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Effects of exercise training on energy balance of ovariectomized rats.

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and ovarian hormones on the regulation of energy balance. Female rats were divided into sedentary and exercise-trained groups. Each group thus formed was further divided into a sham-operated group, an ovariectomized group, or ovariectomized estradiol-treated group. Rats were exercise trained on a rodent motor-driven treadmill. After 33 days of treatment, rats were killed and the energy contents of carcasses, feces, and food were determined. Brown adipose tissue (BAT) thermogenesis was assessed through mitochondrial GDP binding. The results show that ovariectomy led to increases in food intake, body weight, and protein gains, whereas estradiol treatment abolished these effects. The results also show that exercise training reduced fat gain. Exercise training interacted with ovariectomy on energy gain; in sedentary rats ovariectomy enhanced the energy gain, an effect that disappeared in exercise-trained rats. However, exercise training was found to alter neither body weight and protein gains nor energy intake. Ovariectomy did not affect energy expenditure when the results are expressed in relative terms (kJ.kg body wt-0.67.day-1). Similarly, exercise training did not modify energy expenditure (kJ.kg body wt-0.67.day-1) once the cost of the training program was subtracted. BAT mitochondrial GDP binding was not affected by any of the experimental treatments. The present results therefore suggest that neither ovariectomy nor exercise training affect energy expenditure through regulatory forms of BAT-mediated thermogenesis.

Adipose Tissue, Brown↗

Gender influences coronary L-type Ca(2+) current and adaptation to exercise training in miniature swine.

Endurance exercise training increases smooth muscle L-type Ca(2+) current density in both resistance and proximal coronary arteries of female miniature swine. The purpose of the present study was to determine 1) whether gender differences exist in coronary smooth muscle (CSM) L-type Ca(2+) current density and 2) whether endurance training in males would demonstrate a similar adaptive response as females. Proximal, conduit (approximately 1.0 mm), and resistance [~200 microm (internal diameter)] coronary arteries were obtained from sedentary and treadmill-trained swine of both sexes. CSM were isolated by enzymatic digestion (collagenase plus elastase), and voltage-gated Ca(2+)-channel current (I(Ca)) was determined by using whole cell voltage clamp during superfusion with 75 mM tetraethylammonium chloride and 10 mM BaCl(2). Current-voltage relationships were obtained at test potentials from -60 to 70 mV from a holding potential of -80 mV, and I(Ca) was normalized to cell capacitance (pA/pF). Endurance treadmill training resulted in similar increases in heart weight-to-body weight ratio, endurance time, and skeletal muscle citrate synthase activity in male and female swine. I(Ca) density was significantly greater in males compared with females in both conduit (-7.57 +/- 0.58 vs. -4.14 +/- 0.47 pA/pF) and resistance arteries (-11.25 +/- 0.74 vs. -6.49 +/- 0.87 pA/pF, respectively). In addition, voltage-dependent activation of I(Ca) in resistance arteries was shifted to more negative membrane potentials in males. Exercise training significantly increased I(Ca) density in both conduit and resistance arteries in females (-7.01 +/- 0.47 and -9.73 +/- 1.13 pA/pF, respectively) but had no effect in males (-8.61 +/- 0.50 and -12.04 +/- 1.07 pA/pF, respectively). Thus gender plays a significant role in determining both the magnitude and voltage dependence of I(Ca) in CSM and the adaptive response of I(Ca) to endurance training.

Adaptation, Physiological↗

Effects of exercise training on insulin-regulatable glucose-transporter protein levels in rat skeletal muscle.

Exercise training has been shown to enhance the ability of insulin to stimulate glucose uptake in responsive tissues. The purpose of this study was to determine the effects of exercise training on the levels of the insulin-regulatable glucose transporter (IRGT) in rat skeletal muscle. After 6 wk of voluntary running in exercise-wheel cages, male Sprague-Dawley rats were rested for approximately 27 h and fasted overnight before removal of plantaris and soleus muscles. The concentration of glucose transporters per unit of muscle protein or DNA was quantitated by immunoblotting with an anti-IRGT polyclonal antibody raised against a synthetic peptide. The IRGT protein was increased by 60% (141 +/- 14 vs. 229 +/- 24 counts/min [cpm]/25 micrograms protein, P less than 0.01) in plantaris muscle from exercise-trained rats compared with controls. Total protein yield, DNA content, and 5'-nucleotidase activity were not different in plantaris muscle from control and exercise-trained rats. In contrast, there was no significant increase in the IRGT protein in soleus muscle after training when data were expressed per unit of muscle protein (292 +/- 22 vs. 346 +/- 16 cpm/25 micrograms protein). These data indicate that the increase in the IRGT in plantaris muscle is a selective response to exercise training that does not reflect an overall increase in muscle protein. The changes in IRGT for these muscles with exercise training parallel changes observed in insulin-mediated glucose uptake. We propose that this increase in the total number of glucose transporters may be a major component of the increase in insulin-mediated glucose uptake that is observed with exercise training.

Animals↗

[Exercise training improves activities of daily living in elderly patients with congestive heart failure].

Exercise training which is one of the multidisciplinary interventions for elderly patients with congestive heart failure, plays an important role for improving the quality of life and reducing the re-admission rate of these patients. We assessed the validity of exercise training for the improvement of patient's skeletal muscle functions and activities of daily living along with monitoring cardiac functions. Exercise training programs were performed in 12 patients with congestive heart failure (New York Heart Association class III or IV), including 5 with valvular disease, 4 with dilated cardiomyopathy and 3 with ischemic cardiomyopathy (mean 79 +/- 9 years). All patients were admitted because of exacerbation of congestive heart failure and were treated conventionally. The exercise training program was started after stabilization of their cardiac condition. The medication was not changed during the training period. After exercise training programs, the cardio-thoracic ratio decreased from 63.8 +/- 7.9% to 60.1 +/- 6.9% (p < 0.01), ejection fraction on echocardiography increased from 47.4 +/- 18.2% to 56.0 +/- 17.5% (p < 0.01), and brain natriuretic peptide decreased from 404.8 +/- 267.5 pg/ml to 313.6 +/- 239.5 pg/ml (p < 0.05). The quadriceps muscle power increased from 0.77 +/- 0.36 Nm/kg to 0.97 +/- 0.41 Nm/kg (p < 0.01). The maximum walking distance on flat surface increased from 149 +/- 164 m to 456 +/- 394 m (p < 0.05). In most patients, the activities of daily living, especially mobility, improved. Appropriate exercise training for the elderly patients with congestive heart failure improves activities of daily living and also reduces the amount of required care by the patients.

Activities of Daily Living↗

Effect of exercise training on myocardial blood flow in patients with stable coronary artery disease.

BACKGROUND: The mechanisms by which exercise training benefits patients with coronary artery disease (CAD) are unclear but may include improved myocardial circulation. The aim of this study was to investigate the effect of exercise training on myocardial blood flow (MBF) and coronary flow reserve (CFR) in patients with stable CAD. METHODS: Twelve patients with documented CAD and ischemic ST-segment depression during exercise testing were randomized to exercise training (n = 7) or sedentary life style (control; n = 5) and underwent rubidium-82 positron emission tomography pre- and postintervention. Global left ventricle MBF and regional MBF in 17 left ventricular segments were calculated. Segments with <75% uptake (2 SD below normal) on stress uptake images were defined as abnormal. RESULTS: Exercise training increased global CFR by 20.8% +/- 27.9% versus control (10.5 +/- 24.1%, P = .0001). In normal segments (exercise training: n = 91; control: n = 46), exercise training did not change resting MBF (-14.1% +/- 16.3% vs -8.8% +/- 15.6%) and hyperemic MBF (-1.93% +/- 19.1% vs 2.86% +/- 20.5%, P = NS) and increased in CFR compared to control (17.0% +/- 25.5% vs 11.3% +/- 23.5%, P = .01). In abnormal segments, the change in resting MBF was not significantly different (-12.6% +/- 18.5% exercise [28 segments] vs -2.9% +/- 18.0% control [39 segments], P = NS). A significant increase was seen in hyperemic MBF with exercise (12.5% +/- 22.1% vs 2.6% +/- 16.3%, P = .02) and CFR (32.8% +/- 32.3% vs 9.5% +/- 24.8%, P = .001). CONCLUSIONS: Exercise training increased CFR in normal and diseased segments, and increased hyperemic flow in diseased segments. These data provide preliminary evidence in support of a favorable effect of exercise training on blood flow to ischemic myocardium.

Coronary Artery Disease↗

Benefits of exercise training in the treatment of heart failure: study with a control group.

OBJECTIVE: Exercise training programs have been proposed as adjuncts to treatment of heart failure. The effects of a 3-month-exercise-training-program with 3 exercise sessions per week were assessed in patients with stable systolic chronic heart failure. METHODS: We studied 24 patients with final left ventricle diastolic diameter of 70+/-10mm and left ventricular ejection fraction of 37+/-4%. Mean age was 52+/-16 years. Twelve patients were assigned to an exercise training group (G1), and 12 patients were assigned to a control group (G2). Patients underwent treadmill testing, before and after exercise training, to assess distance walked, heart rate, systolic blood pressure, and double product. RESULTS: In G2 group, before and after 3 months, we observed, respectively distance walked, 623+/-553 and 561+/- 460m (ns); peak heart rate, 142+/-23 and 146+/- 33b/min (ns); systolic blood pressure, 154+/-36 and 164+/-26 mmHg (ns); and double product, 22211+/- 6454 and 24293+/-7373 (ns). In G1 group, before and after exercise, we observed: distance walked, 615+/-394 and 970+/- 537m (p<0.003) peak heart rate, 143+/-24 and 143+/-29b/min (ns); systolic blood pressure, 136+/-33 and 133+/-24 mmHg (ns); and double product, 19907+/- 7323 and 19115+/-5776, respectively. Comparing the groups, a significant difference existed regarding the variation in the double product, and in distance walked. CONCLUSION: Exercise training programs in patients with heart failure can bring about an improvement in physical capacity.

Cardiac Output, Low↗

Effects of exercise training and ACE inhibition on insulin action in rat skeletal muscle.

Our laboratory has demonstrated (Steen MS, Foianini KR, Youngblood EB, Kinnick TR, Jacob S, and Henriksen EJ, J Appl Physiol 86: 2044-2051, 1999) that exercise training and treatment with the angiotensin-converting enzyme (ACE) inhibitor trandolapril interact to improve insulin action in insulin-resistant obese Zucker rats. The present study was undertaken to determine whether a similar interactive effect of these interventions is manifest in an animal model of normal insulin sensitivity. Lean Zucker (Fa/-) rats were assigned to either a sedentary, trandolapril-treated (1 mg. kg(-1). day(-1) for 6 wk), exercise-trained (treadmill running for 6 wk), or combined trandolapril-treated and exercise-trained group. Exercise training alone or in combination with trandolapril significantly (P < 0.05) increased peak oxygen consumption by 26-32%. Compared with sedentary controls, exercise training alone or in combination with ACE inhibitor caused smaller areas under the curve for glucose (27-37%) and insulin (41-44%) responses during an oral glucose tolerance test. Exercise training alone or in combination with trandolapril also improved insulin-stimulated glucose transport in isolated epitrochlearis (33-50%) and soleus (58-66%) muscles. The increases due to exercise training alone or in combination with trandolapril were associated with enhanced muscle GLUT-4 protein levels and total hexokinase activities. However, there was no interactive effect of exercise training and ACE inhibition observed on insulin action. These results indicate that, in rats with normal insulin sensitivity, exercise training improves oral glucose tolerance and insulin-stimulated muscle glucose transport, whereas ACE inhibition has no effect. Moreover, the beneficial interactive effects of exercise training and ACE inhibition on these parameters are not apparent in lean Zucker rats and, therefore, are restricted to conditions of insulin resistance.

Angiotensin-Converting Enzyme Inhibitors↗

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits.

Exercise training is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro- and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n = 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n = 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 +/- 8% (n = 6; P < 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 +/- 6% (n = 6; P < 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 +/- 8 and 13 +/- 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n = 6; P > 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 +/- 6 and 38 +/- 5% for ExT and L-NAME + ExT, respectively (n = 6; P < 0.05)]. On the other hand, L-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 +/- 7 and 45 +/- 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n = 6; P < 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO.

Acetylcholine↗

Effect of chronic clenbuterol administration and exercise training on immune function in horses.

Effects of longitudinal exercise training and acute intensive exercise (simulated race test) on immune function have not been reported in horses. Clenbuterol, a beta2-adrenergic agonist, is used to manage inflammatory airway disease in horses. This study investigated the interaction of 8 wk of exercise training with or without 12 wk of clenbuterol administration in horses. Twenty-three untrained standardbred mares (10 +/- 3 yr, Mean +/- SE) were used and divided into four experimental groups. Horses given clenbuterol plus exercise (CLENEX; n = 6) and clenbuterol alone (CLEN; n = 6) received 2.4 microg/kg BW of clenbuterol twice daily (in an average volume of 20 mL) on a schedule of 5 d on and 2 d off for 12 wk. The CLENEX group was also aerobically trained 3 d/wk. Mares given exercise alone (EX; n = 5) were aerobically trained for 3 d/wk, and the control group (CON; n = 6) remained sedentary. Both EX and CON horses were administered similar volumes (approximately 20 mL) of molasses twice daily. A simulated race test (SRT) resulted in an elevation in lymphocyte number postexercise (P < 0.05). There was no significant difference after acute exercise in either monocyte or granulocyte number. Acute exercise resulted in a decrease (P < 0.05) in the percentage of CD4+ and an increase (P < 0.05) in the percentage of CD8+ cells. The SRT resulted in a decreased lymphoproliferative response to pokeweed mitogen (P < 0.05). A SRT had no effect on antibody production in response to equine influenza vaccine. The EX group demonstrated greater cortisol concentrations at rest and at all other time points postexercise after completing the training regimen compared with CLENEX horses (P < 0.05). Preexercise (SRT) peripheral blood monocyte number was lower in CLENEX horses than in other treatment groups (P < 0.05). Clenbuterol and exercise training did not significantly affect post-SRT changes in leukocyte numbers. Exercise training resulted in a decrease (P < 0.05) in the percentage of CD8+ cells post-SRT compared with other groups, but the percentage of CD4+ cells was not altered by either clenbuterol or exercise conditioning. Lymphocyte proliferative response was not affected by clenbuterol or exercise treatment. Horses demonstrated responses to bouts of acute exercise as noted with other species, namely humans and rodents.

Adrenergic beta-Agonists↗

Diet and exercise training restore blood pressure and vasodilatory responses during physiological maneuvers in obese children.

BACKGROUND: The effects of diet and diet plus exercise training on muscle vasodilatation during physiological maneuvers in obese children are unknown. We tested the hypothesis that (1) blood pressure (BP) and forearm vascular conductance (FVC) responses during handgrip exercise and mental stress would be altered in obese children and (2) diet plus exercise training would restore BP and FVC responses during exercise and mental stress in obese children. METHODS AND RESULTS: Thirty-nine obese children (aged 10+/-0.2 years) were randomly divided into 2 groups: diet plus exercise training (n=21; body mass index [BMI]=28+/-0.5 kg/m2) and diet (n=18; BMI=30+/-0.4 kg/m2). Ten age-matched lean control children (BMI=17+/-0.5 kg/m2) were also studied. Forearm blood flow was measured by venous occlusion plethysmography. BP was monitored noninvasively. Handgrip exercise was performed at 30% maximal voluntary contraction for 3 minutes. Stroop color word test was performed for 4 minutes. Baseline BP was significantly higher and FVC was significantly lower in obese children. During exercise and mental stress, BP responses were significantly higher and FVC responses were significantly lower in obese children. Diet and diet plus exercise training significantly reduced body weight. Diet and diet plus exercise training significantly decreased BP levels during exercise and mental stress. Diet plus exercise training, in contrast to diet alone, significantly increased FVC responses during exercise (3.7+/-0.3 versus 5.6+/-0.4 U; P=0.01) and mental stress (3.5+/-0.5 versus 4.5+/-0.4 U; P=0.02). After diet plus exercise training, BP and FVC responses during exercise and mental stress were similar between obese children and the control group. CONCLUSIONS: Obesity exacerbates BP responses and impairs FVC responses during exercise and mental stress in children. Diet and exercise training restore BP and FVC responses in obese children.

Blood Pressure↗

Effects of exercise training on left ventricular function and peripheral resistance in patients with chronic heart failure: A randomized trial.

CONTEXT: Exercise training in patients with chronic heart failure improves work capacity by enhancing endothelial function and skeletal muscle aerobic metabolism, but effects on central hemodynamic function are not well established. OBJECTIVE: To evaluate the effects of exercise training on left ventricular (LV) function and hemodynamic response to exercise in patients with stable chronic heart failure. DESIGN: Prospective randomized trial conducted in 1994-1999. SETTING: University department of cardiology/outpatient clinic in Germany. PATIENTS: Consecutive sample of 73 men aged 70 years or younger with chronic heart failure (with LV ejection fraction of approximately 0.27). INTERVENTION: Patients were randomly assigned to 2 weeks of in-hospital ergometer exercise for 10 minutes 4 to 6 times per day, followed by 6 months of home-based ergometer exercise training for 20 minutes per day at 70% of peak oxygen uptake (n=36) or to no intervention (control group; n=37). MAIN OUTCOME MEASURES: Ergospirometry with measurement of central hemodynamics by thermodilution at rest and during exercise; echocardiographic determination of LV diameters and volumes, at baseline and 6-month follow-up, for the exercise training vs control groups. RESULTS: After 6 months, patients in the exercise training group had statistically significant improvements compared with controls in New York Heart Association functional class, maximal ventilation, exercise time, and exercise capacity as well as decreased resting heart rate and increased stroke volume at rest. In the exercise training group, an increase from baseline to 6-month follow-up was observed in mean (SD) resting LV ejection fraction (0.30 [0.08] vs 0.35 [0.09]; P=.003). Mean (SD) total peripheral resistance (TPR) during peak exercise was reduced by 157 (306) dyne/s/cm(-5) in the exercise training group vs an increase of 43 (148) dyne/s/cm(-5) in the control group (P=.003), with a concomitant increase in mean (SD) stroke volume of 14 (22) mL vs 1 (19) mL in the control group (P=.03). There was a small but significant reduction in mean (SD) LV end diastolic diameter of 4 (6) mm vs an increase of 1 (4) mm in the control group (P<.001). Changes from baseline in resting TPR for both groups were correlated with changes in stroke volume (r=-0.76; P<.001) and in LV end diastolic diameter (r=0.45; P<.001). CONCLUSIONS: In patients with stable chronic heart failure, exercise training is associated with reduction of peripheral resistance and results in small but significant improvements in stroke volume and reduction in cardiomegaly. JAMA. 2000.

Aged↗

Exercise training prevents maturation-induced decrease in insulin sensitivity.

We examined the effects of exercise training initiated before maturation or after maturation on insulin sensitivity and glucose transporter GLUT-4 content in membrane fractions of skeletal muscle. Female Wistar rats (4 wk of age) were divided into sedentary and exercise-trained groups. At 12 wk of age, a subset of the trained animals (Tr) was killed along with a subset of sedentary controls (Sed). One-half of the remaining sedentary animals remained sedentary (Sed-Sed) while the other half began exercise training (Sed-Tr). The remaining rats in the original trained group continued to train (Tr-Tr). Euglycemic clamp (insulin infusion rate at 6 mU.kg body wt-1. min-1) was performed at 4, 12, and 27 wk. After euglycemic clamp in all animals except the 4-wk-old, hindlimb (gastrocnemius and part of quadriceps) muscles were removed for preparation of membrane fractions. In sedentary rats, glucose infusion rate (GIR) during euglycemic clamp was decreased from 15.9 mg.kg-1.min-1 at 4 wk of age to 9.8 mg.kg-1.min-1 at 12 wk of age and 9.1 mg.kg-1.min-1 at 27 wk of age. In exercise-trained rats, the GIR was not significantly decreased by maturation (at 12 wk) and further aging (at 27 wk). Initiation of exercise after maturation restored the GIR at 27 wk of age to the same levels as these for the corresponding exercise-trained rats. GLUT-4 content in plasma and intracellular membrane fractions of hindlimb muscle obtained just after euglycemic clamp showed the same trend as the results of GIR. These results suggest that exercise training prevented the maturation-induced decrease in insulin sensitivity. Improvement of insulin sensitivity caused by exercise training was attributed, at least in part, to the increase in insulin-sensitive GLUT-4 on the plasma membrane in skeletal muscle.

Age Factors↗

Randomised training after myocardial infarction: short and long-term effects of exercise training after myocardial infarction in patients on beta-blocker treatment. A randomized, controlled study.

In this study we assessed the short- and long-term effects of 4-weeks of exercise training (MI) soon after myocardial infarction in patients on beta-blocker treatment. Thirty-seven male patients < or = 65 years of age were included in the study, 19 of them randomized to exercise training (ET) and 18 to a control group (Ctr). Cumulated work (CW), calculated in kiloJoules (kJ), was recorded before immediately after the intervention period and again six months after the MI. In the short term the mean (SD) CW increased by 22% (from 65(20) to 79(25) kJ) in the ET group, compared with no change in the Ctr patients (65(24) vs 65(21) kJ) (p = 0.009). At late follow-up CW was 14% above baseline in the ET patients (65(20) vs 74(20) kJ) p = 0.036, compared with only 6% in the 15 Ctr patients who were still available for follow-up (68(24) vs 72(29) kJ), but without a significant between-group difference. In post-MI patients on beta-blocker treatment, and with a high baseline exercise capacity, physical training improved exercise capacity in the short term, but there was no significant between-group difference at long-term follow-up.

Adrenergic beta-Antagonists↗

Effect of aerobic and resistance exercise training on vascular function in heart failure.

Exercise training of a muscle group improves local vascular function in subjects with chronic heart failure (CHF). We studied forearm resistance vessel function in 12 patients with CHF in response to an 8-wk exercise program, which specifically excluded forearm exercise, using a crossover design. Forearm blood flow (FBF) was measured using strain-gauge plethysmography. Responses to three dose levels of intra-arterial acetylcholine were significantly augmented after exercise training when analyzed in terms of absolute flows (7.0 +/- 1.8 to 10.9 +/- 2.1 ml x 100 ml(-1) x min(-1) for the highest dose, P < 0.05 by ANOVA), forearm vascular resistance (21.5 +/- 5.0 to 15.3 +/- 3.9 ml x 100 ml forearm(-1) x min(-1), P < 0.01), or FBF ratios (P < 0.01, ANOVA). FBF ratio responses to sodium nitroprusside were also significantly increased after training (P < 0.05, ANOVA). Reactive hyperemic flow significantly increased in both upper limbs after training (27.9 +/- 2.7 to 33.5 +/- 3.1 ml x 100 ml(-1) x min(-1), infused limb; P < 0.05 by paired t-test). Exercise training improves endothelium-dependent and -independent vascular function and peak vasodilator capacity in patients with CHF. These effects on the vasculature are generalized, as they were evident in a vascular bed not directly involved in the exercise stimulus.

Acetylcholine↗

Effects of exercise training on the relationship between insulin binding and insulin-stimulated tyrosine kinase activity in rat skeletal muscle.

The effect of exercise training on insulin binding and insulin receptor tyrosine kinase activity was studied using detergent solubilized wheat germ agglutinin (WGA)-agarose purified receptor preparations from rat biceps femoris (BF) and tensor fascia lata (TFL) muscles. Insulin receptor activity, as assessed by A14 [125I] insulin binding, was significantly elevated in BF of exercise-trained rats when compared with similar preparations from a sedentary control group. This increase in binding activity was due to change in Bmax not KD. In contrast, neither the Bmax nor the KD of insulin binding to TFL changed with exercise training. The structure of insulin receptors isolated from BF or TFL was unaltered by exercise training as determined by affinity labeling (alpha-subunit, molecular weight (mol wt) approximately 131 kilodaltons [kDa]) and electrophoretic mobility of the alpha- and beta-subunit. Furthermore, basal tyrosine kinase activity was not affected by exercise training in extracts from either BF or TFL. However, the insulin dependent increase in maximal tyrosine kinase activity (Vmax) of the BF, but not TFL, was enhanced by exercise training. Specifically, insulin stimulated phosphorylation of both the beta-subunit of the insulin receptor (auto phosphorylation) and of a synthetic peptide (exogenous phosphorylation) were increased over control values in BF from exercise-trained rats, whereas both measurements of tyrosine kinase activity of TFL from the two experimental groups were similar. In contrast, both insulin-stimulated autophosphorylation and tyrosine kinase activity were significantly decreased in BF of exercise-trained rats when normalized to insulin binding activity. This disassociation was only seen in BF from exercise-trained rats, and was not true of TFL. These data indicate that exercise training can lead to increases in insulin receptor number and tyrosine kinase activity, as well as modifying the relationship between these two variables. The changes noted are not observed in all exercising muscles, and their development seems to depend upon the fiber composition. These results emphasize the complex relationship that exists in the regulation of insulin action at the level of its receptor.

Adenosine Triphosphate↗

Effects of high-cholesterol diet and parallel exercise training on the vascular function of rabbit aortas: a time course study.

It is plausible to assume that exercise training, when applied early enough, can completely correct atherosclerotic defects. Using rabbit aortic specimens, we examined the effects of chronic exercise and high-cholesterol diet feeding on vascular function for different time periods. Male New Zealand White rabbits were divided into four groups: the normal diet groups with or without exercise training and the high-cholesterol diet groups with or without exercise training. Animals in high-cholesterol diet groups were fed 2% cholesterol rabbit chow for 2, 4, or 6 wk. Those in exercise training groups ran on a treadmill at 0.88 km/h for up to 40 min/day, 5 days/wk for the same period of time as the diet feeding. Thoracic aortas were isolated for functional and immunohistochemical analyses. We found that 1). although high-cholesterol diet feeding (>or=2 wk) elevated serum cholesterol levels and impaired acetylcholine-evoked vasorelaxation, only the latter effect was reversed by exercise training; 2). the effects of diet and exercise on acetylcholine-evoked vasorelaxation were mainly due to altered release of nitric oxide and endothelium-derived hyperpolarizing factor; and 3). diet feeding for 4 or 6 wk caused significant lipid deposition and expression of P-selectin, VCAM-1, monocyte chemoattractant protein-1, and inducible nitric oxide synthase, which were largely reduced by exercise training. In conclusion, parallel exercise training almost completely reverses the early-stage endothelial dysfunction caused by high-cholesterol diet feeding.

Acetylcholine↗

Exercise training increases the activity of pyruvate dehydrogenase complex in skeletal muscle of diabetic rats.

The effects of diabetes and exercise training on the activity of pyruvate dehydrogenase (PDH) complex in skeletal muscle were examined in rats. Male Sprague-Dawley rats were divided into four groups as follows: non-diabetic sedentary, non-diabetic trained, diabetic sedentary, and diabetic trained groups. Diabetic rats were prepared by a bolus injection of intravenous streptozotocin (50 mg/kg body weight). Exercise training was performed by having rats run on a treadmill at a speed of 25 m/min for 45 min/day, 6 days/wk for 4 wks. Exercise training decreased serum concentrations of glucose and non-esterified fatty acid in diabetic rats. GLUT4 content in skeletal muscle in sedentary rats was significantly decreased by diabetes; however, exercise training significantly increased the GLUT4 content in diabetic rats. The total and actual activities and the proportion of actual activity of the PDH complex were decreased in diabetic sedentary rats. Exercise training did not affect the total activity of the PDH complex in non-diabetic rats, whereas it increased the total activity in diabetic rats to the same level as that in non-diabetic rats. In diabetic rats, exercise training tended to increase the proportion of actual activity of the PDH complex from 2.7 +/- 0.4% to 4.7 +/- 0.8%, although the proportion of actual activity in non-diabetic rats was decreased by exercise training. The present study suggests that exercise training may improve glucose metabolism in the skeletal muscle of streptozotocin-induced diabetic rats probably through the mechanisms of increasing both GLUT4 content and the activity of the PDH complex.

Animals↗

Exercise training attenuates cardiovascular adverse remodeling in adult ovariectomized spontaneously hypertensive rats.

OBJECTIVE: To study the combined effects of ovariectomy and regular exercise training on hypertension and on cardiac and aortic remodeling in spontaneously hypertensive rats (SHR). DESIGN: Three-month-old female spontaneously hypertensive rats (SHR) were ovariectomized (ovx) or were left intact (int) and divided in four groups (n = 7): sedentary (sed-ovx), exercise-trained (ex-ovx), sedentary intact (sed-int), and exercise-trained intact (ex-int). The exercise protocol was performed on a motor treadmill for 13 weeks. Blood pressure (BP), left ventricular myocardium and aortic wall were studied by light microscopy and stereology. RESULTS: Exercise-trained SHR showed a BP reduction of more than 15% compared with the matched sedentary SHR (sed-int: 210 +/- 5 mm Hg, sed-ovx: 225 +/- 4 mm Hg, ex-int: 178 +/- 2 mm Hg, ex-ovx: 180 +/- 3 mm Hg, P < 0.001). Ovariectomy caused adverse cardiac and aortic wall remodeling, including cardiomyocyte hypertrophy, myocardial interstitial reparative fibrosis and vascularization impairment with loss of cardiomyocytes, and aortic tunica media hypertrophy. Exercise training showed beneficial effects, mainly reduced BP, decreased cardiac hypertrophy due to hypertension, and increased myocardial vascularization. Ovariectomy accelerated cardiomyocyte loss in SHR while exercise training offset this process. Exercise training was the main factor influencing the improvement of intramyocardial arteries length density and significantly reduced the aortic wall thickness and increased the density of smooth muscle cell nuclei per tunica media unit area. CONCLUSIONS: In ovariectomized SHR, exercise training exerts beneficial effects diminishing adverse cardiac and aortic wall remodeling, mainly by reducing interstitial myocardial fibrosis, improving myocardial vascularization, and sustaining the number of cardiomyocytes.

Animals↗