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Effect of exercise training at different intensities on fat metabolism of obese men.

The present study investigated the effect of exercise training at different intensities on fat oxidation in obese men. Twenty-four healthy male obese subjects were randomly divided in either a low- [40% maximal oxygen consumption (VO(2 max))] or high-intensity exercise training program (70% VO(2 max)) for 12 wk, or a non-exercising control group. Before and after the intervention, measurements of fat metabolism at rest and during exercise were performed by using indirect calorimetry, [U-(13)C]palmitate, and [1,2-(13)C]acetate. Furthermore, body composition and maximal aerobic capacity were measured. Total fat oxidation did not change at rest in any group. During exercise, after low-intensity exercise training, fat oxidation was increased by 40% (P < 0.05) because of an increased non-plasma fatty acid oxidation (P < 0.05). High-intensity exercise training did not affect total fat oxidation during exercise. Changes in fat oxidation were not significantly different among groups. It was concluded that low-intensity exercise training in obese subjects seemed to increase fat oxidation during exercise but not at rest. No effect of high-intensity exercise training on fat oxidation could be shown.

Adult↗

Exercise training increases L-type calcium current density in coronary smooth muscle.

Exercise training produces numerous adaptations in the coronary circulation, including an increase in coronary tone, both in conduit and resistance arteries. On the basis of the importance of voltage-gated Ca2+ channels (VGCC) in regulation of vascular tone, we hypothesized that exercise training would increase VGCC current density in coronary smooth muscle. To test this hypothesis, VGCC current was compared in smooth muscle from conduit arteries (>1.0 mm), small arteries (200-250 micrometer), and large arterioles (75-150 micrometer) from endurance-trained (Ex) or sedentary miniature swine (Sed). After 16-20 wk of treadmill training, VGCC current was determined using whole cell voltage-clamp techniques. In both Ex and Sed, VGCC current density was inversely related to arterial diameter, i.e., large arterioles > small arteries > conduit arteries. Exercise training increased peak inward currents approximately twofold in smooth muscle from all arterial sizes compared with those from Sed (large arteriole, -12.52 +/- 2.05 vs. -5.74 +/- 0.99 pA/pF; small artery, -6.20 +/- 0.97 vs. -3.18 +/- 0.44 pA/pF; and conduit arteries, -4.22 +/- 0.30 vs. -2.41 +/- 0.55 pA/pF; 10 mM Ba2+ external). Dihydropyridine sensitivity, voltage dependence, and inactivation kinetics identified this Ca2+ current to be L-type current in all arterial sizes from both Sed and Ex. Furthermore, peak VGCC current density was correlated with treadmill endurance in all arterial sizes. We conclude that smooth muscle L-type Ca2+ current density is increased within the coronary arterial bed by endurance exercise training. This increased VGCC density may provide an important mechanistic link between functional and cellular adaptations in the coronary circulation to exercise training.

Animals↗

Improved postischemic recovery of cardiac pump function in exercised trained diabetic rats.

This study examined whether exercise training of diabetic rats (streptozocin, 55 mg/kg) would affect the ability of perfused hearts to recover pump function after 75 min of ischemia and 30 min of reperfusion. All hearts were perfused with buffer containing the diabetic plasma concentrations of glucose and free fatty acids. Four groups were studied: sedentary control, trained control, sedentary diabetic, and trained diabetic. Trained control and diabetic rats were exercised on a treadmill at 5% grade, 21 m/min, 90 min/day, 6 days/wk for 8 wk. Sedentary diabetics had significantly lower body weight and elevated plasma glucose, triacylglycerol, and cholesterol relative to both control groups. Hearts from this group exhibited depressed postischemic recovery of pump function during reperfusion. In contrast, trained diabetic rats exhibited significantly lower plasma levels of triacylglycerol and cholesterol relative to sedentary diabetics. The postischemic recovery of cardiac pump function was improved in hearts from trained diabetic rats relative to sedentary diabetics. Exercise training had no effect on control rats. These results suggest that exercise training produces an antihyperlipidemic effect in diabetic rats and improves the tolerance of the diabetic heart to ischemia.

Animals↗

Predictors of noncompliance to exercise training in heart failure.

BACKGROUND/OBJECTIVES: Exercise training is an emerging therapy in heart failure (HF). However, factors influencing noncompliance to exercise have not been evaluated. We assessed clinical factors, functional status, and emotional predictors of noncompliance to a 12-week home walking exercise program. METHODS: Using a correlational design, we evaluated noncompliance of 39 HF patients (aged 63.2 +/- 10.1 years, left ventricular ejection fraction 29.5% +/- 8.0%, peak oxygen consumption 14.1 +/- 3.7 mL/kg/min, HF duration 37.5 +/- 32.9 months, 74% New York Heart Association class II) to home walking exercise. Noncompliance was defined as (1) completion of the 12-week program with 60% or less of prescribed weekly walking duration (noncompliant completers); or (2) failure to complete the 12-week program (dropouts). Univariate analyses (chi-square or t test) and multivariate backward logistic regression were performed to identify clinical factors (body mass index, comorbidities, and HF duration), functional status (peak VO2), and emotional dysphoria (anxiety, hostility, depression) predictive of noncompliance to training. RESULTS: Mean compliance was 35% +/- 30% (945/2700 minutes) for noncompliant patients (n = 13) and 99% +/- 13% (2673/2700 minutes) for compliant patients (n = 26). In the multivariate analysis, higher comorbidity (odds ratio [OR]: 2.7, confidence interval [CI]: 1.11-6.71), longer HF duration (OR: 1.1, CI: 1.01-1.13), lower hostility (OR: 0.47, CI: 0.24-0.91), and lower body mass index (OR: 0.76, CI: 0.58-0.98) were predictive of noncompliance to exercise training in patients with HF. CONCLUSIONS: Noncompliance should be monitored carefully in HF patients with multiple comorbidities, longer HF duration, lower body mass index, and lower hostility scores. In this subgroup of HF patients, tailored exercise prescriptions may enhance compliance to an exercise program.

Activities of Daily Living↗

The effects of exercise training on sympathetic neural activation in advanced heart failure: a randomized controlled trial.

OBJECTIVES: The goal of this study was to test the hypothesis that exercise training reduces resting sympathetic neural activation in patients with chronic advanced heart failure. BACKGROUND: Exercise training in heart failure has been shown to be beneficial, but its mechanisms of benefit remain unknown. METHODS: Sixteen New York Heart Association class II to III heart failure patients, age 35 to 60 years, ejection fraction < or =40% were divided into two groups: 1) exercise-trained (n = 7), and 2) sedentary control (n = 9). A normal control exercise-trained group was also studied (n = 8). The four-month supervised exercise training program consisted of three 60 min exercise sessions per week, at heart rate levels that corresponded up to 10% below the respiratory compensation point. Muscle sympathetic nerve activity (MSNA) was recorded directly from peroneal nerve using the technique of microneurography. Forearm blood flow was measured by venous plethysmography. RESULTS: Baseline MSNA was greater in heart failure patients compared with normal controls; MSNA was uniformly decreased after exercise training in heart failure patients (60 +/- 3 vs. 38 +/- 3 bursts/100 heart beats), and the mean difference in the change was significantly (p < 0.05) greater than the mean difference in the change in sedentary heart failure or trained normal controls. In fact, resting MSNA in trained heart failure patients was no longer significantly greater than in trained normal controls. In heart failure patients, peak VO(2) and forearm blood flow, but not left ventricular ejection fraction, increased after training. CONCLUSIONS: These findings demonstrate that exercise training in heart failure patients results in dramatic reductions in directly recorded resting sympathetic nerve activity. In fact, MSNA was no longer greater than in trained, healthy controls.

Adult↗

Effect of exercise training on serum leptin levels in type 2 diabetic patients.

To evaluate the effect of exercise training on serum leptin levels 50 sedentary subjects with type 2 diabetes were enrolled in either 6 weeks of aerobic exercise training with diet therapy (n = 23) or diet therapy alone (n = 27). The training program consisted of walking and cycle ergometer exercise for 1 hour at least 5 times per week, with the intensity of exercise maintained at 50% of maximum oxygen uptake. Serum leptin levels decreased significantly in the exercise training (TR) group (7.2 +/- 3.6 to 4.6 +/- 2.5 ng/mL, P <.05), but not in the sedentary (SED) group (6.9 +/- 3.4 to 5.6 +/- 2.9 ng/mL). Leptin levels standardized for percentage body fat (dividing serum leptin level by percentage body fat) after treatment were lower in the TR subjects compared with the SED subjects. Body weight and percentage body fat decreased in all patients; however, no significant changes were observed in either group. Fasting concentrations of plasma insulin and cortisol and the urinary excretion of 17-hydroxycorticosteroid (17-OHCS) did not differ between the groups either before or after treatment. Fasting plasma glucose and hemoglobin A(1c) (HbA(1c)) improved significantly in both groups, although no significant differences were observed between the groups either before or after treatment. Ventilatory threshold increased significantly in the exercise training subjects. This study demonstrates that exercise training in type 2 diabetic subjects reduces serum leptin levels independent of changes in body fat mass, insulin, or glucocorticoids.

17-Hydroxycorticosteroids↗

Effect of dietary control and exercise training on daily food intake and serum lipids in postmyocardial infarction patients.

The effects of 12 weeks of exercise training without dietary control (n = 30) and exercise training with dietary control by dietition counseling (n = 30) and exercise training with dietary control by dietition counseling (n = 30) on serum cholesterol, serum triglycerides, and total substrate contents were studied in 60 postmyocardial infarction patients. Both groups showed reductions (P less than 0.01) in mean total daily kilocalories consumed (2867 +/- 82 versus 2088 +/- 77 and 2848 +/- 15 versus 1285 +/- 68, respectively); however, no significant change occurred in total body weight. The dietary control group consumed relatively more kilocalories as protein than the group without dietary control (285 of 1,285 versus 389 of 2,088, respectively) and less (P less than 0.05) as fat (443 of 1285 versus 804 of 2,089, respectively). Both groups had lower (P less than 0.01) mean daily dietary cholesterol after 12 weeks (811 +/- 44 versus 232 +/- 17 mg) versus (325 +/- 18 versus 309 +/- 23 mg, respectively). A reduction in serum cholesterol (P less than 0.05) was seen in the dietary control group (270 +/- 8 versus 243 +/- 7 mg/dl) but not in the group without dietary control (260 +/- 6 versus 261 +/- 7 mg/dl). The dietary control group had a lower mean triglyceride level (P less than 0.05) (229 +/- 24 versus 155 +/- 18 mg/dl)) but no differences were seen in the group without dietary control (189 +/- 15 versus 180 +/- 13 mg/dl). It is concluded that significant reductions in caloric intake and daily cholesterol compliment the effects of exercise training in postmyocardial infarction patients by increasing substrate protein:fat consumption ratio and by reducing serum cholesterol and triglycerides. These effects are not seen with exercise training alone.

Cholesterol↗

Modulation of extracellular matrix genes reflects the magnitude of physiological adaptation to aerobic exercise training in humans.

BACKGROUND: Regular exercise reduces cardiovascular and metabolic disease partly through improved aerobic fitness. The determinants of exercise-induced gains in aerobic fitness in humans are not known. We have demonstrated that over 500 genes are activated in response to endurance-exercise training, including modulation of muscle extracellular matrix (ECM) genes. Real-time quantitative PCR, which is essential for the characterization of lower abundance genes, was used to examine 15 ECM genes potentially relevant for endurance-exercise adaptation. Twenty-four sedentary male subjects undertook six weeks of high-intensity aerobic cycle training with muscle biopsies being obtained both before and 24 h after training. Subjects were ranked based on improvement in aerobic fitness, and two cohorts were formed (n = 8 per group): the high-responder group (HRG; peak rate of oxygen consumption increased by +0.71 +/- 0.1 L min(-1); p < 0.0001) while the low-responder group (LRG; peak rate of oxygen consumption did not change, +0.17 +/- 0.1 L min(-1), ns). ECM genes profiled included the angiopoietin 1 and related genes (angiopoietin 2, tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE1) and 2 (TIE2), vascular endothelial growth factor (VEGF) and related receptors (VEGF receptor 1, VEGF receptor 2 and neuropilin-1), thrombospondin-4, alpha2-macroglobulin and transforming growth factor beta2. RESULTS: neuropilin-1 (800%; p < 0.001) and VEGF receptor 2 (300%; p < 0.01) transcript abundance increased only in the HRG, whereas levels of VEGF receptor 1 mRNA actually declined in the LRG (p < 0.05). TIE1 and TIE2 mRNA levels were unaltered in the LRG, whereas transcription levels of both genes were increased by 2.5-fold in the HRG (p < 0.01). Levels of thrombospondin-4 (900%; p < 0.001) and alpha2-macroglobulin (300%, p < 0.05) mRNA increased substantially in the HRG. In contrast, the amount of transforming growth factor beta2 transcript increased only in the HRG (330%; p < 0.01), whereas it remained unchanged in the LRG (-80%). CONCLUSION: We demonstrate for the first time that aerobic training activates angiopoietin 1 and TIE2 genes in human muscle, but only when aerobic capacity adapts to exercise-training. The fourfold-greater increase in aerobic fitness and markedly differing gene expression profile in the HRG indicates that these ECM genes may be critical for physiological adaptation to exercise in humans. In addition, we show that, without careful demonstration of physiological adaptation, conclusions derived from gene expression profiling of human skeletal muscle following exercise may be of limited value. We propose that future studies should (a) investigate the mechanisms that underlie the apparent link between physiological adaptation and gene expression and (b) use the genes profiled in this paper as candidates for population genetic studies.

Acclimatization↗

Patients with large myocardial infarction gain a greater improvement in exercise capacity after exercise training than those with small to medium infarction.

BACKGROUND: It remains unclear whether patients with large-size myocardial infarction (MI) achieve the same benefit from exercise training as do those with small- to medium-size MI. HYPOTHESIS: This study was designed to determine the magnitude and mechanisms underlying improvement in exercise capacity in patients with large-size MI after cardiac rehabilitation. METHODS: In all, 296 patients who participated in a cardiac rehabilitation program after acute MI were divided into two groups according to the peak serum creatine phosphokinase (CPK) level: the group with large infarction (Group 1) (> or = 5000 U/l peak CPK, 64 patients) and the group with less extensive infarction (Group 2) (< 5000 U/I, 232 patients). Exercise capacity was assessed before and after a 3-month cardiac rehabilitation program that included exercise training. RESULTS: Before exercise training, both the peak work rate (p < 0.05) and peak oxygen uptake (VO2) (p < 0.01) were significantly lower in Group 1 than in Group 2. After exercise training, the changes in peak work rate and peak VO2 were significantly greater in Group 1 than in Group 2 (both p < 0.01). The infarction size measured by the peak CPK level correlated significantly with both the baseline exercise capacity and its improvement after exercise training, although these correlations were insignificant in a multivariate analysis. In the multivariate analysis, the improvement in exercise capacity is determined by age and baseline exercise capacity, which is determined by the duration of inactivity, minute ventilation (VE)/VCO2 slope and left ventricular end-diastolic pressure. CONCLUSIONS: Compared with patients with small- to medium-size myocardial infarction, patients with large infarction gain a greater improvement in exercise capacity after exercise training due to reversal of physical deconditioning and improvement in congestive heart failure.

Adaptation, Physiological↗

Resistance exercise training reduces plasma endothelin-1 concentration in healthy young humans.

Endothelin-1 (ET-1), which is produced by vascular endothelial cells, has potent vasoconstrictor and proliferative activity in vascular smooth muscle cells, and therefore has been implicated in regulation of vascular tonus and progression of atherosclerosis. We recently demonstrated that the plasma ET-1 concentration was significantly decreased by aerobic exercise training in healthy young humans and healthy older humans. However, it is unclear whether the production of ET-1 is altered by resistance exercise training. We measured the plasma ET-1 concentration before and after resistance exercise training in healthy young humans. Six healthy young men (26 +/- 1 years old) performed 8 weeks of resistance exercise training (3 days/week). There were no significant differences in body composition, blood pressure, heart rate, and maximal oxygen consumption before and after resistance exercise training. The girths of the arm and thigh significantly increased after resistance exercise training. The maximal muscle powers in the arm and leg increased after resistance exercise training. After resistance exercise training, the plasma concentration of ET-1 significantly decreased. The present study suggested that resistance exercise training, as well as aerobic exercise training, reduces the plasma ET-1 concentration in healthy young humans, and that this reduction in plasma ET-1 concentration may have beneficial effects on the cardiovascular system.

Adaptation, Physiological↗

Unilateral carotid-cardiac baroreflex responses in exercise trained and untrained men.

To determine effects of aerobic exercise training on individual contributions of the right and left carotid sinus baroreflex control of the cardiac interval, heart rate [expressed as R-R Interval (RRI)] and mean arterial pressure (MAP) responses were elicited by pulsed trains of neck suction and pressure in exercise trained (ET = 8) and untrained (UT = 8) men. ET subjects had a greater (mean +/- SD) maximal oxygen uptake (VO2max) than UT subjects (ET = 64.5 +/- 2.4 ml.kg.min-1 vs UT = 39.8 +/- 3.7 ml.kg.min-1; P < 0.001). A neck collar device was modified for delivery of suction and pressure pulses to only one side of the neck. Carotid-cardiac gains for right, left, and bilateral baroreflexes were determined from the logistic function of RRI responses to changes in estimated carotid sinus pressure (ECSP). There were no significant differences in the maximal gains for bilateral (ET = 6.4 +/- 1.8 vs UT = 5.9 +/- 1.3 ms.mm Hg-1 ECSP), right sided (ET = 5.3 +/- 1.2 vs UT = 4.5 +/- 1.2 ms.mm Hg-1 ECSP) or left sided (ET = 3.3 +/- 1.8 vs UT = 3.6 +/- 1.8 ms.mm Hg-1 ECSP) responses between groups and both groups demonstrated an inhibitory summation of reflexes. We suggest that right and left carotid-cardiac responses, as well as the summation of these reflexes, are quantitatively similar in exercise trained and untrained subjects.

Adult↗

Effects of exercise training on brown adipose tissue thermogenesis in ovariectomized obese rats.

The effect of exercise training on brown adipose tissue (BAT) thermogenesis was studied by measuring cytochrome oxidase activity, as a marker of mitochondrial abundance, mitochondrial guanosine-5'-diphosphate (GDP) binding, as an indicator of thermogenic activity and oxygen consumption in BAT in ovariectomized (OVX) obese rats and sham-operated rats. Six-week exercise training significantly suppressed body weight gain in OVX rats to the level of sedentary control rats, although food intake in exercise trained OVX rats increased more than in the sedentary OVX rats. Exercise training increased cytochrome oxidase activity, mitochondrial GDP binding and oxygen consumption in BAT in OVX rats, which were reduced in a sedentary condition, as well as in the control rats. These results suggest that exercise training potentiates BAT thermogenesis, which may contribute to the reduction of body weight in OVX obese rats.

Adipose Tissue, Brown↗

ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits.

Exercise training elicits a metabolic and cardiovascular response that underlies fitness. The molecular mechanisms that orchestrate this adaptive response and secure the wide-ranging gains of a regimented exercise program are poorly understood. Formed through association of the Kir6.2 pore and the sulfonylurea receptor, the stress-responsive ATP-sensitive K(+) channels (K(ATP) channels), with their metabolic-sensing capability and broad tissue expression, are potential candidates for integrating the systemic adaptive response to repetitive exercise. Here, the responses of mice lacking functional Kir6.2-containing K(ATP) channels (Kir6.2-KO) were compared with wild-type controls following a 28-day endurance swimming protocol. While chronic aquatic training resulted in lighter, leaner, and fitter wild-type animals, the Kir6.2-KO manifested less augmentation in exercise capacity and lacked metabolic improvement in body fat composition and glycemic handling with myocellular defects. Moreover, the repetitive stress of swimming unmasked a survival disadvantage in the Kir6.2-KO, associated with pathologic calcium-dependent structural damage in the heart and impaired cardiac performance. Thus, Kir6.2-containing K(ATP) channel activity is required for attainment of the physiologic benefits of exercise training without injury.

Animals↗

Exercise training for heart failure patients improves respiratory muscle endurance, exercise tolerance, breathlessness, and quality of life.

PURPOSE: Increased respiratory muscle endurance and peak oxygen consumption (VO(2peak)) induced by respiratory muscle training support the relationship between respiratory muscle function and exercise capacity in patients with heart failure. This raises the question whether exercise-training results in increased respiratory muscle function contributing to an increased exercise tolerance, a decreased perception of breathlessness, and an improved quality of life. METHODS: Prospective cohort analysis was completed on 24 patients with New York Heart Association (NYHA) Class III heart failure [18 men, 6 women; aged = 64 (SD 7.9) years; percent ejection fraction (%EF) = 24.0 (SD 7.8)]. Maximal sustainable ventilatory capacity (MSVC), submaximal and peak exercise responses, perception of breathlessness, and quality of life were measured before (baseline) and after (end of study) 12 weeks of exercise training. RESULTS: As a result of exercise training, VO(2peak) (P=.01) and MSVC (P<.001) increased, with MSVC contributing to a larger proportion of the variability for VO(2peak) at study completion (r=0.57 vs 0.42). Although stroke volume did not increase beyond exercise at 25 W and did not change with exercise training, ventilation decreased during exercise (P<.05), perception of breathing difficulty (P<.05) was reduced, and quality of life was enhanced (P=.008). CONCLUSIONS: Despite no increase in cardiac output and stroke volume, respiratory muscle endurance improved with exercise training, contributing to increased exercise capacity, decreased breathlessness, and decreased perception of breathlessness. Practical implications can include less frequent rest periods and fatigue, greater confidence, maintenance of independence, and enhanced quality of life.

Aged↗

Genetic markers of fibrinolytic responses of older persons to exercise training.

We assessed the interactive effect of genetic polymorphisms and exercise training on fibrinolysis in 50 - 75 yr old men (n = 17) and women (n = 28). Subjects had tissue plasminogen activator (t-PA) antigen levels and activity and plasminogen activator inhibitor-1 (PAI-1) activity measured before and after 6 mo of endurance-exercise training. Subject's DNA was typed for the PAI-1 4 G/5 G and t-PA I/D variants. Baseline PAI-1 activity, t-PA activity, and t-PA antigen levels were not different among PAI-1 or t-PA genotype groups. Overall, exercise training did not change PAI-1 activity (- 0.43 +/- 0.81 IU/mL, p = NS), increased t-PA activity (0.37 +/- 0.16 IU/mL, p = 0.02), and decreased t-PA antigen levels (- 0.88 +/- 0.20 ng/mL, p < 0.001). Although the differences in changes with training were not significant among genotype groups, significant t-PA antigen level improvements were evident only in PAI-1 4 G allele carriers and significant t-PA activity increases only in PAI-1 4 G homozygotes. t-PA genotype affected the training-induced t-PA antigen level improvements (p = 0.033) after covarying for gender and baseline t-PA antigen levels, with the smallest and largest reductions in the D homozygotes and I/D heterozygotes, respectively. These findings could have important treatment implications for the use of exercise training to reduce CV disease and thrombotic risk in older men and women.

Aged↗

Long-term exercise training with constant energy intake. 3: Effects on plasma lipoprotein levels.

The composition and concentration of plasma lipoproteins were studied in five young men (mean BMI = 27.5 +/- 2.9 (s.d.] before, during (after 25 and 50 days of training), and after the completion of a 100 day exercise training program that induced daily 4.2 MJ calorie deficit. Along with reductions in body weight (from 86.7 +/- 20.0 to 78.7 +/- 17.1 kg, P less than 0.01) and in fat mass (from 17.0 +/- 9.7 to 10.4 +/- 7.4 kg, P less than 0.01), the exercise training program induced numerous changes in plasma lipoprotein levels. Plasma total cholesterol level fell significantly after 25 days of training (P less than 0.05) and remained significantly reduced at the end of the training experiment (P less than 0.05). This reduction in total plasma cholesterol was accompanied by reductions in plasma apoprotein (apo) B, LDL-cholesterol and LDL-apo B levels (P less than 0.05). There were trends for reductions in plasma triglyceride and VLDL components that were significant only for VLDL-triglycerides (P less than 0.05). Plasma HDL-cholesterol levels increased significantly only at the end of the training program (P less than 0.01). This increase in plasma HDL-cholesterol was not accompanied by an increase in plasma apo A-I levels suggesting that exercise training produced an increase in HDL cholesterol content rather than an increase in HDL particle number. Ratios of HDL-cholesterol/cholesterol (P less than 0.01) and apo A-I/apo B (P less than 0.05) were significantly increased by exercise training, suggesting a decreased risk of cardiovascular disease. These results indicate that a reduction in fat mass solely induced by aerobic exercise training has substantial beneficial effects on plasma lipoprotein levels.

Adult↗

Differential effects of exercise training intensity on blood pressure and cardiovascular responses to stress in borderline hypertensive humans.

BACKGROUND: Psychologic stress has been associated with the development of hypertension. Aerobic exercise training appears to decrease cardiovascular responses to psychologic stress. OBJECTIVE: To determine the efficacy of low-intensity and moderate-intensity exercise training in reducing blood pressure and cardiovascular responses to stress. DESIGN: We sought to compare the cardiovascular responses to a psychologic stressor, the Stroop Color Word Task (Stroop), before and after 12 weeks of low-intensity (about 45% maximal oxygen uptake) and moderate-intensity (about 75% maximal oxygen uptake) aerobic exercise training. METHODS: Eighteen borderline hypertensive subjects (resting blood pressure 139 +/- 9/92 +/- 9 mmHg) were divided randomly into three groups: control (no exercise), low-intensity exercise (40-50% maximal oxygen uptake), and moderate-intensity exercise (70-80% maximal oxygen uptake). Training groups exercised three times per week at the prescribed exercise intensity. Heart rate and blood pressure were recorded during the Stroop before, and after 4 and 8 weeks of exercise training. RESULTS: In the low-intensity exercise group, exercise training attenuated mean blood pressure, systolic blood pressure, and diastolic blood pressure responses to the Stroop and decreased resting blood pressure. The moderate-intensity exercise group demonstrated a reduced diastolic blood pressure response to the Stroop. CONCLUSIONS: These results suggest that, in borderline hypertensive humans, 12 weeks of aerobic exercise training attenuates the cardiovascular responses to the Stroop. Furthermore, low-intensity exercise training appears to be a more effective stimulus than moderate-intensity exercise training in reducing resting blood pressure and blood pressure responses to stress.

Adult↗

Body composition, muscle and fat pad changes following two levels of dietary restriction and/or exercise training in male rats.

This study examined the effects of exercise training on conservation of lean mass during moderate and severe dietary restriction in male Sprague-Dawley rats. Eight rats each (48 total) were assigned to one of three levels of dietary restriction (ad lib., AL; moderate, MR; severe, SR) and to one of two activity levels (cage-confined, CC; or treadmill exercised, E) for a 10-week period. Post-intervention, the AL-E (91 percent), MR-CC (84 percent), MR-E (86 percent), SR-CC (66 percent) and SR-E (68 percent) groups all weighed less than the AL-CC group (427 +/- 4.3 g). Exercise training resulted in conservation of lean mass (protein + water + ash) at the moderate but not severe levels of dietary restriction. Further examination showed that this was mostly water since no between-group differences existed at any given diet level for protein or ash mass. Exercise training did elicit conservation of left ventricular heart muscle mass at both the moderate and severe levels of dietary restriction. In contrast, gastrocnemius muscle mass was conserved or maintained only at the moderate dietary restriction level. Thus, the level of dietary restriction appears to affect the ability of exercise training to elicit conservation of both total lean mass and the mass of individual muscles during diet-induced body mass reduction.

Adipose Tissue↗