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PubMed1997

Walking performance and economy in chronic heart failure patients pre and post exercise training.

The effect of a 3-week exercise programme on performance and economy of walking was analysed in 16 male patients with chronic heart failure [mean age 51.8 (SD 6.9) years, height 174.9 (SD 6.3) cm, body mass 75.3 (SD 11.5) kg, ejection fraction 20.8 (SD 5.0)%]. They were submitted to a cardiopulmonary exercise test on a cycle ergometer and a 6-min walking test on a treadmill before and after the period of exercise training. The training programme consisted of interval cycle (five times a week for 15 min), and treadmill ergometer training (three times a week for 10 min) at approximately 70% cycling peak oxygen uptake (VO2peak) and supplementary exercises (three times a week for 20 min). Compared to the pre values cycling VO2peak [11.9 (SD 2.9) vs 14.0 (SD 2.3) ml. kg-1.min-1], maximal self paced walking speed [0.68 (SD 0.33) vs 1.16 (SD 0.30) m.s-1], and net walking power [2.16 (SD 0.89) vs 2.73 (SD 0.91) W.kg-1] had increased (P < 0.01) while net energy cost [3.31 (SD 0.66) vs 2.33 (SD 0.38) J.kg-1. m-1] had decreased (P < 0.001) after the training period. Approximately 42% of the increase of walking speed resulted from a higher walking power output, whereas approximately 58% corresponded to a positive effect on walking economy. The improvement in walking economy was a function of an increase in walking velocity itself and a result of a more efficient walking technique. These results would indicate that in patients with marked exercise intolerance, adequate exercise training programmes could contribute to favourable metabolic changes with positive effects on the economy of motion.

Cardiac Output, Low↗

PubMed2000

Chronic exercise training preserves prostaglandin-induced dilation of epicardial coronary artery during development of heart failure in awake dogs.

Although it has been shown that long-term exercise training preserves endothelium-mediated nitric oxide vasodilator function in chronic heart failure (CHF), whether exercise training exerts similar beneficial effects on endothelial/prostaglandin-mediated vasodilator capacity in coronary circulation during the development of CHF has not been determined. Fifteen mongrel dogs were surgically instrumented for measurement of left ventricular pressure, aortic pressure, coronary blood flow and left circumflex coronary artery diameter. Dogs (n = 5) who underwent 4 weeks of cardiac pacing (210 b/min for 3 weeks and 240 b/min for the 4th week) developed CHF as characterized by significant reduction in left ventricular systolic pressure, mean arterial pressure and left ventricular dP/dt, increases in left ventricular end-diastolic pressure and heart rate, as well as clinical signs of CHF. Endothelial prostaglandin-mediated vasodilation of the epicardial coronary artery was impaired, as manifested by an attenuated arachidonic acid (AA)-induced dilation of the artery (epicardial artery diameter increased by: 0.78 +/- 0. 84% in CHF versus 4.6 +/- 0.89% in normal, P < 0.05); however, prostacyclin (PGI(2))-induced and nitroglycerin-induced vasodilation of the coronary circulation were not altered. In contrast, dogs (n = 6) with cardiac pacing plus daily exercise training (4.4 +/- 0.3 km/h, 2 h/day) only developed mild cardiac dysfunction, and the response of the epicardial coronary artery diameter to AA was preserved (epicardial artery diameter increased by 4.2 +/- 0.98% from baseline, P 0.05 compared to its respective control). Thus, long-term exercise training preserves endothelial/prostaglandin-mediated dilation of epicardial coronary artery during development of CHF.

Animals↗

PubMed2005

Augmentation of endothelial function following exercise training is associated with increased L-arginine transport in human heart failure.

We have reported previously a decrease in the clearance of the NO (nitric oxide) precursor L-arginine in the forearm circulation of CHF (congestive heart failure) patients, suggesting a potential rate-limiting mechanism contributing to the common finding of endothelial dysfunction in CHF. Given data that show exercise training augments endothelial function in CHF, the aim of the present study was to investigate whether these improvements were due to an increase in L-arginine transport. Measures of L-arginine transport, endothelial function and exercise capacity were repeated before and after 8 weeks of "usual living" or exercise training in 21 CHF patients [NYHA (New York Heart Association) class II/III]. Exercise capacity (6-min walk test) increased following exercise training (496+/-21 to 561+/-17 m; P=0.005), whereas the control group demonstrated no change [488+/-18 to 484+/-21 m; P=ns (not significant)]. Basal FBF (forearm blood flow) remained stable following exercise training (2.68+/-0.55 to 2.46+/-0.32 ml.min(-1).100 ml(-1) of tissue) and "usual living" (2.16+/-0.37 to 2.91+/-0.55 min(-1).100 ml(-1) of tissue). FBF responses to ACh (acetylcholine) increased following exercise by 49.6+/-17.7% (area under curve; P=0.01) demonstrating augmented endothelial function. FBF responses to SNP (sodium nitroprusside) were also improved following exercise training (30.8+/-8.2%; P=0.02). There was no change in vascular function in the "usual living" group. The clearance of L-arginine was significantly increased following involvement in the exercise programme (69.4+/-7.8 to 101.0+/-9.5 ml/min; P=0.04), whereas there was no change in the "usual living" group (78.4+/-17.5 to 81.0+/-14.9 ml/min; P=ns). In conclusion, the augmentation in endothelial function observed following exercise may be due, in part, to an increase in the transport of L-arginine in CHF patients.

Acetylcholine↗

PubMed2005

Exercise training restores uncoupling protein-3 content in limb muscles of patients with chronic obstructive pulmonary disease.

Oxidative capacity and uncoupling protein-3 (UCP3) content are reduced in limb muscles of patients with chronic obstructive pulmonary disease (COPD). It has been hypothesized that the physiological role of UCP3 is to protect mitochondria against lipotoxicity in cases where fatty acid influx exceeds the capacity to oxidize them. Exercise training improves oxidative capacity and reduces UCP3 protein content in healthy subjects, but the response of UCP3 to training in COPD is unknown. We studied the effect of exercise training on UCP3 content in limb muscles of COPD patients. For this, seven healthy age-matched subjects and thirteen patients with COPD were studied. All patients were admitted to an 8-wk exercise training intervention. Exercise capacity was assessed by means of an incremental cycle ergometry test. Biopsies were taken from the vastus lateralis in which UCP3 and lipid peroxidation levels were determined by Western blotting. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase (HAD; an enzyme involved in fatty acid oxidation) were measured as indexes of muscle oxidative capacity. UCP3 in COPD was approximately 50% lower compared with healthy age-matched controls. In COPD, training induced upregulation of UCP3 [from 67.7 (SD 41.8) to 113.8 (SD 104.2) arbitrary units (AU), P = 0.062], especially in the patients who showed no increase in HAD activity [from 80.9 (SD 52.6) to 167.9 (SD 109.1) AU, P = 0.028], whereas lipid peroxidation levels remained unaltered. We conclude that exercise-training can restore muscle UCP3 protein level in COPD, and the nature of this response complies with the hypothesis that UCP3 may protect against lipotoxicity.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2004

Endurance exercise training inhibits activity of plasma GOT and liver caspase-3 of mice [correction of rats] exposed to stress by induction of heat shock protein 70.

A single bout of exercise increases production of heat shock protein 70 (HSP70), which protects cells against various stresses. In this study, we investigated whether endurance exercise training enhances liver level of HSP70 and, if so, whether HSP70 contributes to hepatic protection against stress in vivo. Mice of an exercise-training group performed 60 min of treadmill running 5 days/wk for 4 wk. The resting level of liver HSP70 was 4.5 times higher in the trained than in sedentary mice. After 4 wk of exercise training, both groups of mice were exposed to the following stresses: 1) heat stress, 2) cold stress, 3) oxidative stress, 4) ethanol stress, and 5) exercise stress by compelling the mice to run on a treadmill until exhausted. After exposure to the stresses, the liver was immediately isolated. Elevation of liver HSP70 in the trained mice was evident, whereas no elevation was found in the sedentary mice. On exposure to heat, diethyldithiocarbamate and ethanol, activities of glutanic oxalacetic transaminase in plasma, and liver caspase-3, a key enzyme of apoptotic processing, were elevated in the sedentary mice but not in the trained mice. These results suggest that exercise training enhanced the resting level of liver HSP70 and hepatic protection against various stresses, at least partly attributing to the suppression of caspase-3 activity by the increase in HSP70.

Adaptation, Physiological↗

PubMed1996

Exercise training versus angioplasty for stable claudication. Long and medium term results of a prospective, randomised trial.

OBJECTIVES: To compare percutaneous transluminal angioplasty (PTA) against exercise training in the treatment of stable claudication. DESIGN: Prospective, randomised trial. MATERIALS: Fifty-six patients with unilateral, stable, lower limb claudication assessed prior to randomisation, at 3 monthly intervals for 15 months, and at approximately 6 years follow-up. Thirty-seven patients were available for long term review. OUTCOME MEASURES: Ankle/brachial pressure index (ABPI), treadmill claudication and maximum walking distances, percentage fall in ankle systolic pressure after exercise. RESULTS: Significant increases were seen in ABPI in the patients treated with PTA at all assessment to 15 months. However in terms of improved walking performance, the most significant changes in claudication and maximum walking distance were seen in the exercise training group. At long term follow-up, there was no significant difference between the groups. Subgroup analysis by angiographic site of disease showed greater functional improvement in those patients with disease confined to the superficial femoral artery treated by exercise training. The overall prognosis for the whole group of patients was benign, with only two (4%) undergoing amputation. CONCLUSIONS: Exercise training confers a greater improvement in claudication and maximum walking distance than PTA, especially in patients with disease confined to the superficial femoral artery.

Angioplasty, Balloon↗

PubMed1999

Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure.

BACKGROUND: Patients with chronic heart failure (CHF) have a markedly increased incidence of malignant ventricular arrhythmias. QT dispersion (QTd), defined as the difference between maximal and minimal QT intervals, reflects the regional inhomogeneity of ventricular repolarization dispersion and may mark the presence of malignant ventricular arrhythmias. PURPOSE: To determine the effects of exercise training on QTd in patients with CHF. PATIENTS: Fifteen patients with CHF and ejection fractions < 40% (mean, 28+/-9%) who were on a stable medical regimen. DESIGN AND INTERVENTION: Standardized 12-lead surface ECGs were obtained at the beginning and end of the exercise training program, and QT and JT intervals were measured manually and corrected for heart rate by using Bazett's formula. QTd, heart rate-corrected QTd (QTc-d), JT dispersion (JTd), and heart rate-corrected JTd (JTc-d) were measured in at least eight ECG leads in each patient. RESULTS: Following the cardiac rehabilitation and exercise training programs, patients with CHF had only slight improvements in exercise capacity (results were not significant). However, these patients had marked improvements in QTd (71+/-11 to 59+/-17 ms; p < 0.02), QTc-d (82+/-28 to 63+/-17 ms; p < 0.01), JTd (76+/-19 to 57+/-18 ms; p < 0.002), and JTc-d (84+/-23 to 61+/-18 ms; p < 0.001) following the exercise training programs. CONCLUSION: These data indicate that aerobic exercise training significantly reduces the indices of ventricular repolarization dispersion in patients with CHF. Further studies are needed to evaluate how effectively this reduction in ventricular repolarization dispersion decreases the risk of malignant ventricular arrhythmias and sudden death in patients with CHF.

Aged↗

PubMed1996

Endothelium-dependent relaxation and hyperpolarization evoked by bradykinin in canine coronary arteries: enhancement by exercise-training.

1. Kinins, which are produced locally in arterial walls, stimulate the release of endothelium-derived vasodilator substances. Therefore, they may participate in the metabolic adaptation to chronic exercise that occurs in the coronary circulation. Experiments were designed to compare the reactivity to bradykinin in coronary arteries isolated from sedentary and exercised-trained dogs (for 8-10 weeks). 2. The organ chambers used in this study were designed for measurement of isometric tension and cell membrane potential with glass microelectrodes. Rings of canine isolated coronary arteries with endothelium were suspended in the organ chambers filled with modified Krebs-Ringer bicarbonate solution (37 degrees C, gassed with 5% CO2 in 95 O2), and were all treated with indomethacin to prevent interference from prostaglandins. 3. Bradykinin evoked concentration-dependent relaxations of the coronary arteries. However, the kinin was significantly less potent in relaxing coronary arteries from the sedentary dogs than those from the trained ones. 4. In the presence of NG-nitro-L-arginine (an inhibitor of nitric oxide synthases), concentration-relaxation curves to bradykinin were shifted to the right in both types of preparations. Nonetheless, the peptide was still significantly more potent in arteries from exercise-trained animals. 5. In the electrophysiological experiments, concentration-hyperpolarization curves to bradykinin obtained in arteries from sedentary dogs were also significantly to the right of those in vessels from exercise-trained animals. Thus, in arteries from exercised animals, bradykinin more potently evoked the release of both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). 7. The angiotensin converting enzyme (ACE)-inhibitor, perindoprilat, shifted to the left the concentration-relaxation curves to bradykinin obtained under control conditions and in the presence of NG-nitro-L-arginine. The concentration-hyperpolarization curves to bradykinin were also shifted to the left by perindoprilat. The shift induced by the ACE-inhibitor in either type of preparation was not significantly different. 8. These findings demonstrate that exercise-training augments the sensitivity of the coronary artery of the dog to the endothelium-dependent effects of bradykinin. This sensitization to bradykinin may reflect an increased role of both NO and EDHF, and is not the consequence of differences in ACE activity in the receptor compartment.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1984

Effect of exercise training on plasma high-density lipoprotein cholesterol level at constant weight.

Previous investigations have demonstrated an increase of plasma high-density lipoprotein cholesterol (HDL-Chol) and a decrease in the ratio of low density lipoprotein (LDL)-Chol/HDL-Chol (Atherogenic Index; AI) as a result of exercise training. The question of whether elevation of HDL-Chol was a consequence of weight reduction or physical training itself was unsolved. The present study was designed to prevent the weight reduction that is associated with exercise training. Five healthy and mildly active male volunteers, aged 28-31 years, participated in a 4-week training programme. They ran on a treadmill at 140-160 m/min at 0% grade for 50 min, 5 times a week, equivalent to an energy expenditure of 9 kcal/kg body weight/day. Subjects maintained their body weights by increasing calorie intake to match increased energy expenditure. No changes were observed in mean body weight, skinfold thickness, basal metabolism, and maximal oxygen uptake after the training programme. The HDL-Chol level increased from 54 to 73 mg/dl (P less than 0.05), and the reduction of AI was 30.8% (P less than 0.05) in response to the exercise training. However, the exercise training did not induce changes in plasma total cholesterol and triglyceride (TG) levels. The results of this experiment suggested that moderate physical training itself can be a potent factor for the regulation of HDL-Chol level and improvement of the AI in the absence of alterations in body weight.

Adult↗

PubMed2002

Beneficial effect on blood pressure and lipid profile by programmed exercise training in Taiwanese patients with mild hypertension.

Mild essential hypertensive patients comprise a large portion of the hypertensive population. Previous reports have shown that moderate-intensity regular exercise training in these patients usually reduces blood pressure. By designing programmed exercise to evaluate whether it is effective in reducing blood pressure in mild hypertensive patients and also has beneficial effects on other biochemical parameters. Twenty-three mild hypertensive Taiwanese patients (resting blood pressure 139.1 +/- 11.4/99.5 +/- 8.0 mmHg) were divided randomly into two groups: control (no exercise) and moderate-intensity exercise (average 6.4 +/- 0.7 METs). The training group exercised three times per week at the prescribed exercise intensity by using the Treadmill exercise test. Blood pressure, heart rate and other biochemical parameters were monitored regularly every 4 weeks for 12 weeks. After 12 weeks regular exercise training, the exercise group showed for significant resting blood pressure reduction. Mean maximal reduction of systolic pressure was 18 mmHg. Significant reduction of total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglyceride were found; elevation of high-density lipoprotein cholesterol (HDL-C) was also noted. These data suggest that after 12 weeks of exercise training in mild hypertensive patients, successful reduction of blood pressure and favorable changes of lipid profile will be noted.

Adult↗

PubMed2002

Exercise training increases lipid metabolism gene expression in human skeletal muscle.

The effects of a single bout of exercise and exercise training on the expression of genes necessary for the transport and beta-oxidation of fatty acids (FA), together with the gene expression of transcription factors implicated in the regulation of FA homeostasis were investigated. Seven human subjects (3 male, 4 female, 28.9 +/- 3.1 yr of age, range 20-42 yr, body mass index 22.6 kg/m(2), range 17-26 kg/m(2)) underwent a 9-day exercise training program of 60 min cycling per day at 63% peak oxygen uptake (VO(2 peak); 104 +/- 14 W). On days 1 and 9 of the program, muscle biopsies were sampled from the vastus lateralis muscle at rest, at the completion of exercise, and again 3 h postexercise. Gene expression of key components of FA transport [FA translocase (FAT/CD36), plasma membrane-associated FA-binding protein], beta-oxidation [carntine palmitoyltransferase(CPT) I, beta-hydroxyacyl-CoA dehydrogenase] and transcriptional control [peroxisome proliferator-activated receptor (PPAR)alpha, PPAR gamma, PPAR gamma coactivator 1, sterol regulatory element-binding protein-1c] were unaltered by exercise when measured at the completion and at 3 h postexercise. Training increased total lipid oxidation by 24% (P < 0.05) for the 1-h cycling bout. This increased capacity for lipid oxidation was accompanied by an increased expression of FAT/CD36 and CPT I mRNA. Similarly, FAT/CD36 protein abundance was also upregulated by exercise training. We conclude that enhanced fat oxidation after exercise training is most closely associated with the genes involved in regulating FA uptake across the plasma membrane (FAT/CD36) and across the mitochondrial membrane (CPT I).

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2006

Exercise training attenuates age-induced elevation in Bax/Bcl-2 ratio, apoptosis, and remodeling in the rat heart.

Aging is characterized by loss of myocytes, remodeling, and impaired contractile function in the heart. The rate of programmed cell death, or "apoptosis," in the left ventricle increases with age, and contributes to a 30% reduction in myocytes. Aging may preferentially target the Bcl-2 pathway of apoptosis in the heart. Exercise can protect cardiac function of the aging heart, although the mechanisms are poorly understood. We tested the hypothesis that 12 wk of exercise training would attenuate age-induced increases in remodeling, apoptosis, and Bax/Bcl-2 ratio in rat left ventricle. We found that exercise training provided significant protection against loss of cardiac myocytes, reduction in number of myonuclei, reactive hypertrophy of remaining myocytes, and increased connective tissue in left ventricle of the aging rat heart. Exercise training significantly attenuated age-induced increases of apoptosis in the left ventricle, as indicated by lower DNA fragmentation, TUNEL-positive staining, and caspase-3 cleavage, when compared with left ventricles from the age-matched sedentary group. Further, exercise training in the aging reduced caspase-9 levels and Bax/Bcl-2 ratio by lowering Bax protein expression while increasing Bcl-2 levels. These are the first data to demonstrate protective effects of endurance exercise training against elevated apoptosis and remodeling in the aging heart.

Aging↗

PubMed1986

[Influence of exercise training on left ventricular performance investigated by two-dimensional echocardiography].

The influence of exercise training on left ventricular performance was investigated by exercise two-dimensional echocardiography in 12 top-ranking Japanese volleyball players and 10 untrained subjects. Left ventricular wall thickness and dimension were greater in the athletes than in the nonathletes. The left ventricular wall thickness-internal radius ratio, however, was nearly the same in both groups. At rest, heart rate, the stroke area index, % fractional area and the cardiac index were significantly lower in the athletes than in the nonathletes. During exercise, heart rate was slower in the athletes at every exercise stress stage. The stroke area index, % fractional area and the cardiac index increased linearly in the athletes, although these indices of the nonathletes reached a plateau at the moderate exercise stage. The double product at the last stage was greater in the athletes than in the nonathletes. Both groups did not differ as to segmental fractional area change of left ventricular contraction at rest and during exercise. Serum norepinephrine concentration was significantly lower in the athletes than in the nonathletes at rest. After exercise, however, the difference between the two groups was not apparent. It is suspected that exercise training increased the exercise capacity due to an increase in the left ventricular systolic function reserve, the increment of cardiac VO2 max, and the change of blood flow distribution, and generalized aerobic metabolism in various organs.

Adult↗

PubMed2003

Interaction of exercise training and chronic NOS inhibition on blood pressure, heart rate, NO and antioxidants in plasma of rats.

Many individuals with cardiovascular diseases undergo periodic exercise conditioning with or without medication. Therefore, the purpose of this study was to examine the effect of exercise training on BP and HR under the condition of NOS inhibition and to clarify the mechanism of the effect in regard to oxidative stress, antioxidant enzyme activity, and NO production in the plasma of the rat. Fisher 344 rats were divided into four groups: (1) sedentary control, (2) exercise training for 8 weeks, (3) nitro-L-arginine methyl ester (L-NAME) (10mg/kg, s.c. for 8 weeks) and (4) ET + L-NAME. Blood pressure (BP) and heart rate (HR) were monitored weekly for 8 weeks. The animals were sacrificed 24h after last treatments, plasma isolated and analyzed. The results show that exercise conditioning resulted in enhanced NO production (120% of control), GSH levels (110% of control), GSH/GSSG ratio (124% of control) and the up-regulation of catalase (CAT) (225% of control), glutathione peroxidase (GSH-Px) (161% of control), glutathione reductase (GR) (142% of control) and glutathione-S-transferase (GST) (189% of control) and depression of malondialdehyde (MDA) (90% of control) and lactate (75% of control) in plasma of the rat. These biochemical changes were accompanied by no significant change in BP but slight increase in HR. Chronic L-NAME administration resulted in depression of NO (84% of control), GSH (90% of control), GSH/GSSG ratio (76% of control), the down-regulation of superoxide dismutase (SOD) (67% of control), GST (74% of control), and GR (90% of control). Plasma CAT and GSH-Px activities, MDA and lactate levels were significantly increased in L-NAME treated rats. The biochemical changes were accompanied by increase in blood pressure and heart rate. Interaction of exercise training and chronic NOS inhibitor treatment resulted in normalization of plasma NO levels, GSH/GSSG ratio, SOD and GST activities, and the up-regulation of, CAT, GSH-Px, and GR activities. The interaction resulted in depletion of plasma MDA levels compared to L-NAME treated group. The biochemical changes were accompanied by decrease in BP and HR compared to L-NAME treated group. The data suggest that the exercise training attenuated the oxidative injury caused by NOS inhibitor by increasing the plasma NO levels, GSH/GSSG ratio and up-regulating the antioxidant enzyme and lowering the BP and HR in the rat.

Journal Article↗

PubMed2004

Exercise training enhanced the expression of myocardial proteins related to cell protection in spontaneously hypertensive rats.

Exercise training could potentially exert beneficial effects on the signaling events associated with cardiac cell apoptosis. Spontaneously hypertensive rats (SHR) were trained 5 days/week on a treadmill (18 m/min for 120 min/day) between the ages of 4 weeks and 1 week, corresponding to the hypertensive accelerating phase. The effect of exercise training on the expression of anti-apoptotic proteins HSP-72, Bcl-2 and protein kinase B (PKB), and the apoptotic proteins Bax and glycogen synthase kinase-3 (GSK-3) was examined. Exercise had a significant acute lowering effect on blood pressure, but this decrease did not attenuate the progressive increase in blood pressure. In the left ventricles of exercised SHR, PKB phosphorylation of both Ser473 and Thr308 residues was significantly increased by 166% and 120%, respectively, compared to sedentary SHR. PKB phosphorylation significantly correlated with GSK-3beta phosphorylation. HSP-72 and Bcl-2 protein expression were increased in the left ventricle of exercised SHR, and associated with the concomitant increased expression of the protein Bax. Thus, the Bcl-2/Bax ratio was not changed by exercise training, suggesting that the anti-apoptotic mechanism was effective in compensating the increase in the expression of the pro-apoptotic protein Bax in the myocardium of the SHR.

Animals↗

PubMed1984

Increased conjugated dopamine in plasma after exercise training.

To evaluate the effect of endurance exercise on plasma catecholamines, we exercise trained eight dogs (group T) by treadmill running for 8 weeks. Six sedentary dogs constituted a nontrained control group (group NT). Heart rate response to a graded submaximal stress test was reduced in group T dogs (p less than 0.05), but mean resting aortic blood pressure (NT, 84 +/- 5 mm Hg; T, 82 +/- 4 mm Hg) and heart rate (NT, 87 +/- 1 bpm; T, 84 +/- 2 bpm) were unchanged by exercise, and no cardiac hypertrophy occurred after exercise. Plasma norepinephrine and epinephrine levels were reduced in group T at rest and during a fixed exercise workload. Plasma conjugated dopamine showed a marked increase in group T dogs (NT, 1398 +/- 130 pg/ml; T, 11346 +/- 1291 pg/ml; p less than 0.01) at rest, and no change in conjugated dopamine occurred in either group after short-term exercise stress. No intergroup differences were noted in resting coronary flow or coronary arteriovenous oxygen, or in myocardial oxygen consumption. The data verify previous findings of lower plasma levels of norepinephrine and epinephrine after training, and indicate that a marked rise in conjugated dopamine occurs after training. These findings suggest that norepinephrine and epinephrine metabolism is shifted toward conjugated dopamine by exercise training, thereby reducing active catecholamines in plasma, but retaining a large pool of usable metabolite.

Animals↗

PubMed2003

Exercise training improves ageing-induced decrease in eNOS expression of the aorta.

AIMS: Ageing impairs endothelial function such as the regulation of vascular tone. The release of nitric oxide (NO), which has a potent vasodilator effect and antiatherosclerotic property, is decreased in the aorta of aged rats. Exercise training, however, has been reported to increase the expression of endothelial NO synthase (eNOS) in the aorta of young rats. In aged rats, it is not known whether the expression of eNOS is altered by exercise training. We hypothesized that exercise training would improve the ageing-induced decrease in eNOS expression in vessels, and examined the messenger RNA (mRNA) and protein expression of eNOS in the aorta of sedentary-young rats (sedentary-young group; 4 months old), sedentary-aged rats (sedentary-aged group; 23 months old), and swim-trained aged rats (training-aged group; 23 months old, swimming training for 8 weeks, 5 days week(-1), 90 min day(-1)). RESULTS: Body weight was significantly lower, and citrate synthase activity in the epitrochlearis muscle was significantly higher in the training-aged group compared with the sedentary-aged group. The mRNA expression of eNOS in the aorta was significantly higher in the training-aged group than in the sedentary-aged group, while it was significantly lower in both the sedentary-aged and training-aged groups than in the sedentary-young group. The expression of eNOS protein in the aorta was also significantly higher in the training-aged group than in the sedentary-aged group, while it was also significantly lower in the sedentary-aged group, but not in the training-aged group, than in the sedentary-young group. CONCLUSION: The present results revealed that the production of eNOS in the aorta decreases with ageing, and that the decreased production is increased by exercise training in aged rats, which may produce beneficial effects on the impaired cardiovascular system caused by ageing.

Aging↗

PubMed1990

Effects of exercise training on the menstrual cycle: existence and mechanisms.

This review evaluates the status of the evidence that exercise training affects the menstrual cycle beginning with evidence for the existence of delayed menarche, amenorrhea, and luteal suppression in athletes. A later age of menarche and a higher prevalence of amenorrhea and luteal suppression have been observed in athletes, but there is no experimental evidence that athletic training delays menarche, and alternative sociological and statistical explanations for delayed menarche have been offered. Cross-sectional studies of amenorrheic athletes have revealed abnormal reproductive hormone patterns, suggesting that the GnRH pulse generator in the hypothalamus is failing to initiate normal hypothalamic-pituitary-ovarian function. Longitudinal data show that the abrupt initiation of a high volume of aerobic training can disrupt the menstrual cycle in at least some women, but these women may be more susceptible to reproductive disruption than others, and some aspect of athletic training other than exercise (such as caloric deficiency) may be responsible for the observed disruption. Luteal suppression may be an intermediate condition between menstrual regularity and amenorrhea in athletes, or it may be the endpoint of a successful acclimation to exercise training. A potential endocrine mechanism of menstrual disruption in athletes involving the hypothalamic-pituitary-adrenal axis is discussed. Finally, promising future directions for research on this topic are described.

Adolescent↗