carnitine) may also build up in cells and damage the liver, heart, and muscles. (nih.gov)
- Hardest hit are organs and tissues that need a lot of energy, like muscles, brain, heart, kidneys and liver. (nih.gov)
- Feeding chickens with oral contraceptive steroids at the dose used by some poultry growers in Egypt has led to the formation of high estrogen residues in the muscles and the liver compared with controls. (who.int)
- The purpose of this study is to assess the formation of residues in the muscle and liver of chickens of contraceptive steroids applied orally at the same dose used by poultry growers and the resultant level of estrogen in chickens. (who.int)
- Three duplicate samples of muscles and liver were separately analysed for estrogen (17-estradiol) content by using high pressure liquid chromatography (HPLC) as described earlier [3]. (who.int)
Long-chain3
- A group of fats called long-chain fatty acids must be attached to a substance known as carnitine to enter mitochondria. (nih.gov)
- Without enough functional CACT protein, long-chain fatty acids cannot be transported into mitochondria. (nih.gov)
- It is what transports long-chain fatty acids into the mitochondria (thereby increasing energy production via beta-oxidation). (timesofisrael.com)
Endoplasmic reticulum2
Cellular6
- In this process-known as cellular respiration or oxidative phosphorylation-the mitochondria act like small cellular batteries, using an electrical voltage across their membranes as an intermediate energy source to produce ATP. (nih.gov)
- Mitochondrial reticulum for cellular energy distribution in muscle. (nih.gov)
- Mitochondria are cellular structures that generate most of the energy needed by cells. (nih.gov)
- They found that one important benefit involves the cellular power plant - the mitochondria - which creates the fuel so the body can function properly. (medicalxpress.com)
- For example, researchers in NICHD's Division of Intramural Research (DIR) study MD at the cellular level to determine whether membrane composition can be improved to stabilize muscle cells. (nih.gov)
- Within the DIR, the Section on Cellular and Membrane Biophysics focuses on understanding how membrane dynamics affect the structure and function of muscle cells and ways to alter those effects. (nih.gov)
Mitophagy5
- A new study shows that exercise triggers a process called mitophagy, where the muscle disposes of damaged mitochondria, making the muscle and cells healthier. (medicalxpress.com)
- They discovered that this "stress test" induced by aerobic exercise triggers a process called mitophagy, where the muscle disposes of the damaged or dysfunctional mitochondria, making the muscle healthier. (medicalxpress.com)
- Yan's lab also deleted the Ulk1 gene in mouse skeletal muscle and found that, without the gene, the removal of damaged or dysfunctional mitochondria is dramatically inhibited, suggesting a new role for the Ulk1 gene in exercise and mitophagy. (medicalxpress.com)
- Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy, Nature Communications (2017). (medicalxpress.com)
- 13. PGC-1α overexpression via local transfection attenuates mitophagy pathway in muscle disuse atrophy. (nih.gov)
Biogenesis3
- SIRT3) in skeletal muscle, both of which are regulators of mitochondria biogenesis. (nih.gov)
- 9. Expression of nuclear-encoded genes involved in mitochondrial biogenesis and dynamics in experimentally denervated muscle. (nih.gov)
- 10. Role of p53 in mitochondrial biogenesis and apoptosis in skeletal muscle. (nih.gov)
Cells30
- The findings reveal a major mechanism for energy distribution in skeletal muscle cells, and could provide new insights into diseases linked to energy use in muscle. (nih.gov)
- Skeletal muscles are made of long, thin cells that are packed with highly organized proteins and organelles. (nih.gov)
- To meet this energy demand, muscle cells contain mitochondria. (nih.gov)
- Scientists have long believed that the energy produced by mitochondria is distributed through muscle cells by some type of diffusion mechanism. (nih.gov)
- A team led by Drs. Robert S. Balaban and Sriram Subramaniam from NIH's National Heart, Lung, and Blood Institute (NHLBI) and National Cancer Institute (NCI), respectively, hypothesized that some other faster, more efficient energy pathway must spread energy throughout muscle cells. (nih.gov)
- With isolated mitochondrial preparations, we confirmed that a known mitochondrial protein, prohibitin, was present in mitochondria, and by co-immunoprecipitation analysis that ERα36 was associated with prohibitin in ht-UtLM cells. (nih.gov)
- The distinctive colocalization pattern of ERα36 with mitochondria in ht-UtSMC and ht-UtLM cells, and the association of ERα36 with a mitochondrial-specific protein suggest that ERα36 is localized primarily in mitochondria and may play a pivotal role in non-genomic signaling and mitochondrial functions. (nih.gov)
- Comparison of ERα36 and ERα66 domain structures and subcellular ERα36 staining patterns in human uterine smooth muscle (ht-UtSMC) and leiomyoma cells (ht-UtLM). (nih.gov)
- As a byproduct of energy production, mitochondria make unstable molecules called free radicals that can damage cells. (medlineplus.gov)
- Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. (nih.gov)
- It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle. (nih.gov)
- By tagging mitochondria in the skeletal tissue of rats with different colors, the researchers were able to observe the process in action and confirm that mitochondrial fusion occurs in muscle cells. (nih.gov)
- The focus of the Muscle Energetics Laboratory, led by Dr. Brian Glancy, is to determine how mitochondria are optimized within muscle cells to help maintain energy homeostasis during the large change in energy demand caused by muscle contraction. (nih.gov)
- 3D rendering of red blood cells (various colors) within a skeletal muscle capillary of a newborn mouse. (nih.gov)
- There's a malfunction in the tiny capsule-shaped structures-called mitochondria Known as the cell's "powerhouse," they convert food molecules into a form of energy your cells can use. (nih.gov)
- Depending on which cells are affected, people with mitochondrial diseases may have muscle weakness and pain, digestive problems, heart disease, seizures and many other symptoms. (nih.gov)
- Mitochondria produce about 90% of the energy that cells need to function. (nih.gov)
- These tasks include promoting migration of endothelial cells and protecting heart muscle cells from cell death, also known as apoptosis. (medicalnewstoday.com)
- The aerobic fitness definition is a measure of your body's ability to take oxygen from the atmosphere and use it to produce energy for your muscle cells. (livestrong.com)
- The secondary component involves the ability of your muscle cells to extract oxygen from your blood and use it to make adenosine triphosphate, or ATP, the fundamental carrier of energy in cells. (livestrong.com)
- Regardless of how efficiently your heart pumps blood, aerobic fitness is also dependent on the ability of your muscle cells to extract oxygen from your blood and use it to make energy. (livestrong.com)
- Aerobic energy is produced in the mitochondria of your muscle cells, using carbohydrates and fats for fuel. (livestrong.com)
- By borrowing a tool from bacteria that infect plants, scientists have developed a new approach to eliminate mutated DNA inside mitochondria-the energy factories within cells. (nih.gov)
- Mitochondria convert fuel from food into a form of energy that cells can use. (nih.gov)
- Researchers created a mouse model with tissues that appear similar to and function similarly to those of MD patients, as well as an inability to exercise or repair muscle cells. (nih.gov)
- Older muscles lose their mitochondria, the power engines of the cells. (ucdavis.edu)
- If people use 3 grams of Korean ginseng daily, the number of mitochondria in their cells increases. (ergo-log.com)
- Supplementation with ginseng caused a sharp increase in the number of mitochondria in the cells of the test subjects. (ergo-log.com)
- It can help maintain the health of the mitochondria of the cells. (keine-ruhe.org)
- It may also help keep mitochondria in cells healthy. (keine-ruhe.org)
Bioenergetics2
- Carnitine in Human Muscle Bioenergetics: Can Carnitine Supplementation Improve Physical Exercise? (nih.gov)
- Considering the important role of fatty acids in muscle bioenergetics, and the limiting effect of free carnitine in fatty acid oxidation during endurance exercise, l-carnitine supplementation has been hypothesized to improve exercise performance. (nih.gov)
Mouse skeletal6
- The group analyzed high-resolution 3-D images of mouse skeletal muscle. (nih.gov)
- A fly-through rendering of the mitochondrial network within an oxidative mouse skeletal muscle cell. (nih.gov)
- Fly-through rendering of the interior structures of a newborn mouse skeletal muscle highlighting cell and organelle membrane as well as myosin filaments. (nih.gov)
- 3D rendering of the branching contractile structures within a newborn mouse skeletal muscle. (nih.gov)
- 3D rendering of the interior of a mouse skeletal muscle mitochondrion. (nih.gov)
- 3D rendering of mitochondria (various colors) and the sarcotubular network (green) in an oxidative mouse skeletal muscle. (nih.gov)
Cardiac muscle1
- and positive regulation of cardiac muscle hypertrophy. (nih.gov)
Apoptosis2
Powerhouses1
- Mitochondria are often called the powerhouses of the cell. (medicalnewstoday.com)
Biochemical1
- We will collect muscle specimens from the vastus lateralis and blood at baseline and 90 days for biochemical analyses, as well as monitor blood chemistries and adverse events at monthly clinic visits. (nih.gov)
Reactive oxygen1
- More recent reports suggest that mitochondrial dysfunction is not an early event in the development of insulin resistance, but rather a complication of the hyperlipidemia-induced reactive oxygen species (ROS) production in skeletal muscle, which might promote mitochondrial alterations, lipid accumulation and inhibition of insulin action. (unina.it)
Organelles2
- Mitochondria have diverse functions and are essential organelles that require continuous surveillance to maintain their function. (nature.com)
- Once within these organelles, it triggered tasks vital for the repair of heart muscle following a heart attack . (medicalnewstoday.com)
Exercise16
- During strenuous exercise, the rate of energy use in skeletal muscles can increase by more than 100-fold almost instantly. (nih.gov)
- Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). (oregonstate.edu)
- These findings suggest that the NO3 (-)-NO2 (-)-NO pathway is a significant modulator of muscle energetics and O2 delivery during hypoxic exercise and subsequent recovery. (nih.gov)
- As a basic rule of thumb, it is best not to eat immediately before a exercise as a result of while your muscle tissue are trying to do their "thing," your stomach is making an attempt to concurrently digest the meals in your abdomen. (samsungsummerkrush.com)
- The researchers made their unexpected finding while working with healthy, specially-bred mice, some of which had two genes in muscle essential for exercise removed. (mcmaster.ca)
- The researchers found the mice without the muscle AMPK genes had lower levels of mitochondria and an impaired ability for their muscles to take up glucose while they exercise. (mcmaster.ca)
- When you exercise you get more mitochondria growing in your muscle. (mcmaster.ca)
- If you don't exercise, the number of mitochondria goes down. (mcmaster.ca)
- And exercise capacity, mainly determined by muscle size and function, is the best predictor of mortality in the general population. (medicalxpress.com)
- Yan and colleagues have completed a study in mice that, for the first time, shows that just one bout of moderate-to-intense exercise acts as a "stress test" on mitochondria in muscles. (medicalxpress.com)
- Aerobic exercise removes damaged mitochondria in skeletal muscle," Yan said. (medicalxpress.com)
- Aerobic exercise training increases your total blood volume, heart muscle size and contractility, resulting in a greater volume of blood being injected per heart beat. (livestrong.com)
- In response to repeated bouts of aerobic exercise, the density and number of mitochondria increase. (livestrong.com)
- High-intensity exercise that challenges your aerobic limit has a more profound effect on mitochondria adaptations and oxygen extraction than low- to moderate-intensity activity. (livestrong.com)
- Both exercise and a keto diet can increase the number of mitochondria in muscles. (ucdavis.edu)
- Supplementation with Panax ginseng may protect muscles against breakdown caused by intensive exercise. (ergo-log.com)
Weakness5
- He also suggested that identifying the proteins involved in mitochondrial fusion may aid in drug development for alcohol-related muscle weakness. (nih.gov)
- Simply writing, "R/O polymyositis" or "weakness", or worse, "muscle weakness" (we would not be concerned about weakness of character here, so using the term muscle weakness in this context seems oddly redundant) does not provide the pathologist with any useful clinical information and is a disservice to the patient. (medscape.com)
- These abnormal mitochondria cause extreme fatigue and weakness in his legs, trouble breathing and a host of other problems. (nih.gov)
- Mitochondrial gene mutations can lead to a variety of health problems including muscle weakness, heart disease, and blindness in the case of LHON. (nih.gov)
- Therefore, a deficiency in this vitamin might explain why some people experience weakness or muscle aching. (timesofisrael.com)
Mechanisms2
Disuse5
- Here, we demonstrate that LONP1, a major mitochondrial protease resides in the matrix, plays a role in controlling mitochondrial function as well as skeletal muscle mass and strength in response to muscle disuse. (nature.com)
- In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. (nature.com)
- Thus, these findings reveal a role of LONP1-dependent mitochondrial protein quality-control in safeguarding mitochondrial function and preserving skeletal muscle mass and strength, and unravel a link between mitochondrial protein quality and muscle mass maintenance during muscle disuse. (nature.com)
- 8. Effect of denervation-induced muscle disuse on mitochondrial protein import. (nih.gov)
- 16. Muscle apoptotic response to denervation, disuse, and aging. (nih.gov)
Mitochondrial function6
- The working hypothesis in the lab is that mitochondrial function within a muscle cell is dictated not only by the amount and composition of mitochondria but also by spatial relationships between mitochondria and the sites of energy storage, utilization, and signaling. (nih.gov)
- 70 years), whether 90 days of resveratrol supplementation is associated with (i) increases in muscle mitochondrial function (State 3 & 4 respiration), (ii) increases in levels of PGC-1a, AMP-activated protein kinase (AMPK), and Sirtuins (i.e. (nih.gov)
- If our hypotheses are supported, this study will be the first to show that resveratrol improves mitochondrial function in muscle, and that these changes are associated with increased levels of physical function in moderate to low functioning older adults ¿ the population who is at greatest risk of functional decline and physical disability. (nih.gov)
- 2. Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle. (nih.gov)
- 6. Mitochondrial function and apoptotic susceptibility in aging skeletal muscle. (nih.gov)
- 11. The role of PGC-1alpha on mitochondrial function and apoptotic susceptibility in muscle. (nih.gov)
Contraction4
- However, studies have shown that these diffusion pathways alone are not sufficient to support normal muscle contraction. (nih.gov)
- Initiating and maintaining muscle contraction requires rapid, coordinated movement of signals and material within and among various structures located throughout the relatively large muscle cell. (nih.gov)
- The Muscle Energetics Laboratory focuses on the energy distribution aspect of continued muscle contraction, deficits in which have been implicated in many pathologies including diabetes and muscular dystrophy as well as aging. (nih.gov)
- In particular, we aim to determine how mitochondria are optimized as part of the integrated muscle cell to maintain energy homeostasis during the large change in energy demand caused by the onset of muscle contraction. (nih.gov)
Lysosomes1
- The mitochondria fluoresce green when they are healthy and turn red when damaged and broken down by the cell's waste-disposal system, the lysosomes. (medicalxpress.com)
Microscopic1
- This high-resolution 3-D microscopic image shows a network of interconnected mitochondria within a mouse muscle cell. (nih.gov)
Convert1
- Healthy mitochondria can help convert fat into energy quickly. (keine-ruhe.org)
Energy11
- Researchers found that mitochondria in mouse muscles not only produce energy, but can quickly distribute it across the muscle cell through a grid-like network. (nih.gov)
- The mitochondria were electrically coupled and able to rapidly distribute the mitochondrial membrane voltage-the primary energy for ATP production-throughout the cell. (nih.gov)
- The discovery of this mechanism for rapid distribution of energy throughout the muscle cell will change the way scientists think about muscle function and will open up a whole new area to explore in health and disease," Balaban says. (nih.gov)
- Ongoing efforts are centered around the structure, function, composition, and developmental regulation of mitochondrial networks with the goal of gaining better control of and understanding the functional consequences of altering spatial relationships within the muscle energy distribution system. (nih.gov)
- Fatty acids are a major source of energy for the heart and muscles. (nih.gov)
- Scientists have learned that among the genes in mtDNA are instructions for making 13 proteins that mitochondria need to produce energy. (nih.gov)
- Mitochondria won their title because, within their membranes, adenosine triphosphate - which is the energy currency of life - is produced. (medicalnewstoday.com)
- Mitochondria not only produce energy, they also help the body break down harmful metabolites known as kynurenines . (ucdavis.edu)
- The more fit we are, the more muscle mitochondria we have, and the more energy our muscles can make from fat, the better we are at breaking down potential neurotoxins . (ucdavis.edu)
- Myoglobin transports oxygen to the mitochondria in your muscles, which in turn produce ATP to give your muscles energy. (runkeeper.com)
- So, as you increase your myoglobin, you improve your body's ability to quickly transport oxygen to the muscles for energy, making you able to run faster. (runkeeper.com)
Inability1
- Human muscle contains high amounts of carnitine but it depends on the uptake of this compound from the bloodstream, due to muscle inability to synthesize carnitine. (nih.gov)
Protein4
- Skeletal muscle-specific ablation of LONP1 in mice resulted in impaired mitochondrial protein turnover, leading to mitochondrial dysfunction. (nature.com)
- Once these fatty acids are joined with carnitine, the CACT protein transports them into mitochondria. (nih.gov)
- Using exon skipping, researchers restored up to 90% of dystrophin protein throughout the skeletal and heart muscles in a mouse model of DMD. (nih.gov)
- Speed workouts also increase your production of myoglobin, which is a protein found in your muscles. (runkeeper.com)
Apoptotic6
- Although both autophagic and apoptotic signaling are active in skeletal muscle during various diseases and atrophy, their specific roles here are somewhat unique. (qigonginstitute.org)
- 3. Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle. (nih.gov)
- 5. Differential susceptibility of subsarcolemmal and intermyofibrillar mitochondria to apoptotic stimuli. (nih.gov)
- 7. Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle. (nih.gov)
- 14. Decreased DNA fragmentation and apoptotic signaling in soleus muscle of hypertensive rats following 6 weeks of treadmill training. (nih.gov)
- 20. Mitochondria in skeletal muscle: adaptable rheostats of apoptotic susceptibility. (nih.gov)
AMPK1
- By removing these genes we identified the key regulator of the mitochondria is the enzyme AMPK," said Steinberg. (mcmaster.ca)
FIBERS1
- During speed workouts, you maximally activate your slow-twitch muscles and intermediate muscle fibers, which increases your aerobic capacity. (runkeeper.com)
Pathway4
- 1. Regulating effect of mitochondrial lactate dehydrogenase on oxidation of cytoplasmic NADH via an "external" pathway in skeletal muscle mitochondria. (nih.gov)
- 2. Oxidation of NADH via an "external" pathway in skeletal-muscle mitochondria and its possible role in the repayment of lactacid oxygen debt. (nih.gov)
- 6. Oxidation of NADH by a rotenone and antimycin-sensitive pathway in the mitochondrion of procyclic Trypanosoma brucei brucei. (nih.gov)
- 18. [Activation of the external pathway of NADH oxidation in mitochondria at decreased pH]. (nih.gov)
Glycolytic1
- Electron microscopy image of a mitochondrion with a donut hole (cyan) as well as sarcoplasmic reticulum (magenta), transverse tubules (orange), and contractile A-bands (green), I-bands (red), and Z-disks (blue) from a mouse glycolytic skeletal muscle. (nih.gov)
Respiration1
- Substrate-Specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults. (oregonstate.edu)
Role3
- Skeletal muscle insulin resistance: role of mitochondria and other ROS sources. (unina.it)
- 3. The NADH oxidase system (external) of muscle mitochondria and its role in the oxidation of cytoplasmic NADH. (nih.gov)
- Although the etiology of age-related physical disability is complex and multi-factorial, emerging evidence implicates the mitochondria as playing a key role in the initial onset and progression of functional decline in many older adults. (nih.gov)
Molecules1
- that lead to flawed proteins or other molecules in the mitochondria. (nih.gov)
Oxygen1
- The central component involves the ability of your lungs, heart and vascular system to deliver oxygen to your muscles via your blood stream. (livestrong.com)
Researchers4
- The researchers traced the paths of mitochondria and found that they formed a network, or reticulum. (nih.gov)
- Even in healthy people, researchers have found, mitochondria can gradually deteriorate as we grow older. (nih.gov)
- Over the last decades, though, researchers have learned a lot about mitochondria. (nih.gov)
- The researchers - led by Judith Haendeler and Joachim Altschmied - found that caffeine caused p27 to move into mitochondria. (medicalnewstoday.com)
FAST-TWITCH1
- Your body will become more efficient at recruiting your fast-twitch muscles. (runkeeper.com)
Fatty1
- 19. Effect of fatty acids and ketones on the activity of pyruvate dehydrogenase in skeletal-muscle mitochondria. (nih.gov)
Increases1
- This is due to capsaicin, which is found in the peppers and increases uncoupling proteins found in the muscle. (self.com)
Pathology1
- Knowledge of the fundamentals of muscle biopsy pathology is useful to promote understanding of the pathogenesis of many types of neuromuscular disorders and assists the non-pathologist clinician to understand reports that he or she receives for the muscle biopsies from his or her patients. (medscape.com)
Disorders2
- The remainder of this article addresses the key clinical characteristics and pathologic findings on muscle biopsy of selected examples of disorders from 4 different categories of muscle disease: immune-mediated (inflammatory) myopathies, muscular dystrophies, metabolic myopathies, and congenital myopathies. (medscape.com)
- The article Muscle Biopsy and Clinical and Laboratory Features of Neuromuscular Disease provides information about the procedure of muscle biopsy and background about the general features of the clinical presentations of neuromuscular disorders. (medscape.com)
Enzyme1
- 17. Lactate dehydrogenase is not a mitochondrial enzyme in human and mouse vastus lateralis muscle. (nih.gov)
Electron1
- 17. Pyrroloquinoline Quinone Resists Denervation-Induced Skeletal Muscle Atrophy by Activating PGC-1α and Integrating Mitochondrial Electron Transport Chain Complexes. (nih.gov)
Functional2
- The safeguard of a functional mitochondrial system is particularly important for skeletal muscle, the largest metabolically active and highly structured tissue that is often affected in diseases of mitochondrial dysfunction. (nature.com)
- 14. Physical and functional association of lactate dehydrogenase (LDH) with skeletal muscle mitochondria. (nih.gov)
Tissue1
- Skeletal muscle is the most abundant tissue in humans and faces near instantaneous changes in demand for force production lasting from seconds to minutes to hours. (nih.gov)
Function5
- By supporting and conducting research, NICHD aims to improve our understanding of MD as a way to develop targeted treatments and therapies to slow or stop muscle degeneration, improve muscle strength and function, and optimize overall health for people with MD. (nih.gov)
- Several DER components support research on MD, muscle development, and muscle function. (nih.gov)
- Some of this work includes simulators that help model muscle function in people with MD, to allow providers to fine-tune general rehabilitation techniques for the needs to individuals with MD. Other NCMRR-led activities focus on improving assistive technology to help people with MD function better in their surroundings. (nih.gov)
- A new UC Davis Health study found that a ketogenic (keto) diet improves muscle function in older animals by preventing muscle mass loss due to age ( sarcopenia ). (ucdavis.edu)
- A keto diet therefore prevents muscle deterioration and even restores muscle function. (ucdavis.edu)
Diseases1
- But mitochondria have importance beyond rare diseases. (nih.gov)
Involved in mitochondrial1
- In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. (nih.gov)
Health1
- In this Q&A, he shares his latest research on the keto diet, its effect on muscle growth and brain health, and its potential side effects. (ucdavis.edu)
Found1
- They found that the mitochondrial "wires" were electrically conductive and that most of the mitochondria were in direct electrical communication through the interconnecting network. (nih.gov)
Structures1
- Mitochondria are colored according to their location relative to the adjacent contractile structures. (nih.gov)
Muscular dystrophies1
- New mouse model for muscular dystrophies shows defects in repairing muscles. (nih.gov)
Cell2
- When its turned on, Ulk1 activates other components in the cell to execute the removal of dysfunctional mitochondria," Yan said. (medicalxpress.com)
- Each cell in the body contains dozens or even hundreds of mitochondria. (nih.gov)