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PubMed2005

Vulnerability of the mid aged rat myocardium to the age-induced oxidative stress: influence of exercise training on antioxidant defense system.

This study investigated the onset of age-related changes in the myocardial antioxidant defense system (ADS) and the vulnerability of the myocardium to oxidative stress following exercise training. Few studies have investigated the influence of the most prevalent life-prolonging strategy physical exercise, on the age-dependent alterations in the myocardial antioxidant enzyme system of female rats at mid age and to determine whether exercise-induced ADS could attenuate lipid peroxidation. Two age groups young (3 months old) and mid age (12 months old) Wistar strain female albino rats were given chronic exercise training for a period of 12 weeks. We found a striking decrease (p < 0.01) in the activity levels of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) in the myocardium of mid aged rats when compared to young rats by 36, 50 and 29%, respectively, suggesting the onset of age-dependent decrease in the myocardial ADS. A similar age-related decrease (p < 0.01) was observed in the reduced glutathione (GSH) content (36%). Despite the reduction in ADS, lipid peroxidation (LPO) (20%) was also decreased. In contrast, exercise training significantly elevated (p < 0.01) these antioxidant enzyme activities and the content of GSH. The increase in SOD and CAT activities were more pronounced in the mid aged rats when compared to younger rats, but increased the level of lipid peroxidation to higher levels in the mid-age group following the training regimen. The findings of the present study suggest that, although the activity levels of the myocardial antioxidant enzymes were elevated with the 12 weeks of exercise training, the changes were not sufficient enough in attenuating oxidative stress in the myocardium of female rats during this short period of exercise training.

Aging↗

PubMed2002

Possible mechanisms by which adipocyte lipolysis is enhanced in exercise-trained rats.

A possible mechanism(s) behind exercise training-enhanced lipolysis was investigated in rat adipocytes. Exercise training (9 weeks; running) enhanced the activity of cAMP-dependent protein kinase (PKA) and the protein expressions of PKA subunits (catalytic, RII alpha, and RII beta) in P(40) fraction (sedimenting at 40,000g), but not in I(40) fraction (infranatant of 40,000g) of adipocyte homogenate. The expression of PKA-anchoring protein 150 (AKAP150) in P(40) fraction was greater in exercise-trained (TR) than in control (C) rats. Hormone-sensitive lipase (HSL) activities in both fractions were also greater in TR. On the other hand, stimulated lipolysis was accompanied by increased activities of HSL in P(40) but not in I(40) fraction. The decreases in stimulated lipolysis due to St-Ht31 were greater in TR rats. Thus, the mechanisms behind exercise training-enhanced adipocyte lipolysis could involve the increased activities of PKA and HSL with enhanced expressions of AKAP150 and some subunits of PKA, all of which may be compartmentalized within adipocytes.

Adipocytes↗

PubMed1995

Effects of exercise-training on hypoxia and angiotensin II-induced pulmonary vasoconstrictions.

The present study was undertaken to determine whether exercise-training for 6 weeks would inhibit pulmonary vasoconstriction induced by hypoxia in isolated, blood-perfused rat lungs. Hypoxic pulmonary vasoconstriction (HPV) and angiotensin II (AII)-induced pulmonary vasoconstriction were significantly less in the exercise-trained (ET) group than in the control (cont) group with all challenges. Normoxic pulmonary arterial and capillary pressures in the ET group were significantly lower than those in the cont group and capillary pressor response to hypoxia was less in the ET group than in the cont group. In conclusion, it appears that HPV and AII-induced vasoconstrictions can be reduced by exercise-training, because it would seem that exercise-training repeated responses to increased shear-stress resulting from elevated blood flow in pulmonary vessels.

Angiotensin II↗

PubMed2001

Exercise training and axonal regeneration after sciatic nerve injury.

In the present study, we aimed to investigate the relationship between exercise training and peripheral nerve regeneration after crush injury. For this purpose, HRP neurohistochemistry and modified Pal-Weigert methods were used to assess the axonal regeneration. In the 2nd and 3rd regeneration week groups, myelin debris was observed, and there was no significant difference between exercise trained and sedentary groups. In the 4th regeneration week group, it was seen that myelin debris was removed, and some myelinated fibers were observed in the exercise trained group. On the other hand, there was no myelinated fiber in the sedentary group, and there was a significant difference between exercise trained and sedentary groups. Consequently, we think that exercise is effective in the 4th regeneration week.

Animals↗

PubMedDate not supplied

Effects of exercise training on insulin sensitivity in adolescents with type I diabetes.

We investigated the influence of a program of exercise training consisting of three weekly sessions, each 45 min long, for 12 wk, on indices of physical fitness, glycemic control, and insulin sensitivity in nine adolescents with type I diabetes; six age-matched adolescents with diabetes of equivalent duration served as nonexercised controls. All subjects were instructed not to change dialy insulin dose or caloric intake. In the exercised group, maximal oxygen uptake during graded cycle ergometry to volitional exhaustion increased by 9 +/- 2.7% (P less than 0.01) and lean body mass increased by 4 +/- 1.8% (P less than 0.05). Insulin sensitivity, assessed via the euglycemic clamp technique at insulin infusion rates of 100 mU/M2/min, showed an increase of insulin-mediated glucose disposal from 274 +/- 33 to 338 +/- 28 mg/M2/min, representing an increase in insulin sensitivity of 23 +/- 5% (P less than 0.01). None of these indices changed in the control group. Despite increased insulin sensitivity, glycohemoglobin levels remained at 12 +/- 1% before and after the 12 wk of exercise training, indicating no improvement in overall glycemic control. No increase in hypoglycemic reactions was reported in either group. We conclude that exercise training may be a valuable adjunct in managing type I diabetes providing there is concomitant attention to diet and insulin. Exercise training alone, however, does not improve glycemic control, although it improves physical fitness and insulin sensitivity.

Adolescent↗

PubMed2005

Outcome of exercise training on the long-term burden of hospitalisation in patients with chronic heart failure. A retrospective study.

AIMS: Heart failure is a major cause of hospitalisation, particularly in patients more than 65 years of age in the western world. A common endpoint in studies designed to evaluate treatment effects in heart failure is mortality and morbidity, often reported as an event of hospitalisation. It has recently been reported that this endpoint is misleading with respect to the burden of the disease with regard to the patient, the health service and costs. Furthermore, it can be hypothesized that different treatment effects are better evaluated using more sensitive parameters than those traditionally used in clinical studies. Short-term beneficial effects of exercise training in heart failure patients have previously been showed. Therefore, the aim of this study was to evaluate the long-term effects of exercise training in heart failure patients with regard to different outcome parameters. METHOD AND STUDY GROUP: Patients with chronic heart failure, stabilised on pharmacological treatment, who had participated in a physical training program for 8 weeks, were analysed retrospectively after 5 years. The study group was compared to a matched control group which received conventional treatment and was diagnosed during the same period but not participating in a training program. RESULTS: Exercise training in heart failure patients resulted in significantly less hospitalisation events (2+/-3 vs. 3+/-3, p<0.05) and hospitalisation days (10+/-17 vs. 20+/-27, p<0.05) due to cardiac problems at 5 years after follow-up. Exercise training did not effect mortality. CONCLUSION: Long-term effects of exercise training on burden of disease in chronic heart failure patients is associated with significantly less events and days of hospitalisation due to worsening of cardiac disease.

Aged↗

PubMed2000

Exercise training for claudicants: changes in blood flow, cardiorespiratory status, metabolic functions, blood rheology and lipid profile.

OBJECTIVE: Exercise training improves the walking distance of claudicants. The aim of this study was to investigate factors associated with the improvement in the maximum walking distance (MWD) in respect to cardiovascular, respiratory and metabolic adaptations. METHODS: Forty claudicants were studied. Common femoral artery blood flow (BF), heart rate (HR), oxygen consumption (VO(2)), respiratory exchange ratio (RER), lactate levels, blood rheology and lipid profiles were measured. Tests were repeated after 3 months of exercise training. RESULTS: Fifteen patients did not complete the exercise program. For patients who did complete the program, MWD improved by 82%. A significant reduction in HR and VO(2)during exercise was demonstrated. No significant changes occurred in BF or RER. Although MWD increased significantly, there was no increase in recovery VO(2)(oxygen debt). A significant reduction in post-exercise lactate levels occurred. Blood rheology was unchanged, but an improvement in HDL levels was noted. CONCLUSIONS: Many claudicants could not complete an exercise program, mainly due to osteoarthritis. Exercise training improved exercise tolerance significantly without any increase in BF. The HR and oxygen cost of similar exercise was reduced. An improved MWD did not correlate with a higher oxygen debt or lactate load. Favourable changes in lipid profiles occurred.

Aged↗

PubMed2004

Expression of MHC-beta and MCT1 in cardiac muscle after exercise training in myocardial-infarcted rats.

To evaluate the hypothesis that increasing the potential for glycolytic metabolism would benefit the functioning of infarcted myocardium, we investigated whether mild exercise training would increase the activities of oxidative enzymes, expression of carbohydrate-related transport proteins (monocarboxylate transporter MCT1 and glucose transporter GLUT4), and myosin heavy chain (MHC) isoforms. Myocardial infarction (MI) was produced by occluding the proximal left coronary artery in rat hearts for 30 min. After the rats performed 6 wk of run training on a treadmill, the wall of the left ventricle was dissected and divided into the anterior wall (AW; infarcted region) and posterior wall (PW; noninfarcted region). MI impaired citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities in the AW (P < 0.01) but not in the noninfarcted PW. No differences in the expression of MCT1 were found in either tissues of AW and PW after MI, whereas exercise training significantly increased the MCT1 expression in all conditions, except AW in the MI rats. Exercise training resulted in an increased expression of GLUT4 protein in the AW in the sham rats and in the PW in the MI rats. The relative amount of MHC-beta was significantly increased in the AW and PW in MI rats compared with sham rats. However, exercise training resulted in a significant increase of MHC-alpha expression in both AW and PW in both sham and MI rats (P < 0.01). These findings suggest that mild exercise training enhanced the potential for glycolytic metabolism and ATPase activity of the myocardium, even in the MI rats, ensuring a beneficial role in the remodeling of the heart.

Adaptation, Physiological↗

PubMed2001

The effect of exercise training on glucose tolerance and skeletal muscle triacylglycerol content in rats fed with a high-fat diet.

The aim of the present study was to evaluate the effect of exercise training on glucose tolerance and glycogen and triacylglycerol (TG) content in different types of skeletal muscles and in the liver of rats fed with a high-fat diet. From 8 to 11 weeks of age male Wistar rats were fed with isocaloric standard (control) or high-fat diet (HFD--59% calories as fat) and were additionally assigned to a sedentary or trained group (4 weeks of training on a treadmill). An intravenous glucose tolerance test (IVGTT) with the determination of basal and post load insulin was performed before the final tissue sampling. HFD rats developed marked hyperinsulinemia. Exercise training improved glucose tolerance and insulin response in the control group only (AUC for glucose in control sedentary vs control trained, p<0.05; AUC for insulin: control sedentary vs control trained, p<0.005). Liver glycogen was significantly lower in the HFD group (p<0.05 vs control sedentary) and did not increase after exercise training. Muscle and liver TG content was markedly higher in the HFD group in comparison to control (p<0.0001 in all cases). Exercise training increased TG content in the control group in all examined tissues except white gastrocnemius (p<0.001 in all cases compared to sedentary controls), and did not affect tissue TG in the HFD group. After exercise training there was still markedly higher tissue TG content in the HFD group vs control (p<0.0001 in all cases). We conclude that beneficial metabolic effects of training are impaired in high-fat fed rats and that training does not completely reverse metabolic disturbances in this group of animals.

Animals↗

PubMed2003

Differential effects of exercise training in men and women with chronic heart failure.

BACKGROUND: Abnormalities of myosin heavy chain (MHC) isoforms, enzyme activity, and capillarity contribute to the exercise intolerance that is characteristic of patients with heart failure. To what extent these changes can be reversed with exercise training and whether differences exist in the responses of men and women remains uncertain. We described and compared the effects of exercise training on exercise capacity and skeletal muscle histochemistry in men and women with chronic heart failure. METHODS: Fifteen patients (10 male) undergoing standard medical therapy completed a 14- to 24-week exercise training program. Peak oxygen consumption, MHC isoforms, capillary density, and selected metabolic enzymes were assessed before and after training. RESULTS: Peak oxygen consumption was improved 14% (P <.05); however, this increase was mostly because of the improvement observed in men versus women (+20% versus +2%, respectively, P <.01). At baseline, MHC I content was lower in men than in women (33% +/- 3% vs 49.6% +/- 5.5%, P <.05). MHC I improved with training in men, to 45.6% +/- 4.5% (+38%, P <.05), versus women (-3%, P =.82), and the increase in men tended (P =.12) to be significant when compared with that in women. There were no significant changes in capillary density or muscle enzyme activity with training in the group as a whole or in men and women separately. CONCLUSION: Among patients with chronic heart failure, improvements in peak exercise capacity may be more pronounced in men than in women. This difference in response of functional capacity to training paralleled differences observed between men and women for changes in MHC I isoforms.

Exercise Therapy↗

PubMed2004

Exercise training meta-analysis of trials in patients with chronic heart failure (ExTraMATCH).

OBJECTIVE: To determine the effect of exercise training on survival in patients with heart failure due to left ventricular systolic dysfunction. DESIGN: Collaborative meta-analysis. Inclusion criteria Randomised parallel group controlled trials of exercise training for at least eight weeks with individual patient data on survival for at least three months. Studies reviewed Nine datasets, totalling 801 patients: 395 received exercise training and 406 were controls. MAIN OUTCOME MEASURE: Death from all causes. RESULTS: During a mean (SD) follow up of 705 (729) days there were 88 (22%) deaths in the exercise arm and 105 (26%) in the control arm. Exercise training significantly reduced mortality (hazard ratio 0.65, 95% confidence interval, 0.46 to 0.92; log rank chi(2) = 5.9; P = 0.015). The secondary end point of death or admission to hospital was also reduced (0.72, 0.56 to 0.93; log rank chi(2) = 6.4; P = 0.011). No statistically significant subgroup specific treatment effect was observed. CONCLUSION: Meta-analysis of randomised trials to date gives no evidence that properly supervised medical training programmes for patients with heart failure might be dangerous, and indeed there is clear evidence of an overall reduction in mortality. Further research should focus on optimising exercise programmes and identifying appropriate patient groups to target.

Exercise Therapy↗

PubMed2000

Effect of endurance exercise training on left ventricular size and remodeling in older adults with hypertension.

BACKGROUND: It is not known whether exercise training can induce a reduction of blood pressure (BP) and a regression of left ventricular hypertrophy (LVH) in older hypertensive subjects. This study was designed to determine whether endurance exercise training, by lowering BP, can induce regression of LVH and left ventricular (LV) concentric remodeling in older hypertensive adults. METHODS: We studied 11 older adults with mild to moderate hypertension (BP 152.0 +/- 2.5/91.3 +/- 1.5 mm Hg, mean +/- SE), 65.5 +/- 1.2 years old, who exercised for 6.8 +/- 3.8 months. Seven sedentary hypertensive (BP 153 +/- 3/89 +/- 2 mm Hg) subjects, 68.5 +/- 1 years old, served as controls. LV size and geometry and function were assessed with the use of two-dimensional echocardiography. RESULTS: Exercise training increased aerobic power by 16% (p < .001), and it decreased systolic (p < .05) and diastolic (p < .05) BP, LV wall thickness (from 12.8 +/- 0.4 mm to 11.3 +/- 0.3 mm; p < .05), and the wall thickness-to-radius (h/r) ratio (from 0.48 +/- 0.02 to 0.41 +/- 0.01; p < .05). There were no significant changes in the controls. The changes in LV mass index (deltaLVMI) were different between the two groups. LV mass index decreased in the exercise group (deltaLVMI - 14.3 +/- 3.3 g) but not in the controls (deltaLVMI 1.4 +/- 4.1 g; p = .009). A multiple stepwise regression analysis showed that among clinical and physiological variables including changes in resting systolic BP, aerobic power, body mass index, and systolic BP during submaximal and maximal exercise, only the reduction in resting systolic BP correlated significantly with a regression of concentric remodeling (delta h/r ratio r = .80; p = .003). The other variables did not add to the ability of the model to predict changes in the h/r ratio. CONCLUSIONS: The data suggest that exercise training can reduce BP and induce partial regression of LVH and LV concentric remodeling in older adults with mild or moderate hypertension.

Aged↗

PubMedDate not supplied

The cost-effectiveness of exercise training for the primary and secondary prevention of cardiovascular disease.

BACKGROUND: Although exercise training improves cardiovascular disease (CVD) risk factors, few studies have evaluated its potential long-term cost-effectiveness. METHODS: Using the Cardiovascular Disease Life Expectancy Model, a validated disease simulation model, we calculated the life expectancy of average 35- to 74-year-old Canadians found in the 1992 Canadian Heart Health Survey. The impacts of exercise training on cardiovascular risk factors were estimated as a 4% decrease in low-density lipoprotein (LDL) cholesterol, a 5% increase in high-density lipoprotein (HDL) cholesterol, and a 6 mm Hg decrease in both systolic and diastolic blood pressure. Exercise adherence was estimated at 50% for the first year and 30% for all additional years. Costs for a supervised exercise program determined from Canadian sources and converted to US dollars were estimated at $605 for the first year (medical evaluation, stress test, exercise prescription, and program costs) and $367 for all additional years (program costs). For an unsupervised program, the costs were estimated at $311 for the first year and $73 for all additional years. RESULTS: The cost-effectiveness (CE) of an unsupervised exercise program (1996 U.S. dollars) was less than $12,000 per year of life saved (YOLS) for all individuals. The CE of a supervised exercise program was less than $15,000/YOLS for men with CVD, and between $12,000 and $43,000 for women with CVD and men without CVD. CONCLUSIONS: Given the relatively few risks, substantial long-term benefits, and modest costs, an unsupervised exercise training program represents good value for all. A more expensive supervised exercise program is also cost-effective for most individuals with CVD.

Adult↗

PubMed2003

Exercise-trained but not untrained rats maintain free carnitine reserves during acute exercise.

Exercise training is known to induce physiological adaptations that improve exercise performance and alter patterns of energy substrate utilization to favour fatty acid oxidation. L-Carnitine is an essential cofactor for the oxidation of fatty acids under all physiological conditions, including exercise. This study evaluated the effect of acute exercise on carnitine concentrations in tissue and serum, liver carnitine palmitoyltransferase-I activity and expression, and serum lipids in both trained and untrained rats as compared to non-exercised rats. Serum acyl- and total carnitine was significantly higher in the trained animals, whether exercised or not, suggesting an exercise-induced increase in a renal threshold for carnitine. Untrained rats had significantly higher acylcarnitine in skeletal muscle and an acyl/free carnitine ratio of 0.63 +/- 0.06 compared with 0.31 +/- 0.16 in trained animals receiving an identical acute bout of exercise, demonstrating that untrained animals utilized a significantly higher percentage of free carnitine reserves during exercise. This study suggests that free carnitine reserves may be reduced during exercise in untrained rats, an effect that has the potential to impair both carbohydrate and fat metabolism during exercise.

Adaptation, Physiological↗

PubMed1990

Skeletal muscle limits the exercise tolerance of renal transplant recipients: effects of a graded exercise training program.

Sixteen renal transplant recipients were studied before and after they had participated in a 24-week exercise training program to determine (1) the nature of the factors explaining their impaired exercise tolerance, and (2) their adaptative responses to exercise training. During progressive treadmill exercise to exhaustion prior to training, renal transplant recipients stopped exercising at lower peak rates of oxygen consumption (VO2max) (29.0 +/- 7.8 47.9 +/- 9.1 mL O2.kg-1.min-1; P less than 0.001) and ventilation (55.9 +/- 13.2 v 124.0 +/- 22.2 L.min-1; P less than 0.0001), and at lower peak heart rates (169 +/- 22 v 196 +/- 9 beats.min-1; P less than 0.05) and peak blood lactate concentrations (5.0 +/- 2.1 v 11.5 +/- 4.0 mmol.L-1; P less than 0.001) than did controls. None showed a plateau in oxygen consumption with increasing workload. Exercise time to exhaustion was also significantly shorter in renal transplant recipients (9.5 +/- 1.8 v 16.0 +/- 1.3 min; P less than 0.0001). After training, exercise time to exhaustion (12.0 +/- 2.0 min; P less than 0.001), VO2max (37.5 +/- 4.8 mL O2.kg-1.min-1; P less than 0.05), maximum ventilation rate (68.5 +/- 14.0 L.min-1; P less than 0.05), peak blood lactate concentrations (7.8 +/- 1.8 mmol-L-1; P less than 0.001), and the rate of oxygen consumption at a blood lactate concentration of 2.0 mmol.L-1 (22.5 +/- 2.5 v 16.5 +/- 2.2 mL O2.kg-1.min-1; P less than 0.001) had all increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed2005

Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction.

OBJECTIVE: This study examined the cardiovascular adaptations of an exercise training program and evaluated the role of peripheral vasodilator capacity in contributing to these adaptations after myocardial infarction. DESIGN: A total of 44 consecutive patients with uncomplicated myocardial infarction underwent 3 wks of exercise training. Controls (n = 12) with comparable myocardial infarction were selected from our database and were restricted to a program with minimal activity. All patients performed cardiopulmonary exercise testing with hemodynamic measurements. Forearm and calf reactive hyperemic flow were measured by venous occlusive plethysmography as indices of peripheral vasodilator capacity. RESULTS: Despite no change in arteriovenous oxygen difference at peak exercise after training, training resulted in significant increases in oxygen consumption, cardiac output, and stroke volume and a significant decrease in systemic vascular resistance at peak exercise (overall, P < 0.05). Calf reactive hyperemic flow increased significantly after training (P < 0.001), but forearm reactive hyperemic flow did not. Furthermore, increase in calf reactive hyperemic flow after training had a positive correlation with increases in peak cardiac output, stroke volume, and oxygen consumption after training and an inverse correlation with peak systemic vascular resistance. CONCLUSIONS: Exercise training improved exercise tolerance by improving hemodynamic responses to exercise after myocardial infarction. This improved exercise performance was linked to a training-induced increase in calf vasodilator capacity.

Adaptation, Physiological↗

PubMedDate not supplied

Heredity and changes in plasma lipids and lipoproteins after short-term exercise training in men.

The aims of this controlled experiment were to investigate the effects of short-term aerobic exercise training on plasma lipid and lipoprotein concentrations and the role of heredity in determining the individual variation observed in the lipoprotein-lipid response. Six pairs of male monozygotic (MZ) twins were subjected to an exercise training program that induced a 22,000 kcal energy deficit after 22 consecutive days of training. This program significantly reduced body weight, percent body fat, and subcutaneous fat and significantly increased maximal oxygen consumption (VO2max) (p less than 0.005). The plasma insulin response to an oral glucose challenge was markedly reduced after training (p less than 0.001). Plasma triglyceride concentration decreased and the high density lipoprotein cholesterol (HDL-CHOL)/CHOL ratio increased with training (p less than 0.05). Subjects also displayed substantial individual variation in their response to exercise training, but the changes in plasma CHOL, apolipoprotein (apo) B low density lipoprotein cholesterol (LDL-CHOL), HDL-CHOL, and the HDL-CHOL/CHOL ratio tended to be similar within MZ twin pairs (0.67 less than or equal to ri less than or equal to 0.92; 0.05 greater than p less than 0.0001) thus indicating a significant effect of heredity on the sensitivity of plasma lipids and lipoproteins to exercise training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2002

Exercise training alters skeletal muscle mitochondrial morphometry in heart failure patients.

BACKGROUND: Previous research has demonstrated that exercise intolerance in heart failure patients is associated with significant alterations in skeletal muscle ultrastructure and oxidative metabolism that may be more consequential than cardiac output. DESIGN: To examine the effect of exercise training on skeletal muscle mitochondrial size in chronic heart failure patients. METHODS: Six heart failure patients participated in 16-weeks of supervised upper and lower extremity exercise training. At the conclusion of training, percutaneous needle biopsies of the vastus lateralis were taken and electron microscopy was used to assess mitochondrial sizes. RESULTS: The exercise programme resulted in a significant increase in peak maximal oxygen consumption ( P< 0.05) and anaerobic threshold (P < 0.04). Knee extension muscle force increased following training ( P< 0.02). After exercise training, the average size of the mitochondria increased by 23.4% (0.036 to 0.046 mu(2), P< 0.015) and the average shape was unaltered. CONCLUSION: Exercise training with heart failure patients alters skeletal muscle morphology by increasing mitochondrial size, with no change in shape. This may enhance oxidative metabolism resulting in an increased exercise tolerance.

Aged↗