Nitro-oxidative stress biomarkers in active and inactive men.

Oxidative stress markers are novel factors shown to be related to cardiovascular (CVD) risk. We examined the effects of long-term exercise, age, and their interaction on plasma oxidized LDL (ox-LDL), nitrotyrosine, and myeloperoxidase (MPO) levels, all biomarkers of oxidative stress, and determined their association with plasma nitric oxide (NOx) levels as an index of NO bioavailability. Older (62±2 yr) active men (n=12) who had exercised for >30 years and young (25±4 yr) active men (n=7) who had exercised for >3 years were age- and BMI-matched to older (n=11) and young (n=8) inactive men. Young subjects had lower plasma nitrotyrosine levels than older subjects (P=0.047). Young inactive subjects had higher ox-LDL levels than either the young active (P=0.042) or the older active (P=0.041) subjects. In addition, plasma oxidative stress levels, particularly ox-LDL, were correlated with various conventional plasma lipoprotein-lipid levels, and in older subjects were associated with Framingham risk score (r=0.49, P=0.015). We found no relationships between plasma oxidative stress markers and NOx levels. The findings suggest that a sedentary lifestyle may be associated with higher ox-LDL levels and that the levels of oxidative stress markers are related to levels of other conventional CVD risk factors and overall CVD risk.

Effects of endurance exercise training on markers of cholesterol absorption and synthesis.

Abnormal cholesterol metabolism, including low intestinal cholesterol absorption and elevated synthesis, is prevalent in diabetes, obesity, hyperlipidemia, and the metabolic syndrome. Diet-induced weight loss improves cholesterol absorption in these populations, but it is not known if endurance exercise training also improves cholesterol homeostasis. To examine this, we measured circulating levels of campesterol, sitosterol, and lathosterol in 65 sedentary subjects (average age 59 years; with at least one metabolic syndrome risk factor) before and after 6 months of endurance exercise training. Campesterol and sitosterol are plant sterols that correlate with intestinal cholesterol absorption, while lathosterol is a marker of whole body cholesterol synthesis. Following the intervention, plant sterol levels were increased by 10% (p<0.05), but there was no change in plasma lathosterol. In addition, total and LDL-cholesterol were reduced by 0.16 mmol and 0.10 mmol, respectively (p<0.05), while HDL-C levels increased by 0.09 mmol (p<0.05). Furthermore, the change in plant sterols was positively correlated with the change in VO2max (r=0.310, p=0.004), independent of other metabolic syndrome risk factors. These data indicate that exercise training reduces plasma cholesterol despite increasing cholesterol absorption in subjects with metabolic syndrome risk factors.

The effect of 7 years of intense exercise training on patients with coronary artery disease.

The purpose of this study was to evaluate the effects of long-term exercise training on maximal aerobic exercise capacity, evidence of myocardial ischemia and plasma lipid-lipoprotein concentrations in patients with coronary artery disease. Nine men with coronary artery disease, aged 57 +/- 2 years, who had completed 12 months of supervised intense exercise training were restudied after 6 additional years during which they continued to exercise. The first 12 months of training resulted in a 44% increase in maximal oxygen consumption (VO2max) from 25.0 +/- 1.3 to 35.9 +/- 1.5 ml X kg-1 X min-1 (p less than 0.001). The VO2max after 6 additional years (total 7 years) of intense training was 36.8 +/- 2.4 ml X kg-1 X min-1. Plasma high density lipoprotein (HDL)-cholesterol concentration increased from 38 +/- 3 to 45 +/- 4 mg X dl-1 at 12 months and rose further to 53 +/- 5 mg X dl-1 at 6 years of follow-up (p less than 0.05). The atherogenic index (total cholesterol/HDL-cholesterol ratio) decreased from 5.8 +/- 0.4 to 4.9 +/- 0.4 by 12 months (p less than 0.01) and to 4.1 +/- 0.4 after 6 additional years of training (p less than 0.05). Although the maximal heart rate-pressure product was 14% higher after 12 months of training, maximal ST segment depression was significantly less, 0.27 +/- 0.06 versus 0.19 +/- 0.04 mV (p less than 0.05); this improvement was maintained after 6 years of additional training. These data provide evidence that the beneficial effects of a program of intense exercise training can be maintained for long periods in some motivated patients with coronary artery disease who continue to exercise.

Effect of exercise intensity on glucose and insulin metabolism in obese individuals and obese NIDDM patients.

OBJECTIVE: The primary purpose of this study was to evaluate the acute effect of exercise of differing intensity on plasma glucose and insulin responses to an oral glucose challenge. RESEARCH DESIGN AND METHODS: Six obese men and six obese men with NIDDM of similar age, weight, percentage body fat, and VO2peak participated in the study. Each subject underwent two 7-day exercise programs in a counterbalanced order at 2-week intervals. During each 7-day exercise period, the subjects cycled every day at a power output corresponding to 50% VO2peak for 70 min or 70% VO2peak for 50 min. Muscle glycogen utilization was estimated during exercise on day 7 using a [3H]glucose infusion technique in conjunction with indirect calorimetry. During the day before and after each 7-day exercise period, a 3-h oral glucose tolerance test (OGTT) was administered after a 12-h overnight fast. RESULTS: The average caloric expenditure did not differ between exercise at 50 and 70% VO2peak in both obese and obese NIDDM subjects. However, the carbohydrate oxidation was higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (77 +/- 5 vs. 68 +/- 6 g) and obese NIDDM subjects (70 +/- 4 vs. 58 +/- 6 g). Muscle glycogen utilization was also higher (P < 0.05) during exercise at 70 than 50% VO2peak in obese subjects (59 +/- 9 vs. 30 +/- 7 g) and in obese NIDDM subjects (48 +/- 5 vs. 24 +/- 5 g). In obese subjects, plasma glucose response area during the OGTT did not change after 7 days of exercise at either 50 or 70% VO2peak. Plasma insulin response area during the OGTT also did not change after 7 days of exercise at 50% VO2peak. However, plasma insulin response area was reduced (P < 0.05) after 7 days of exercise at 70% VO2peak (9,644 +/- 1,783 vs 7,538 +/- 1,522 microU.ml-1.180 min-1). In obese NIDDM subjects, both plasma glucose and insulin response areas during the OGTT did not decrease after 7 days of exercise at either 50 or 70% VO2peak. CONCLUSIONS: It is concluded that the exercise-induced improvement in insulin sensitivity is influenced by exercise intensity in obese individuals. The improved insulin sensitivity after 7 days of exercise at 70% VO2peak in obese individuals may be related to greater muscle glycogen utilization during exercise. The lack of improvement in glucose tolerance and insulin sensitivity after 7 days of exercise at either 50 or 70% VO2peak in obese NIDDM patients may be due to the fact that the NIDDM patients selected in the present study were relatively hypoinsulinemic.

Improvement in glucose tolerance after 1 wk of exercise in patients with mild NIDDM.

We investigated the effects of 1 wk of intense exercise on glucose tolerance in 10 men with abnormal glucose tolerance [7 had mild non-insulin-dependent diabetes mellitus (NIDDM), and 3 had impaired glucose tolerance]. The 7 days of exercise did not result in significant changes in body weight or maximal oxygen uptake. Plasma glucose concentration at 120 min averaged 227 +/- 23 mg/dl in an oral glucose tolerance test (OGTT) before and 170 +/- 18 mg/dl after the 7 days of exercise (P less than .001). There was a 36% reduction in the area under the glucose tolerance curve. Plasma insulin concentration at 120 min of the OGTT averaged 172 +/- 27 microU/ml before and 106 +/- 13 microU/ml after 7 days of exercise (P less than .001); the area under the insulin curve was decreased by 32%. In contrast to the response to 7 days of exercise, one bout of exercise did not result in an improvement in glucose tolerance. These results provide evidence that regularly performed, vigorous exercise can be effective in decreasing insulin resistance and improving glucose tolerance within 7 days in some patients with mild NIDDM.

Insulin sensitivity in postmenopausal women: independent and combined associations with hormone replacement, cardiovascular fitness, and body composition.

OBJECTIVE: The effects of combined physical activity and hormone replacement therapy (HRT) on insulin sensitivity in postmenopausal (PM) women are unclear. The purpose of the study was to test the following hypotheses: 1) PM women who have undergone vigorous exercise training have greater insulin sensitivity than PM women who are physically active and PM women who are sedentary, and 2) PM women using HRT have greater insulin sensitivity than PM women not using HRT. We also sought to determine whether body composition or cardiovascular fitness was the stronger predictor of insulin sensitivity in these women. RESEARCH DESIGN AND METHODS: Three groups of PM women classified as sedentary (n = 18), physically active (n = 19), and athletic (n = 23) underwent an insulin-modified frequently sampled intravenous glucose tolerance test to determine the insulin sensitivity index (SI) and dual-energy X-ray absorptiometry to determine body composition. RESULTS: There was a significant association between both physical activity (P = 0.036) and HRT (P = 0.007) and fasting plasma insulin levels. The athletic PM women had the lowest plasma insulin levels and the highest SI. Across all physical activity levels, PM women using HRT (n = 29) had significantly lower fasting plasma insulin levels and a lower SI than PM women not using HRT (n = 31). HRT was significantly (P = 0.025) associated with intravenous glucose tolerance (KG); the women not using HRT had a higher K(G); than the PM women using HRT (0.83 +/- 0.08 vs. 0.60 +/- 0.05% per minute). Percent body fat (r = -0.37, P = 0.004) and VO2max (r = 0.35, P = 0.007) were similar predictors of SI. CONCLUSIONS: We conclude that, although overall HRT was associated with an attenuated SI, vigorous exercise training was independently associated with the greatest SI. In addition, PM women using HRT may benefit from having lower plasma insulin levels, but they may also have a lower SI.

APO E gene and gene-environment effects on plasma lipoprotein-lipid levels.

Apolipoprotein E (apo E) is important in plasma lipid metabolism and is a component of several plasma lipoprotein-lipid particles. Three major apo E isoforms are encoded by three common alleles at the APO E locus. The E2 allele is associated with lower and the E4 allele with higher total plasma cholesterol and LDL cholesterol levels compared with the E3 allele. Available data generally indicate that APO E2, and possibly E3, genotype individuals reduce plasma total and low-density lipoprotein (LDL) cholesterol levels more than APO E4 individuals with statin therapy. Some evidence also indicates that APO E2 individuals are more likely to respond favorably to gemfibrozil and cholestyramine. On the other hand, it appears that with probucol, APO E4 genotype individuals may improve plasma lipoprotein-lipid profiles more than APO E3 individuals. APO E2 and E3 genotype perimenopausal women appear to improve plasma lipoprotein-lipid profiles more with hormone replacement therapy than APO E4 women. On the other hand, low-fat diet interventions tend to reduce plasma LDL cholesterol and, perhaps, plasma total cholesterol levels more in APO E4 than in APO E2 or E3 individuals. Both cross-sectional and longitudinal studies generally indicate that APO E2 and E3 individuals improve plasma lipoprotein-lipid profiles more with exercise training than APO E4 individuals. Although these data are hardly definitive, they lend strong support for the possibility that in the near future individuals will be directed to what might be their optimal therapy for improving plasma lipoprotein-lipid profiles and cardiovascular disease risk based partially on APO E genotype.

Impaired insulin sensitivity and maximal responsiveness in older hypertensive men.

This study examines the relation between blood pressure and insulin resistance in obese, sedentary middle-aged and older men. Eleven hypertensive and 17 normotensive subjects of comparable age (58.6 +/- 1.0 years, mean +/- SEM), percent body fat (27.7 +/- 0.7%), and maximal aerobic capacity (30.2 +/- 0.9 mL.kg-1.min-1) participated in this study. Glucose disposal (M, milligrams per kilogram of fat-free mass per minute) determined during a three-dose hyperinsulinemic euglycemic clamp was lower in the hypertensive than normotensive subjects at the low (M at 120 pmol/m2.min: 2.3 +/- 0.2 versus 3.2 +/- 0.3, P = .06), intermediate (M at 600 pmol/m2.min: 8.0 +/- 0.6 versus 10.4 +/- 0.6, P = .02), and high (M at 3000 pmol/m2.min: 13.5 +/- 0.5 versus 15.5 +/- 0.7, P = .04) insulin infusion rates. The calculated insulin concentration necessary for a half-maximal effect (EC50) was greater in the hypertensive than normotensive subjects (1164 +/- 168 versus 864 +/- 66 pmol/L, P = .03). In this population of normotensive and hypertensive men, systolic, diastolic, and mean arterial blood pressures were related to glucose disposal at these insulin infusion rates (r = -.35 to -.46, P < .05) as well as the EC50 (r = .42 to .44, P < .05). Thus, hypertensive obese, sedentary older men have a reduction in both sensitivity and maximal responsiveness to insulin that is directly related to the severity of hypertension independent of obesity and physical fitness.

Improvement of insulin sensitivity by short-term exercise training in hypertensive African American women.

African American women have a high prevalence of insulin resistance, non-insulin-dependent diabetes mellitus, obesity, and hypertension that may be linked to low levels of physical activity. We sought to determine whether 7 days of aerobic exercise improved glucose and insulin metabolism in 12 obese (body fat >35%), hypertensive (systolic blood pressure > or =140 and/or diastolic blood pressure > or =90 mmHg) African American women (mean age 51+/-8 years). Insulin-assisted frequently-sampled intravenous glucose tolerance tests were performed at baseline and 14 to 18 hours after the 7th exercise session. There was no significant change in maximal oxygen consumption, body composition, or body weight after the 7 days of aerobic exercise. The insulin sensitivity index increased (2.68+/-0.45 x 10[-5] to 4.23+/-0.10 x 10[-5] [min(-1)/pmol/L], P=.02). Fasting (73+/-9 to 50+/-9 pmol/L, P=.02) and glucose-stimulated (332+/-58 to 261+/-45 pmol/L, P=.05) plasma insulin levels decreased. Additional measures related to the insulin resistance syndrome also changed with the 7 days of exercise: basal plasma norepinephrine concentrations were reduced (2.46+/-0.27 to 1.81+/-0.27 nmol/L, P=.02) and sodium excretion rate increased from 100+/-13 to 137+/-7 mmol/d (P=.03); however, there was no change in potassium excretion or 24-hour ambulatory blood pressure. We conclude that a short-term aerobic exercise program improves insulin sensitivity in African American hypertensive women independent of changes in fitness levels, body composition, or body weight. The present study indicates that short-term exercise can improve insulin resistance in hypertensive, obese, sedentary African American women and confirms previous reports that a portion of the exercise-induced improvements in glucose and insulin metabolism may be the result of recent exercise.

Exercise training-induced blood pressure and plasma lipid improvements in hypertensives may be genotype dependent.

Exercise training improves cardiovascular disease risk, but individual responses are highly variable. We hypothesized that common polymorphic gene variations would affect these responses. Sedentary obese hypertensive older men who had undergone exercise training were typed at the apolipoprotein (apo) E, angiotensin-converting enzyme (ACE), and lipoprotein lipase (LPL) loci. Individuals of all genotype subgroups were generally similar before training; they also changed body weight, body composition, and &f1;O(2)max similarly with training. ACE insertion/insertion (II) and insertion/deletion (ID) genotype individuals (n=10) tended to reduce systolic blood pressure more with training than deletion/deletion (DD) individuals (n=8) (-10 versus -5 mm Hg, P=0. 16). ACE II and ID individuals decreased diastolic blood pressure more with training than DD individuals (-10 versus -1 mm Hg, P<0. 005). Systolic blood pressure reductions with training were also larger in apoE3 and E4 (n=15) than apoE2 men (n=3) (-10 versus 0 mm Hg, P<0.05). The same trend was evident for diastolic blood pressure (-7 versus -3 mm Hg), but the difference was not significant. Systolic (14 versus -6 mm Hg, P=0.08) and diastolic (-9 versus -5 mm Hg, P=0.10) blood pressure reductions tended to be greater in LPL PvuII +/+ (n=4) than +/- and -/- individuals (n=14). Systolic (-10 versus 3 mm Hg, P<0.05) and diastolic (-9 versus 2 mm Hg, P<0.05) blood pressure reductions were larger in LPL HindIII +/+ and +/- (n=15) than -/- persons (n=3), respectively. LPL PvuII -/- individuals (n=3) had larger increases in HDL cholesterol (11 versus 2 mg/dL, P<0.05) and HDL(2) cholesterol (8 versus 0 mg/dL, P<0.05) than LPL PvuII +/- and +/+ individuals (n=15). These results are consistent with the possibility that apoE, ACE, and LPL genotypes may identify hypertensives who will improve blood pressure, lipoprotein lipids, and cardiovascular disease risk the most with exercise training.

Altered hemodynamics during exercise in older essential hypertensive subjects.

This study was designed to compare the resting and exercise hemodynamics of older adults with moderate hypertension with those of age-matched normotensive controls. Thirty-one hypertensive (20 men, 11 women; mean age, 63.9 +/- 2.8 years) and 28 normotensive subjects (15 men, 13 women; mean age, 62.6 +/- 2.4 years) were studied. There were no differences between the groups in terms of body weight, body composition, and maximal O2 consumption (VO2). At rest, there were no differences in VO2, cardiac output, stroke volume, or heart rate between the two groups, although systolic (158 +/- 13 vs 121 +/- 12 mm Hg) and diastolic blood pressures (94 +/- 7 vs 79 +/- 8 mm Hg) were higher in the hypertensive subjects. The hypertensive subjects' elevated blood pressure at rest was the result of a higher total peripheral resistance. During exercise, the hypertensive subjects had a lower cardiac output and stroke volume, no difference in heart rate and VO2, higher systolic, diastolic, and mean blood pressures, and a higher total peripheral resistance compared with their normotensive peers. The results indicate that older hypertensive persons have an altered cardiovascular response to exercise as compared with age-matched normotensive subjects. The responses also indicate that older essential hypertensive persons do not undergo excessive myocardial demands during exercise of the intensity usually prescribed in rehabilitation programs.

Bicycle ergometry and gas exchange measurements in neuromuscular diseases.

Using bicycle ergometry with computerized respiratory gas exchange measurements, we compared exercise capacities in patients with various neuromuscular diseases to those in normal controls. As expected, male and female patients had significantly reduced maximum work capacities (kilopond-meters per minute per kilogram of body weight) and maximal oxygen consumptions. The oxygen cost of exercise was normal in the majority of patients, although some appeared to have abnormally high oxygen consumptions during exercise. Breathing patterns during exercise, particularly in regard to onset of hyperventilation, were similar in patients and controls.

Endurance exercise training in a patient with central core disease.

A 36-year-old man with central core disease underwent endurance exercise training on a bicycle ergometer for 9 months. The training resulted in an increase in work capacity and maximal oxygen consumption of approximately 50%. Further improvement in his exercise capacity seemed limited by the primary disease. These results suggest that some neuromuscular disease patients may benefit from endurance exercise training.

The prolonged exercise test.

The response to a standardized exercise test was investigated in 12 volunteers and 13 patients with aches, cramps, and pains. In men, creatine kinase (CK) levels peaked (up to 1600 mU per milliliter) between 10 and 20 hours after exercise. High levels of blood lactate during exercise were related to the intensity of work and to high levels of CK after exercise. The patients could be divided into several groups: (1) those with no change in blood metabolites (psychogenic); (2) those with a disproportionate rise in CK (metabolic myopathies); (3) those with a disproportionate rise of lactate (mitochondrial abnormalities); and (4) in one patient with exercise-related pains, subnormal elevation of fatty acid levels. The correlation of changes in blood lactate, CK, and fatty acids may be useful, whereas an isolated measurement, even if outside the normal range, is often meaningless.

Riboflavin-responsive lipid myopathy and carnitine deficiency.

We used riboflavin to treat a patient with lipid myopathy, reduced exercise capacity, intolerance to fasting, and reduced concentrations of carnitine in muscle and serum. Although carnitine concentrations did not change, exercise capacity doubled, and response to fasting improved. Muscle enzyme assay showed that palmityl CoA dehydrogenase activity with and without added flavin adenine dinucleotide (a riboflavin product) was normal. Another riboflavin derivative, electron transfer flavoprotein, could be the site of the defect.

McArdle's disease with myoadenylate deaminase deficiency: observations in a combined enzyme deficiency.

Exercise and work potential of a patient with coexistent myophosphorylase and myoadenylate deaminase (AMPDA) deficiency was compared with that of three patients with myophosphorylase deficiency alone. The patient with the combined defect failed to produce an abnormal rise in serum ammonia or hypoxanthine as seen in the other patients after forearm exercise. Maximum oxygen consumption and work rates during cycle ergometer testing were similar in all patients, but well below controls. The occurrence of two defects involving short-term energy metabolism in muscle presents an opportunity to define further the metabolic role of AMPDA.

Carnitine "deficiency": lack of response to carnitine therapy.

A 29-year-old women had muscle weakness, low concentrations of carnitine in muscle and serum, and abnormally low urinary excretion of carnitine. During a fast, exercise capacity declined, ketone body concentrations rose, metabolic acidosis worsened, and she became hypoglycemic. After treatment with oral carnitine, serum carnitine content returned to normal and blood glucose was maintained during fasting, but ketone body concentrations in blood were even higher. Muscle carnitine content and exercise capacity did not improve. This patient demonstrated features of both systemic and muscle carnitine deficiency, suggesting that the current classification of carnitine-deficiency syndromes is inadequate.

Effect of exercise training in 60- to 69-year-old persons with essential hypertension.

This study sought to determine whether 9 months of low- or moderate-intensity exercise training could decrease blood pressure (BP) in hypertensive men and women (mean age 64 +/- 3 years). Patients underwent weekly BP evaluations for 1 month to ensure that they had persistently elevated BP and then completed a maximal treadmill exercise test to exclude those with overt coronary artery disease. The low- and moderate-intensity groups trained at 53 and 73% of maximal oxygen consumption (VO2 max), respectively; however, total caloric expenditure per week was similar in both groups. VO2 max did not increase in the low-intensity group with training, but increased 28% in the moderate-intensity group. Diastolic BP decreased 11 to 12 mm Hg in both training groups. Systolic BP decreased 20 mm Hg in the low-intensity group with training, which was significantly greater than the change in the control and the moderate-intensity groups. Although systolic BP decreased 8 mm Hg in the moderate-intensity training group, this reduction was not significant. Training resulted in a somewhat lower cardiac output at rest in the low-intensity group, whereas total peripheral resistance decreased slightly in the moderate-intensity training group. Plasma and blood volumes, plasma renin levels and urinary sodium excretion did not change in either group with training. Both groups manifested lower plasma norepinephrine levels after training during standing rest, but not while supine. Thus, low-intensity training may lower BP as much or more than moderate-intensity training in older persons with essential hypertension, but the underlying mechanisms are unclear.

Effects of training on systolic time intervals at rest and during isometric exercise in men and women 61 to 64 years old.

To determine whether regular exercise improves left ventricular (LV) contractile function in persons 60 years and older, systolic time intervals (STIs) were measured in 10 healthy men and women (mean age 62 +/- 1 year [+/- standard deviation]) before and after 6 months of intense endurance training. STIs, systolic and diastolic blood pressure (BP) and heart rate (HR) were determined at rest and in response to isometric handgrip exercise. Systolic BP, diastolic BP and HR increased acutely from rest in response to handgrip (p less than 0.002). The indexes of total electromechanical systole and LV ejection time (ET) index increased (p less than 0.01), preejection period (PEP) index increased (p less than 0.05) or remained unchanged and PEP/LVET did not change from values at rest in response to handgrip. Training resulted in an 18% increase in maximal oxygen uptake (p less than 0.01). After training, systolic and diastolic BP were reduced at rest (p less than 0.002) and, along with HR, were lower in response to handgrip (p less than 0.002). However, training did not alter STIs at rest or during handgrip. These findings indicate that healthy persons in their 60s have a normal LV response to isometric exercise. Prolonged, intense endurance training does not alter LV contractile function at rest or in response to isometric exercise. However, training can significantly reduce BP at rest, and markedly lower the HR-systolic BP product attained during acute isometric stress, even in normotensive older subjects.

Effect of exercise training on the blood pressure and hemodynamic features of hypertensive adolescents.

Twenty-five adolescents (aged 16 +/- 1 years) whose blood pressure (BP) was persistently above the 95th percentile for their age and sex were studied before and after 6 +/- 1 months of exercise training and again 9 +/- 1 months after the cessation of training. Maximal oxygen consumption (VO2) increased significantly with training. There was no change in body weight or sum of skinfolds. Both systolic and diastolic BP decreased significantly with training; however, complete BP normalization was not achieved. When the subjects were retested 9 +/- 1 months after cessation of training, systolic BP and VO2 max had returned to pretraining levels; however, diastolic BP was still below pretraining levels in the subjects who had diastolic hypertension initially. Except in subjects who initially had an elevated cardiac output, no consistent hemodynamic changes were found with training or cessation of training to account for the reductions in BP. The subjects whose resting cardiac outputs were high initially had significantly lower cardiac outputs after training as a result of decreases in both heart rate and stroke volume; however, vascular resistance remained unchanged. Sedentary control subjects with similar BP had no significant change in any of the variables measured over a similar period. These data indicate that moderate endurance exercise training can lower BP in otherwise healthy hypertensive adolescents as an initial therapeutic intervention.