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PubMed1992

Exercise training improves left ventricular contractile response to beta-adrenergic agonist.

To determine whether endurance exercise training can improve left ventricular function in response to beta-adrenergic stimulation, young healthy sedentary subjects (10 women and 6 men) were studied before and after 12 wk of endurance exercise training. Training consisted of 3 days/wk of interval training (running and cycling) and 3 days/wk of continuous running for 40 min. The training resulted in an increase in maximal O2 uptake from 41.0 +/- 2 to 49.3 +/- 2 ml.kg-1.min-1 (P less than 0.01). Left ventricular function was evaluated by two-dimensional echocardiography under basal conditions and during beta-adrenergic stimulation induced by isoproterenol infusion. Fractional shortening (FS) under basal conditions was unchanged after training (36 +/- 1 vs. 36 +/- 2%). During the highest dose of isoproterenol, FS was 52 +/- 1% before and 56 +/- 1% after training (P less than 0.05). At comparable changes in end-systolic wall stress (sigma es), the increase in FS induced by isoproterenol was significantly larger after training (13 +/- 1 vs. 17 +/- 2%, P less than 0.01). Furthermore there was a greater decrease in end-systolic dimension at similar changes in sigma es in the trained state during isoproterenol infusion (-4.6 +/- 0.1 mm before vs. -7.0 +/- 0.1 mm after training, P less than 0.01). There were no concurrent changes in end-diastolic dimension between the trained and untrained states during isoproterenol infusion, suggesting no significant changes in preload at comparable levels of sigma es.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2000

Psychological response to exercise training and/or energy restriction in obese women.

OBJECTIVE: The effect of 12 weeks of exercise training (five 45-minute walking sessions/week at 60% to 75% maximum heart rate) and/or moderate energy restriction (4.19 to 5.44 MJ or 1200 to 1300 kcal/day) on psychological general well-being (GWB) and profile of mood states (POMS) was studied in obese women (n = 91, age 45.6 +/- 1.1 years, body mass index 33.1 +/- 0.6 kg/m2). METHODS: Subjects were randomized to one of four groups: control (C); exercise (E); diet (D); and exercise and diet (ED). Psychological variables were measured in all subjects at three timepoints--prestudy, 3 weeks, and poststudy--and analyzed using a 4 x 3 repeated measures design. RESULTS: GWB but not POMS was improved in ED (but not E or D) relative to C poststudy, especially in four of six subscales: freedom from health concern or worry, life satisfaction; cheerful versus depressed mood; and relaxed versus tense feelings. CONCLUSION: These data demonstrate that the combination of moderate energy restriction and exercise training during a 12-week period improves psychological general well-being scores but not mood states in obese subjects.

Adult↗

PubMed1997

Gender-dependent effects of exercise training on serum leptin levels in humans.

Leptin, the product of the ob gene, is elevated in obese humans and appears to be closely related to body fat content. The purpose of the present investigation was to determine the effect of aerobic exercise training on systemic leptin levels in humans. Eighteen sedentary middle-aged men (n = 9) and women (n = 9) who did not differ in aerobic capacity (29.4 +/- 1.2 vs. 27.5 +/- 1.2 ml x kg(-1) x min(-1)) or insulin sensitivity index (3.41 +/- 1.12 vs. 4.88 +/- 0.55) were studied. Fat mass was significantly lower in females vs. males (21.83 +/- 2.25 vs. 26.99 +/- 2.37 kg, P < 0.05). Despite this, fasting serum leptin was significantly higher in the females vs. males (18.27 +/- 2.55 vs. 9.88 +/- 1.26 ng/ml, P < 0.05). Serum leptin concentration decreased 17.5% in females (P < 0.05) after 12 wk of aerobic exercise training (4 day/wk, 30-45 min/day) but was not significantly reduced in males. Fat mass was not altered after training in either group. In contrast, both aerobic capacity (+13% males, +9.1% females) and insulin sensitivity (+35% males, +82% females) were significantly improved subsequent to training. These data suggest that 1) women have higher circulating leptin concentrations despite lower fat mass and 2) exercise training appears to have a greater effect on systemic leptin levels in females than in males.

Adult↗

PubMed1976

Exercise training as a therapeutic modality.

At present we have no data to assure us that physical activity changes or prevents the development of coronary atherosclerosis or that it changes the progression of the disease which is already present. The data are excellent that in about 85% of patients with coronary disease, exercise training has beneficial personal and societal effects. However, even this opinion must be subjected to critical scrutiny. Several (controlled and randomized) studies of the effects of exercise training on arteriosclerotic heart disease subjects are in progress, in the United States, in Canada, and in Europe. The National Exercise and Heart Disease Project in the U.S.A has already accessed 600 arteriosclerotic heart disease subjects and expects to attain the target study population of 800 subjects by 1 June 1976. We msut be prepared and willing to accept the results of such rigorously controlled studies. In another four to five years of follow-up, the basis for our present views will be either confirmed or rejected -- although most of us anticipate a validation of our present opinion, viz., exercise training enhances the quality of life, and coping capacity, even though the direct effects on the course of coronary atherosclerosis have not been demonstrated.

Adult↗

PubMed1996

Exercise training mode affects the hemodynamic responses to lower body negative pressure in women.

To determine if different exercise modes used to improve cardiovascular fitness result in differing cardiovascular responses to lower body negative pressure (LBNP) in exercise-trained women, seven chronically exercising female runners (RUN) and 11 swimmers (SWIM) of similar fitness levels maximal oxygen uptake, [VO(2max), mean (SEM) = 50 (2) and 45 (2) ml*kg(-1)*min(-1), respectively; P > 0.05] underwent serial exposures to LBNP at pressures of 0, -1.3, -2.7 and -5.3 kPa (referenced to ambient barometric pressure). Forearm vascular resistance (venous occlusion plethysmography) increased with LBNP but did not differ between groups at any level of LBNP. At 0 and - 1.3 kPa, the total peripheral resistance index (TPRI; impedance cardiography) was significantly (P <0.05) higher in RUN than SWIM [1.118(0.028) vs 0.787 (0.040) at 0 kPa and 1.245 (0.100) vs 0.840 (0.040) 2 kPa*l* min(-1)*m(-2) at -1.3kPa]. At an LBNP of -2.7kPa, stroke index (SI) was significantly higher in SWIM than RUN [57.8(4.6) vs 41.9 (4.0) ml*beat(-1)*m(-2)] while TPRI remained greater in RUN than SWIM. At -5.3 kPa, SWIM exhibited a higher cardiac index [3.232 (0.209) vs 2.447 (0.189) l*min(-1)*m(-2)] and SI [49.4 (4.4) vs 31.0 (4.5) ml *beat(-1)*m(-2)] but reduced heart rate [71(3) vs 83(5) beats . min(-1)] and TPRI [0.968 (0.043) vs 1.655 (0.128) kPa*1*min(-1)* m(-2)]. Mean arterial pressure declined significantly at an LBNP of -5.3 kPa in both groups; pulse pressure was lower (P <0.05) in RUN than SWIM at LBNP values of -2.7 and -5.3 kPa. These data suggest that: (1) female runners experience a greater increase in systemic vasoconstriction even though female swimmers can better maintain their cardiac index at high levels of LBNP, and (2) training mode appears to affect the pulse pressure responses to LBNP in exercise-trained women.

Adult↗

PubMed1990

High-repetitive submaximal treadmill exercise training: effect on normal and dystrophic mice.

Exercise as a treatment for muscular dystrophy is controversial. Whereas vigorous high-resistive exercise increases skeletal muscle degeneration in animals with neuromuscular disorders, the effect of low-intensity, high-repetitive exercise has been conflicting. The purpose of this study was to determine if low-intensity, high-repetitive exercise has a beneficial effect on dystrophic mice. Dystrophy mice and unaffected littermates were exercised daily starting at age three weeks on a treadmill (4 m/min, 18 degrees incline, 100 meters, three weeks' duration). Exercise increased the dystrophic soleus twitch tension, the rate of twitch tension development, and the rate of twitch tension relaxation by 55%, 58%, and 48%, respectively (p less than .05). The twitch:tetanus ratio increased by 57% (p less than .05). Both the soleus and the extensor digitorum longus from the exercised dystrophic mice had significantly less degeneration (as shown by reduced internal nuclei, necrosis, fiber splitting, and moth-eaten fibers) than the nonexercised dystrophic mice (p less than .05). This study suggests that exercise training programs can be beneficial or at least not result in further muscle fiber degeneration if (1) the exercise program is started early in the course of the disease; (2) submaximal high-repetitive or even high-resistive exercise is used; and (3) the histopathologic degeneration is slowly progressive or in an arrested state.

Animals↗

PubMedDate not supplied

Exercise training and mouse mammary tumour metastasis.

The present study was designed to address whether exercise influences the experimental metastasis of a mouse mammary tumour; a related issue was the impact of timing of exercise onset relative to tumour exposure on NK and LAK mediated cytotoxicity. After 8 weeks of forced treadmill exercise or voluntary wheel running or remaining sedentary, female BALB/c mice received an intravenous (i.v.) injection of female BALB/c mice received an intravenous (i.v.) injection of MMT line 66 tumour cells. Mice were then randomized into continuation of activity (TT, WW), cessation of activity (TS, WS), initiation of activity (ST, SW) and maintenance of sedentary condition (SS) for three weeks. Tumour control (TC) mice, who were matched to the SS mice for age, received an i.v. injection of heat-killed MMT 66 tumour cells. In total there were 8 groups including the tumour control. The average number of lung tumours did not differ by activity condition; however, the mice in the continuous treadmill group (TT) tended to have a higher tumour multiplicity (162 +/- 22) and those in the treadmill x sedentary condition (TS) tended to have lower tumour multiplicity (109 +/- 16) compared with the other groups except the SW group (95 +/- 15). The lymphokine activated killer activity in the spleen was significantly elevated in the TS (49 +/- 3%) and WS (44 +/- 3%) mice compared with the sedentary animals (30 +/- 3%) (p < 0.003 and 0.05, respectively). NK activity was lower in the mice that had stopped exercising (TS and WS) after injection of tumour compared with sedentary animals. These data suggest that although exercise training influences natural immune cytotoxic mechanisms in vitro, this may not translate into clinically significant changes in tumour burden. The dissociation between natural immunity and tumour outcome may reflect the relative resistance of the tumour line to lysis by natural killer cells. It remains to be tested if infusion of IL-2 (to induce LAK activity) in exercise trained animals results in fewer tumour metastases.

Animals↗

PubMed2006

Moderate exercise training improves functional capacity, quality of life, and endothelium-dependent vasodilation in chronic heart failure patients with implantable cardioverter defibrillators and cardiac resynchronization therapy.

BACKGROUND: The objective of this study was to determine the effects of a moderate exercise training program on functional capacity, quality of life, and hospital readmission rate in chronic heart failure patients with implantable cardioverter defibrillators and cardiac resynchronization therapy. METHODS AND RESULTS: We studied 52 men (mean age 55+/-10 years, ejection fraction 31+/-7%) in chronic heart failure II (n=29) and III (n=23) NYHA functional class with ischemic cardiomyopathy who received implantable cardioverter defibrillators with or without cardiac resynchronization therapy. Patients were randomized into two groups. Group T (n=30 patients, 15 implantable cardioverter defibrillator, 15 implantable cardioverter defibrillator+cardiac resynchronization therapy) underwent a supervised exercise training program at 60% of peak VO2 three times a week for 8 weeks. Group C (n=22 patients, 12 implantable cardioverter defibrillator, 10 implantable cardioverter defibrillator+cardiac resynchronization therapy) avoided physical training. At 8 weeks, only trained patients had improvements in peak VO2 (P<0.01 versus C), endothelium-dependent dilatation of the brachial artery (P<0.001 versus C) and quality of life (P<0.001 versus C). Among trained patients, those with cardiac resynchronization therapy had greater improvements in peak VO2 and quality of life. During the follow-up (24+/-6 months), eight controls had sustained ventricular tachycardia requiring hospital readmission, while no trained patients had adverse events (log rank 8.56; P<0.001). The improvement in peak VO2 was correlated with the improvement in endothelium-dependent dilatation (r=0.65). CONCLUSION: Moderate exercise training is safe and has beneficial effects after implantable cardioverter defibrillator implantation, especially when cardiac resynchronization therapy is present. These effects are associated with improvement in quality of life and outcome.

Adult↗

PubMed1994

Influence of endurance exercise training on distribution of vascular adaptations in rat skeletal muscle.

We hypothesized that an exercise training program consisting of treadmill running at 32 m/min up a 15% incline, 90 min/day, 5 days/wk for 12-14 wk, would elicit vascular adaptation in skeletal muscle of all fiber types in rats. This hypothesis was based on previous reports that this intensity and duration of training caused increases in oxidative capacity in rat skeletal muscle of all fiber types. Skeletal muscle vascular transport capacity was examined with measurements of total and regional (radiolabeled microspheres) flow capacity, capillary filtration coefficient (CFC), and permeability-surface area product (PS) for 51Cr-EDTA in maximally vasodilated (papaverine) hindquarters of control (C; n = 25) and exercise-trained (ET; n = 26) rats. CFC was increased in ET (0.038 +/- 0.001 vs. 0.030 +/- 0.001 ml.min-1 x mmHg-1 x 100 g-1; P < or = 0.001). PS was greater in ET than C (7.80 +/- 0.33 vs. 6.39 +/- 0.37 ml.min-1 x 100 g-1; P < or = 0.01). Citrate synthase activity was increased in the soleus (25%; P < or = 0.05), the medial head (35%; P < or = 0.05), and the red portion of the long head (45%; P < or = 0.005) but not in the white portion of the long head of triceps brachii (P = 0.14) of ET rats. Pressure-flow relationships indicate that total flow was greater (P < or = 0.05) in ET hindquarters at all perfusion pressures. Regional flow data revealed that increases in flow capacity were not evident in muscles composed of all fiber types as predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1996

One year of exercise training does not alter resting left ventricular systolic or diastolic function.

Few studies have examined the effect of prolonged exercise training on left ventricular diastolic function in previously sedentary subjects. We performed M-mode, 2-D, and Doppler echocardiography on 16 previously sedentary men before and after 1 yr of exercise training. Six men served as controls. Exercise subjects participated in four 1-h supervised sessions weekly at 60-80% of their measured maximal heart rate. Maximal oxygen uptake, maximal exercise cardiac output, and resting left ventricular systolic and diastolic function were determined before and after training. Maximal oxygen uptake and peak cardiac output increased 27.3% and 8.5% in the trainers (P < 0.001 for both) and 1.3% and 1.0% in the controls. Left ventricular diastolic and systolic dimensions changed slightly in both groups. Maximal early inflow velocity decreased in both trainers (-9.9 +/- 14.0 cm.s-1, mean +/- SD, P < or = 0.01) and controls (-7.2 +/- 10.2 cm.s-1). Maximal atrial inflow velocity decreased (-7.8 +/- 10.9 cm.s-1, P < or = 0.01) only in the trainers possibly because of a reduction in resting heart rate (-6 +/- 11 beats.m-1, P < or = 0.05). Acceleration and deceleration times were unchanged in both groups. These results demonstrate that substantial increases in exercise performance and exercise cardiac output can occur without detectable changes in resting cardiac dimensions or left ventricular systolic and diastolic function.

Cardiac Output↗

PubMed1996

Interaction of exercise training and clenbuterol on GLUT-4 protein in muscle of obese Zucker rats.

Chronic administration of clenbuterol, a beta 2-adrenergic agonist, attenuates the exercise training-induced improvement in muscle insulin resistance of the obese Zucker rat. The present study was conducted to determine whether clenbuterol also attenuates the increase in muscle GLUT-4 protein that occurs with exercise training and whether the action of clenbuterol is related to its ability to downregulate the beta-adrenergic receptors. Female obese Zucker rats were randomly assigned to one of the following four groups: control (CON, n = 7), clenbuterol (CL, n = 8), exercise training (TR, n = 8), and clenbuterol with exercise training (CL+TR, n = 8). Rats assigned to the training groups were run on a rodent motor-driven treadmill for 6-7 wk. Rats receiving clenbuterol were intubated with 0.8 mg/kg body weight 30 min before running each day. Red quadriceps (RQ) and white quadriceps (WQ) GLUT-4 protein concentrations of TR rats were significantly greater than those of CON and CL+TR rats. The RQ GLUT-4 protein concentration of the CL+TR rats was significantly greater than that of CON rats, but this difference did not occur in the WQ. GLUT-4 protein concentrations were not different between the CON and CL rats. The patterns of RQ and WQ GLUT-4 mRNA were similar to those of their respective GLUT-4 proteins. Rats receiving daily injections of propranolol (30 mg/kg body wt), a beta-adrenergic receptor antagonist, demonstrated no increase in GLUT-4 protein in RQ or WQ after 6 wk of exercise training. These results indicate that 1) clenbuterol can attenuate the increase in muscle GLUT-4 protein associated with exercise training and 2) this effect is likely mediated by a downregulation of the beta-adrenergic receptors.

Adrenergic beta-Agonists↗

PubMed1995

Fiber type-specific effects of clenbuterol and exercise training on insulin-resistant muscle.

The interrelationships among glucose uptake, GLUT-4 protein, and citrate synthase activity in insulin-resistant skeletal muscle were investigated. Female obese (fa/fa) Zucker rats were randomly assigned to treadmill training, ingestion of the selective beta 2-adrenergic agonist clenbuterol, or sedentary control groups. After 7-8 wk of treatment, hindlimbs were perfused to determine maximal insulin-stimulated (10 mU/ml) 2-[3H]deoxy-D-glucose (2-DG) uptake. Exercise training significantly enhanced 2-DG uptake and GLUT-4 protein in red gastrocnemius and plantaris. Alternatively, 2-DG uptake was not altered in soleus after exercise training despite a 52% increase in GLUT-4 protein. The increases in GLUT-4 protein in red gastrocnemius, plantaris, and soleus of the trained rats were accompanied by increases in citrate synthase activity. In contrast to exercise training, clenbuterol administration decreased citrate synthase activity in red and white gastrocnemius, yet had no effect on GLUT-4 protein levels or maximal insulin-stimulated 2-DG uptake. Clenbuterol treatment did, however, increase citrate synthase activity and GLUT-4 protein in soleus. These findings indicate that total GLUT-4 protein largely determines the maximal rate of insulin-stimulated glucose uptake in fast-twitch muscle, whereas in slow-twitch muscle it does not. In addition, the results demonstrate that coordination of proteins governing glucose uptake and disposal may be disrupted in a fiber type-specific manner. Overall, the findings raise important questions as to whether regulation of proteins governing glucose uptake and disposal differs significantly among fiber types.

Animals↗

PubMed2000

Exercise training restores ischemic preconditioning in the aging heart.

OBJECTIVES: To investigate the effects of ischemic preconditioning in hearts from adult and both sedentary and trained senescent rats. BACKGROUND: Ischemic preconditioning does not prevent postischemic dysfunction in the aging heart, probably because of reduction of cardiac norepinephrine release. Exercise training can reverse the age-related decrease of norepinephrine production. METHODS: We investigated the effects on mechanical parameters of ischemic preconditioning against 20 min of global ischemia followed by 40 min of reperfusion in isolated perfused hearts from adult (six months) and sedentary or trained (six weeks of graduated swim training) senescent (24 months) rats. Norepinephrine release in coronary effluent was determined by high-performance liquid chromatography. RESULTS: Final recovery of percent-developed pressure was significantly improved after preconditioning in adult hearts (91.6+/-9.6%) versus unconditioned controls (54.2+/-5.1%, p<0.01). The effect of preconditioning on developed pressure recovery was absent in sedentary but present in trained senescent hearts (39.6+/-4.1% vs. 64.3+/-7.1%, p<0.05). Norepinephrine release significantly increased after preconditioning in adult and in trained but not in sedentary senescent hearts. The depletion of myocardial norepinephrine stores by reserpine abolished preconditioning effects in adult and trained senescent hearts. CONCLUSIONS: In adult and trained but not in sedentary senescent hearts, preconditioning reduces postischemic dysfunction and is associated with an increase in norepinephrine release. Preconditioning was blocked by reserpine in both adult and trained senescent hearts. Thus, exercise training may restore preconditioning in the senescent heart through an increase of norepinephrine release.

Aging↗

PubMed2001

Short-term effects of weight loss with or without low-intensity exercise training on fat metabolism in obese men.

BACKGROUND: Energy restriction is known to induce a decline in fat oxidation during the postdiet period. Reduced fat oxidation may contribute to weight regain. OBJECTIVE: The present study investigated the effect of the addition of low-intensity exercise training to energy restriction on postdiet fat oxidation and on the contribution of the sympathetic nervous system to fat oxidation. DESIGN: Forty obese men were divided randomly into 2 groups: diet (D) and diet plus exercise (DE). Both groups followed an energy restriction program for 10 wk. Subjects in the DE group also participated in a low-intensity exercise training program [40% maximal oxygen uptake (VO2max)] for 12 wk. Before the intervention and after 12 wk, with subjects at stable body weights, we measured body composition, VO2max, and substrate oxidation at rest, during exercise at 50% VO2max, and during recovery. Measurements were made with and without administration of the beta-adrenergic antagonist propranolol. RESULTS: Both interventions led to significant decreases in body weight, fat mass, and fat-free mass (P < 0.001); these decreases did not differ significantly between the D and DE groups. Neither intervention significantly affected VO2max. The effect of the intervention on the respiratory exchange ratio differed significantly between the D and DE groups [two-way analysis of variance (ANOVA), P < 0.05]. The effect on the beta-adrenergic-mediated respiratory exchange ratio tended to be different between the 2 groups (two-way ANOVA, P = 0.09). CONCLUSION: Addition of low-intensity exercise training to energy restriction counteracts the decline in fat oxidation during the postdiet period.

Adrenergic beta-Antagonists↗

PubMed1995

Effects of exercise training and deconditioning on platelet function in men.

Platelets play an important role in the pathogenesis of cardiovascular disease. It has also been noticed that regular exercise can reduce the risk of cardiovascular disease. This is the first study to demonstrate that endurance exercise training may suppress platelet adhesiveness and aggregation and that deconditioning may reverse the training effects. Healthy male sedentary subjects were randomly divided into control and training groups. The trained men were trained on a bicycle ergometer at about 60% of maximal oxygen consumption for 30 minutes per day, 5 days per week for 8 weeks, then deconditioned for 12 weeks. During the experimental period, blood samples of the trained subjects were collected before and immediately after a progressive exercise test every 4 weeks. The same experiments were applied to the controls at the beginning of this study and 8 weeks thereafter. A tapered parallel-plate chamber was used to assess platelet adhesiveness. Platelet aggregation induced by ADP was evaluated by the percentage of reduction in single platelet count. Our results showed that (1) platelet adhesiveness and aggregability were increased by short-term strenuous exercise in both control and trained groups, but the enhancement of platelet aggregability was decreased after exercise training in the trained subjects; (2) at rest and immediately after strenuous exercise, platelet adhesiveness and aggregability were decreased by training, whereas they were unchanged in the control group; and (3) deconditioning reversed the training effects on resting and postexercise platelet adhesiveness and aggregability back to the pretraining state. These results suggest that platelet adhesiveness and aggregability may be depressed by exercise training but be reversed back to the pretraining state after deconditioning.

Blood Platelets↗

PubMed1989

The effect of detraining and reduced training on the physiological adaptations to aerobic exercise training.

In previously sedentary individuals, regularly performed aerobic exercise results in significant improvements in exercise capacity. The development of peak exercise performance, as typified by competitive endurance athletes, is dependent upon several months to years of aerobic training. The physiological adaptations associated with these improvements in both maximal exercise performance, as reflected by increases in maximal oxygen uptake (VO2max), and submaximal exercise endurance include increases in both cardiovascular function and skeletal muscle oxidative capacity. Despite prolonged periods of aerobic training, reductions in maximal and submaximal exercise performance occur within weeks after the cessation of training. These losses in exercise performance coincide with declines in cardiovascular function and muscle metabolic potential. Significant reductions in VO2max have been reported to occur within 2 to 4 weeks of detraining. This initial rapid decline in VO2max is likely related to a corresponding fall in maximal cardiac output which, in turn, appears to be mediated by a reduced stroke volume with little or no change in maximal heart rate. A loss in blood volume appears to, at least partially, account for the decline in stroke volume and VO2max during the initial weeks of detraining, although changes in cardiac hypertrophy, total haemoglobin content, skeletal muscle capillarisation and temperature regulation have been suggested as possible mediating factors. When detraining continues beyond 2 to 4 weeks, further declines in VO2max appear to be a function of corresponding reductions in maximal arterial-venous (mixed) oxygen difference. Whether reductions in oxygen delivery to and/or extraction by working muscle regulates this progressive decline is not readily apparent. Changes in maximal oxygen delivery may result from decreases in total haemoglobin content and/or maximal muscle blood flow and vascular conductance. The declines in skeletal muscle oxidative enzyme activity observed with detraining are not causally linked to changes in VO2max but appear to be functionally related to the accelerated carbohydrate oxidation and lactate production observed during exercise at a given intensity. Alternatively, reductions in submaximal exercise performance may be related to changes in the mean transit time of blood flow through the active muscle and/or the thermoregulatory response (i.e. degree of thermal strain) to exercise. In contrast to the responses observed with detraining, currently available research indicates that the adaptations to aerobic training may be retained for at least several months when training is maintained at a reduced level. Reductions of one- to two-thirds in training frequency and/or duration do not significantly alter VO2max or submaximal endurance time provided the intensity of each exercise session is maintained.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗

PubMed1986

Effects of exercise training on regional adipose tissue metabolism in pregnant rats.

To investigate the effects of intense exercise training on maternal adiposity and fetal development, normal lean Zucker (Fa/Fa) rats were divided into three groups: control nonpregnant (CNP), control pregnant (CP), and exercise-trained pregnant (TRP). Trained rats swam three continuous hours per day, 6 days/wk, throughout pregnancy. Food efficiency increased with pregnancy, the highest values being observed during the last trimester of the gestation period. On day 21, pup number, weight, and body composition were similar for CP and TRP. By day 21 of gestation, in both TRP and CP rats, inguinal adipose tissue weight, cell size, and lipoprotein lipase (LPL) activity increased; although TRP values were smaller (P less than 0.05). In CP rats, parametrial and retroperitoneal adipose tissue weights, cell size, and LPL activities increased throughout pregnancy, whereas TRP values were similar to CNP (P less than 0.05). Parametrial fat cell lipolysis showed, however, no effect of training. These results indicate that the extensive energy expenditure occurring during endurance training selectively reduced the dams' adiposity in a regionally specific fashion without any apparent alteration in pup development. The increased substrate utilization required by training during pregnancy did not, however, modify fat cell lipolysis but rather prevented lipid filling through suppression of LPL activity of some depots.

Adipose Tissue↗

PubMed2005

Low-intensity exercise training during doxorubicin treatment protects against cardiotoxicity.

Doxorubicin (Dox) is a highly effective antineoplastic antibiotic associated with a dose-limiting cardiotoxicity that may result in irreversible cardiomyopathy and heart failure. The purpose of this study was to examine the effects of low-intensity exercise training (LIET) during the course of Dox treatment on cardiac function, myosin heavy chain expression, oxidative stress, and apoptosis activation following treatment. Male Sprague-Dawley rats either remained sedentary or were exercise trained on a motorized treadmill at 15 m/min, 20 min/day, 5 days/wk (Monday through Friday) for 2 wk. During the same 2-wk period, Dox (2.5 mg/kg) or saline was administered intraperitoneally to sedentary and exercised rats 3 days/wk (Monday, Wednesday, Friday) 1-2 h following the exercise training sessions (cumulative Dox dose: 15 mg/kg). Five days following the final injections, hearts were isolated for determination of left ventricular (LV) function, lipid peroxidation, antioxidant enzyme protein expression, 72-kDa heat shock protein expression, caspase-3 activity, and myosin heavy chain isoform expression. Dox treatment significantly impaired LV function and increased caspase-3 activity in sedentary animals (P < 0.05). LIET attenuated the LV dysfunction and apoptotic signal activation induced by Dox treatment and increased glutathione peroxidase expression, but it had no significant effect on lipid peroxidation, protein expression of myosin heavy chain isoforms, 72-kDa heat shock protein, or superoxide dismutase isoforms. In conclusion, our data suggest that LIET applied during chronic Dox treatment protects against cardiac dysfunction following treatment, possibly by enhancing antioxidant defenses and inhibiting apoptosis.

Animals↗