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At least 523 records · Page 29Linked to original sources
PubMed1992

Effect of exercise training on the total ischaemic burden: an assessment by 24 hour ambulatory electrocardiographic monitoring.

OBJECTIVE: To examine the effect of prolonged high intensity exercise training on total ischaemic burden in men with chronic stable angina pectoris. DESIGN: A randomised controlled trial based on 24 hour ambulatory electrocardiographic monitoring of patients on two occasions a year apart. SETTING: Cardiology department of a large general hospital. SUBJECTS: 40 men under 60 years of age with chronic stable angina pectoris and no previous myocardial infarction. RESULTS: After training the exercise group showed a 30% reduction in frequency of ST segment depression. There were significant reductions in painful episodes of ischaemia and those triggered by changes in heart rate. There was also a trend towards a reduction in silent ischaemia and episodes not triggered by changes in heart rate. The duration of ischaemic episodes was also reduced. No significant change in frequency or severity of dysrhythmia was shown. CONCLUSIONS: Exercise training reduces total ischaemic burden in patients with angina pectoris by reducing the frequency and duration of all types of ischaemic episode.

Adult↗
PubMed2001

Exercise training and autonomic nervous system activity in obese individuals.

PURPOSE: This study was designed to investigate the effects of 12 wk of exercise training on autonomic nervous system (ANS) in 18 obese middle-aged men (N = 9) and women (N = 9) (age: 41.6 +/- 1.2 yr; BMI: 27.3 +/- 0.4 kg x m(-2); %fat: 29.6 +/- 1.3%, mean +/- SE). METHODS: Each subject participated in an aerobic exercise training at anaerobic threshold (AT), consisting of 30 min/session, 3 times/wk, for 12 consecutive weeks. The ANS activities were assessed by means of power spectral analysis of heart rate variability (HRV) at resting condition before, at 5 wk, and after the exercise program. RESULTS: The exercise training resulted in a significant decrease in body mass, BMI, and % fat (P < 0.01) but not in lean body mass (P > 0.05) together with a significant increase in the AT VO2 (P < 0.01). Our power spectral data indicated that there were significant increases in the low-frequency component associated with the sympathovagal activity (0.03--0.15 Hz, 348.5 +/- 66.8 vs 694.7 +/- 91.5 ms(2), P < 0.01), the high-frequency vagal component (0.15--0.4 Hz, 146.3 +/- 30.4 vs 347.7 +/- 96.5 ms(2), P < 0.05), and the overall autonomic activity as evaluated by total power (0.03--0.4 Hz, 494.8 +/- 88.5 vs 1042.4 +/- 180.9 ms(2), P < 0.01) of HRV after the training. CONCLUSIONS: Twelve weeks of exercise training has significantly improved both the sympathetic and parasympathetic nervous activities of the obese individuals with markedly reduced ANS activity, suggesting a possible reversal effect of human ANS functions. These favorable changes may also have an influence on the thermoregulatory control over the obesity.

Adult↗
PubMed2006

Exercise training attenuates acute doxorubicin-induced cardiac dysfunction.

The use of doxorubicin, a highly effective antitumor antibiotic, is limited by a dose-dependent cardiotoxicity. The purpose of this study was to determine whether chronic exercise training (ET) prior to doxorubicin treatment would preserve cardiac function and reduce myocardial oxidative stress following treatment. Rats were exercise trained on a motorized treadmill or confined to sedentary cage activity for 12 weeks, then administered an intraperitoneal injection of doxorubicin (15 mg/kg) or 0.9% saline. Five days following the injections, hearts were isolated and Langendorf perfused to assess cardiac function and then processed for biochemical analyses. Doxorubicin treatment induced significant inotropic, lusitropic, and chronotropic cardiac dysfunction, reduced coronary flow, and increased cardiac lipid peroxidation in the sedentary animals. Doxorubicin treatment was also associated with a decrease in cardiac manganese superoxide dismutase protein expression and an increase in heat shock protein-72 (Hsp72) compared with saline-treated animals. Exercise training attenuated doxorubicin-induced cardiac dysfunction, and lipid peroxidation, and led to a greater cardiac expression of Hsp72 compared with the sedentary animals. The results of this study demonstrate for the first time that chronic exercise training before doxorubicin treatment protects against cardiac dysfunction following treatment, and provide evidence for a sustained increase in myocardial Hsp72 following exercise training and doxorubicin treatment in vivo.

Animals↗
PubMed2006

Exercise training increases insulin-stimulated glucose disposal and GLUT4 (SLC2A4) protein content in patients with type 2 diabetes.

AIMS/HYPOTHESIS: Exercise enhances insulin-stimulated glucose transport in skeletal muscle through changes in signal transduction and gene expression. The aim of this study was to assess the impact of acute and short-term exercise training on whole-body insulin-mediated glucose disposal and signal transduction along the canonical insulin signalling cascade. METHODS: A euglycaemic-hyperinsulinaemic clamp, with vastus lateralis skeletal muscle biopsies, was performed at baseline and 16 h after an acute bout of exercise and short-term exercise training (7 days) in obese non-diabetic (n=7) and obese type 2 diabetic (n=8) subjects. RESULTS: Insulin-mediated glucose disposal was unchanged following acute exercise in both groups. Short-term exercise training increased insulin-mediated glucose disposal in obese type 2 diabetic (p<0.05), but not in obese non-diabetic subjects. Insulin activation of (1) IRS1, (2) IRS2, (3) phosphotyrosine-associated phosphatidylinositol-3 kinase activity and (4) the substrate of phosphorylated Akt, AS160, a functional Rab GTPase activating protein important for GLUT4 (now known as solute carrier family 2 [facilitated glucose transporter], member 4 [SLC2A4]) translocation, was unchanged after acute or chronic exercise in either group. GLUT4 protein content was increased in obese type 2 diabetic subjects (p<0.05), but not in obese non-diabetic subjects following chronic exercise. CONCLUSIONS/INTERPRETATION: Exercise training increased whole-body insulin-mediated glucose disposal in obese type 2 diabetic patients. These changes were independent of functional alterations in the insulin-signalling cascade and related to increased GLUT4 protein content.

Biopsy↗
PubMed1997

Nonselective beta-adrenergic blockade with carvedilol does not hinder the benefits of exercise training in patients with congestive heart failure.

BACKGROUND: Long-term beta-adrenergic blockade does not appear to be associated with drug-induced training in patients with congestive heart failure (CHF); whether exercise training can increase peak aerobic capacity in patients with CHF who are treated with beta-adrenergic blockers is currently unknown. METHODS AND RESULTS: We studied 23 patients with CHF who were treated with carvedilol or propranolol in addition to ACE inhibitors, furosemide, and digoxin. Of the patients treated with carvedilol, 8 underwent exercise training and 8 remained sedentary. All 7 patients treated with propranolol underwent exercise training. Peak oxygen consumption (mL.kg-1.min-1) was serially measured in trained and sedentary patients. Peak reactive hyperemia (mL.min-1.100 mL-1) was determined in the calf and forearm immediately before and after 12 weeks of training. The peak oxygen consumption of trained patients treated with either carvedilol or propranolol increased from 12.9 +/- 1.4 to 16.0 +/- 1.6 (P < .001) and 12.4 +/- 1.0 to 15.7 +/- 0.9 (P < .001) mL.kg-1.min-1, respectively, whereas it did not change in the sedentary patients. Peak reactive hyperemia increased significantly in the calves but not the forearms of trained patients. CONCLUSIONS: Long-term, nonselective beta-adrenergic blockade with carvedilol or propranolol does not prevent patients with CHF from deriving systemic and regional benefits from physical training.

Adaptation, Physiological↗
PubMed1996

Exercise training decreases dyspnea and the distress and anxiety associated with it. Monitoring alone may be as effective as coaching.

STUDY OBJECTIVE: To determine whether exercise training with coaching is more effective than exercise training alone in reducing dyspnea and the anxiety and distress associated with it and improving exercise performance, self-efficacy for walking, and dyspnea with activities of daily living. DESIGN: Randomized clinical trial of 51 dyspnea-limited patients with COPD assigned to monitored (n = 27) or coached (n = 24) exercise groups. SETTING: Outpatient area of university teaching hospital. INTERVENTION: Both groups completed 12 supervised treadmill training sessions (phase 1) over 4 weeks followed by 8 weeks of home walking (phase 2). The CE group also received coaching during training. MEASUREMENTS: Perceived work of breathing, dyspnea intensity, distress associated with dyspnea, and anxiety associated with dyspnea were rated on a visual analog scale during incremental treadmill testing and after 6-min walks before and after phase 1. Dyspnea with activities of daily living, self-efficacy for walking, state anxiety, and 6-min walks were measured before and after both phases. RESULTS: Dyspnea and the associated distress and anxiety improved significantly for both groups relative to work performed and in relation to ventilation (p < 0.05). There were no significant differences between groups in any outcomes. The phase 1 improvement in laboratory dyspnea was accompanied by improvements in dyspnea with activities of daily living (p < 0.01) and self-efficacy for home walking (p < 0.01) that were sustained during the home phase. CONCLUSIONS: Coaching with exercise training was no more effective than exercise training alone in improving exercise performance, dyspnea, and the anxiety and distress associated with it, dyspnea with activities, and self-efficacy for walking.

Aged↗
PubMed2003

Long-term cardiorespiratory results of exercise training following cardiac transplantation.

The long-term influence of exercise training after heart transplantation remains unclear. Accordingly, we performed a 12-year follow-up study of 36 patients who underwent heart transplantation. Findings for survivors were compared with those of age-matched controls over the same period. Comparisons were also made between survivors and deceased patients. The sample comprised 36 men (aged 47 +/- 9 years) and a group of healthy age-matched controls. The patients received 16 months of outpatient exercise training; physiologic data were collected initially and at discharge. At 12 years, further data were collected on 20 of 23 survivors and their controls; 3 of the survivors were unavailable for final assessment, and 13 patients had died in the interim. The survivors' peak oxygen intake (V*O(2peak)) increased 26% after training and decreased 0.39 mlkg(-1)min(-1) per year (27.9 +/- 7 to 23.7 +/- 6), which was a similar rate as the controls (0.37 mlkg(-1)min(-1) per year; 33.7 +/- 7 to 29.2 +/- 7). Lean body mass (LBM) increased 3 kg by 16 months and a further 2.5 kg by 12 years, but ultimately was 3 kg below the controls. Although there was no difference in entry data between deceased patients and survivors, the latter attained greater gains in V*O(2peak) and LBM over the 16 months of training. Thus, in heart transplantation patients who undergo training, gains in exercise capacity are lost over 12 years at a rate commensurate with normal aging. A reduced training response in V*O(2peak) and LBM contributes to a poorer prognosis.

Adult↗
PubMed2004

Exercise training increases glycogen synthase activity and GLUT4 expression but not insulin signaling in overweight nondiabetic and type 2 diabetic subjects.

Exercise training improves insulin sensitivity in subjects with and without type 2 diabetes. However, the mechanism by which this occurs is unclear. The present study was undertaken to determine how improved insulin signaling, GLUT4 expression, and glycogen synthase activity contribute to this improvement. Euglycemic clamps with indirect calorimetry and muscle biopsies were performed before and after 8 weeks of exercise training in 16 insulin-resistant nondiabetic subjects and 6 type 2 diabetic patients. Training increased peak aerobic capacity (Vo(2peak)) in both nondiabetic (from 34 +/- 2 to 39 +/- 2 mL O(2)/kg fat-free mass [FFM]/min, 14% +/- 2%, P <.001) and diabetic (from 26 +/- 3 to 34 +/- 3 mL O(2)/kg FFM/min, 32% +/- 4%) subjects. Training also increased insulin-stimulated glucose disposal in nondiabetic (from 6.2 +/- 0.5 to 7.1 +/- 0.7 mg/kg FFM/min) and diabetic subjects (from 4.3 +/- 0.6 to 5.5 +/- 0.6 mg/kg FFM/min). Total glycogen synthase activity was increased by 46% +/- 17% and 45% +/- 12% in nondiabetic and diabetic subjects, respectively, in response to training (P <.01 v before training). Moreover, after training, glycogen synthase fractional velocity was correlated with insulin-stimulated glucose storage (r = 0.53, P <.05) and the training-induced improvement in glucose disposal was accounted for primarily by increased insulin-stimulated glucose storage. Training also increased GLUT4 protein by 38% +/- 8% and 22% +/- 10% in nondiabetic and diabetic subjects, respectively (P <.05 v. before training). Akt protein expression, which was decreased by 29% +/- 3% (P <.05) in the diabetic subjects before training (compared to the nondiabetics), increased significantly in both groups (P <.001). In contrast, exercise training did not enhance the ability of insulin to stimulate insulin receptor substrate-1 (IRS-1)-associated phosphatidylinositol 3 (PI 3)-kinase activity. The present data are consistent with a working model whereby 8 weeks of exercise training increases insulin-stimulated glucose disposal primarily by increasing GLUT4 protein expression without enhancing insulin-stimulated PI 3-kinase signaling, and that once the glucose enters the myocyte, increased glycogen synthase activity preferentially shunts it into glycogen synthesis.

Adult↗
PubMed1996

Interaction between exercise training and ejection fraction in predicting prognosis after a first myocardial infarction.

BACKGROUND: Although recent meta-analysis trials have shown that exercise training may improve survival after myocardial infarction, the mechanism of this beneficial effect is still unknown. The purpose of this study was to detect possible interactions between exercise training and predictors of prognosis after a first myocardial infarction. METHODS AND RESULTS: Patients with uneventful clinical courses after a first myocardial infarction were randomly assigned to a 4-week training period (125 patients, group 1) or to a control group (131 patients, group 2). Before randomization, all patients underwent a symptom-limited exercise test (28 +/- 2 days after myocardial infarction), 24-hour Holter monitoring, and coronary arteriography (31 +/- 3 days after the acute episode). After a mean follow-up period of 34.5 months, 18 patients had cardiac deaths (5 in group 1 and 13 in group 2). Multivariate analysis by Cox regression model showed that ejection fraction was the only independent prognostic indicator (P = .03). Evidence existed of an interaction between ejection fraction and exercise training, showing an effect of physical training on survival that depended on the patient's ejection fraction. Among patients with ejection fractions < 41%, the relative risk for an untrained patient was 8.63 times higher than for a trained patient (P = .04), whereas for ejection fractions > 40%, the estimated risks for trained and untrained patients were similar. CONCLUSIONS: These data show that exercise training may prolong survival in post-myocardial infarction patients with depressed left ventricular function. A randomized trial in such patients seems warranted.

Adult↗
PubMed2001

Exercise training alters the effect of chronic hypoxia on myocardial adrenergic and muscarinic receptor number.

Chronic hypoxic exposure results in elevated sympathetic activity leading to downregulation of myocardial alpha(1)- and beta-adrenoceptors (alpha(1)-AR, beta-AR). On the other hand, it has been shown that sympathetic activity is reduced by exercise training. The objective of this study was to determine whether exercise training could modify the changes in receptor expression associated with acclimatization. Four groups of rats were studied: normoxic sedentary rats (NS), rats living and training in normoxia (NTN), sedentary rats living in hypoxia (HS, inspired PO(2) = 110 Torr), and rats living and training in hypoxia (HTH, inspired PO(2) = 110 Torr). Training consisted of running in a treadmill at 80% of maximal O(2) uptake during 10 wk. Myocardial receptor density was measured by radioactive ligand binding. Right ventricular (RV) hypertrophy occurred in HS but not in HTH. No effect of exercise was detected in RV weight of normoxic rats. Acclimatization to hypoxia (HS vs. NS) resulted in a decrease in both alpha(1)- and beta-AR density, whereas muscarinic receptor (M-Ach) expression increased. Hypoxic exercise training (HS vs. HTH) moderated beta-AR downregulation and M-Ach upregulation and prevented the fall in alpha(1)-AR density. Normoxic training (NS vs. NTN) did not change beta-AR density. On the other hand, densities of alpha(1)-AR in both ventricles as well as RV M-Ach increased in NTN vs. NS. The data show that exercise training in hypoxia 1) prevents RV hypertrophy, 2) suppresses the downregulation of alpha(1)-AR in the left ventricle (LV) and RV, and 3) attenuates the changes in both beta-AR and M-Ach receptor density in LV and RV. Exercise training in normoxia increases M-Ach receptor expression in the RV.

Animals↗
PubMedDate not supplied

Dyspnea and the affective response during exercise training in obstructive pulmonary disease.

BACKGROUND: Dyspnea (SOB), dyspnea-related anxiety (DA), and exercise performance have been shown to improve after exercise training in patients with Chronic Obstructive Pulmonary Disease (COPD). However, there are no published descriptions of the changes in dyspnea intensity or dyspnea-related anxiety during or across the exercise training sessions. OBJECTIVES: To describe and compare the differences in the patterns of change in SOB, DA, and exercise performance during 12 exercise training sessions with and without nurse coaching. METHODS: Forty-five dyspnea-limited patients with COPD were randomly assigned to nurse-monitored (ME) or nurse-coached exercise (CE). SOB and DA were rated on a 200 mm VAS every 2 minutes during each of 12 treadmill training sessions. RESULTS: Warm-up, peak, cool-down, mean SOB, and peak SOB/stage remained constant over the exercise sessions, with increasing exercise performance for both groups over the 12 sessions (p < .001). There was a significant difference in the pattern of mean SOB over time between the ME and CE group (p < . 05). Mean, peak DA, and peak DA/stage showed a rapid decrease within the first 4 sessions (p < . 05) with no significant differences between the groups. Warm-up and cool-down DA remained constant. There were large intra- and inter-subject variations in the rating of dyspnea and dyspnea-related anxiety within and across sessions. CONCLUSIONS: As theoretically proposed, both groups significantly decreased their DA over the training sessions. This decrease was early in the sessions and was not accompanied by a decrease in the SOB. In contrast, subjects maintained a nearly constant mean and peak SOB with increasing exercise performance, suggesting that people may have a dyspnea threshold above which they are unable to tolerate greater dyspnea. Description of the changes in dyspnea and the affective response during training need to be expanded, while studying the type and timing of strategies to enhance the improvement in dyspnea and dyspnea-related anxiety.

Aged↗
PubMed2002

The effects of exercise training on walking function and perception of health status in elderly patients with peripheral arterial occlusive disease.

OBJECTIVE: To determine the effects of 12-week exercise programme on ambulatory function, free-living daily physical activity and health-related quality of life in disabled older patients with intermittent claudication. DESIGN: Prospective, randomized controlled trial. SETTING: University Medical Center and Veterans Affairs Medical Center, Taipei, Taiwan. SUBJECTS: Thirty-two of 64 patients with Fontaine stage II peripheral arterial occlusive disease (PAOD) were randomized to exercise training and 32 to usual care control. Five patients from the exercise group and six patients from the control group dropped out, leaving 27 and 26 patients, respectively, completing the study in each group. INTERVENTIONS: Twelve weeks of treadmill exercise training. MAIN OUTCOME MEASURES: Treadmill walking time to onset of claudication pain and to maximal claudication pain, 6-min walk distance, self-reported ambulatory ability and perceived health-related quality of life (QOL). RESULTS: Compliance of exercise programme was 83% of the possible sessions. Exercise training increased treadmill walking time to onset of claudication pain by 88% (P < 0.001), time to maximal pain by 70% (P < 0.001), and 6-min walk distance by 21% (P < 0.001). SUBJECTS: Perception of health-related QOL improved from 12% to 178% in the exercise group. These improvements were significantly better than the changes in the control group (P < 0.05). CONCLUSIONS: Significant improvements in claudication following 12-week exercise training in elderly PAOD patients were observed. Increase in treadmill walking time to maximal claudication pain in these patients translated into the improvement of perceived physical health, which enabled the patients to become more functionally independent.

Aged↗
PubMed1981

Decreased vascular sensitivity to norepinephrine following exercise training.

Twenty Sprague-Dawley rats (230 +/- 9 g; mean +/- SE) were exercised daily for 6 wk by swimming 1 h/day with weights (5% of body wt) attached to their tails. Nineteen additional rats (237 +/- 8 g) remained sedentary in their cages. All animals were anesthetized with urethan (800 mg/kg) and alpha-chloralose (60 mg/kg). In the first series of experiments, increasing doses of norepinephrine were injected into the jugular vein and the responses in mean arterial blood pressure was recorded from a cannulated femoral artery. Exercise training had no effect on the maximal increase in blood pressure, but significantly decreased blood pressure sensitivity to norepinephrine, expressed as a pD2 value (=-log ED 50), from 5.64 +/- 0.07 to 5.20 +/- 0.06. In the second series, the cremaster muscle with intact circulation and innervation was suspended in a tissue bath and norepinephrine in increasing concentrations was added to the cremaster bath. The responses of the main arteriole (approximately 110 micron) and venule (approximately 170 micron) were recorded by television microscopy. Exercise training had no effect on vessel diameters of resting muscle or on the maximal vessel constrictions obtained in response to high concentrations of norepinephrine. Arteriole sensitivity to norepinephrine was significantly decreased (pD2 of 6.69 +/- 0.24 vs. 5.96 +/- 0.18) and there was some tendency for reduced venule sensitivity. These data suggest that exercise training in rats produces a decrease in alpha- or an increase in beta-adrenergic receptor sensitivity.

Animals↗
PubMed2005

Impact of exercise training on muscle function and ergoreflex in Fontan patients: a pilot study.

BACKGROUND: Several studies have demonstrated persistent reduced exercise capacity in Fontan patients even after surgical intervention. The purpose of this study was to evaluate if the skeletal muscle function of these patients is abnormal, if it correlates with exercise tolerance and if it can be improved by exercise training. METHODS: We evaluated the functional capacity of seven patients who underwent Fontan procedure (age:16+/-5 years, mean+/-SD) and seven healthy children (19+/-7 years) paired for age, sex, height and weight. Evaluation included pulmonary evaluation, neuromuscular function and exercise tolerance. Secondly, an 8-week exercise training program was performed by five of these patients. RESULTS: The ergoreflex contribution to absolute diastolic blood pressure was higher (12.5+/-4.8 vs. 5.6+/-4.2 mmHg; p=0.04) in Fontan patients vs. healthy subjects whereas a trend was encountered regarding the ergoreflex contribution to absolute systolic blood pressure (9.0+/-7.0 vs. 0.4+/-9.0 mmHg; p=0.09). Furthermore, time to fatigue of the non-dominant forearm muscles was shorter in Fontan patients vs. healthy subjects (431+/-290 vs. 847+/-347 s; p=0.03). Following exercise training, there was a significant reduction of the ergoreflex contribution to absolute values of systolic blood pressure (9.8+/-0.9 vs. 0.3+/-2.7 mmHg; p<0.05). There was an association between muscle strength and VO2 peak in Fontan patients (upper limb: r=0.895; p<0.01; lower limb: r=0.838; p<0.05, respectively). CONCLUSIONS: Skeletal muscle function in Fontan patients is abnormal which may have an impact in the reduced exercise tolerance encountered in these patients. Exercise training may have beneficial impacts on the skeletal muscle function in this population.

Adolescent↗
PubMed1987

Select cardiovascular and metabolic responses of diabetic rats to moderate exercise training.

The combined influence of diabetes and moderate treadmill exercise training on select metabolic and cardiovascular parameters was investigated with mature male Sprague-Dawley rats assigned to either control diabetic or diabetic groups receiving exogenous insulin. Experimental diabetes was induced with streptozotocin (80 mg.kg-1, i.v.) and verified by blood glucose concentrations greater than 16 mmol. The animals were designated as control, insulin-injected (5 U.kg-1, twice daily), or saline-injected (twice daily), and assigned to either non-trained or trained sub-groups. Insulin treatment partially restored the measured physiological functions to within normal limits. All animals were trained at 60 to 70% maximal oxygen consumption for 9 wk and exhibited higher maximal oxygen consumption values and cytochrome oxidase activity of the soleus muscles. Diabetes caused lower (P less than 0.05) reductions in resting heart rate but training-induced bradycardia did not occur in any group. Heart rate response to atropine sulfate (1 mg.kg-1, atrial choline acetyltransferase activity, atrial acetylcholine concentration, and quinuclidinyl benzilate binding was measured to evaluate changes in the parasympathetic nervous system. Atropine-induced cardiac acceleration was most pronounced in control and least effective in diabetic animals. Endurance training had no meaningful influence on this response to cholinergic inhibition. Quinuclidinyl benzilate binding for the diabetic and the diabetic groups receiving insulin revealed no change in receptor number, receptor affinity, or training effects. These findings indicated that 9 wk of exercise training improves the aerobic capability of insulin-deficient rats without changing cardiovascular characteristics associated with the parasympathetic nervous system.

Acetylcholine↗
PubMed2001

Insulin-like growth factors and leucine kinetics during exercise training in children with cystic fibrosis.

BACKGROUND: Little is known about the metabolic effects of exercise training in children with cystic fibrosis. The hypothesis for the current study was that in patients with declining clinical status, exercise increases circulating insulin-like growth factors (IGFs) and improves protein kinetics. METHODS: This was a prospective intervention study in 10 children with cystic fibrosis who participated in a structured isoenergetic exercise (cycling) training program for 3 months. Measurements of IGFs, protein kinetics (using intravenous [13C]-1-leucine tracer infusions) and nutritional balance studies were conducted at baseline and after 3 months. RESULTS: Standard deviation scores of plasma IGF-I, IGF-II, and IGF binding protein (BP)-3 were all decreased at baseline (mean +/- SE: -2.0+/-0.2, -2.0+/-0.2. -0.6+/-0.2, respectively). IGF-I and IGF-II concentrations were significantly higher after exercise training (standard deviation scores -1.4+/-0.3 and -1.3 +/-0. 1, respectively; compared with baseline: one-tailed t-test P = 0.03 and 0.002). The standard deviation score of the IGF-I/IGF BP-3 ratio, an indicator of free IGF-I in the circulation, normalized during exercise training (0.0+/-0.6 vs. -1.3+/-0.2 SD units at baseline, one-tailed t-test P = 0.04). There was no significant difference in protein intake and fasting protein breakdown, oxidation, and protein synthesis or in energy balance and fat absorption. CONCLUSIONS: These results show that isoenergetic exercise training can be safely recommended to patients with cystic fibrosis. It provides a positive anabolic stimulus to IGF status but is not sufficient to adequately augment protein accretion in patients with diminished nutritional status.

Adolescent↗
PubMed1994

Vasodilator responses of coronary resistance arteries of exercise-trained pigs.

BACKGROUND: The purpose of this study was to test the hypothesis that vasodilator responses of porcine coronary resistance arteries are increased by exercise training. METHODS AND RESULTS: Yucatan miniature swine were randomly divided into groups of exercise-trained (ET) and sedentary (SED) control pigs. ET pigs were placed on a progressive treadmill training program lasting 16 to 20 weeks, and SED pigs remained inactive during the same time period. Coronary resistance arteries 64 to 157 microns in diameter were isolated for in vitro evaluation of relaxation responses to the endothelium-independent dilators sodium nitroprusside (1 x 10(-10) to 1 x 10(-4) mol/L) and adenosine (1 x 10(-10) to 1 x 10(-5) mol/L) and to bradykinin (1 x 10(-13) to 3 x 10(-7) mol/L), an endothelium-dependent agent. Relaxation responses to adenosine and sodium nitroprusside were not altered by exercise training. Endothelium-dependent relaxation to bradykinin was enhanced in coronary resistance arteries from ET pigs (IC50: ET, 0.07 +/- 0.02 nmol/L; SED, 1.59 +/- 0.09 nmol/L). To determine whether prostanoids and/or the nitric oxide synthase pathway were involved in the ET-induced changes in bradykinin-induced vasodilation, responses to bradykinin were examined in coronary resistance arteries from both ET and SED pigs in the presence of indomethacin and in the presence of nitro-monomethyl L-arginine (L-NMMA). Both indomethacin and L-NMMA produced significant inhibition of the bradykinin-induced relaxation in vessels from both groups. Despite decreased bradykinin-induced relaxation after indomethacin, bradykinin-induced vasodilation was still enhanced in vessels from the ET group. L-NMMA caused greater inhibition of the bradykinin-induced relaxation in coronary resistance arteries from ET pigs relative to arteries from SED pigs and eliminated the training-induced enhancement of the bradykinin responses. CONCLUSIONS: These results suggest that exercise training enhances bradykinin-induced vasodilation through increased endothelium-derived relaxing factor/nitric oxide production by the L-arginine/nitric oxide synthase pathway.

Adenosine↗