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A 30-year follow-up of the Dallas Bedrest and Training Study: II. Effect of age on cardiovascular adaptation to exercise training.

BACKGROUND: Aerobic power declines with age. The degree to which this decline is reversible remains unclear. In a 30-year longitudinal follow-up study, the cardiovascular adaptations to exercise training in 5 middle-aged men previously trained in 1966 were evaluated to assess the degree to which the age-associated decline in aerobic power is attributable to deconditioning and to gain insight into the specific mechanisms involved. Methods and Results-- The cardiovascular response to acute submaximal and maximal exercise were assessed before and after a 6-month endurance training program. On average, VO(2max) increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, VO(2max) increased 16% when indexed to total body mass (31 versus 36 mL/kg per minute) or fat-free mass (44 versus 51 mL/kg fat-free mass per minute). Maximal heart rate declined (181 versus 171 beats/min) and maximal stroke volume increased (121 versus 129 mL) after training, with no change in maximal cardiac output (21.4 versus 21.7 L/min); submaximal heart rates also declined to a similar degree. Maximal AVDO(2) increased by 10% (13.8 versus 15.2 vol%) and accounted for the entire improvement of aerobic power associated with training. CONCLUSIONS: One hundred percent of the age-related decline in aerobic power among these 5 middle-aged men occurring over 30 years was reversed by a 6-month endurance training program. However, no subject achieved the same maximal VO(2) attained after training 30 years earlier, despite a similar relative training load. The improved aerobic power after training was primarily the result of peripheral adaptation, with no effective improvement in maximal oxygen delivery.

Adaptation, Physiological↗

Weight-bearing exercise training and lumbar bone mineral content in postmenopausal women.

STUDY OBJECTIVE: To assess the effect of weight-bearing exercise training and subsequent detraining on lumbar bone mineral content in postmenopausal women. DESIGN: Non-randomized, controlled, short-term (9 months) trial and long-term (22 months) exercise training and detraining (13 months). SETTING: Section of applied physiology at a university school of medicine. PATIENTS: Thirty-five healthy, sedentary postmenopausal women, 55 to 70 years old. All women completed the study. There was 90% compliance with exercise training. INTERVENTIONS: All women were given calcium, 1500 mg daily. The exercise group did weight-bearing exercise (walking, jogging, stair climbing) at 70% to 90% of maximal oxygen uptake capacity for 50 to 60 min, 3 times weekly. MEASUREMENTS AND MAIN RESULTS: Bone mineral content increased 5.2% (95% confidence interval [CI], 2.0% to 8.4%; P = 0.0037) above baseline after short-term training whereas there was no change (-1.4%) in the control group. After 22 months of exercise, bone mineral content was 6.1% (95% CI, 3.9% to 8.3% above baseline; P = 0.0001) in the long-term training group. After 13 months of decreased activity, bone mass was 1.1% above baseline in the detraining group. CONCLUSIONS: Weight-bearing exercise led to significant increases above baseline in bone mineral content which were maintained with continued training in older, postmenopausal women. With reduced weight-bearing exercise, bone mass reverted to baseline levels. Further studies are needed to determine the threshold exercise prescription that will produce significant increases in bone mass.

Aged↗

Effect of short-term exercise training on muscle glycogen in resting conditions in rats fed a high fat diet.

It has been reported that exercise training increases muscle glycogen storage in rats fed a high carbohydrate (CHO) diet in resting conditions. The purpose of this study was to examine whether a 3-week swimming training programme would increase muscle glycogen stores in rats fed a high-fat (FAT) diet in resting conditions. Rats were fed either the FAT or CHO diet for 7 days ad libitum, and then were fed regularly twice a day (between 0800 and 0830 hours and 1800 and 1830 hours) for 32 days. During this period of regular feeding, half of the rats in both dietary groups had swimming training for 3 weeks and the other half were sedentary. The rats were not exercised for 48 h before sacrifice. All rats were killed 2 h after their final meal (2030 hours). The glycogen contents in red gastrocnemius muscle, heart and liver were significantly higher in sedentary rats fed the CHO diet than in those fed the FAT diet. Exercise training clearly increased glycogen content in soleus, red gastrocnemius and heart muscle in rats fed the CHO diet. In rats fed the FAT diet, however, training did not increase glycogen content in these muscles or the heart. Exercise training resulted in an 87% increase of total glycogen synthase activity in the gastrocnemius muscle of rats fed the CHO diet. However, this was not observed in rats fed the FAT diet. The total glycogen phosphorylase activity in the gastrocnemius muscle of the rats of both dietary groups was increased approximately twofold by training.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Metabolic effects of treadmill exercise training on the diabetic heart.

This study determined whether exercise training in rats would prevent the accumulation of lipids and depressed glucose utilization found in hearts from diabetic rats. Diabetes was induced by intravenous streptozotocin (60 mg/kg). Trained diabetic rats were run on a treadmill for 60 min, 27 m/min, 10% grade, 6 days/wk for 10 wk. Training of diabetic rats had no effect on glycemic control but decreased plasma lipids. In vivo myocardial long-chain acylcarnitine, acyl-CoA, and high-energy phosphate levels were similar in sedentary control, sedentary diabetic, and trained diabetic groups. The levels of myocardial triacylglycerol were similar in sedentary control and diabetic rats but decreased in trained diabetic rats. Hearts were perfused with buffer containing diabetic concentrations of glucose (22 mM) and palmitate (1.2 mM). D-[U-14C] glucose oxidation rates (14CO2 production) were depressed in hearts from sedentary diabetic rats relative to sedentary control rats. Hearts from trained diabetic rats exhibited increased glucose oxidation relative to those of sedentary diabetic rats, but this improvement was below that of the sedentary control rats. [9,10(-3)H]palmitate oxidation rates (3H2O production) were identical in all three groups. These findings suggest that exercise training resulted in a partial normalization of myocardial glucose utilization in diabetic rats.

Animals↗

Exercise training in chronic heart failure: effects on pro-inflammatory markers.

BACKGROUND: Acute bouts of exercise have been shown to induce inflammatory cytokine activation and peripheral hypoxia in patients with chronic heart failure (CHF). In this study, we set out to investigate the impact of chronic exercise training on pro-inflammatory cytokines and markers of endothelial damage. METHODS AND RESULTS: We measured tumor necrosis factor alpha (TNFalpha), its soluble TNF-receptors 1 and 2, interleukin 6 (IL-6), soluble e-selectin, soluble intracellular adhesion molecule-1 (sICAM) and sCD14 in 18 patients with CHF and 9 age-matched controls in a randomized cross-over study of 8 weeks of exercise training (5 days/week, submaximal bicycle ergometer training, 30 min/day; calisthenics 9 min/day) versus 8 weeks of rest. At baseline, patients had a lower peak Vo(2) (p=0.009) and a trend for higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly elevated levels of sICAM (p=0.02), TNFalpha (p=0.02) and TNF-R2 (p=0.002); TNF-R1 and IL-6 were not elevated. Although exercise training was effective and led to an increase in peak Vo(2) in CHF (p<0.003), there was no activation of any of the above variables observed, neither in patients nor controls. CONCLUSIONS: Chronic heart failure is associated with increased levels of TNFalpha and markers of endothelial damage. Whereas acute bouts of exercise have been reported to lead to an increase in pro-inflammatory cytokines and markers of endothelial damage, these effects are not seen when exercise is performed chronically.

Adult↗

Muscle insulin resistance amended with exercise training: role of GLUT4 expression.

PURPOSE: Muscle insulin resistance is characterized by the inability of a normal insulin concentration to produce a favorable rate of glucose uptake. The muscle of the obese Zucker rat is highly insulin resistant. The purpose of this review is to discuss the cellular defects associated with the muscle insulin resistance of the obese Zucker rat, as well as the mechanisms by which exercise training alleviates or compensates for these defects. Emphasis will be given to the importance of an increased GLUT4 expression on alleviating muscle insulin resistance. METHODS: A review of the relative research from my laboratory and the scientific literature was performed to obtain information on the muscle insulin resistance of the obese Zucker rat and its response to exercise training. RESULTS: The insulin resistance of the obese Zucker rat results from defects in the insulin signaling cascade, which limits translocation of the glucose transporter GLUT4 to the plasma membrane upon insulin binding to its receptor. Exercise training improves the muscle insulin resistance of obese Zucker rat but does not correct the defects in insulin signaling or GLUT4 translocation. The improvement in insulin resistance, i.e., glucose transport, is correlated with an increased expression of GLUT4 protein. Preventing GLUT4 overexpression during exercise training will inhibit the improvement in insulin-stimulated glucose transport. CONCLUSION: Exercise training does not correct but compensates for the defects in muscle insulin resistance by increasing expression of GLUT4. This increase in GLUT4 protein is essential for the improvement in muscle insulin resistance.

Animals↗

Effects of exercise training on left ventricular mass in patients with ischemic heart disease.

To determine whether exercise training results in increased left ventricular mass in patients with ischemic heart disease, we obtained echocardiograms in 14 coronary patients before and after an average of seven months (range 3 to 14 months) of supervised arm and leg exercise. Each echocardiogram was interpreted jointly by two blinded observers, using three different measurement conventions and a semiautomated method of analysis to minimize errors of interpretation. Exercise training led to subjective improvement in all 14 patients, and to an objective increase in functional capacity in 13 of 14 patients, as evidenced by an increase in maximal oxygen consumption estimated from symptom-limited treadmill exercise testing (8.8 +/- 2.7 (SD) and 10.7 +/- 2.5 METS before and after training, respectively, p less than 0.01). However, this functional improvement was not accompanied by any significant change in left ventricular end-diastolic diameter, or posterior wall or interventricular septal thickness. Likewise, left ventricular cross-sectional area (CSA), an index of left ventricular mass which corrects for altered ventricular volume and theoretically reflects directional changes in mass despite nonuniform wall thickness, did not change significantly after training by any measurement convention (CSA = 18.0 +/- 6.5 and 17.6 +/- 6.5 cm2 before and after training, respectively, by American Society of Echocardiography measurements). These data strongly suggest that improved functional capacity after exercise training in patients with ischemic heart disease is not due to exercise-induced left ventricular hypertrophy.

Adult↗

Effects of exercise training on baroreflex control of the cardiovascular system.

Dynamic exercise training has been recommended as an antihypertensive therapy and as a way to modify the effects of many cardiovascular risk factors (Arakawa, 1993; Arroll and Beaglehole, 1992; Kelly and McClellan, 1994: see references 1-3 in the paper). However, the mechanisms underlying the blood-pressure lowering effect of chronic exercise are still poorly understood. It has been suggested that a decrease in sympathetic tone is one of the major effects elicited by chronic exercise on the cardiovascular system. The importance of the sympathetic component is confirmed in this review, since it was found that in spontaneously hypertensive rats (SHR) a marked decrease in sympathetic activity occurred after exercise training. Moreover, our findings suggest that this effect is mediated by improving the depressed baroreceptor function, which is, in part, responsible for the attenuation of the baroreflex sensitivity observed in the sedentary SHR (Krieger et al., 1998, 1999; see references 4 and 5 in the paper).

Animals↗

Exercise training enhances endogenous fibrinolysis in peripheral arterial disease.

PURPOSE: Acute clinical events resulting from atherosclerosis (myocardial infarction, stroke) are associated with impaired endogenous fibrinolysis, the system by which the body lyses inappropriately formed thrombus. Endurance exercise training improves fibrinolysis in normal subjects and those with coronary artery disease. The hypothesis of this study was that exercise training would improve fibrinolysis in subjects with peripheral arterial disease (PAD). METHODS AND RESULTS: Twenty-one men with intermittent claudication (IC-EX) underwent treadmill exercise training for 6 months. Twenty age-matched male subjects with IC were followed for the same period (IC-NONEX). Fibrinolytic activity was measured prior to entry into exercise or "usual care," and at the completion of the study period. Fibrinolysis was quantified by measurement of the activity levels of tissue plasminogen activator (tPA, the activator of fibrinolysis) and its inhibitor plasminogen activator inhibitor-1 (PAI-1), using an amidolytic method. Fibrinolysis, quantified as increased PAI-1 activity, was reduced in both claudicant groups relative to healthy controls at baseline. After 6 months of exercise, subjects in the IC-EX group experienced significant improvements in fibrinolytic activity, manifested as a 23% decrease in PAI-1 activity and a 28% increase in tPA activity. No changes occurred in the IC-NONEX group. In the IC-EX group, subjects with the highest initial PAI-1 values experienced the greatest decreases in PAI-1 activity and thus the greatest benefit from exercise. CONCLUSIONS: Patients with PAD have impaired fibrinolytic activity, manifested primarily as increases in the inhibitor of fibrinolysis, PAI-1. Six months of exercise training reduced these impairments, and may serve as an intervention to reduce cardiovascular mortality and morbidity in these patients.

Aged↗

Changes in blood lipids consequent to aerobic exercise training related to changes in body fatness and aerobic fitness.

The contribution of changes in body fatness and aerobic fitness to changes in blood lipids after aerobic exercise training was investigated. The sample included 295 men (77 black, 218 white) and 355 women (131 black, 224 white), aged 17 to 65 years, from the HERITAGE Family Study. Participants underwent measurements at baseline and after 20 weeks of supervised exercise training on a cycle ergometer. Body fat mass (FM, in kilograms) was determined by underwater weighing, and aerobic fitness (maximal oxygen uptake, VO(2max), in milliliters per minute) was assessed by cycle ergometry. Blood lipid measurements included fasting plasma levels of high-density lipoprotein cholesterol (HDL-C), HDL(2)-C, HDL(3)-C, low-density lipoprotein cholesterol (LDL-C), total cholesterol (CHOL), CHOL/HDL, and triglycerides (TG). A composite lipid change index (LCI) was derived by subjecting the Delta scores for the individual blood lipids to principal components analysis. The exercise training was accompanied by a mean increase of 17.5% in VO(2max) and a mean decrease of 3.3% in FM. Partial correlations, controlled for age, between absolute changes in VO(2max) and changes in the blood lipids were consistently low and nonsignificant. On the other hand, absolute changes in FM were significantly (P <.05) associated with changes in HDL-C (r = -.23), HDL(2)-C (r = -.17), and CHOL/HDL (r =.24) and the LCI (r = -.27) in men and with changes in LDL-C (r =.22), CHOL (r =.19), and CHOL/HDL (r =.15) and the LCI (r = -.19) in women. Forward stepwise regression confirmed that the change in FM was a better predictor of changes in blood lipids than the change in VO(2max), entering as a predictor in 4 of 8 regressions in both men and women. Change in VO(2max) did not enter as a significant predictor in any regression. Further, there were no differences in LCI between the upper and lower quartiles of VO(2max) change. On the other hand, there were significant differences between the low and high quartiles of FM change. No race effects were observed in any of the relationships, except that race was a significant predictor of changes in TG in both men and women. In conclusion, changes in blood lipids associated with aerobic exercise training do not appear to be related to changes in aerobic fitness per se; rather, they are weakly to moderately associated with changes in body fatness.

Adipose Tissue↗

Exercise training enhances tumor necrosis factor-alpha-induced expressions of anti-apoptotic genes without alterations in caspase-3 activity in rat epididymal adipocytes.

The effect of exercise training on tumor necrosis factor-alpha (TNF-alpha) signaling was investigated in rat epididymal adipocytes. Incubation of isolated adipocytes with TNF-alpha (20 ng/ml) for 5 h enhanced the expression of the inhibitor apoptosis protein 2 (IAP2) gene without any enhancement of caspase-3 activity in both the sedentary control (C) and exercise-trained (TR) groups. However, the ability of TNF-alpha to enhance IAP2 gene expression was significantly greater in TR than in C rats. The basal expression of the IkappaB kinase beta (IKK beta) gene and that of the BCL-x(L) gene were also higher in TR than in C rats. Mn-superoxidedismutase contents in adipocytes were higher in TR than in C rats. Moreover, no apoptotic nucleuses of adipocytes in response to acute exercise were observed in either group at least up to 5 h after exercise. Exercise training also enhanced the inhibitory effect of TNF-alpha on the gene expression of the fatty acid synthase (FAS), a lipogenic enzyme, suggesting that fatty acid synthesis may be reduced. Thus, exercise training enhanced TNF-alpha signaling directed toward the expressions of survival signals and the suppression of FAS gene expression.

Adipocytes↗

Effects of cardiac rehabilitation and exercise training on autonomic regulation in patients with coronary artery disease.

BACKGROUND: Although cardiovascular rehabilitation and exercise training have substantial benefits in various ischemic heart disease (IHD) risk factors and subsequent prognosis after major IHD events, there is a paucity of information about its effects on autonomic regulation (such as heart rate variability [HRV] and baroreflex gain), particularly considering its arterial and cardiopulmonary components. METHODS: We studied 40 patients (aged 60 +/- 6 y) after major IHD events, including 29 who underwent a comprehensive phase II cardiac rehabilitation and exercise training program and 11 controls who did not attend cardiac rehabilitation. Specifically, we determined whether active training improves prognostic indices of autonomic regulation of the SA node and whether changes in baroreflex gain could be ascribed to the arterial or to the cardiopulmonary component of the overall arterial pressure/heart period baroreflex. RESULTS: Only patients with IHD undergoing active rehabilitation demonstrated a significant increase in R-R interval, in its variance, in overall gain of arterial pressure/heart period baroreflex (7.44 +/- 1.20 ms/mm Hg to 12.12 +/- 1.48 ms/mm Hg, P <.001) and in peak oxygen consumption (Delta = 2.45 mL/kg/min, P <.001). Separate examination of the selective arterial and cardiopulmonary components showed that only the latter increased significantly (6.17 +/- 1.09 ms/mm Hg to 10.62 +/- 1.56 ms/mm Hg; P <.01). CONCLUSIONS: Cardiac rehabilitation is associated with significant improvements in autonomic markers of neural regulation of the SA node, such as increases in R-R variance and the gain of the overall spontaneous baroreflex, with specific improvements in the cardiopulmonary component as opposed to the arterial baroreflex component of this system. These improvements may further explain the reduction in morbidity and mortality noted after formal cardiac rehabilitation and exercise training programs.

Angioplasty, Balloon, Coronary↗

Effects of physical exercise training on cardiac function and graft patency after coronary artery bypass grafting.

The effects of physical exercise training after coronary artery bypass grafting on recovery of cardiac function and graft patency were studied in 115 patients. The patients were divided into Group I (N = 60) with and Group II (N = 55) without a scheduled rehabilitation program. The rate of graft patency was 98% in Group I and 80% in Group II. After operation, the exercise cardiac index and stroke index were significantly higher in Group I than in Group II. The exercise stroke index increased significantly in Group I, but not in Group II. The variables affecting graft patency, examined by a stepwise method, included double product, cardiac index, stroke index, and left ventricular end-diastolic pressure during postoperative exercise conditions, and postoperative exercise training. The multiple coefficient for these five variables was 0.459 (p less than 0.01). Our findings suggest that physical exercise training should be started as early as possible after coronary artery bypass grafting to improve graft patency and recovery of cardiac function.

Cardiac Output↗

A pilot study of exercise training in adult patients with repaired tetralogy of Fallot.

BACKGROUND: Positive effects of physical training in adults with acquired heart disease have been reported. The role of exercise training in adults with congenital heart disease, however, is less well defined. OBJECTIVES: To assess the level of physical activity in adult patients with repaired tetralogy of Fallot (TOF), as well as the safety and effect of exercise training in these patients. PATIENTS AND METHODS: A questionnaire of physical activity was filled upon entering the study by the participants. Eighteen adult patients with repaired TOF were then randomly assigned to participate in a three-month structured exercise program (exercise group, nine patients) or to continue their usual exercise routine (control group, nine patients). Each patient in the exercise group received an individualized exercise program to be performed three times a week, whereas the control group was told to continue living their life as usual. Cardiopulmonary testing was performed in all patients at baseline (before randomization) and at the end of the study. RESULTS: No death or incidents occurred during the study period. All patients but one were physically inactive at the onset of the study. There was a significant increase in peak oxygen consumption in the exercise group by the end of the study (22.1 mL/kg/min [6 metabolic equivalents (METS)] versus 24.3 mL/kg/min [7 METS], P=0.049), whereas it remained unchanged in the control group (21.8 mL/kg/min [6 METS] versus 22.1 mL/kg/min [6 METS], P=0.825). CONCLUSION: In clinically stable adult patients with repaired TOF, a moderate level of exercise training improves aerobic capacity. Regular exercise should be encouraged in these sedentary patients.

Adult↗

Role of exercise-training in the prevention of hyperinsulinemia caused by high energy diet.

The present study was undertaken to determine whether exercise-training done in combination with feeding a high energy diet could modulate carbohydrate metabolism. Male rats were divided into exercise-trained or sedentary groups that received either a palatable high energy diet or merely standard laboratory diet. After 10 weeks of training, the animals were subjected to an intravenous glucose tolerance test. Body weight, epididymal fat pads, and adipocyte volume were reduced following training. The results also showed that exercise-training protects against deterioration of glucose tolerance produced by high energy diet. Training prevented the elevation of basal as well as glucose challenged insulin levels induced by the high energy diet in spite of a high fat as well as high overall energy intake. A highly significant coefficient of correlation (r = 0.78, P less than 0.01) was observed between the size of adipocytes and the insulin response to glucose load and suggests that the prevention of hyperinsulinemia in rats fed high energy foods while training could be associated with the ability to prevent obesity.

Adipose Tissue↗

Cardiorespiratory exercise training in children.

Definitive statements concerning the cardiorespiratory effects of exercise training in children cannot be made. Few carefully controlled and well-defined exercise training studies including important cardiorespiratory variables have been conducted. Generally, it appears that the response to training in pubescent and postpubescent children is not different from what is observed in adults.

Adolescent↗

Enlargement glycogen store in rat liver and muscle by fructose-diet intake and exercise training.

This study investigated the effect of long-term intake of a fructose diet and exercise training on glycogen content in liver and skeletal muscle in female rats. Thirty-six rats (8 wk old) were divided into two dietary groups and were fed with a control (chow) diet or fructose diet (containing 20%) fructose) for 12 wk. During this period, one-half of the rats in each dietary group were trained by using a motor-driven treadmill (running speed of 25 m/min and duration of 90 min/day, 5 days/wk). The liver glycogen was increased by intake of a fructose diet and exercise training, and the content was in the following order: control-diet and sedentary rats < fructose-diet and sedentary rats < or = control-diet and trained rats < fructose-diet and trained rats in the ratio of 1:3.4:3.6:5.0. The glycogen content in gastrocnemius muscle showed the same trend as that in liver; the ratio was 1:1.3:1.3:1.6. These results indicate that both long-term intake of the fructose diet and exercise training synergistically increased glycogen in both tissues.

Animals↗

[Effects of upper extremity exercise training using biofeedback and constraint-induced movement on the upper extremity function of hemiplegic patients].

PURPOSE: The purpose of this study was to investigate the effects of exercise training using biofeedback and constraint-induced movement on the upper extremity function of hemiplegic patients. METHOD: A non-equivalent pretest-posttest design was used. Study subjects were a conveniently selected group of 40 hemiplegic patients(20 experimental subjects, 20 control subjects) who have been enrolled in two community health centers. After biofeedback training the subjects of experimental group were given constraint-induced movement, involving restraint of unaffected U/E in a sling for about 6 hours in a day over a period of two weeks, while at the same time intensively training the affected U/E. Outcomes were evaluated on the basis of the U/E motor ability(hand function, grip power, pinch power, U/E ROMs), and motor activity(amount, quality). RESULT: 1. After 2 weeks of treatment, the motor abilities of affected U/E(hand function, grip power, pinch power, ROMs of wrist flexion, elbow flexion and shoulder flexion/extension) were significantly higher in subjects who participated in exercise training than in subjects in the control group with no decrement at 4-week follow-up. However, there was no significant difference in wrist extension between experimental or control group. 2. After 2 weeks of treatment, the amount of use and the quality of motor activity of affected U/E were significantly higher in subjects who participated in exercise training than in subjects in the control group with no decrement at 4-week follow-up. CONCLUSION: The above results state that exercise training using biofeedback and constraint-induced movement could be an effective intervention for improving U/E function of chronic hemiplegic patients. Long-term studies are needed to determine the lasting effects of constraint-induced movement.

English Abstract↗