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The effects of exercise training of different intensities on neuromuscular junction morphology.

Little is known about the effects of exercise training on neuromuscular junction morphology in skeletal muscle. The objectives of this investigation were: 1) to determine if exercise training would elicit changes in neuromuscular junction morphology, 2) to determine if exercise training of different intensities would evoke specific changes in neuromuscular junction morphology, and 3) to determine whether changes in neuromuscular junction structure occur independently of changes in muscle fibre type and size. Twenty-four age and size matched male Sprague-Dawley rats were randomly assigned to three groups: high-intensity trained (HIT), low-intensity trained (LIT), or untrained. Neuromuscular junction morphology of the soleus muscle was determined via immunofluorescent staining. Presynaptic acetylcholine vesicles were visualized with SV-2 antibody in conjunction with fluorescein isothiocyanate labelled secondary secondary antibody. Postsynaptic acetylcholine receptors were identified with rhodamine labelled alpha-bungarotoxin. Laser scanning microscopy was used to produce images of synapses, which were used to quantitate the following: total area of SV-2 and alpha-bungarotoxin staining, density of acetylcholine vesicles and receptors, structural complexity, and synaptic coupling. To visualize nerve terminal branching, a smaller number of neuromuscular junctions were stained with C-2 antibody, which reacts with a neurofilament epitope, in conjunction with fluorescein isothiocyanate labelled secondary antibody. Total length of branching, number of branches, average length of branches, and ratio of secondary to primary branches per neuromuscular junction were determined. Citrate synthase activity, fibre type composition and fibre cross-sectional areas of the soleus muscle were assessed to determine the presence of a training effect in that muscle. Results indicate that training did induce hypertrophy of the neuromuscular junction that was independent of muscle hypertrophy. Although the HIT and LIT groups exhibited similar hypertrophic responses of the neuromuscular junction, the HIT group displayed more dispersed synapses than the LIT group. Neither exercise training program, however, resulted in altered densities of acetylcholine vesicles or receptors, nor did training significantly change synaptic coupling. Nerve terminal branching was also affected by exercise training. Neuromuscular junctions from the HIT group demonstrated a greater total length of branching, average length per branch, and number of finer, or secondary, branches than those of the LIT group.

Acetylcholine↗

Effects of athletic strength and endurance exercise training in young humans on plasma endothelin-1 concentration and arterial distensibility.

Strength exercise training induces a decrease in arterial distensibility, whereas endurance exercise training causes an increase in arterial distensibility. Endothelin-1 (ET-1), which is produced by vascular endothelial cells, has potent vasoconstrictor and proliferative activity on vascular smooth muscle cells. We hypothesized that endogenous ET-1 participates in alteration of arterial distensibility by different exercise training types (i.e., strength and endurance exercise training). The purpose of the present study was to investigate plasma ET-1 concentration and arterial distensibility in strength- and endurance-trained athletes. Subjects were male strength-trained athletes (discus, hammer, or javelin throwers; 22.2 years; SA), male endurance-trained athletes (long- or middle-distance runners; 20.7 years; EA), and sedentary healthy men (20.6 years; sedentary control, SC). Maximum hand-grip strength was markedly greater in SA compared with EA and SC (55.3 vs. 41.1 vs. 40.5 kg, P < 0.05). Maximum oxygen uptake was markedly greater in EA than in SA and SC (60.9 vs. 43.1 vs. 43.6 ml/kg/min, P < 0.05). Arterial pulse wave velocity (PWV), which is an index of arterial distensibility, was significantly higher in SA than in EA and SC (688 vs. 529 vs. 601 cm/sec, P < 0.05). In EA, PWV was significantly lower in comparison to that in SC (P < 0.05). Thus arterial distensibility was lower in SA than in EA and SC and higher in EA than in SC. Plasma ET-1 concentration was significantly higher in SA compared with EA and SC (1.64 vs. 1.12 vs. 1.24 pg/ml, P < 0.05). Plasma ET-1 concentration tended to be lower in EA than in SC. These results suggest that the difference in plasma ET-1 level may participate in the mechanism underlying different adaptation of arterial distensibility between strength- and endurance-trained athletes.

Adult↗

Exercise training improves aging-induced downregulation of VEGF angiogenic signaling cascade in hearts.

Exercise training improves aging-induced deterioration of angiogenesis in the heart. However, the mechanisms underlying exercise-induced improvement of capillary density in the aged heart are unclear. Vascular endothelial growth factor (VEGF) is implicated in angiogenesis, which activated angiogenic signaling cascade through Akt and endothelial nitric oxide synthase (eNOS)-related pathway. We hypothesized that VEGF angiogenic signaling cascade in the heart contributes to a molecular mechanism of exercise training-induced improvement of capillary density in old age. With the use of hearts of sedentary young rats (4 mo old), sedentary aged rats (23 mo old), and exercise-trained aged rats (23 mo old, swim training for 8 wk), the present study investigated whether VEGF and VEGF-related angiogenic molecular expression in the aged heart is affected by exercise training. Total capillary density in the heart was significantly lower in the sedentary aged rats compared with the sedentary young rats, whereas that in the exercise-trained rat was significantly higher than the sedentary aged rats. The mRNA and protein expressions of VEGF and of fms-like tyrosine kinase-1 (Flt-1) and fetal liver kinase-1 (Flk-1), which are main VEGF receptors, in the heart were significantly lower in the sedentary aged rats compared with the sedentary young rats, whereas those in the exercise-trained rats were significantly higher than those in the sedentary aged rats. The phosphorylation of Akt protein and eNOS protein in the heart corresponded to the changes in the VEGF protein levels. These findings suggest that exercise training improves aging-induced downregulation of cardiac VEGF angiogenic signaling cascade, thereby contributing to the exercise training-induced improvement of angiogenesis in old age.

Aging↗

Greater effect of diet than exercise training on the fatty acid profile of rat skeletal muscle.

We determined the interaction of diet and exercise-training intensity on membrane phospholipid fatty acid (FA) composition in skeletal muscle from 36 female Sprague-Dawley rats. Animals were randomly divided into one of two dietary conditions: high-carbohydrate (64.0% carbohydrate by energy, n = 18) or high fat (78.1% fat by energy, n = 18). Rats in each diet condition were then allocated to one of three subgroups: control, which performed no exercise training; low-intensity (8 m/min) treadmill run training; or high-intensity (28 m/min) run training. All exercise-trained rats ran 1,000 m/session, 4 days/wk for 8 wk and were killed 48 h after the last training bout. Membrane phospholipids were extracted, and FA composition was determined in the red and white vastus lateralis muscles. Diet exerted a major influence on phospholipid FA composition, with the high-fat diet being associated with a significantly (P < 0.01) elevated ratio of n-6/n-3 FA for both red (2.7-3.2 vs. 1.0-1.1) and white vastus lateralis muscle (2.5-2.9 vs. 1.2). In contrast, alterations in FA composition as a result of either exercise-training protocol were only minor in comparison. We conclude that, under the present experimental conditions, a change in the macronutrient content of the diet was a more potent modulator of skeletal muscle membrane phospholipid FA composition compared with either low- or high-intensity treadmill exercise training.

Animals↗

Effects of exercise training on glucose control, lipid metabolism, and insulin sensitivity in hypertriglyceridemia and non-insulin dependent diabetes mellitus.

Exercise training has potential benefits for patients with hyperlipidemia and/or non-insulin dependent diabetes mellitus. In nondiabetic, nonobese subjects with hypertriglyceridemia, exercise training alone increased insulin sensitivity, improved glucose tolerance, and lowered serum triglyceride and cholesterol levels. These improvements did not occur when exercise training alone was given to similar patients with impaired glucose tolerance. In severely obese (X = 125 kg) subjects without diabetes melitus, a 600 calorie diet alone decreased glucose and insulin concentrations and improved glucose tolerance but did not increase insulin sensitivity. The addition of exercise training improved insulin sensitivity. Obese, non-insulin dependent diabetes mellitus subjects on sulfonylurea therapy alone increased insulin levels but failed to improve insulin sensitivity or glucose levels. In contrast, the addition of exercise training to this medication resulted in improved insulin sensitivity and lowered glucose levels. We conclude that exercise training has major effects on lowering triglyceride levels in hyperlipidemic subjects and can potentiate the effect of diet or drug therapy on glucose metabolism in patients with non-insulin dependent diabetes mellitus.

Blood Glucose↗

Disruption of estrous cycles in exercise-trained rats.

The female Sprague-Dawley rat was evaluated as an animal model for the menstrual irregularities that are common in women athletes. Daily vaginal smears revealed that estrous cycles were markedly disrupted in rats during a 10-week exercise training program, while cycles remained normal in sedentary rats. Compared to 9 sedentary rats, the 10 exercise-trained rats had longer mean cycle lengths and fewer estrus smears. Six of the exercise-trained rats, but none of the sedentary rats, had an "anestrus period" with more than twice the normal interval between estrus smears; one exercise-trained rat became essentially acyclic. Weight gain during the 10-week training program was lower in exercise-trained rats than in sedentary rats. Colonic temperatures, monitored at rest and during 30 min of exercise, were slightly lower in exercise-trained rats with irregular estrous cycles than in exercise-trained rats with regular cycles, indicating that unusually elevated body temperatures during exercise are not responsible for exercise-related reproductive acyclicity. It is concluded that the female Sprague-Dawley rat may be a useful animal model for the study of menstrual irregularities associated with exercise training.

Anestrus↗

Exercise training during rehabilitation of patients with COPD: a current perspective.

Patients with chronic obstructive pulmonary disease (COPD) suffer frequently from physiologic and psychological impairments, such as dyspnea, peripheral muscle weakness, exercise intolerance, decreased health-related quality of life (HRQOL) and emotional distress. Rehabilitation programmes have shown to result in significant changes in perceived dyspnea and fatigue, utilisation of healthcare resources, exercise performance and HRQOL. Exercise training, which consists of whole-body exercise training and local resistance training, is the cornerstone of these programmes. Regrettably, the positive effects of respiratory rehabilitation deteriorate over time, especially after short programmes. Hence, attention should be given to the aftercare of these patients to prevent them to revert again to a sedentary lifestyle. On empirical basis three possibilities seem to be clinically feasible: (1) continuous outpatient exercise training; (2) exercise training in a home-based or community-based setting; or (3) exercise training sessions in a group of asthma and COPD patients.

Aftercare↗

Effects of exercise training on vascular function and myocardial perfusion.

It has long been unclear how exercise training improves myocardial perfusion in patients with stable CAD. Regression of coronary atherosclerosis and collateral formation have been favorite theories; however, angiographic techniques have so far failed to document any significant increase in coronary collaterals at rest. Although net regression of stenotic lesions may be achieved in high-intensity exercise training, it is unlikely that it causes the significant improvement in myocardial perfusion that is seen much earlier than plaque regression. The novel tools to examine coronary endothelial function in vivo and in vitro have now made it clear that exercise training enhances myocardial perfusion by increasing both eNOS and ecSOD expression, which attenuates the premature breakdown of NO by ROS. These increases in local NO production and half-life improve endothelium-dependent vasodilation in response to flow or acetylcholine. These functional changes will occur rather rapidly after the initiation of an exercise training program, although no studies are available on their precise time course. Anatomic changes, such as augmentation of the capillary bed and slowing of the progression of coronary atherosclerosis, may require more extended periods of training (Fig. 4). Recently, first reports about a possible association between endothelial dysfunction and the frequency of clinical events has been documented. Further prospective studies are needed to establish whether endothelial dysfunction is just an indicator of plaque instability or an independent prognostic marker. If it turns out to be the latter, exercise training may be promoted from a symptomatic intervention to a preventive strategy with long-term prognostic benefits.

Animals↗

Effects of exercise training on skeletal muscle glucose uptake and transport.

Exercise training increases the concentration of GLUT-4 protein in skeletal muscle that is associated with an increase in maximal insulin-stimulated glucose transport. The purpose of this study was to determine whether exercise training results in a long-lasting increase in insulin-stimulated glucose transport in rat skeletal muscle. Glucose uptake and skeletal muscle 3-O-methyl-D-glucose (3-MG) transport were determined during hindlimb perfusion in the presence of a maximally stimulating concentration of insulin (10 mU/ml). Hindlimb glucose uptake was approximately 29% above sedentary (Sed) levels in rats examined within 24 h (24H) of their last exercise session. However, when rats were examined 48 h (48H) after their last exercise session, hindlimb glucose uptake was not different from Sed levels. Maximal 3-MG transport was enhanced, above Sed levels, in red (RG; 72% increase) and white (WG; 44% increase) gastrocnemius and plantaris (Plan; 67% increase) muscles, but not soleus (Sol), of 24H rats. GLUT-4 protein content was significantly elevated in those muscles that exhibited enhanced 3-MG transport in 24H rats. GLUT-4 protein content was also elevated in RG, WG, and Plan of 48H rats and was not different from 24H rats. Despite the elevated GLUT-4 protein content, 3-MG transport in 48H rats was only slightly, although statistically not significantly, higher than in Sed rats. These results provide evidence that exercise training does not result in a persistent increase in skeletal muscle glucose uptake or transport, despite an increase in GLUT-4 protein content.

3-O-Methylglucose↗

Effect of exercise training upon left ventricular systolic performance and effort capacity in patients with old myocardial infarction.

Recent studies suggested an improving of left ventricular (LV) systolic function during exercise training in patients with old myocardial infarction. Twenty patients with old myocardial infarction (3-6 weeks) were included in an exercise training programme (mainly cycloergometer) for 2 to 8 weeks. Before and after the exercise training programme, the effort capacity and LV systolic function were determined through exercise testing on cycloergometer and echocardiography. The peak effort raised from 4.39 to 5.27 METs (p < 0.05) and the difference DAF-DAM was reduced from 25% to 12% (p < 0.05). The double product (DP) at peak effort raised nonsignificantly (4.91%, p > > 0.05), but at submaximal effort levels DP decreased significantly on each effort step (12.16%, p < < 0.05). In turn, LV systolic function calculated parameters were practically the same before and after the exercise training programme. (EDD 54.3 vs 5.3 mm, ESD 39.3 vs 38 mm, EDV 160 vs 169 ml, ESV 60.6 vs 54.8 ml, EF 54.1% vs 57.8%, SF 27.6% vs 31.2%). It is concluded that exercise training raised the effort capacity in patients with old myocardial infarction, mainly through peripheral mechanisms, LV systolic function being unchanged. It is also important that exercise training have not any detrimental effect upon LV systolic function and consequently exercise training programmes can be applied and can be useful also in patients with old myocardial infarction and impaired LV systolic function.

Adult↗

[Effects of exercise training on mobilization of BM-CPCs and migratory capacity as well as LVEF after AMI].

BACKGROUND AND PURPOSE: Bone marrow-derived circulating progenitor cells (BM-CPCs) are mobilized in adult peripheral blood (PB) during the acute myocardial infarction (AMI) period and contribute to the regeneration of infarcted myocardium. In this study, the influence of physical training on the mobilization and the migratory activity of the BM-CPCs as well as on the left ventricular function (LVEF) after AMI was examined. PATIENTS AND METHODS: 26 patients with AMI were analyzed in two groups. The first group comprised 17 patients with standardized exercise training for 3 weeks 14 +/- 4 days after AMI, the second group nine control subjects without exercise training. PB concentrations of CD34/45+ and CD133/45+ were measured by FACS. The migratory activity of BM-CPCs was analyzed by migration assay. B-type natriuretic peptide (BNP) in PB and the functional investigations spiroergometry (VO2 and PaO2) and stress echocardiography (LVEF) were determined in both groups. RESULTS: A significant increase in both concentrations, CD34/45+ and CD133/45+, as well as in migratory capacity of BM-CPCs was found after 3 weeks of exercise training, which was significantly decreased 3 months after completion of exercise training. No significant difference was observed in the control group without exercise training. In the functional investigations a significant increase in VO2 as well as PaO2 was shown spiroergometrically after exercise training. There was no difference in stress echocardiographic LVEF at rest in both groups. On the other hand, interestingly, the findings showed that the increase of LVEF at peak stress was significantly higher after exercise training as compared to the control group. Moreover, a significant decrease in BNP values was found after exercise training as well as 3 months after AMI. No difference was found in the control group. CONCLUSION: This study demonstrates that exercise training for 3 weeks after AMI leads to a significant mobilization as well as increase of functional activation of BM-CPCs in humans. Moreover, regular exercise training might contribute to the positive effects on the regenerative potency after AMI.

Aged↗

Physical activity and exercise training prescriptions for patients.

The dominant outcome from exercise prescription is an increase in various markers of exercise capacity. A very large group of studies have demonstrated that the VO2max is increased in response to exercise performed according to well-accepted principles of exercise prescription. Other markers of exercise capacity, such as the VT, also improve substantially following exercise training. Finally, improvement in exercise capacity is generally related to improved quality of life, particularly in patients with exercise capacity limited by various disease processes. Beyond the specific physiologic gains from training, exercise contributes to a better overall clinical outcome. Although there are few data conclusively demonstrating that exercise independently causes favorable changes in other risk factors, it should be recognized that exercise can contribute indirectly to modulation of other risk factors. Exercise represents positive health advice. Since most of our other recommendations to patients are in the nature of negative advice (e.g., don't smoke, don't eat high-fat foods), and since people are infamous for ignoring negative advice, the value of using a positive recommendation that may indirectly lead the patient to discontinue bad behaviors can hardly be overstated.

Cardiac Rehabilitation↗

Short-term exercise training enhances reflex cholinergic nitric oxide-dependent coronary vasodilation in conscious dogs.

The effects of exercise training on the coronary vasodilation following activation of the Bezold-Jarisch reflex were examined in conscious dogs. Mongrel dogs were chronically instrumented using sterile techniques for measurements of systemic hemodynamics and left circumflex coronary blood flow (CBF). With the heart rate controlled (150 bpm), veratrine (0.5 to 20 micrograms/kg) caused dose-dependent increases in CBF; eg, 5 micrograms/kg of veratrine increased CBF by 61 +/- 6% from 31 +/- 1.3 mL/min (P < .05). After exercise training, the dose-response curve of CBF in response to veratrine was shifted to the left; eg, 5 micrograms/kg of veratrine increased CBF by 101 +/- 12% (P < .05 compared with control) from 34 +/- 2.3 mL/min. The enhanced coronary vasodilation was blunted by nitro-L-arginine (NLA, 35 mg/kg). In anesthetized dogs after exercise training, electrical stimulation of the left vagus nerve caused greater increases in CBF, and NLA inhibited increases in CBF. Acetylcholine, norepinephrine, angiotensin II, and bradykinin caused greater increases in NO2- production in coronary microvessels from exercise-trained dogs compared with those from normal dogs. Our results indicate that the coronary vasodilation following activation of the Bezold-Jarisch reflex is enhanced in conscious dogs after exercise training. Since electrical stimulation of the vagus nerve caused greater coronary vasodilation and since the agonists resulted in greater increases in NO production in coronary microvessels from exercise-trained dogs, the mechanism responsible for the enhanced coronary vasodilation following activation of the Bezold-Jarisch reflex is most likely due to the increased release of NO from the endothelial cells.

Acetylcholine↗

Exercise training regulates SOD-1 and oxidative stress in porcine aortic endothelium.

Vascular oxidative stress contributes to endothelial dysfunction. Aerobic exercise training improves vascular function. The purpose of this study was to test the hypothesis that exercise training would improve the balance of antioxidant to prooxidant enzymes and reduce markers of oxidative stress in aortic endothelial cells (AEC). Female Yucatan miniature pigs either remained sedentary (SED) or were exercise trained (EX) for 16-19 wk. EX pigs had increased AEC SOD-1 protein levels and Cu/Zn SOD activity of the whole aorta compared with SED pigs. Protein levels of other antioxidant enzymes (SOD-2, catalase) were not affected by exercise training. Protein levels of p67(phox), a subunit of the prooxidant enzyme NAD(P)H oxidase, were reduced in EX vs. SED AEC. These EX adaptations were associated with lower AEC malondialdehyde levels and decreased phosphorylation of ERK-1/2. Endothelial nitric oxide synthase protein, protein nitrotyrosine content, and heme oxygenase-1 protein were not different in EX vs. SED pigs. We conclude that chronic aerobic exercise training influenced both antioxidant and prooxidant enzymes and decreased indexes of oxidative stress in AEC. These adaptations may contribute to improved endothelial function with exercise training.

Animals↗

Effect of exercise training on ANP receptors.

To clarify whether exercise-training affects ANP function, we trained male Wistar rats by treadmill running for nine weeks and measured ANP receptor number and affinity in the kidney, lung and adrenal. We also measured guanylate cyclase activity, by which second messenger cGMP accumulates. The number of adrenal ANP receptor significantly increased after exercise-training. There was no significant difference of affinity for all the organs examined between the training group and the control group. Guanylate cyclase activity tended to decrease in the kidney in the training group. A significant difference was found when the samples were stimulated by C-type natriuretic peptide (CNP). There was no significant difference in guanylate cyclase activity in the lung and adrenal. These findings are consistent with the exercise-induced hypervolemia, but not with the anti-hypertensive role of exercise-training.

Adrenal Glands↗

Vasoconstrictor responses of coronary resistance arteries in exercise-trained pigs.

Coronary resistance arteries isolated from exercise-trained pigs have been shown to exhibit enhanced myogenic reactivity (J. M. Muller, P. R. Myers, and M. Harold Laughlin. J. Appl. Physiol. 75: 2677-2682, 1993). The purpose of this study was to test the hypothesis that exercise training results in enhanced vasoconstrictor responses of these arteries to all vasoconstrictor stimuli [specifically acetylcholine (ACh), endothelin-1 (ET-1), KCl, and the Ca2+ channel-agonist Bay K 8644]. Female Yucatan miniature swine were trained (Trn) on a motor-driven treadmill (n = 16) or remained sedentary (Sed, n = 15) for 16-20 wk. Arteries 50-120 micron in diameter were isolated and cannulated with micropipettes, and intraluminal pressure was set at 60 cmH2O throughout experiments. Vasoreactivity was evaluated by examining constrictor responses to increasing concentrations of ACh (10(-9) to 10(-4) M), ET-1 (10(-10) to 10(-8) M), KCl (bath replacement with isotonic physiological saline solution containing 30 or 80 mM), and Bay K 8644 (10(-9) to 10(-6) M). Constricted diameters are expressed relative to the passive diameter observed after 100 microM SNP. All four constrictors produced similar decreases in diameter in arteries from both groups [ACh: 0.52 +/- 0.07 (Trn) and 0.54 +/- 0,06 (Sed); ET-1: 0.66 +/- 0.05 (Trn) and 0.70 +/- 0.07 (Sed); KCl: 0.66 +/- 0.05 (Trn) and 0.70 +/- 0.07 (Sed); Bay K 8644: 0.86 +/- 0.05 (Trn) and 0. 76 +/- 0.05 (Sed)]. Present results combined with previous observations indicate that exercise training does not alter vasoconstrictor responses of porcine coronary resistance arteries but specifically increases myogenic reactivity. Thus the underlying cellular mechanisms for myogenic tone are altered by training but not receptor-mediated mechanisms (ACh and ET-1) nor voltage-gated Ca2+ channels (KCl and Bay K 8644) in coronary resistance arteries.

Acetylcholine↗

The effect of exercise training in a cold environment on thermoregulation in adult and aged C57BL/6J mice.

We studied the effect of exercise training in cold environment (six weeks of daily, one-hour runs on a treadmill at ambient temperature of 6 +/- 1 degrees C at 60-65% of VO2max) on cold-induced metabolic heat production, heat loss, and cold tolerance in adult and aged C57BL/6J male mice. In adult mice, exercise training in cold environment resulted in greater cold-induced heat production and cold tolerance without changes in heat loss, similar to the effects of daily cold exposure without exercise. In aged mice, daily cold exposures did not affect cold tolerance and cold-induced heat production, but exercise training in the cold resulted in greater cold-induced heat production and cold tolerance. Heat loss in aged mice increased similarly after both repeated cold exposures and exercise training in the cold. Therefore, mechanisms of effect of exercise training on cold tolerance are different in adult and aged animals. Exercise training in cold environment does not affect cold-induced heat production and cold tolerance in adult mice, but improves them in aged animals.

Acclimatization↗

A review to develop an effective exercise training for heart failure patients.

The patient with heart failure relies on varied physiological adaptations to exercise training. Although, the cardiovascular adaptations may be limited, the patient with heart failure relies on changes in the pulmonary system as well as peripheral muscular adaptations. Therefore, the intent of this review is to outline effective exercise program design and to discuss the effects of exercise training on the patient with heart failure, including cardiovascular, pulmonary, and peripheral musculature adaptations. As a result of exercise training, patients with heart failure can improve their exercise capacity and quality of life, despite no or reduced improvement in central hemodynamics. Respiratory muscle endurance improves with exercise training which contributes to patients' increased exercise capacity, decreased breathlessness, and decreased perception of breathlessness. In addition, peripheral muscle adaptations result in an enhanced ability for oxygen extraction and utilization, a delayed onset of anaerobic metabolism during physical activity, and less fatigue as a result of physical activity and activities of daily living. Many of the physiological sequela associated with reduce functional ability in heart failure patients are correctable with exercise training. The practical implications (and maybe the most important to the patient) of these positive adaptations include less frequent rest periods, lesser overall fatigue, greater confidence to embark on physical tasks, maintenance of independence, and enhanced quality of life.

Adaptation, Physiological↗