Effects of physical training and its cessation on the hemostatic system of obese children.
(9/816)
BACKGROUND: Physical training can improve hemostatic function in adults, thereby reducing heart disease risk, but no information is available in children on whether physical training can enhance hemostatic function. OBJECTIVE: The purpose of this investigation was to examine the effects of a physical training program on hemostatic variables in a biethnic group of obese children. DESIGN: Children were randomly assigned to 2 groups. Group 1 participated in physical training for 4 mo and then ceased physical training for 4 mo, whereas group 2 did no physical training for the first 4 mo and then participated in physical training for 4 mo. Plasma hemostatic variables [fibrinogen, plasminogen activator inhibitor 1 (PAI-1), and D-dimer) were measured at months 0, 4, and 8. RESULTS: Analyses of variance revealed no significant group-by-time interactions for the hemostatic variables. When data from both groups were combined there was a significant decrease in D-dimer after 4 mo of physical training (P < 0.05). Factors explaining individual differences in responsiveness to the physical training revealed that individuals with greater percentage fat before physical training showed greater reductions in fibrinogen and D-dimer, and that blacks showed greater reductions in D-dimer than whites (P < 0.05). Stepwise multiple linear regression showed that only higher prephysical training concentrations of fibrinogen, PAI-1, and D-dimer explained significant proportions of the variation in changes in these variables. CONCLUSIONS: In obese children, 4-mo periods of physical training did not lead to significant changes in hemostatic variables. Children with greater adiposity and concentrations of hemostatic factors before physical training showed greater reductions in hemostatic variables after physical training than did children with lesser values. (+info)
Effect of 14 weeks of resistance training on lipid profile and body fat percentage in premenopausal women.
(10/816)
OBJECTIVES: To study the effects of a supervised, intensive (85% of one repetition maximum (1-RM)) 14 week resistance training programme on lipid profile and body fat percentage in healthy, sedentary, premenopausal women. SUBJECTS: Twenty four women (mean (SD) age 27 (7) years) took part in the study. Subjects were randomly assigned to either a non-exercising control group or a resistance exercise training group. The resistance exercise training group took part in supervised 45-50 minute resistance training sessions (85% of 1-RM), three days a week on non-consecutive days for 14 weeks. The control group did not take part in any structured physical activity. RESULTS: Two way analysis of variance with repeated measures showed significant (p < 0.05) increases in strength (1-RM) in the exercising group. There were significant (p < 0.05) decreases in total cholesterol (mean (SE) 4.68 (0.31) v 4.26 (0.23) mmol/1 (180 (12) v 164 (9) mg/dl)), low density lipoprotein (LDL) cholesterol (2.99 (0.29) v 2.57 (0.21) mmol/l (115 (11) v 99 (8) mg/dl), the total to high density lipoprotein (HDL) cholesterol ratio (4.2 (0.42) v 3.6 (0.42)), and body fat percentage (27.9 (2.09) v 26.5 (2.15)), as well as a strong trend towards a significant decrease in the LDL to HDL cholesterol ratio (p = 0.057) in the resistance exercise training group compared with their baseline values. No differences were seen in triglycerides and HDL cholesterol. No changes were found in any of the measured variables in the control group. CONCLUSIONS: These findings suggest that resistance training has a favourable effect on lipid profile and body fat percentage in healthy, sedentary, premenopausal women. (+info)
Exercise training-induced blood pressure and plasma lipid improvements in hypertensives may be genotype dependent.
(11/816)
Exercise training improves cardiovascular disease risk, but individual responses are highly variable. We hypothesized that common polymorphic gene variations would affect these responses. Sedentary obese hypertensive older men who had undergone exercise training were typed at the apolipoprotein (apo) E, angiotensin-converting enzyme (ACE), and lipoprotein lipase (LPL) loci. Individuals of all genotype subgroups were generally similar before training; they also changed body weight, body composition, and &f1;O(2)max similarly with training. ACE insertion/insertion (II) and insertion/deletion (ID) genotype individuals (n=10) tended to reduce systolic blood pressure more with training than deletion/deletion (DD) individuals (n=8) (-10 versus -5 mm Hg, P=0. 16). ACE II and ID individuals decreased diastolic blood pressure more with training than DD individuals (-10 versus -1 mm Hg, P<0. 005). Systolic blood pressure reductions with training were also larger in apoE3 and E4 (n=15) than apoE2 men (n=3) (-10 versus 0 mm Hg, P<0.05). The same trend was evident for diastolic blood pressure (-7 versus -3 mm Hg), but the difference was not significant. Systolic (14 versus -6 mm Hg, P=0.08) and diastolic (-9 versus -5 mm Hg, P=0.10) blood pressure reductions tended to be greater in LPL PvuII +/+ (n=4) than +/- and -/- individuals (n=14). Systolic (-10 versus 3 mm Hg, P<0.05) and diastolic (-9 versus 2 mm Hg, P<0.05) blood pressure reductions were larger in LPL HindIII +/+ and +/- (n=15) than -/- persons (n=3), respectively. LPL PvuII -/- individuals (n=3) had larger increases in HDL cholesterol (11 versus 2 mg/dL, P<0.05) and HDL(2) cholesterol (8 versus 0 mg/dL, P<0.05) than LPL PvuII +/- and +/+ individuals (n=15). These results are consistent with the possibility that apoE, ACE, and LPL genotypes may identify hypertensives who will improve blood pressure, lipoprotein lipids, and cardiovascular disease risk the most with exercise training. (+info)
Initial aerobic power does not alter muscle metabolic adaptations to short-term training.
(12/816)
To investigate the hypothesis that training-induced increases in muscle mitochondrial potential are not obligatory to metabolic adaptations observed during submaximal exercise, regardless of peak aerobic power (VO(2 peak)) of the subjects, a short-term training study was utilized. Two groups of untrained male subjects (n = 7/group), one with a high (HI) and the other with a low (LO) VO(2 peak) (means +/- SE; 51.4 +/- 0.90 vs. 41.0 +/- 1.3 ml. kg(-1). min(-1);P < 0.05), cycled for 2 h/day at 66-69% of VO(2 peak) for 6 days. Muscle tissue was extracted from vastus lateralis at 0, 3, and 30 min of standardized cycle exercise before training (0 days) and after 3 and 6 days of training and analyzed for metabolic and enzymatic changes. During exercise after 3 days of training in the combined HI + LO group, higher (P < 0.05) concentrations (mmol/kg dry wt) of phosphocreatine (40.5 +/- 3.4 vs. 52.2 +/- 4.2) and lower (P < 0.05) concentrations of P(i) (61.5 +/- 4.4 vs. 53.3 +/- 4.4), inosine monophosphate (0.520 +/- 0.19 vs. 0.151 +/- 0.05), and lactate (37.9 +/- 5.5 vs. 22.8 +/- 4.8) were observed. These changes were also accompanied by reduced levels of calculated free ADP, AMP, and P(i). All adaptations were fully expressed by 3 min of exercise and by 3 days of training and were independent of initial VO(2 peak) levels. Moreover, maximal activity of citrate synthase, a measure of mitochondrial capacity, was only increased with 6 days of training (5.71 +/- 0.29 vs. 7.18 +/- 0.37 mol. kg protein(-1). h(-1); P < 0. 05). These results demonstrate that metabolic adaptations to prolonged exercise occur within the first 3 days of training and during the non-steady-state period. Moreover, neither time course nor magnitude of metabolic adaptations appears to depend on increases in mitochondrial potential or on initial aerobic power. (+info)
Muscle net glucose uptake and glucose kinetics after endurance training in men.
(13/816)
We evaluated the hypotheses that alterations in glucose disposal rate (R(d)) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative workload (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) before training elicited 54.0 +/- 1.7% after training. Whole body glucose R(d) decreased posttraining at ABT (5.45 +/- 0.31 mg. kg(-1). min(-1) at 65% pretraining to 4.36 +/- 0.44 mg. kg(-1). min(-1)) but not at RLT (5.94 +/- 0.47 mg. kg(-1). min(-1)). Net glucose uptake was attenuated posttraining at ABT (1.87 +/- 0.42 mmol/min at 65% pretraining and 0.54 +/- 0.33 mmol/min) but not at RLT (2.25 +/- 0. 81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose R(d) and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65% VO(2 peak)) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65% VO(2 peak)) promotes a glucose shunt from inactive tissues to active muscle. (+info)
Resistance exercise training increases mixed muscle protein synthesis rate in frail women and men >/=76 yr old.
(14/816)
Muscle atrophy (sarcopenia) in the elderly is associated with a reduced rate of muscle protein synthesis. The purpose of this study was to determine if weight-lifting exercise increases the rate of muscle protein synthesis in physically frail 76- to 92-yr-old women and men. Eight women and 4 men with mild to moderate physical frailty were enrolled in a 3-mo physical therapy program that was followed by 3 mo of supervised weight-lifting exercise. Supervised weight-lifting exercise was performed 3 days/wk at 65-100% of initial 1-repetition maximum on five upper and three lower body exercises. Compared with before resistance training, the in vivo incorporation rate of [(13)C]leucine into vastus lateralis muscle protein was increased after resistance training in women and men (P < 0.01), although it was unchanged in five 82 +/- 2-yr-old control subjects studied two times in 3 mo. Maximum voluntary knee extensor muscle torque production increased in the supervised resistance exercise group. These findings suggest that muscle contractile protein synthetic pathways in physically frail 76- to 92-yr-old women and men respond and adapt to the increased contractile activity associated with progressive resistance exercise training. (+info)
Female-related skeletal muscle phenotype in patients with moderate chronic heart failure before and after dynamic exercise training.
(15/816)
This study hypothesized that female patients with chronic heart failure (CHF), similarly as previously reported for male patients, have a decreased proportion of type I (slow twitch) muscle fibers combined with fiber atrophy, and respond to exercise training with an increased muscular fiber area and performance, and with an unaltered fiber type distribution. METHODS: Sixteen women [age 62 +/- 10 years (mean +/- SD)] with stable, moderate CHF (left ventricular ejection fraction 28 +/- 8%) underwent percutaneous needle biopsies of the lateral vastus muscle, and assessments of isokinetic muscle strength and exercise tests with respiratory gas and blood lactate analyses, before and after 8 weeks of intensive knee extensor endurance training. RESULTS: When compared to healthy age-matched women, the women with CHF unexpectedly had a normal proportion of type I fibers (51 +/- 15%), but a decreased cross-sectional area in both type I and II fibers. Exercise training increased the cross-sectional area of muscle fibers up to the reference range (21%, p < 0.04), while the relative number of type I fibers decreased (12%, p < 0.03). Training also increased muscle strength (16%, p < 0.0001) and peak oxygen uptake (20%, p < 0.0001). The increase in peak oxygen uptake was directly related to the training-induced increase in fiber areas (r = 0.63; p < 0.03), and decrease in lactate accumulation was inversely related to the training-induced decrease in the relative number of type I fibers (r = -0.62; p < 0.02). CONCLUSIONS: As for men with CHF, a skeletal muscle atrophy was found in women, but contrary to the hypothesis, the proportion of type I muscle fibers was normal. Exercise training counteracted the atrophy suggesting skeletal muscle trainability in female CHF patients. (+info)
Endurance exercise training does not alter lipolytic or adipose tissue blood flow sensitivity to epinephrine.
(16/816)
We evaluated the relationship between lipolysis and adipose tissue blood flow (ATBF) in response to epinephrine and the effect of endurance exercise training on these responses. Five healthy untrained men underwent a four-stage incremental epinephrine infusion (0.00125, 0.005, 0.0125, and 0.025 microgram. kg fat free mass(-1). min(-1)) plus hormonal clamp before and after 16 wk of cycle ergometry exercise training. Whole body glycerol and free fatty acid (FFA) rates of appearance (R(a)) in plasma were determined by stable isotope methodology, and ATBF was assessed by (133)Xe clearance. After each training session, subjects were fed the approximate number of calories expended during exercise to prevent changes in body weight. Glycerol R(a), FFA R(a), and ATBF increased when plasma epinephrine concentration reached 0.8 nM, but at plasma epinephrine concentrations >1.6 nM ATBF plateaued, whereas lipolysis continued to increase. Exercise training increased peak oxygen uptake by 24 +/- 7% (2.9 +/- 0.2 vs. 3.6 +/- 0.1 l/min; P < 0. 05) but did not alter body weight [70.5 +/- 3.8 vs. 72.0 +/- 3.8 kg; P = nonsignificant (NS)] or percent body fat (18.4 +/- 1.6 vs. 17.8 +/- 1.9%; P = NS). Lipolytic and ATBF responses to epinephrine were also the same before and after training. We conclude that the lipolytic and ATBF responses to epinephrine are coordinated when plasma epinephrine concentration is +info)