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PubMed1991

Exercise training depletes sarcoplasmic reticulum calcium in coronary smooth muscle.

We examined the effects of chronic exercise training on sarcoplasmic reticulum (SR) Ca uptake, spontaneous SR Ca release, and whole-cell currents in coronary smooth muscle cells. Single coronary artery smooth muscle cells demonstrated increases in intracellular free Ca (Cai) during depolarization (measured with fura-2) that were abolished by diltiazem (10(-4) M). Diltiazem significantly inhibited (80%) refilling of the SR Ca store. The SR Ca store of exercise-trained pigs was 64% less after 11 min vs. 2 min of recovery, whereas cells from sedentary pigs showed no depletion. Exercise-training-induced depletion of the SR Ca store was abolished when ryanodine (10(-5) M) was applied during the recovery, but depletion was enhanced by low concentrations of ryanodine (10(-8) M). In smooth muscle from sedentary pigs, 10(-8) M ryanodine mimicked the effects of exercise training by depleting the SR Ca store during 11 min of recovery (54% depletion). When allowed a longer recovery without ryanodine (14 min or without prior depolarization), the SR Ca store in cells from exercise-trained pigs returned toward peak levels. The outward K current vs. voltage relationship did not differ in cells from exercise-trained or sedentary pigs. Exercise training reduced the number of spontaneous transient outward currents normally found in cells from sedentary pigs. We introduce a model that provides a rational basis to explain the results obtained in this study.

Animals↗

PubMed2003

Altered single cell force-velocity and power properties in exercise-trained rat myocardium.

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. The ability of the myocardium to perform external work is a critical aspect of ventricular function, but previous studies of myocardial adaptation to exercise training have been limited to measurements of isometric tension or unloaded shortening velocity, conditions in which work output is zero. We measured force-velocity properties in single permeabilized myocyte preparations to determine the effect of exercise training on loaded shortening and power output. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from T and C hearts, chemically skinned, and attached to a force transducer. Shortening velocity was determined during loaded contractions at 15 degrees C by using a force-clamp technique. Power output was calculated by multiplying force times velocity values. We found that unloaded shortening velocity was not significantly different in T vs. C myocytes (T = 1.43 muscle lengths/s, n = 46 myocytes; C = 1.12 muscle lengths/s, n = 43 myocytes). Training increased the velocity of loaded shortening and increased peak power output (peak power = 0.16 P/P(o) x muscle length/s for T myocytes; peak power = 0.10 P/P(o) x muscle length/s for C myocytes, where P/P(o) is relative tension). We found no effect of training on myosin heavy chain isoform content. These results suggest that training alters power output properties of single cardiac myocytes and that this adaptation may improve the work capacity of the myocardium.

Algorithms↗

PubMed1978

Adrenocortical function in response to myocardial necrosis in exercise-trained rats.

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone was determined in exercise-trained rats. Virgin, male rats, 100 days of age, were trained for an 11-wk period by treadmill running. Following the training program, rats were subjected to two subcutaneous injections of l-isoproterenol 24 h apart and killed 24 h after the second injection. All exercise-trained rats survived isoproterenol treatment, while 44% of the control rats died. Plasma corticosterone concentrations were elevated only in exercise-trained rats treated with isoproterenol. Control rats treated with isoproterenol had plasma corticosterone concentrations similar to that in control and exercise-treated rats given placebo injections. Exercise training reduced adrenocortical responsiveness to ACTH in vitro, but isoproterenol treatment increased in vitro responsiveness to ACTH in exercise-trained and control rats. Total unstimulated corticosterone secretion rates in vitro were similar. The reason for better rat survival in exercise-trained rats is unknown; however, improved energy metabolism, depressed aldosterone secretion, or both are suggested as reasons for the better survival of exercise-trained rats.

Adrenal Cortex↗

PubMed1983

Effects of exercise training on muscle protein catabolism in uremia.

The effects of exercise training on muscle protein catabolism in uremia were studied in female rats. Rats made uremic by 3/4 nephrectomy were compared with sham-operated control female rats under conditions of exercise training by swimming or no exercise. The release of amino acids from epitrochlearis muscle in vitro was measured. Body weight epitrochlearis muscle weight, and epitrochlearis protein content were similar among groups. Uremia increased the release of phenylalanine and tyrosine 33% and alanine 50% from muscle of sedentary rats. Citrate synthase activity and glycogen content of muscle were increased twofold by exercise in both controls and uremics. Exercise increased the release of alanine (60%), glutamine (50%), and pyruvate (30%) from muscles of control rats, but it decreased to control levels the release of phenylalanine and tyrosine in uremic rats. Alanine release remained elevated. To determine if exercise training increases in vitro muscle sensitivity to insulin, we incubated muscle with and without 0.01 U/ml of insulin. Phenylalanine and tyrosine release was reduced minimally by insulin in both sedentary uremic and control groups. Glucose uptake was enhanced by 55% in both groups. But in the exercised uremic and control groups, insulin reduced phenylalanine and tyrosine release by 50% and increased glucose uptake by 75%. These results suggest that exercise training reduces muscle protein catabolism in uremia; and this reduction is associated with enhanced muscle response to pharmacologic doses of insulin in control and uremic rats.

Amino Acids↗

PubMedDate not supplied

Interaction of exercise training and chronic ethanol ingestion on testicular antioxidant system in rat.

Recent evidence has indicated that exercise as well as ethanol exerts oxidative stress on vital organs/tissues of the body. However, the combination of both on the testicular antioxidant system is not known. This study investigates the interactive effects of exercise training and chronic ethanol ingestion on the testicular antioxidant system in rats. Male Fisher-344 rats were treated as follows: sedentary control (SC); exercise training (ET) for 6.5 weeks; ethanol (2 g kg(-1), p.o.) for 6.5 weeks; and ET plus ethanol for 6.5 weeks. Exercise training significantly decreased copper-zinc superoxide dismutase (CuZn-SOD) activity and enzyme protein concentration (73% and 67% of SC), whereas manganese SOD (Mn-SOD) and catalase (CAT) activity significantly increased (157% and 141% of SC) in the testes of rat. Exercise training significantly decreased the testicular malondialdehyde (MDA) concentration (70% of SC). Chronic ethanol ingestion significantly decreased testicular CuZn-SOD activity, enzyme protein concentration and CAT activity (65, 70 and 47% of SC) in rats. Ethanol significantly increased the testicular MDA level (129% of SC). The combination of exercise training and chronic ethanol ingestion significantly decreased testicular CuZn-SOD protein, MDA and the reduced glutathione oxidized glutathione ratio (GSH/GSSG) by 62, 70 and 79%, respectively. The data suggest that exercise training provides protection whereas chronic ethanol ingestion exerts oxidative damage to the testes of rat. Exercise training seems to reduce the extent of oxidative damage caused by ethanol on the testes of rats.

Animals↗

PubMed2000

Effects of high-fat diet and exercise training on intracellular glucose metabolism in rats.

We examined the effects of high-fat diet (HFD) and exercise training on insulin-stimulated whole body glucose fluxes and several key steps of glucose metabolism in skeletal muscle. Rats were maintained for 3 wk on either low-fat (LFD) or high-fat diet with or without exercise training (swimming for 3 h per day). After the 3-wk diet/exercise treatments, animals underwent hyperinsulinemic euglycemic clamp experiments for measurements of insulin-stimulated whole body glucose fluxes. In addition, muscle samples were taken at the end of the clamps for measurements of glucose 6-phosphate (G-6-P) and GLUT-4 protein contents, hexokinase, and glycogen synthase (GS) activities. Insulin-stimulated glucose uptake was decreased by HFD and increased by exercise training (P < 0.01 for both). The opposite effects of HFD and exercise training on insulin-stimulated glucose uptake were associated with similar increases in muscle G-6-P levels (P < 0.05 for both). However, the increase in G-6-P level was accompanied by decreased GS activity without changes in GLUT-4 protein content and hexokinase activities in the HFD group. In contrast, the increase in G-6-P level in the exercise-trained group was accompanied by increased GLUT-4 protein content and hexokinase II (cytosolic) and GS activities. These results suggest that HFD and exercise training affect insulin sensitivity by acting predominantly on different steps of intracellular glucose metabolism. High-fat feeding appears to induce insulin resistance by affecting predominantly steps distal to G-6-P (e.g., glycolysis and glycogen synthesis). Exercise training affected multiple steps of glucose metabolism both proximal and distal to G-6-P. However, increased muscle G-6-P levels in the face of increased glucose metabolic fluxes suggest that the effect of exercise training is quantitatively more prominent on the steps proximal to G-6-P (i.e., glucose transport and phosphorylation).

Animals↗

PubMed1996

The interaction between short-term exercise training and a diuretic-induced hypovolemic stimulus.

Nine healthy untrained males [mean (SEM) age, 20.2 (1) years; peak oxygen uptake (VO2max, 48.2 (2) ml.kg-1.min-1] took part in a study to examine whether short-term exercise training (cycle exercise 2 h.day-1 for 3 days at 60% VO2max), which normally results in an expansion of plasma volume (PV), can counteract a diuretic-induced hypovolemic stimulus (100 mg triamterene + 50 mg hydrochlorothiazide.day-1 for 5 days concurrent with exercise training) and restore PV to control levels. Resting and exercise responses (90 min, 60% VO2max) in the diuretic plus exercise training condition (D+E) were compared to a control (C) and a diuretic (D) condition in which no exercise was performed. Following the short-term training, PV was still decreased (P < 0.05) below C by -8.3 (3)% in D+E and was similar (P > 0.05) to the reduction in D [-12.4 (2)%]. The reduced PV in response to the diuretic was associated with similar (P > 0.05) elevations in resting aldosterone (ALDO) and norepinephrine (NOREPI) levels (ng.100 ml-1) in D [101 (12), 61 (4)] and D+E [85 (16), 60 (10)] above (P < 0.05) C [22 (5), 37 (4)]. During exercise, ALDO levels were increased (P < 0.05) by 66 (5) and 70 (10) ng.100 ml-1 in D and D+E, respectively, and the increase was greater (P < 0.05) than C [44 (8) ng.100 ml-1]. The rise in NOREPI during exercise was lower (P < 0.05) in D+E [164 (44) ng.100 ml-1] than in D [244 (24) ng.100 ml-1] with levels similar to C [176 (25) ng.100 ml-1]. Thus, the ALDO response to the diuretic was heightened at rest and during exercise but was not additionally affected by the short-term training session. Results suggest that 3 days of exercise training are unable to counteract the hypovolemic effects of a diuretic and restore PV to control levels despite chronic elevations in NOREPI and ALDO.

Adult↗

PubMed2006

Effect of aerobic exercise training on blood pressure sensitivity to dietary sodium in older hypertensives.

Although aerobic exercise training has been shown to lower blood pressure (BP) in older adults, its effect on BP sensitivity to dietary sodium (Na(+)) is unknown. Therefore, the present study was undertaken to examine the effect of aerobic exercise training on BP sensitivity to dietary Na(+) in older hypertensive individuals. Blood pressure was measured after 8 days of low (20 mEq) and high (200 mEq) Na(+) diets in 31 older (63+/-7 years, mean+/-standard deviation), hypertensive (152+/-11/88+/-5 mm Hg) individuals at baseline and following 6 months of aerobic exercise training (at 75% VO(2)max, 3 times/week, 40 min/session). Subjects were grouped on the basis of the difference in mean arterial BP (MAP) between diets (Na(+) sensitive: >or=5 mm Hg increase in MAP on high Na(+), n=20; Na(+) resistant: <5 mm Hg increase in MAP on the high Na(+) diet, n=11). Following 6 months of aerobic exercise training, there was a significant increase in maximal aerobic capacity (VO(2)max: 18.3+/-3.8 vs 20.7+/-4.2 ml/kg/min, P<0.017). Aerobic exercise training had a significant (P=0.02) effect on Na(+) sensitivity status, with the proportion of Na(+)-resistant individuals increasing from 35% at baseline to 61% following the 6-month aerobic exercise training programme. This study demonstrates the importance of physical activity on BP sensitivity to dietary Na(+).

Aging↗

PubMed1993

Effect of exercise training on left ventricular performance in older women free of cardiopulmonary disease.

Endurance exercise training increases aerobic exercise capacity (maximal oxygen consumption rate [VO2max]) and attenuates the age-related decline in left ventricular (LV) function during exercise in older men. To determine whether similar adaptations occur in older women, 10 subjects (aged 63 +/- 4 years mean +/- SE) were studied before and after 9 to 12 months of endurance exercise training. They exercised 3.85 +/- 0.06 days/week at 81 +/- 0.3% of maximal heart rate. LV function at rest and during supine exercise was assessed by radionuclide ventriculography. VO2max was increased by 21% (from 1.40 +/- 0.1 to 1.7 +/- 0.1 liter/min; p < 0.001) in response to training. Maximal heart rate and systolic blood pressure during treadmill exercise were unchanged (161 +/- 5 beats/min before vs 164 +/- 3 beats/min after; p = NS, and 208 +/- 7 mm Hg before vs 214 +/- 8 mm Hg after; p = NS, respectively) after training. LV ejection fraction at rest (70.4 +/- 2% before vs 70 +/- 1% after) and during peak exercise (78.6 +/- 2% before vs 79.3 +/- 2% after) did not change in response to training. Furthermore, the increases in ejection fraction from rest to exercise were similar before and after training (change: 8.8 +/- 1 vs 9.1 +/- 1%). Stroke volume and cardiac output at peak exercise also did not change in response to training.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed2001

Effects of exercise training of 8 weeks and detraining on plasma levels of endothelium-derived factors, endothelin-1 and nitric oxide, in healthy young humans.

Vascular endothelial cells produce nitric oxide (NO), which is a potent vasodilator substance and has been proposed as having antiatherosclerotic property. Vascular endothelial cells also produce endothelin-1 (ET-1), which is a potent vasoconstrictor peptide and has potent proliferating activity on vascular smooth muscle cells. Therefore, ET-1 has been implicated in the progression of atheromatous vascular disease. Because exercise training has been reported to produce an alteration in the function of vascular endothelial cells in animals, we hypothesized that exercise training influences the production of NO and ET-1 in humans. The purpose of the present study was to examine whether chronic exercise could influence the plasma levels of NO (measured as the stable end product of NO, i.e., nitrite/nitrate [NOx]) and ET-1 in humans. Eight healthy young subjects (20.3 +/- 0.5 yr old) participated in the study and exercised by cycling on a leg ergometer (70% VO2max for 1 hour, 3-4 days/week) for 8 weeks. Venous plasma concentrations of NOx and ET-1 were measured before and after (immediately before the end of 8-week exercise training) the exercise training, and also after the 4th and 8th week after the cessation of training. The VO2max significantly increased after exercise training. After the exercise training, the plasma concentration of NOx significantly increased (30.69 +/- 3.20 vs. 48.64 +/- 8.16 micromol/L, p < 0.05), and the plasma concentration of ET-1 significantly decreased (1.65 +/- 0.14 vs. 1.23 +/- 0.12 pg/mL, p < 0.05). The increase in NOx level and the decrease in ET-1 level lasted to the 4th week after the cessation of exercise training and these levels (levels of NOx and ET-1) returned to the basal levels (the levels before the exercise training) in the 8th week after the cessation of exercise training. There was a significant negative correlation between plasma NOx concentration and plasma ET-1 concentration. The present study suggests that chronic exercise causes an increase in production of NO and a decrease in production of ET-1 in humans, which may produce beneficial effects (i.e., vasodilative and antiatherosclerotic) on the cardiovascular system.

Adult↗

PubMed2005

Functional coupling of adenine nucleotide translocase and mitochondrial creatine kinase is enhanced after exercise training in lung transplant skeletal muscle.

Mechanisms responsible for limitation of exercise capacity in lung transplant recipients (LR) and benefits gained by exercise training were studied. Mitochondrial respiration parameters, energy transfer, and cell structure were assessed in vastus lateralis biopsies using the permeabilized fiber technique with histochemical and morphometric measurements. Twelve male controls (C) and 12 LR performed exercise training over 12 wk. Before exercise training, there were strong correlations between exercise capacity (maximal O(2) consumption and endurance time at 70% maximal power output) and cellular events, as assessed by percentage of type I fibers and apparent K(m) for exogenous ADP. Anticalcineurins were not involved in LR exercise limitation, since there were no differences in maximal mitochondrial rate of respiration before exercise training and no abnormalities in respiratory chain complexes compared with C. Training resulted in a significant increase in physiological parameters both at the cellular (apparent K(m) for exogenous ADP and stimulating effect of creatine) and integrated (maximal O(2) consumption, power output at ventilatory threshold, maximal power output, and endurance time at 70% maximal power output) levels in LR and C. After the training period, improvements in maximal O(2) consumption and in maximal mitochondrial rate of respiration were noted, as well as changes in endurance time and percentage of type I fibers. Because there were no changes in diameters and fiber types, baseline alteration of apparent K(m) for exogenous ADP and its improvement after training might be related to changes within the intracellular energetic units. After the training period, intracellular energetic units exhibited a higher control of mitochondrial respiration by creatine linked to a more efficient functional coupling adenine nucleotide translocase-mitochondrial creatine kinase, resulting in better exercise performances in C and LR.

Adaptation, Physiological↗

PubMed2000

Effects of exercise training on LV performance and mortality in a murine model of dilated cardiomyopathy.

Dilated cardiomyopathy (DC) is a leading cause of cardiovascular morbidity, and nonpharmacological therapies, such as exercise training, have been suggested. The effects of exercise on left ventricular (LV) function and mortality remain controversial. Using a recently described murine model of DC, which involves a dominant-negative form of the cAMP response element binding protein (CREB) transcription factor (CREB(A133)) under the control of the cardiac myocyte-specific alpha-myosin heavy chain promoter, we sought to assess the effects of moderate-intensity exercise training on LV performance and mortality. Thirty-two transgenic mice were subjected to exercise training and compared with sedentary controls. There was progressive enlargement in LV dimensions in both the sedentary and exercise-trained mice. LV performance was progressively impaired, and exercise training did not prevent this decline. The sedentary CREB(A133) mice displayed a significantly increased rate of death, and exercise training did not prevent or delay this excess mortality. The CREB(A133) murine model of inherited DC demonstrated progressive ventricular dilatation and dysfunction with increased mortality, which was not altered with 12 wk of moderate-intensity exercise training.

Animals↗

PubMed2003

Enhanced expression of neuronal nitric oxide synthase in islets of exercise-trained rats.

It is well known that glucose-stimulated insulin secretion (GSIS) decreases after exercise training. In the present study, we investigated the effects of exercise training (9 weeks of running) on the activity of glucokinase (GK), the production of nitric oxide (NO), and the protein expressions of both glucose transporter-2 (GLUT-2) and NO synthase (NOS) in rat pancreatic islets. Exercise training significantly reduced GSIS, with decreases in GK activity and GLUT-2 protein expression. The NO releases and cGMP contents were higher in the islets of trained rats than in those of control rats. Exercise training enhanced cNOS activity, the protein expression of both neuronal nitric oxide synthase (nNOS) and calmodulin, and NADPH-cytochrome c reductase activity in the homogenates of islets. Thus, exercise training-induced reduction of GSIS would result from, at least in part, decreases in both glucose entry and the first step in glycolytic utilization of glucose. Moreover, exercise training could enhance the protein expression of nNOS, which in turn enhances two catalytic activities of nNOS, an NO production and a cytochrome c reductase activity.

Animals↗

PubMed1983

Effect of confinement in small space flight size cages on insulin sensitivity of exercise-trained rats.

Previous studies on men under conditions of total bed rest, and laboratory animals under limited physical activity, have shown resistance to insulin-induced glucose uptake and, conversely, increased sensitivity to insulin with exercise training. To determine whether the beneficial effects of exercise training on increasing insulin sensitivity are lost following end of exercise and confinement in small cages, oral glucose tolerance tests (OGTT) were given to control and exercise-trained rats before and after placement in small space flight size cages (11 X 4 X 4 1/2 in) for 7 d. The product of the area of the insulin and glucose curves of the OGTT (IG index) provides a measure of insulin resistance. Values obtained, before confinement, were one-half as high in exercise-trained rats as those in control rats (p less than 0.001), reflecting increased sensitivity to insulin with exercise training. After 7 d confinement, the IG index was not significantly different from initial values for both control and exercise-trained rats. These findings indicate that increased insulin sensitivity in exercise-trained rats persists 7 d after cessation of running activity. Furthermore, the data suggest that exercise training, before flight, may be beneficial in minimizing the loss of insulin sensitivity expected with decreased use of gravity dependent muscles during exposure to hypogravity in space flight.

Animals↗

PubMed2005

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats.

Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure (CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well-defined animal model of heart failure (HF), using the lean male spontaneously hypertensive HF (SHHF) rat. In this model, animals typically present with decompensated, dilated HF between approximately 18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise-trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low-intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival (P < 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain (MyHC) isoform shift from alpha- to beta-MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length (approximately 6%), width, and area and prevented the increase in the length-to-width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low-intensity exercise training. No significant alterations in sarco(endo)plasmic reticulum Ca2+ ATPase, phospholamban, or Na+/Ca2+ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low-intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF.

Animals↗

PubMed1989

Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance.

We have recently demonstrated that exercise training can induce important hemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examines the accompanying changes in submaximal exercise performance and the ventilatory response to exercise in these patients. Before and after 16-24 weeks of exercise training, subjects underwent two symptom-limited bicycle exercise tests, one with an incremental graded workload, and one with a constant workload that represented 79 +/- 11% of the pretraining peak oxygen consumption. Breath-by-breath expired gas analysis was performed continuously during each test, and central hemodynamic, leg blood flow, and blood lactate measurements were obtained during the incremental protocol. The ventilatory anaerobic threshold was determined during the incremental exercise study from coplotted breath-by-breath ventilatory data with standard criteria by observers who were unaware of patient identity or training status. As previously reported, exercise training increased peak oxygen consumption by 23% from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min and reduced blood lactate levels during submaximal exercise. The training-induced decrease in lactate accumulation was accompanied by a decrease in carbon dioxide production, respiratory exchange ratio, and ventilation during submaximal exercise. The ventilatory anaerobic threshold was delayed from 284 +/- 43 to 352 +/- 91 seconds of exercise (p = 0.02), and it occurred at an increased oxygen consumption (10.1 +/- 1.2 vs. 12.1 +/- 2.6 ml/kg/min, p = 0.01). Exercise duration during the constant workload protocol increased from 938 +/- 410 to 1,429 +/- 691 seconds (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1996

Antioxidant enzymes response to endurance exercise training and dietary proteins in rat skeletal muscle and liver.

This study was conducted to observe the effects of endurance exercise training on antioxidant enzyme activity in the liver and gastrocnemius muscle of rats being fed dietary casein and soy protein. The respective influences of dietary casein and soy protein on the activity of antioxidant enzymes were also compared. Thirty-nine male Wistar rats, aged 3 weeks, were randomly assigned to six groups: a normal protein control group, a normal protein endurance training group, a casein protein control group, a casein protein endurance training group, a soy protein control group, and a soy protein endurance training group. The endurance exercise training groups were adapted to a treadmill for 2 weeks prior to the date the rats were forced to run for 60 min at 25 m/min, 5 days/week for 12 weeks. We found that antioxidant enzyme activity in the gastrocnemius muscle was neither effected by the dietary proteins (casein and soy protein) nor by the above endurance exercise training load. However, hepatic Cu,Zn-SOD activity increased significantly for the dietary casein and soy protein diet groups as compared with the normal protein diet group (P < 0.01). Furthermore, significant increases both in hepatic Cu,Zn-SOD activity in the normal protein group and hepatic GSHpx activity in the casein and soy protein groups were observed when rats were loaded with 25 m/min of endurance exercise training (P < 0.01). These results suggest that, under the above experimental conditions, a casein or soy protein diet increase hepatic Cu,Zn-SOD activity, while endurance exercise training is effective in increasing hepatic Cu;Zn-SOD activity on a normal protein diet and in increasing hepatic GSHpx activity for cysteine and methionine deficient diets.

Animals↗

PubMed1998

Effects of short-term forearm exercise training on resistance vessel endothelial function in normal subjects and patients with heart failure.

BACKGROUND: Exercise training improves endothelium-dependent vasodilation in animals. This study was designed to determine whether forearm exercise training improves endothelium-dependent vasodilation in control subjects and patients with heart failure, a disease associated with abnormal endothelium-dependent vasodilation. METHODS AND RESULTS: We used strain gauge plethysmography to assess the effects of short-term forearm exercise training on resistance vessel function in 11 control subjects and 7 patients with New York Heart Association class II and III heart failure. Subjects performed 30 minutes of handgrip exercise four times a week for 4-6 weeks. In the control subjects, exercise training increased forearm blood flow (FBF) responses to intra-arterial acetylcholine (20 microg/min) from 6.9 +/- 3.1 to 12.2 +/- 3.0 mL/min/100 mL and peak reactive hyperemic FBF responses from 38.1 +/- 5.6 to 47.4 +/- 5.6 (P < .05). Basal FBF and responses to nitroprusside, L-N-monomethyl arginine and acute forearm exercise were not significantly changed. In the patients with heart failure, chronic forearm exercise did not significantly change any of the above-measured parameters. CONCLUSION: Forearm exercise training improves endothelium-dependent vasodilation and peak hyperemic FBF in control subjects but not in patients with heart failure. These data suggest that resistance vessel abnormalities may not be as readily modifiable by exercise training in patients with heart failure compared with control subjects.

Acetylcholine↗