The effects of exercise and diet manipulation on the capacity to perform prolonged exercise in the heat and in the cold in trained humans.
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1. This study examined the effects of exercise and diet manipulation intended to alter initial muscle glycogen levels on the capacity to perform prolonged exercise at two ambient temperatures. 2. Six well-trained cyclists participated in randomized order in two diet and exercise regimens each lasting 8 days and comprising four cycle tests to exhaustion at 70 % of maximum oxygen uptake. On days 1 and 5, subjects exercised to exhaustion to deplete muscle glycogen. Three days after each depletion trial a diet providing 10 % (low carbohydrate (CHO)) or 80 % (high CHO) of energy as CHO was consumed, and each diet was followed by a performance trial at the same ambient temperature, either 10 or 30 C (days 4 and 8). This schedule was repeated after a week, but performance trials were carried out at the other ambient temperature. 3. In the cold, cycling time increased (median (range)) from 89.2 min (78.0-129.5 min) on the low CHO trial to 158.2 min (116.9-165.6 min) on the high CHO trial (P < 0.01). In the heat, cycling time increased from 44.0 min (31.8-51.4 min) on the low CHO trial to 53.2 min (50.2-82.2 min) on the high CHO trial (P = 0.02). Total CHO oxidized during exercise in the cold after the low CHO diet was higher than in the heat after either diet suggesting that exercise in the heat was terminated before all available CHO stores had been emptied. (+info)
Leptin actions on food intake and body temperature are mediated by IL-1.
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Leptin regulates energy balance through its actions in the brain on appetite and energy expenditure and also shares properties with cytokines such as IL-1. We report here that leptin, injected into rats intracerebroventricularly or peripherally, induces significant dose-dependent increases in core body temperature as well as suppression of appetite. Leptin failed to affect food intake or body temperature in obese (fa/fa) Zucker rats, which posses a defective leptin receptor. Furthermore, injection of leptin increased levels of the proinflammatory cytokine IL-1beta in the hypothalamus of normal Sprague-Dawley rats. Central injection of IL-1 receptor antagonist (IL-1ra) inhibited the suppression of food intake caused by central or peripheral injection of leptin (60 and 84%, respectively) and abolished the leptin-induced increase in body temperature in both cases. Mice lacking (gene knockout) the main IL-1 receptor (80 kDa, R1) responsible for IL-1 actions showed no reduction in food intake in response to leptin. These data indicate that leptin actions in the brain depend on IL-1, and we show further that the effect of leptin on fever, but not food intake, is abolished by a cyclooxygenase inhibitor. Thus, we propose that in addition to its role in body weight regulation, leptin may mediate neuroimmune responses via actions in the brain dependent on release of IL-1 and prostaglandins. (+info)
Work stress and menstrual patterns among American and Italian nurses.
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OBJECTIVES: This study assessed whether job stress alters menstrual patterns among nurses working in 2 different settings: a tertiary care hospital in New York (99 nurses) and a university hospital in Rome (25 nurses). METHODS: Data on menstrual patterns were collected by a daily diary in which the nurses recorded their basal body temperature (BBT) and their menstrual bleeding status for a 3-month period. The BBT curves were used to classify cycles as biphasic or monophasic, and as adequate or inadequate with respect to the luteal phase. Job stress was evaluated by both objective (environmental and work characteristics) and subjective (perceived stress) criteria. RESULTS: The American nurses, especially those assigned to high stress units, had an increased risk for long and monophasic cycles [relative risk (RR) 4.3, 95% confidence interval (95% CI) 1.1-16.2 and RR 5.5, 95% CI 1.2-25.5, respectively]. Among those who perceived their stress at work to be high or reported strenuous work activity, the risk for longer cycles was also raised (RR 2.3, 95% CI 0.6-8.0 and RR 1.6, 95% CI 0.7-4.2, respectively). Luteal phase inadequacy followed the same pattern. Similar trends were observed in the Italian data. In addition, the rotating shiftwork pattern prevalent in the Italian group was possibly associated with higher rates of short cycles and inadequate luteal phases when compared with those of nurses working fixed shifts either day or night. CONCLUSIONS: Menstrual function may be affected by stressful work conditions. (+info)
Cardiovascular phenotype and temperature control in mice lacking thyroid hormone receptor-beta or both alpha1 and beta.
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We have used a telemetry system to record heart rate, body temperature, electrocardiogram (ECG), and locomotor activity in awake, freely moving mice lacking thyroid hormone receptor (TR)-beta or TR-alpha1 and -beta (TR-alpha1/beta). The TR-alpha1/beta-deficient mice had a reduced heart rate compared with wild-type controls. The TR-beta-deficient mice showed an elevated heart rate, which, however, was unresponsive to thyroid hormone treatment regardless of hormonal serum levels. ECG revealed that the TR-beta-deficient mice had a shortened Q-Tend time in contrast to the TR-alpha1/beta-deficient mice, which exhibited prolonged P-Q and Q-Tend times. Mental or pharmacological stimulation of the sympathetic nervous system resulted in a parallel increase in heart rate in all animals. A single injection of a nonselective beta-adrenergic-receptor blocker resulted in a parallel decrease in all mice. The TR-alpha1/beta-deficient mice also had a 0.4 degrees C lower body temperature than controls, whereas no difference was observed in locomotor activity between the different strains of mice. Our present and previous results support the hypothesis that TR-alpha1 has a major role in determining heart rate under baseline conditions and body temperature and that TR-beta mediates a hormone-induced increase in heart rate. (+info)
Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive.
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Hypoglycemic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption (CMRO2) increases during hypoglycemia in piglets, whereas CMRO2 decreases in adult pig models. We tested the hypothesis that increased CMRO2 during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF), CMRO2, and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5 degrees C). In unwarmed animals brain temperature was allowed to fall (37.6 degrees C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals; CMRO2 increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycemic coma in the immature brain, CMRO2 and glutamate are increased in a temperature-dependent manner. (+info)
Exposure to febrile temperature upregulates expression of pyrogenic cytokines in endotoxin-challenged mice.
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Fever is a phylogenetically ancient response that is associated with improved survival in acute infections. In endothermic animals, fever is induced by a set of pyrogenic cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, and IL-6] that are also essential for survival in acute infections. We studied the influence of core temperature on cytokine expression using an anesthetized mouse model in which core temperature was adjusted by immersion in water baths. We showed that raising core temperature from basal (36.5-37.5 degrees C) to febrile (39.5-40 degrees C) levels increased peak plasma TNF-alpha and IL-6 levels by 4.1- and 2. 7-fold, respectively, and changed the kinetics of IL-1beta expression in response to lipopolysaccharide challenge. TNF-alpha levels were increased predominantly in liver, IL-1beta levels were higher in lung, and IL-6 levels were widely increased in multiple organs in the warmer mice. This demonstrates that the thermal component of fever may directly contribute to shaping the host response by regulating the timing, magnitude, and tissue distribution of cytokine generation during the acute-phase response. (+info)
Effects of slow and rapid cooling on catecholamine concentration in arterial plasma and the skin.
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Norepinephrine (NE) and epinephrine (Epi) concentrations in arterial plasma and in skin tissue were measured chromatographically before and after external cooling. Urethan-anesthetized rats were cooled either slowly (0.004-0.006 degrees C/s) or rapidly (0.03- 0.05 degrees C/s). Blood samples were drawn three times from each animal: 1) before cooling and at a rectal temperature decreased 2) by 0.5 degrees C and 3) by 3-4 degrees C. Skin samples were taken from controls and from rapidly or slowly cooled rats at a rectal temperature lowered by 0.5 degrees C. The resting mean values were 36.7 +/- 0.3 degrees C for rectal temperature, 0.62 +/- 0.079 and 1. 09 +/- 0.203 ng/ml for plasma NE and Epi, and 85.6 +/- 4.1 and 137.6 +/- 34.3 ng/g for skin NE and Epi. A decrease in rectal temperature by 0.5 degrees C at rapid cooling produced a 2.6-fold increase of NE and a 2.8-fold increase of Epi in plasma. Concomitantly, there was a significant decrease in skin NE concentration by 28% and Epi by 86%. At a rectal temperature decreased by 0.5 degrees C after slow cooling, plasma catecholamines did not change; at unaltered skin NE concentration, there was a reduction in skin Epi concentration (60%). When rectal temperature was lowered by 3-4 degrees C, the increase in plasma NE was virtually the same at both cooling rates and only plasma Epi increased more after deep rapid cooling than slow cooling. Thus the sympathoadrenal system may be differently activated depending on cooling rate. Rapid cooling, when the dynamic activity of the skin cold receptors is involved in the cold response, may provide conditions for an earlier activation of the sympathoadrenal system. This may evidence the functional significance of the dynamic activity of the skin cold receptors in the formation of the cold defense responses. (+info)
Temperature modulation reveals three distinct stages of Wallerian degeneration.
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After peripheral nerve transection, axons distal to the cut site rapidly degenerate, a process termed Wallerian degeneration. In wild-type mice the compound action potential (CAP) disappears by 3 d. Previous studies have demonstrated that cold temperatures and lower extracellular calcium ion (Ca2+) concentrations can slow the rate of Wallerian degeneration. We have incubated isolated sciatic nerve segments from wild-type and C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37 degrees C. At 25 degrees C we found that the degeneration rate of wild-type axons was slowed dramatically, with the CAP preserved up to 7 d post-transection. In contrast, at 37 degrees C the CAPs were minimal at 2 d. When the temperature of wild-type nerves was raised to 37 degrees C after 24-72 hr at 25 degrees C, degeneration occurred within the subsequent 24 hr. Wld nerves, too, were preserved longer at 25 degrees C but, on return to 37 degrees C, degenerated promptly. Cooling the nerve within 12 hr after axotomy enhanced axonal preservation. Neither wild-type nor Wld nerves showed different degeneration rates when they were incubated with 250 microM or 5 or 10 mM extracellular Ca2+ for 1-2 d, suggesting that an abrupt increase in intracellular Ca2+ occurs at the time of axonal destruction. Wallerian degeneration, thus, appears to progress through three distinct stages. Initiation occurs at the time of injury with subsequent temperature-dependent and -independent phases. Nerves appear to remain intact and are able to exclude Ca2+ from entering until an as yet unknown process finally increases axolemmal permeability. (+info)