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PubMed2001

Metformin, but not exercise training, increases insulin responsiveness in skeletal muscle of Sprague-Dawley rats.

We assessed the effects of combined metformin treatment and exercise training on body composition, on insulin concentration following glucose loading, on insulin-stimulated glucose transport in skeletal muscle, and on muscle glycogen content. Male Sprague-Dawley rats were treated for 35 days with or without metformin (320 mg/kg/day) and/or treadmill exercise training (20 min at 20 m/min, 5 days/wk). Because metformin reduces food intake, pair-fed controls were included. Metformin, training, and pair-feeding all decreased food intake, body weight, and insulin concentration following glucose loading. Metformin and training reduced intra-abdominal fat, but pair feeding did not. In isolated strips derived from soleus, epitrochlearis and extensor carpi ulnaris muscles, metformin increased insulin-stimulated transport of [3H]-2-deoxyglucose by 90%, 89% and 125%, respectively (P < 0.02) and training increased [3H]-2-deoxyglucose transport in the extensor carpi ulnaris muscle only (66%, P < 0.05). Pair-feeding did not alter [3H]-2-deoxyglucose transport. Training increased gastrocnemius muscle glycogen by 100% (P < 0.001). Metformin and pair-feeding did not alter muscle glycogen. We conclude that metformin reverses the maturation-induced impairment of insulin responsiveness in Sprague-Dawley rats by increasing insulin-stimulated glucose transport in skeletal muscle and that this effect is not secondary to reduced food intake. We also conclude that metformin and exercise training may increase insulin sensitivity by different mechanisms, with training causing increased glucose transport only in some muscles and also causing increased muscle glycogen storage.

Aging↗

PubMed1985

Levels of serum sex hormones and risk factors for coronary heart disease in exercise-trained men.

On the basis of previous findings, it has been hypothesized that hyperestrogenemia may be the major predisposing factor for coronary heart disease and that an elevation in the estradiol-to-testosterone ratio, or a closely related hormonal alteration, may cause the expression of risk factors for coronary heart disease. The present study was carried out to investigate whether exercise training, which has been reported to reduce risk factors for coronary heart disease, affects the serum sex hormone levels. The serum sex hormone levels, established risk factors for coronary heart disease, and physical fitness were measured in 10 men who had undergone at least six months of intensive exercise training and in 10 sedentary men of similar age. Despite evidence for a strikingly higher level of physical fitness and a lower level of risk factors in the trained group, no significant difference in mean serum estradiol level was found. Nor did three subjects from the sedentary group show a decrease in estradiol level after three to four months of exercise training. The mean estradiol-to-testosterone ratio, however, was significantly lower in the trained group and might account for the lower level of risk factors in that group. If the hypothesis is correct, exercise training may decrease established risk factors for coronary heart disease without decreasing the risk of coronary heart disease.

Adult↗

PubMed2002

Back extension endurance and strength: the effect of variable-angle roman chair exercise training.

STUDY DESIGN: A pre- and postintervention randomized, controlled trial was conducted. OBJECTIVE: To evaluate the effect of progressive resistance exercise training using a variable-angle Roman chair on the development of lumbar extensor endurance and strength. SUMMARY OF BACKGROUND DATA: Progressive resistance exercise for the lumbar extensors has been used successfully for low back pain rehabilitation, but the limitations of currently available back exercise devices have negatively affected its use. METHODS: For this study, 36 healthy volunteers were randomized into one of two groups: a variable-angle Roman chair exercise group (n = 18) that performed one set of 15 to 25 repetitions of dynamic progressive resistance back extension exercise on a variable-angle Roman chair three times per week for 8 weeks or a control group (n = 18) that did not perform resistance exercise. Before training and after 4 and 8 weeks of training, static back extension endurance (seconds) and isometric lumbar extension strength (Newton.meters) were recorded. RESULTS: The variable-angle Roman chair exercise group displayed a 42% increase in static back extension endurance at the 4-week and 8-week tests relative to the pretraining measure (P < 0.05). The control group did not increase back endurance time at either the 4-week or 8-week tests (P > 0.05). Neither the variable-angle Roman chair exercise group nor the control group displayed an increase in lumbar extension strength at the 4-week or 8-week tests (P > 0.05). CONCLUSIONS: Dynamic progressive resistance exercise training on a variable-angle Roman chair is capable of developing back extension endurance. Future research is needed to determine the clinical applicability of variable-angle Roman chair exercise training for patients with low back pain patients.

Adult↗

PubMed1986

Effect of exercise training in patients with essential hypertension.

After 12 weeks of regular exercise training in 34 patients with moderate essential hypertension, supine systolic blood pressure at rest decrease from 152 +/- 2 (means +/- SEM) to 149 +/- 2 mmHg (p less than 0.05), and diastolic blood pressure from 106 +/- 1 to 102 +/- 1 mmHg (p less than 0.001). At corresponding submaximal exercise levels, diastolic blood pressure also decreased significantly from 110 +/- 2 to 98 +/- 3 mmHg (p less than 0.001), but no significant reduction in systolic blood pressure was observed. Heart rate at the same submaximal work load was significantly reduced (p less than 0.01). This data shows that exercise training might have blood pressure lowering effect in patients with moderate essential hypertension, and might in some patients be an alternative to pharmacological treatment.

Adult↗

PubMed1992

Preventive effect of exercise training on recurrent stenosis after percutaneous transluminal coronary angioplasty (PTCA).

The purpose of this study is to evaluate whether exercise training for 12 weeks prevents the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Symptom-limited treadmill exercise with thallium-201 myocardial single photon emission computed tomography (SPECT) was performed one and 13 weeks after PTCA in 18 patients with exercise training and in 20 patients without. For quantitative analysis, the average count of region of interest in the hypoperfused area on the polar map was calculated. A percentage T1 uptake was determined by dividing average count of the hypoperfused area by that of a normal reference area at an initial image (%IU) and a delayed image (%DU). A percentage redistribution (%RD) was obtained by subtracting %IU from %DU as the parameter of residual ischemia in the hypoperfused area. Total treadmill exercise duration and maximal pressure rate product 13 weeks after PTCA increased significantly (p less than 0.01) in the trained group, whereas there was no significant change in the untrained group. %DU increased significantly (p less than 0.01) in the trained group, whereas there was no significant change in the untrained group. %RD decreased significantly (p less than 0.01) in the trained group, whereas there was no significant changes in the untrained group. The restenosis rates at the third month after PTCA was 17% (3/18) in the trained group and 40% (8/20) in the untrained group. These findings suggest that in patients with coronary artery disease exercise training improves myocardial perfusion by preventing the progression of coronary artery stenosis after PTCA.

Aged↗

PubMed2004

Eight weeks of moderate-intensity exercise training increases heart rate variability in sedentary postmenopausal women.

BACKGROUND: Regular exercise is associated with increased heart rate variability (HRV). However, results from studies examining the effect of exercise training on HRV in postmenopausal women are inconclusive. In addition, the effect of hormone replacement therapy (HRT) on HRV remains a subject of speculation. METHODS: We examined 88 sedentary postmenopausal women in a randomized controlled trial who were assigned to exercise (n = 49) or control (n = 39) groups. The exercising women performed 8 weeks of aerobic exercise training at a heart rate equivalent to 50% of VO2max, consisting on average of 44 minutes per session, 3 to 4 times per week. Resting HRV was measured in each participant at baseline and after 8 weeks of intervention. Ten minutes of resting R-R intervals were analyzed by time (standard deviation of mean R-R intervals, root of mean square successive differences) and frequency domain methods: low-frequency (LF) was defined as 0.04 to 0.15 Hz, high-frequency (HF) as 0.15 to 0.40 Hz, and total spectral power as 0.00 to 0.40 Hz. The LF and HF components in normalized units were also calculated. RESULTS: At baseline, there were no significant differences in HRV between control and exercise groups. Additionally, there were no differences in any HRV variables when women were grouped by HRT use (no HRT, estrogen-only HRT, and progestin-containing HRT). After 8 weeks, women randomly assigned to the exercise group increased all absolute time and frequency domain indexes (all P <.001) and reduced resting heart rate (P =.002) compared with women in the control group. The LF and HF components expressed as normalized units remained unchanged after exercise intervention. Additionally, HRT use did not modify the exercise-induced changes in HRV. CONCLUSIONS: We conclude that moderate aerobic exercise increases HRV in sedentary postmenopausal women. This benefit is not influenced by the use of HRT.

Analysis of Variance↗

PubMed2002

Exercise training and endothelial dysfunction in coronary artery disease and chronic heart failure. From molecular biology to clinical benefits.

Endothelial dysfunction (ED) has been documented in patients with both coronary artery disease (CAD) and chronic heart failure (CHF)-being responsible for exercise-induced myocardial ischemia in the former and increased afterload in the latter. In the last two decades exercise training has assumed a major role in both cardiovascular disorders. In CAD exercise training has established positive effects on myocardial perfusion. Recently, exercise training has been shown to attenuate paradoxical vasoconstriction in CAD. The improved ED after training explains the improvement of myocardial perfusion in the absence of changes in baseline coronary artery diameter. Since ED has been identified as a predictor of coronary events exercise may contribute to long-term reductions of cardiovascular mortality. In CHF the increased peripheral vascular resistance - especially during exercise - is more important. ED contributes to the peripheral vasoconstriction. Training programs have shown to improve ED in CHF. A long-term study of hemodynamic effects of training in CHF revealed a significant reduction of total peripheral resistance (TPR) that after 6 months with a concomitant increase in stroke volume. In a subgroup analysis a significant correlation between changes in TPR and changes in peripheral ED was observed. Cell culture and animal experiments suggest that shear stress increases the endothelial L-arginine uptake, enhances NO synthase activity and expression, and upregulates the production of extracellular superoxide dismutase, which prevents premature NO breakdown. All these molecular effects converge on a reduction of myocardial ischemic events in CAD and a decrease of afterload in CHF.

Chronic Disease↗

PubMed2006

The effects of exercise training on myocardial adrenergic and muscarinic receptors.

We investigated the effects of exercise training on heart rate variability (HRV) and myocardial adrenergic and muscarinic receptors in rats. Exercise training induced a decrease in body mass while ventricular size remained unchanged, a development we considered as a relative cardiac hypertrophy. In addition, there was a reduction in the density of myocardial beta(1)-adrenergic receptors. These structural changes were associated with functional adaptations, as illustrated by the increased response of the sinus node to sympathetic blockade.

Animals↗

PubMed2003

Exercise training in women with heart disease: influence of hormone replacement therapy.

PURPOSE: To examine the central and peripheral cardiovascular effects of exercise training in postmenopausal women with CAD with and without hormone replacement therapy (HRT and N-HRT). METHODS: Thirty-eight female cardiac patients referred for cardiac rehabilitation were divided into HRT ( N= 18) or N-HRT (N = 20) groups. Peak oxygen uptake (VO2) peak and ventilatory anaerobic thresholds (AT) were determined, in addition to submaximal cardiac output (Q). Peripheral measures of resting and peak ischemic blood flows (BF) were also measured. Measurements were all repeated after 12 and 26 wk of exercise training consisting of 1 h of walking at 75-80% of the measured VO2peak at baseline (T1) for 5 d.wk(-1). RESULTS: VO2peak mL.kg(-1).min(-1) at baseline (14.9 +/- 0.4) increased by 5% after 12 wk (15.6 +/- 0.4) and significantly by 15% (17.2 +/- 0.5) after 26 wk of exercise training (P < 0.001). The HRT group was significantly younger than the N-HRT group (58 vs 65 yr; P < 0.01) and had significantly higher VO2peaks at baseline (15.7 vs 14.2 mL.kg(-1).min(-1); P < 0.05), yet either did not influence changes in other variables. At fixed submaximal work rates, there was a significant training bradycardia ( P < 0.01), but insignificant changes in Q or stroke volume regardless of HRT status. Resting and peak ischemic calf BF and vascular conductance increased significantly ( P < 0.001) at 12 and 26 wk, with no difference found according to HRT status. CONCLUSIONS: The cardiovascular responses to training in postmenopausal women with CAD appear to be consistent regardless of HRT status and dominated by peripheral adaptations.

Aged↗

PubMed1984

Causes of the triglyceride-lowering effect of exercise training in rats.

Serum triglyceride (TG) levels are lower in exercise-trained (ET) compared with control rats throughout a 24-h period (P less than 0.01-0.001). To understand this phenomenon, the relationship between serum TG concentration and hepatic very low density lipoprotein (VLDL)-TG secretion rate was studied in intact rats. In addition, hepatic TG secretion was measured in isolated perfused liver and TG removal by isolated perfused hindlimbs at rest and during simulated exercise. In vivo, low TG levels are consistently associated with decreased serum insulin concentration and periodic decrease in free fatty acid (FFA) levels. At rest, with comparable FFA levels, VLDL-TG secretion was 50% lower in ET rats, proportionate to the reduction in serum TG levels. Hepatic TG secretion by perfused livers of ET and control rats was similar when studied at comparable FFA and insulin levels suggesting the fall in VLDL-TG secretion with exercise training was not the result of intrinsic change in the ability of the liver to esterify and secrete TG. Perfused muscle of ET and control rats remove TG at equal rates when perfused at rest. However, during simulated exercise, TG removal was increased only in hindlimbs from ET rats. Thus, low serum TG levels in ET rats seem to be due to a combined effect of decreased hepatic TG secretion, secondary to reduced substrate and insulin supply to the liver, and increased TG removal by muscle during exercise.

Animals↗

PubMed1998

Relative EMG levels in training exercises for abdominal and hip flexor muscles.

The main purpose of our study was to compare systematically EMG levels in sub-maximal training exercises for the trunk and hip flexor muscles with those voluntarily attainable in corresponding situations. Six healthy subjects performed three types of standardized training exercises, whose static positions, movement velocity and range of motion were reproduced during maximal voluntary isokinetic strength tests. EMG was recorded with wire electrodes from the iliacus muscle and with surface electrodes from the rectus femoris, sartorius, rectus abdominis, obliquus externus and internus muscles. The relative EMG values demonstrated a task dependency which could differ between individual muscles. The maximal voluntary activation levels were relatively constant across conditions. Exceptions were present, particularly for the rectus femoris and iliacus muscles. These findings highlight the consequences of using different methods of normalizing EMG. The relative EMG values presented may serve as guidelines when selecting training exercises for specific trunk and hip flexor muscles in sports and rehabilitation.

Abdominal Muscles↗

PubMed1989

Orthostatic responses following 30-day bed rest deconditioning with isotonic and isokinetic exercise training.

To determine if intensive isotonic or isokinetic exercise training during 30 d of -6 degrees head-down bed rest (BR) would accentuate orthostatic intolerance, 19 men (32-42 years) were divided into a no-exercise control group (N = 5), and isotonic (Quinton ergometer, N = 7) and isokinetic (Lido ergometer, N = 7) exercise groups. Training was two 30-min periods per day for 5 days per week. Changes (* = p less than 0.05) in peak VO2 uptake (L/min) from control day 2 to BR day 29 were: isotonic +1.4%, isokinetic -10.2%*, no exercise -20.1%*. Changes in resting plasma volume (ml) from control day 1 to BR day 30 were: isotonic -3.7%, isokinetic -18.0%*, and no exercise -17.2%*. A 60 degrees head-up tilt test was administered on control day 1 and BR day 30; the test was terminated at 60 min or when presyncopal signs and/or symptoms occurred. Changes in means tilt tolerance were: isotonic, 42 to 34 min (delta = -8 min*); isokinetic, 53 to 30 min (delta = -23 min*); and no exercise, 46 to 30 min (delta = -16 min*). Mean day 30 group tolerances were all significantly lower than day 1 tolerances, but the reductions were not different between groups. Because there was no obvious relationship between type of exercise, exercise energy expenditure, change in peak VO2, or change in resting plasma volume and the consistent reduction in post-BR tilt tolerances, it appears that the orthostatic intolerance was due mainly to the reduction in body hydrostatic pressure from the -6 degrees head-down body position, and was not related to the level of physical fitness. Thus, factors other than training status are probably involved.

Adult↗

PubMed1995

Endothelium-dependent vasodilation of proximal coronary arteries from exercise-trained pigs.

We recently reported that alpha-adrenergic vasoconstriction is blunted and adenosine-induced vasodilation is enhanced in proximal coronary arteries of exercise-trained miniature swine [C. L. Oltman, J. L. Parker, H. R. Adams, and M. H. Laughlin. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H372-H382, 1992]. The purpose of the present study was to determine whether this model of exercise training also alters endothelium-dependent vasodilator responses of proximal coronary arteries. Female Yucatan miniature swine were exercise trained (ET) on a motor-driven treadmill or were cage confined (Sed) for 13-20 wk. Exercise tolerance, heart weight-to-body weight ratios, and skeletal muscle oxidative capacity were all significantly greater in ET than in Sed animals. Vasodilator responses were evaluated in vitro by determining concentration-response curves by using vascular rings (3.5-4 mm in axial length) isolated from right and left coronary arteries. Vasorelaxation responses were determined, after tone had been produced with either 30 microM prostaglandin F2 alpha, 30 mM KCl, or 30 nM endothelin. Concentration-response curves were obtained to endothelium-dependent vasodilators including bradykinin (10(-9)-10(-6) M), substance P (10(-12)-10(-6) M), clonidine (10(-9)-10(-6) M), serotonin (10(-10)-10(-5) M), and the Ca2+ ionophore A-23187 (10(-10)-10(-6) M). Endothelium-independent vasodilator responses to sodium nitroprusside (10(-9)-10(-4) M) were not different between arteries from Sed and ET. Bradykinin, substance P, and A-23187 were potent vasodilators in arteries from both groups, whereas serotonin and clonidine did not consistently produce vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Intermittent claudication: functional capacity and quality of life after exercise training or percutaneous transluminal angioplasty--systematic review.

PURPOSE: To systematically review published data about the short- and long-term effects of exercise training and angioplasty on functional capacity and quality of life of patients with intermittent claudication. MATERIALS AND METHODS: Articles published between January 1980 and February 2003 were included if patients had intermittent claudication treated with exercise training or angioplasty and if both functional capacity and quality-of-life scores from Medical Outcomes Study 36-Item Short Form health survey were reported for at least 3 months of follow-up. Data were pooled by using a random effects model and weighted means. Pooled results were compared between the treatment groups by using the chi2 test and the Student t test (alpha = .05, two sided). RESULTS: In the analyses, five studies (202 patients) were included in the exercise group, and three studies (470 patients), in the angioplasty group. At 3 months of follow-up, the ankle-brachial index was significantly improved in the angioplasty group (mean change, 0.18; P < .01) but not in the exercise group (mean change, 0.01; P = .29). At 3 months, quality of life was significantly improved with regard to ratings of physical functioning and bodily pain in the exercise group (mean change, 18 and 10, respectively; P < .01) and physical role functioning in the angioplasty group (mean change, 30; P = .03). Mean change in ankle-brachial index significantly differed between the two treatment groups at 3 and 6 months (P < .01); mean change in quality-of-life scores did not. CONCLUSION: Improvement in quality of life was demonstrated after both exercise training and angioplasty, whereas functional capacity showed significant improvement after angioplasty. The ankle-brachial index significantly differed between the two treatment groups at 3 and 6 months, whereas the quality-of-life scores did not.

Angioplasty, Balloon↗

PubMed2002

Effects of exercise training on cardiovagal and sympathetic responses to Valsalva's maneuver.

PURPOSE: We tested the hypothesis that a strictly-controlled program of aerobic conditioning would increase vagal and decrease sympathetic responses to Valsalva straining. METHODS: Eleven young men performed a maximal aerobic capacity test, controlled frequency breathing (0.25 Hz), and three Valsalva maneuvers before and after 4 wk of exercise training on a cycle ergometer (30 min at > or = 70% max heart rate, 3 sessions. week-1). During controlled breathing and Valsalva straining, we recorded the electrocardiogram, noninvasive beat-by-beat arterial pressure, and peroneal nerve muscle sympathetic traffic at the popliteal fossa (pre- and postexercise sympathetic recordings were obtainable in 7 of 11 subjects). Vagal-cardiac tone was estimated from R-R interval standard deviations during controlled frequency breathing. Cardiovagal baroreflex sensitivity was derived from increases of R-R intervals as functions of increases in systolic pressures with linear regression analysis during phase IV pressure increases, and sympathetic sensitivity was derived from the quotient of total muscle sympathetic nerve activity and diastolic pressure changes during phase II pressure reductions. RESULTS: Exercise training increased VO2 max (3.38 +/- 0.10 pre-, and 3.64 +/- 0.11 L. min-1 postexercise; mean +/- SE; P = 0.04), R-R interval standard deviations (75 +/- 0.12 pre- and 94 +/- 0.14 ms postexercise; mean +/- SE; P = 0.03), and cardiovagal baroreflex sensitivity (15.0 +/- 1.1 pre-, and 25.0 ms. mm Hg-1 +/- 4.0 postexercise; mean +/- SE; P = 0.03). Exercise training did not change baseline sympathetic traffic (P = 0.31) or sympathetic nerve responses to diastolic pressure reductions (P = 0.12). CONCLUSIONS: Exercise training affects vagal and sympathetic mechanisms differently: cardiovagal baroreflex sensitivity is increased, but sympathetic responses to arterial pressure decreases are unchanged.

Adult↗

PubMed2002

Exercise training does not reduce hyperlipidemia in pigs fed a high-fat diet.

The pig is often used as a model for studying lipoprotein metabolism as it relates to human atherosclerosis, but few studies have examined the complete lipoprotein profile and related enzymes in swine ingesting an atherogenic diet. We examined whether exercise training would moderate the effects of an atherogenic diet on lipoproteins and lipoprotein lipase (LPL) activity in miniature swine. Male (n = 30) and female (n = 32) swine were initially divided into 2 dietary groups: one consumed low-fat (8%) pig chow, and one consumed pig chow supplemented with 2% cholesterol, 17.1% coconut oil, 2.3% corn oil, and.7% sodium cholate (46% kcal from fat). Following 30 days on the diets, pigs from each diet group were further divided into sedentary and exercise trained subgroups, each cell with 6 to 8 pigs. Training occurred 5 days per week on a treadmill in which the intensity and duration were progressively increased during the 16- to 20-week training period to 75 minutes of aerobic running per session. A 4-way analysis of variance (ANOVA) with repeated measures on time indicated that at the conclusion of the study the atherogenic diet caused significantly (P <.05) increased cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and subfractions, low-density lipoprotein cholesterol (LDL-C) and subfractions, and LPL activity in both genders. For cholesterol, TG, HDL-C, HDL(2)-C, LDL-C, LDL(1&2)-C, and hepatic lipase, the female response to the diet was exaggerated compared to the male response. Exercise training produced no group differences or interactions on any lipoprotein variable. These results suggest that an atherogenic diet has a greater impact on the lipoproteins of female miniature swine than males. Furthermore, under the conditions of this study, exercise training does not moderate the effects of an atherogenic diet on lipoproteins.

Animals↗

PubMedDate not supplied

Exercise training in heart failure.

Patients with heart failure challenge the clinician with a constellation of difficult clinical, pathophysiologic, and psychologic issues. As a result, until recently, exercise training was not considered a safe and effective treatment strategy to be used in these patients. However, in the past 10 years, data from both randomized and nonrandomized trials showed that regular exercise training in patients with stable Class II and III heart failure can safely improve exercise tolerance, attenuate an overactivated sympathetic nervous system, partially reverse skeletal muscle abnormalities, and enhance health-related quality of life. These outcomes are achievable with a relatively moderate dose of physical activity, such as 30 to 60 minutes of walking or cycling 3 to 5 days per week at an intensity equivalent to 60% to 70% of peak oxygen consumption. Sufficiently powered trials are needed to assess morbidity, mortality, and cost-effectiveness endpoints relative to exercise training in patients with heart failure.

Cardiac Output↗

PubMed1988

Comparison of high- and low-intensity exercise training early after acute myocardial infarction.

The effects of the intensity of exercise training on cardiorespiratory variables were investigated in a consecutive series of men with recent (median 8 weeks) acute myocardial infarction. Forty-five patients were randomly assigned either to a high- (65 to 75% maximum oxygen consumption rate [VO2max]) or to a low-intensity (less than 45% VO2max) exercise group. Patients engaged in medically supervised aerobic training 3 sessions a week for 12 weeks. With training, mean VO2max significantly increased by 11% (2.09 to 2.31 liters/min) within the high group and by 14% (1.93 to 2.21 liters/min) within the low group. Differences between groups were not statistically significant. Both groups also had comparable changes in heart rate, blood pressure and double-product at submaximal and maximal workloads. Analysis of blood lipids revealed that both groups experienced a significant increase in high density lipoprotein cholesterol. There were no significant changes in total serum cholesterol or triglycerides. These findings suggest that within an unselected population of patients after acute myocardial infarction referred for cardiac rehabilitation, low- and high-intensity exercise training produces relatively similar changes in cardiorespiratory variables during the initial 3 months of exercise training.

Adult↗