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Effects of exercise training during hemodialysis.

Fourteen maintenance hemodialysis patients volunteered to participate in a 6-month program of exercise training. The exercise was performed on a stationary bicycle during the hemodialysis treatment. Six maintenance hemodialysis patients served as control without exercise training. Exercising patients participated in 91% of all possible exercise sessions. The exercise group showed a significant (23%) increase in maximal oxygen consumption over the 6 months. No change in exercise capacity resulted in the control group. Five of eight hypertensive patients in the exercise group decreased or discontinued antihypertensive medications. No changes occurred in hematocrit or lipid profiles in either group. We conclude that exercise training during the hemodialysis treatment is technically feasible and safe for appropriately screened patients and will increase exercise capacity, and in some patients improve blood pressure control. Exercise during dialysis also improves compliance to regular exercise and facilitates supervised exercise sessions, which are desirable in this patient group.

Antihypertensive Agents↗

Influence of Pro12Ala peroxisome proliferator-activated receptor gamma2 polymorphism on glucose response to exercise training in type 2 diabetes.

AIMS/HYPOTHESIS: Exercise training improves glycaemic control in some but not all individuals and little research has been done regarding genetic impact on the exercise training response in type 2 diabetes. The purpose of this study was to investigate the influence of the Pro(12)Ala variant of the peroxisome proliferator-activated receptor (PPAR) gamma2 gene on changes in fasting plasma glucose in response to exercise training. METHODS: The study population comprised 139 sedentary type 2 diabetic patients (age: 54.4+/-7.2; HbA(1)c: 7.7+/-0.9%) who completed 3 months of supervised exercise training. The primary outcome variable in our analysis was the post-intervention change in blood glucose. Other assessments included measures of body composition, insulin sensitivity indices and maximal oxygen uptake (VO(2max)). RESULTS: The frequency of the Ala allele was 8.3% and the genotypes were in Hardy-Weinberg equilibrium. At baseline, neither body composition variables (weight, BMI, waist circumference), glucose homeostasis variables (glucose, insulin, HbA(1)c, homeostasis model assessment method) nor VO(2max) were different between genotypes (wild-type: Pro(12)Pro n=117, Ala carriers: X(12)Ala n=22). The exercise-training intervention led to similar improvements in body composition and glucose homeostasis variables in both genotype groups (p<0.05). The change in fasting plasma glucose was significantly different between PPARgamma2 genotypes (-1.66 mmol/l vs -0.54 mmol/l, Ala carriers and wild-type, respectively) (p=0.034 unadjusted and p=0.089 including baseline glucose) and the significant association between genotype and glucose response remained after adjusting for statistically significant predictors (age, changes in insulin and BMI [p=0.015]) and including baseline glucose, insulin and BMI (p=0.031). CONCLUSIONS/INTERPRETATION: These data suggest that the Pro(12)Ala polymorphism may influence the glycaemic response to exercise in type 2 diabetes.

Adult↗

Exercise training down-regulates ob gene expression in the genetically obese SHHF/Mcc-fa(cp) rat.

The recently cloned obesity gene (ob) encodes a protein, leptin, which is secreted from adipose tissue and interacts with hypothalamic receptors to decrease appetite, increase energy expenditure, and reduce body lipid stores. The levels of ob mRNA are increased in several models of obesity, consistent with the hypothesis that obese animals may be resistant to the actions of leptin. The present study examined the impact of increased energy expenditure through exercise training on ob mRNA gene expression and body composition in the SHHF/Mc-fa(cp) male rat, a rodent model of obesity, insulin resistance, and type II diabetes. Six week old lean and obese animals were trained 8-12 weeks by treadmill running at 70% peak oxygen uptake, 5 days/wk, for 1.5 hr/day. After endurance training, exercised rats had significantly lower total body fat compared to sedentary rats of the same age, despite maintaining the same body weight. In the obese SHHF/Mcc-fa(cp) rat, the level of ob mRNA expression was markedly increased by four fold in subcutaneous adipose tissue compared to lean controls (p<0.05). In response to exercise training, there was a significant 85 % decrease in ob mRNA in exercised-training lean rats (p < 0.05) compared with non-exercised controls, while in obese-exercised rats, ob gene expression was significantly reduced only by 50% relative to non-exercised obese rats (p < 0.05). These results demonstrate that exercise training reduces fat mass and ob mRNA in lean and obese rats, and supports the hypothesis of a feedback loop between the adipocyte and hypothalamus that attempts to maintain body weight at a constant level by reducing ob gene expression in response to increased energy expenditure.

Adipose Tissue↗

Effect of insulin on adipocyte lipolysis in exercise-trained rats.

The effect of exercise training on the antilipolytic action of insulin was studied in rat adipocytes. Exercise training enhanced lipolysis induced by norepinephrine. Insulin dose dependently inhibited norepinephrine- (1 microM) stimulated lipolysis in both groups. Its inhibition rate was significantly greater in the trained than in the control group. Thus, exercise training enhanced the antilipolytic action of insulin. In the control group, insulin (1,000 microU/ml) reduced the displacement rate of [3H]CGP-12177 binding to adipocytes by low concentrations of (-)-norepinephrine. The slope factor without insulin was 0.76, whereas that with insulin was 0.95. In the trained group, insulin did not affect the competition binding of (-)-norepinephrine for [3H]CGP-12177. The displacement rate of [3H]CGP-12177 binding from adipocytes by low concentrations of (-)-norepinephrine was significantly greater in the trained than in the control group. The number of surface beta-adrenergic receptors per adipocyte was smaller in the trained than in the control group. Cilostamide, which blocks the antilipolytic action of insulin, restored lipolysis in both groups. The recovery rate was significantly greater in the trained than in the control group. These findings suggest that the enhanced antilipolytic action by insulin in the trained group occurs at a site distal to the binding of norepinephrine to beta-adrenergic receptors and that it is due to the increased activity of particulate low-Michaelis constant phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗

Attenuation of hypercapnic carbon dioxide chemosensitivity after postinfarction exercise training: possible contribution to the improvement in exercise hyperventilation.

OBJECTIVE: To elucidate the responsible mechanisms of increased slope of minute ventilation relative to carbon dioxide production (VE/VCO(2)) during exercise after acute myocardial infarction without overt signs of heart failure, patients who had an acute myocardial infarction were examined after participating in a three month supervised exercise training programme. DESIGN: Exercise testing, hypercapnic CO(2) chemosensitivity measurement (rebreathing method), and pulmonary function test were repeated at entry and after three months in 50 acute myocardial infarction patients with neither symptoms nor signs of heart failure who completed the training programme. Ten patients who performed initial inhospital training served as controls. RESULTS: Age, peak oxygen uptake, left ventricular ejection fraction, CO(2) chemosensitivity, respiratory parameters (percentage of predicted normal vital capacity (%VC), forced expiratory volume in one second, and carbon monoxide transfer factor (%TLCO)) were all significantly correlated with VE/VCO(2) slope. Multivariate regression analysis showed that age (beta = 0.29, p = 0.01), %TLCO (beta = -0.27, p = 0.01), and CO(2) chemosensitivity (beta = 0.49, p < 0.001) were independent determinants of VE/VCO(2) slope. After three months, there was no significant change in these parameters in the control group. Peak oxygen uptake, %TLCO, and %VC and attenuation in CO(2) chemosensitivity increased significantly in the training group. The VE/VCO(2) slope decreased marginally (p = 0.11). The changes in VE/VCO(2) slope were correlated only with those in CO(2) chemosensitivity (r = 0.50, p < 0.001). CONCLUSION: After acute myocardial infarction, exercise hyperventilation is seen in association with aging, enhanced hypercapnic CO(2) chemosensitivity, and reduced TLCO, even in the absence of overt heart failure. The correlation of VE/VCO(2) attenuation after training with the reduction in CO(2) chemosensitivity suggests that exercise training may reduce increased VE/VCO(2) slope, at least partially by reducing CO(2) chemosensitivity.

Breath Tests↗

Effects of exercise training on left ventricular filling at rest and during exercise in patients with ischemic cardiomyopathy and severe left ventricular systolic dysfunction.

The aim of our study was to determine whether exercise training can augment left ventricular diastolic filling at rest and during exercise in patients with ischemic cardiomyopathy and whether any correlation exists between changes in diastolic filling and changes in exercise tolerance. Forty-three consecutive patients (mean age, 54 +/- 8 years) with ischemic cardiomyopathy and severe left ventricular systolic dysfunction (election fraction <30%) were studied. Group T (29 patients) was exercised on a cycle ergometer 3 times a week for 8 weeks at 60% of peak oxygen uptake. Group C (14 patients) was not exercised. All patients underwent an exercise test and a radionuclide ventriculography at baseline and after 8 weeks. At the end, no changes were found in group C. In group T, exercise training increased peak oxygen uptake (1 5%; p < 0.0001), work rate (1 5%; p < 0.005), peak early filling rate (10%; p < 0.02), and peak filling rate (1 1%; p < 0.03). At submaximal exercise, peak filling rate increased at all matched heart rates. The increase in peak filling rate was correlated with the increase in cardiac index (r= 0.72; p < 0.0001) at peak exercise. The independent predictors of the increase in peak oxygen uptake were changes in work capacity and peak early filling rate. The data demonstrate that exercise training can improve the exercise capacity of patients with ischemic cardiomyopathy and severe systolic-dysfunction. The increase in early diastolic filling at rest and during exercise may contribute to the improvement in peak oxygen uptake.

Cardiac Output↗

Clinical significance of coronary vascular adaptations to exercise training.

Coronary vascular adaptations to exercise training have been extensively studied at the microscopic level in animals and correlated with direct and indirect measurements of myocardial blood flow in patients with coronary artery disease. Animals have permitted more extensive study. These findings have generally supported an increased blood flow to the myocardium with exercise training. However, consistent positive structural and functional adaptations to training have not been observed in large animals. Clinical studies have been limited by methodological problems related to techniques for detecting ischemia and measuring myocardial blood flow and the variability in exercise stimulus. Well-established ischemia and high-intensity, long-duration training were the factors that promoted vascular growth in exercising patients with coronary artery disease. Animals studies also have demonstrated the necessity for myocardial ischemia to be present to induce coronary collateral development with exercise training. Optimal promoters of vascular growth in patients with coronary disease may consist of pharmacological interventions combined with exercise training.

Adaptation, Physiological↗

Comparison of single versus multiple lifestyle interventions: are the antihypertensive effects of exercise training and diet-induced weight loss additive?

Although aerobic exercise training and diet-induced weight loss each have been shown to individually lower elevated blood pressure (BP), it is currently not known whether their combined use produces an additive antihypertensive effect. In this randomized clinical trial we therefore compared the effect on resting BP of exercise training only and dietary modification only with that of exercise training plus dietary modification in 55 sedentary, overweight patients with high normal BP or stage 1 or 2 hypertension. After baseline testing, patients were randomized to 1 of the following 3 interventions for 12 weeks: exercise training only (aerobic exercise; 30 to 45 minutes; 3 to 5 days/week; 60% to 85% of maximal heart rate), dietary modification only (aimed primarily at weight loss via restriction of energy intake and dietary fat), or exercise training plus dietary modification. Forty-eight patients completed the study. In these patients, exercise training plus dietary modification elicited a greater reduction (p < or = 0.001) in body weight (-7.1 +/- 2.9 vs -1.0 +/- 1.8 kg) than exercise training only, and a greater increase (p < or = 0.05) in maximal oxygen uptake (4.3 +/- 2.6 vs 1.9 +/- 2.0 ml/kg/min) versus dietary modification only. However, the reduction in BP with exercise training plus dietary modification (-12.5 +/- 6.3/7.9 +/- 4.3 mm Hg) did not differ significantly from that with exercise training only (-9.9 +/- 6.4/5.9 +/- 4.6 mm Hg) or dietary modification only (-11.3 +/- 12.1/7.5 +/- 4.3 mm Hg). These data indicate that the antihypertensive effects of exercise training and diet-induced weight loss are not additive. This finding has important public health and clinical implications for the millions of overweight persons with high normal BP or stage 1 or 2 hypertension.

Adult↗

Changes in rest and exercise myocardial perfusion and left ventricular function 3 to 26 weeks after clinically uncomplicated acute myocardial infarction: effects of exercise training.

The effects of exercise training on exercise myocardial perfusion and left ventricular (LV) function in the first 6 months after clinically uncomplicated acute myocardial infarction (AMI) were assessed in 53 consecutive men aged 55 +/- 9 years. Symptom-limited treadmill exercise with thallium myocardial perfusion scintigraphy and symptom-limited upright bicycle ergometry with equilibrium gated radionuclide ventriculography were performed 3, 11 and 26 weeks after AMI by 23 men randomized to training and 30 randomized to no training. Peak cycle capacity increased in both groups between 3 and 26 weeks (p less than 0.01), but reached higher levels in trained than in untrained patients (803 +/- 149 vs 648 +/- 182 kg-m/min, p less than 0.01). Reversible thallium perfusion defects were significantly more frequent at 3 than at 26 weeks: 59% and 36% of patients, respectively (p less than 0.05), without significant inter-group differences. Values of LV ejection fraction at rest, submaximal and peak exercise did not change significantly in either group. The increase in functional capacity, i.e., peak treadmill or bicycle workload, that occurred 3 to 26 weeks after infarction was significantly correlated with the increase in peak exercise heart rate (p less than 0.001), but not with changes in myocardial perfusion or LV function determined by radionuclide techniques. Changes in myocardial perfusion or LV function do not appear to account for the improvement in peak functional capacity that occurs within the first 6 months after clinically uncomplicated AMI.

Coronary Circulation↗

Acute and chronic effects of strenuous exercise on glucose metabolism in isolated, incubated soleus muscle of exercise-trained rats.

Male and female Wistar rats were exercise-trained for 6 or 11 weeks respectively, to examine the effects of acute exercise or exercise training per se on insulin-stimulated glucose utilization in soleus muscles isolated and incubated in vitro. The maximal activities of hexokinase and 2-oxoglutarate dehydrogenase were significantly elevated (by greater than 50%) in gastrocnemius muscle of exercise-trained male and female rats, indicating an adaptation to the training regime. No significant differences in any of the variables studied were observed between appropriately matched male and female rats. There were no significant differences in the sensitivity or responsiveness of the rates of lactate formation or glycogen synthesis in soleus muscles isolated from exercise-trained and sedentary animals at rest (exercise-trained animals were studied 40 h after the last exercise bout). On the other hand, acute exercise caused significant changes in soleus muscle glucose metabolism. Basal and insulin-stimulated rates of glycogen synthesis were significantly elevated in soleus muscles incubated from both sedentary and exercise-trained rats immediately after an exercise bout. In addition, the responsiveness of glucose utilization to insulin in soleus muscles from exercise-trained rats was significantly increased after acute exercise. The results indicate that significant changes in the control of glucose metabolism by insulin in soleus muscle occur as a result of an acute exercise bout, while no adaptive changes in insulin sensitivity occur in soleus muscle after exercise training.

Animals↗

Canine cardiac sarcoplasmic reticulum is not altered with endurance exercise training.

To investigate the effect of exercise training on calcium movements by isolated cardiac sarcoplasmic reticulum (SR), mongrel dogs either remained sedentary (S) or were exercise-trained (E) via running for a period of 8-10 wk. The trained state was confirmed by the increase in skeletal muscle citrate synthase activity and decreases in submaximal exercise heart rates in the E group but not in the S dogs. The properties of isolated cardiac SR were identical between the groups. The variables tested included ATP-dependent calcium transport and calcium-stimulated ATPase activity. Importantly, there was no difference in spontaneous calcium release which occurred after peak ATP-dependent calcium accumulation was reached. Calcium release from passively loaded vesicles induced by calcium and ionophore also did not differ in the SR isolated from the E dogs. The change in the affinity of the SR Ca ATPase for calcium after the addition of the polyanion, heparin, was similar in both groups, indicating that the regulation of calcium-stimulated ATPase activity by the SR protein, phospholamban, is not modified by exercise training. We conclude that exercise training of 8-10 wk duration does not alter the calcium handling properties of cardiac SR isolated from mongrel dogs.

Animals↗

Physical responses to different modes of interval exercise in patients with chronic heart failure--application to exercise training.

METHOD: In exercise training with chronic heart failure patients, working muscles should be stressed with high intensity stimuli without causing cardiac overstraining. This is possible using interval method exercise. In this study, three interval exercise modes with different ratios of work/ recovery phases (30/60 s, 15/60 s and 10/60 s) and different work rates were compared during cycle ergometer exercise in heart failure patients. Work rate for the three interval modes was 50% (30/60 s), 70% (15/60 s) and 80% (10/60 s) of the maximum achieved during a steep ramp test (increments of 25 w/10 s) corresponding to 71, 98 and 111 watts on average. Metabolic and cardiac responses to the three interval exercises were then examined including catecholamine levels and perceived exertion. Parameters measured during interval exercise were compared with an intensity level of 75% peak VO2, determined during an ordinary ramp exercise test (increments of 12.5 W.min-1). RESULTS: (mean +/- SEM) (1) In all three interval modes, VO2, ventilation and lactate did not increase significantly during the course of exercise. Mean values during the last work phase were between 754 +/- 30 and 803 +/- 46 ml.min-1 for VO2, between 26 +/- 3 and 28 +/- 1 l.min-1 for ventilation and between 1.24 +/- 0.14 and 1.29 +/- 0.10 mmol.l-1 for lactate. (2) In mode 10/60 s, heart rate and systolic blood pressure increased significantly (82 +/- 4 --> 85 +/- 4 beats.min-1; 124 +/- 5 --> 134 +/- 5 mmHg; P < 0.05 each), while in mode 15/60 s catecholamines increased significantly (norepinephrine 0.804 +/- 0.089 --> 1.135 +/- 0.094 nmol.l-1; P < 0.008; epinephrine 0.136 +/- 0.012 --> 0.193 +/- 0.019 nmol.l-1; P < 0.005). (3) In all three modes, rating of leg fatigue and dyspnoea increased significantly during exercise but remained within the range of values considered 'very light to fairly light' on the Borg scale. (4) Compared to an intensity level of 75% peak VO2, work rate during interval work phases was between 143 and 221%, while cardiac stress (rate-pressure product) was significantly lower (83-88%). CONCLUSION: All three interval modes resulted in physical response in an acceptable range of values, and thus can be recommended.

Chronic Disease↗

Microvascular and myocardial contractile responses to ischemia: influence of exercise training.

We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Short-term exercise training in patients with chronic atrial fibrillation: effects on exercise capacity, AV conduction, and quality of life.

PURPOSE: A randomized study was conducted to determine whether short-term exercise training in patients with chronic atrial fibrillation (AF) might improve exercise capacity and quality of life (QOL), and influence atrioventricular conduction. METHODS: Atrial fibrillation patients (age 64 +/- 7 years) were randomized to exercise training (n = 15) or a 2-month control period (n = 15) followed by the training program. Twenty-four training sessions consisted of aerobic exercise and muscle strengthening. A cycle ergometer test and a 15-minute resting high-frequency spectral electrocardiogram analysis were performed and a QOL questionnaire (SF-36) was completed before and after training. Because there were no changes after 2 months in the control group, pooled data for all patients are presented before and after training. RESULTS: Cumulated work at Borg scale 17 increased by 41% +/- 36%. Heart rate at rest and after 10 minutes of exercise decreased from 75 +/- 14 to 68 +/- 14 bpm and 145 +/- 19 to 137 +/- 21 bpm, respectively. HF increased from 81 +/- 17 to 91 +/- 22 milliseconds. Four of the 8 scales and 1 of the 2 summary scales of the Short-Form-36 improved. P <.05 for all results. CONCLUSIONS: Exercise capacity, heart rate variability, and QOL improved after 2 months of exercise training in patients with chronic AF. Heart rates at rest and during exercise decreased.

Aged↗

Hormonal factors in reduced postprandial heat production of exercise-trained subjects.

The influence of exercise training on postprandial heat production was investigated in human subjects. Whereas resting metabolic rate was comparable for trained and nontrained subjects, the heat increment of feeding (HIF) after subjects consumed a meal containing 755 kcal was approximately 50% smaller in the trained subjects. Measurements of respiratory quotient also indicated a reduction of about 50% in glucose oxidation associated with exercise training. The levels of plasma norepinephrine increased significantly (P less than 0.01) from 200 to 300 pg/ml in the sedentary subjects, but the changes observed in trained subjects were not significant. During the early phase of the meal, plasma levels of insulin were increased, even before nutrients appeared in the blood. Throughout the study the enhanced sensitivity to insulin of the trained subjects was confirmed. the postprandial heat production was diminished in exercise-trained subjects, and it is suggested that this could be related to a reduced activity of the sympathetic nervous system. Another possibility is that this reduction in HIF is related to a facilitation of glucose disposal in the form of glycogen rather than in the form of lipids.

Adult↗

Glucose and insulin responses following 16 months of exercise training in overweight adults: the Midwest Exercise Trial.

The current study examined the insulin and glucose response during an oral glucose tolerance test (OGTT) in overweight young adults prior to and following exercise training in the Midwest Exercise Trial (MET). Subjects (N = 66) were randomly assigned to non-exercise control (CON; 16 females, 13 males) or exercise (EX; 22 females, 15 males) groups. EX performed supervised and verified exercise on 3 to 5 days per week in 20- to 45-minute sessions at 60% to 75% of heart rate reserve. OGTTs and assessments for body mass, body composition, and maximal oxygen consumption (Vo(2) max) were performed at baseline, and after 9 and 16 months of training. Blood was collected during a 75-g OGTT and analyzed for glucose and insulin concentrations with the total area under the glucose and insulin curves used in the analysis. The EX males had significant decreases from baseline to 9 months in body mass (94.8 +/- 12.5 to 89.2 +/- 9.8 kg) and percent fat (28.3 +/- 4.8 to 24.2 +/- 3.9) with no further changes at 16 months. CON females had significant increases in body mass (78.2 +/- 6.4 to 81.1 +/- 8.1 kg) and percent fat (36.6 +/- 4.2 to 37.8 +/- 4.7) from baseline to 16 months. Vo(2) max increased significantly from baseline to 9 months in the EX males (3.67 +/- 0.62 to 4.36 +/- 0.55 L/min) and EX females (2.53 +/- 0.32 to 2.99 +/- 0.42 L/min). For glucose area under the curve, there were no significant differences between EX or CON across the 16 months of the study. For insulin area under the curve, there was a significant decrease for male EX from baseline to 9 months (12,535 +/- 6,114 to 8,390 +/- 4,231 microU/L/180 min). We conclude that regular exercise in healthy, previously sedentary overweight adult males leads to improvements in Vo(2) max and weight loss and a reduction in the insulin concentration required to dispose of a set glucose load. In females, improvement in Vo(2) max without weight loss does not lead to improvement in insulin sensitivity.

Adolescent↗

Exercise training and responsiveness of isolated coronary arteries.

Exercise is associated with release of catecholamines and vasoactive intestinal polypeptides. Recurrent exposure to catecholamines modifies the sensitivity of adrenoceptors. To test the hypothesis that exercise training may affect the sensitivity of the epicardial coronary arteries, we performed studies on isolated coronary arteries from male dogs capable of running on a treadmill. The animals were separated randomly into two groups: sedentary and exercise training. After 11 wk, rings of left circumflex and left anterior descending coronary arteries were studied in vitro. Contractions to alpha 1-adrenergic agonists (norepinephrine and phenylephrine) were not affected by exercise training. During contractions with prostaglandin F2 alpha, endothelium-dependent relaxations to alpha 2-adrenergic agonists (norepinephrine and UK 14304) were not reduced significantly by exercise training. The concentration-relaxation curves to beta-adrenergic agonists (norepinephrine, isoproterenol, and epinephrine) were shifted to the right after training. The concentration-response curves to vasoactive intestinal polypeptide, but not that to substance P, were shifted to the right in rings with endothelium from exercise-trained animals. These findings demonstrate a decrease in responsiveness of canine vascular smooth muscle to beta-adrenergic agonists and to vasoactive intestinal polypeptide after exercise training.

Animals↗

Exercise training and substrate utilisation in obesity.

Together with diet and behavioural modification, regular exercise is one of the key components of programs for the treatment of obesity. It appears to be one of the major factors determining the long-term success of weight loss programs. One of the mechanisms that may underlie this and other beneficial effects of regular exercise is the effect of exercise training on substrate utilisation. Exercise training increases fat oxidation in lean subjects. The capacity to mobilise and oxidise fat has been shown to be impaired in obese and post-obese subjects. Thus, an increase in the capacity for fat oxidation may help to maintain fat and energy balance at a lower fat mass in individuals with a predisposition for obesity. However, in view of the impaired fat oxidation in obese and post-obese individuals the question arises whether exercise training also increases fat oxidation in the obese. Few studies have addressed this question and have investigated the effect of exercise training on substrate utilisation in obesity. Addition of an exercise training program has been shown to prevent the reduction of basal fat oxidation that is associated with diet-induced weight loss in two studies. No effect of additional exercise training on substrate oxidation during exercise was found. In post-obese subjects exercise training caused no change in 24 h substrate oxidation in one study and increased carbohydrate, rather than fat oxidation in another. In obese subjects neither low (40% maximal aerobic fitness (VO2max)) nor high (70% VO2max) intensity training was found to affect resting substrate oxidation. During exercise fractional fat oxidation was increased after low, but not after high intensity training. The question, whether exercise training increases fat oxidation in obese and post-obese as in lean subjects therefore cannot be answered conclusively at this point in time and requires further study. The role of exercise intensity and type of exercise needs to be studied as well.

Adipose Tissue↗