Left ventricular function is not impaired in weight-lifters who use anabolic steroids.

Recent reports suggest that anabolic steroid use might deleteriously affect left ventricular function. To examine this possibility, the present study measured left ventricular size and function with use of Doppler echocardiographic techniques in 23 weight lifters: 12 who were currently using anabolic steroids and 11 who reported that they had never used these drugs. Drug users had administered anabolic steroids to themselves for at least three cycles over the past year. All studies were interpreted by blind review and group assignment was confirmed by urine testing. Average age, years of exercise training and body weight, as well as heart rate and blood pressure at rest were similar in both groups. Cardiac dimensions (mean +/- SD) including left ventricular diastolic cavity diameter (57 +/- 3 vs. 56 +/- 5 mm), septal thickness (10 +/- 2 vs. 9 +/- 1 mm), posterior wall thickness (8 +/- 1 vs. 8 +/- 1 mm) and myocardial mass (149 +/- 27 vs. 135 +/- 21 g) did not differ between the anabolic steroid users and nonusers, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Training, diet and physical characteristics of distance runners with low or high concentrations of high density lipoprotein cholesterol.

We examined possible determinants of serum high density lipoprotein cholesterol (HDL-C) concentrations in 56 male distance runners (aged 20-56 years) by comparing runners whose HDL-C were either above or below the group median of 63 +/- 13 (+/- SD) mg/dl. HDL-C averaged 53 +/- 7 mg/dl for runners below and 73 +/- 11 mg/dl for runners above the median. Neither exercise training (miles run per week, years of running), physical characteristics (height, weight, adiposity), or dietary factors (total daily caloric intake and daily caloric intake from protein, fat, saturated fat, polyunsaturated fat, carbohydrate, and alcohol) differed between the two groups (P greater than 0.05, MANOVA). Apo A-I (P less than 0.01) was higher and triglyceride concentrations lower (P = 0.07) in the high HDL-C group. The data were also analyzed by comparing runners in the lowest and highest tertiles for HDL-C values and essentially the same results were obtained. When all runners were combined, neither training, physical characteristics nor dietary intake was significantly related to HDL-C (P greater than 0.05). Total cholesterol and apo A-I were directly related (r = 0.35 and r = 0.66, respectively, P less than 0.01) and triglycerides inversely related (r = -0.31, P less than 0.05) to HDL-C. Plasma post-heparin lipoprotein lipase activity (LPLA), hepatic triglyceride lipase activity (HTGLA), and HDL-C subfractions were measured in 22 runners.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of atenolol or prazosin on maximal exercise performance in hypertensive joggers.

We evaluated maximal performance during cycle ergometry and treadmill exercise in 14 hypertensive male joggers treated with prazosin or atenolol in an unblinded, placebo-controlled, crossover design. Maximal oxygen uptake was measured during both exercise modalities; cardiac output was measured only during cycle ergometry using the acetylene rebreathing technique. Both drugs reduced resting systolic and diastolic blood pressures. Prazosin reduced total peripheral resistance during submaximal exercise but had little effect on maximal cycle and treadmill performance. Atenolol, in contrast, reduced treadmill duration, maximal oxygen uptake, and heart rate compared with placebo. Atenolol also increased stroke volume and the arterial venous oxygen difference and reduced cardiac output during cycle exercise. Both drugs produced similar reductions in exercise diastolic pressure, but exercise systolic pressure was lower only during atenolol treatment. Prazosin was better tolerated by the subjects and was preferred by 10 of the men. We conclude that both drugs effectively reduced resting blood pressure, but that atenolol decreased exercise cardiac output and may impede exercise performance in physically active hypertensive subjects.

Elevated high-density lipoprotein cholesterol in endurance athletes is related to enhanced plasma triglyceride clearance.

We compared the clearance rate (K2) of plasma triglycerides (TG) following the intravenous (IV) infusion of a fat emulsion in 13 male endurance athletes (age 33 +/- 5.6 years, mean +/- SD) and 12 sedentary men (33 +/- 5.6 years). The athletes had lower fasting triglycerides (TG) (75 +/- 30.4 mg/dL v 125 +/- 52.5 mg/dL) and higher high-density lipoprotein (HDL) cholesterol concentrations (64 +/- 16.2 mg/dL v 42 +/- 9.4 mg/dL) than the sedentary subjects (P less than .01 for all). The higher HDL concentrations were due to increases in both the HDL2 and HDL3 subfractions. K2 in the athletes was 92% higher than that in the sedentary men (4.8 +/- 2.3%/min v 2.5 +/- 0.7%/min, P less than .01), but there was no difference in postheparin lipoprotein lipase activity (LPLA) between the groups (P greater than .05). K2 was positively correlated with LPLA (r = .51) and inversely related to fasting TG concentrations (r = -.73, P less than .01 for both). Furthermore, K2 was directly related to HDL (r = .75), HDL2 (r = .72), and HDL3 (r = .60) cholesterol concentrations (P less than .01 for all). These data suggest that the low TG levels in endurance athletes result at least in part from increased TG removal and that the elevated HDL concentrations of endurance athletes are related to enhanced fat clearance.

The effects of caloric restriction or exercise cessation on the serum lipid and lipoprotein concentrations of endurance athletes.

The interaction of exercise and diet in determining the lipid profiles of endurance athletes is poorly defined. Since active men consume more calories than sedentary individuals, we examined the effects of caloric restriction alone or in combination with exercise cessation on the serum lipid levels of men running 16 km daily. For seven days before each study, subjects consumed diets composed of 15% protein, 32% fat, and 53% carbohydrate. During ten-day experimental periods, one group (n = 10) continued running and consumed the same diet containing 3670 kcal/day, while two other groups consumed an identical diet containing 20% fewer calories and either continued (n = 16) or stopped (n = 15) exercise training. High-density lipoprotein cholesterol (HDL-C) concentrations decreased 1% to 5% in all groups during the seven-day preliminary diet. Additional reductions in total HDL-C concentrations were similar in the control and exercise cessation groups, but HDL2-C level decreased 15% during exercise cessation. During caloric restriction and continued running, in contrast, HDL-C concentration increased 8% and the HDL2-C subfraction increased 23%. There was little change in levels of apolipoprotein A-I concentrations during any of the protocols, demonstrating that changes in HDL-C are not necessarily attended by changes in the major HDL apoprotein. Low-density lipoprotein cholesterol (LDL-C) level decreased 10% to 15% in all groups during the preliminary period. Only small additional reductions occurred in men who continued running. Exercise cessation, however, was associated with a 10% increase in LDL-C level after only two days of inactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of high-carbohydrate and high-fat diets on the serum lipid and lipoprotein concentrations of endurance athletes.

We examined the effects of high-carbohydrate and high-fat diets on the serum lipid levels of distance runners. For seven days before each study, subjects consumed a diet containing 15% protein, 32% fat, and 53% carbohydrate. During 14-day experimental periods, a control group (n = 10) continued the same diet while two other groups consumed 69% of their calories as either carbohydrate (n = 13) or fat (n = 14). High-density lipoprotein (HDL)-cholesterol decreased 9% during the high-carbohydrate diet because of a 26% fall in the HDL2 fraction (1.063 to 1.125 g/mL). These changes were not accompanied by changes in the levels of apolipoproteins (apo) A-I or A-II. Total and low-density lipoprotein (LDL)-cholesterol initially decreased but subsequently exceeded pre-diet values while triglyceride concentrations increased 30% to 50%. Postheparin lipoprotein lipase activity (LPLA) fell 20%. Despite these dietary effects, HDL and HDL2 cholesterol concentrations in the athletes remained above values typical of sedentary men. The high-fat diet produced different effects on the serum lipids and lipoprotein levels of the athletes. HDL levels changed little during the study although HDL-cholesterol and apo A-I on the last diet day were both slightly above initial values. The high-fat diet provided 111 g of saturated fat per day but had surprisingly little effect on total and LDL-cholesterol whereas serum triglycerides fell by 10% to 20%. Postheparin LPLA increased 30% with fat feeding and the changes in LPLA correlated with alterations in triglyceride levels (r = -0.53, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute increase in lipoprotein lipase following prolonged exercise.

We investigated the acute effects of prolonged exercise on lipoprotein metabolism. Serum lipid and lipoprotein concentrations and plasma postheparin lipolytic activity were measured in ten well-trained men (ages 21 to 39) the day before and after a 42 km foot race. LDL cholesterol decreased by 10% (113 +/- 31 to 103 +/- 32 mg/dL, P less than 0.01) and total HDL-cholesterol levels increased by 9% (65 +/- 18 to 71 +/- 19 mg/dL, P less than 0.01) the day after the race. No changes in the concentration of apolipoprotein A-I or A-II occurred. Triglyceride levels decreased by 39% (95 +/- 38 to 58 +/- 23 mg/dL, P less than 0.001). Two days after the race, total HDL cholesterol (74 +/- 21 mg/dL, P less than 0.05) and the HDL2 subfraction (37 +/- 19 mg/dL, P less than 0.05) remained significantly elevated compared to pre-race values. Most dramatically, the level of lipoprotein lipase activity measured in postheparin plasma nearly doubled after the race, demonstrating that vigorous exercise acutely increases this enzyme activity. The increase in lipoprotein lipase activity probably mediated the fall in serum triglycerides after exercise and may also account for the increase in HDL cholesterol.

Exercise acutely increases high density lipoprotein-cholesterol and lipoprotein lipase activity in trained and untrained men.

We studied the effects of a single exercise session on lipid and lipoprotein concentrations and on postheparin plasma lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase activities (HTGLA) in 11 trained (T) and ten untrained (UT) men. Subjects exercised on a bicycle ergometer at 80% of their maximal heart rate for one (UT) or two hours (T). Blood samples were drawn 24 hours before and at ten minutes and 24, 48, and 72 hours after exercise. Values were analyzed before and after adjustment for estimated changes in plasma volume (PV). High density lipoprotein cholesterol (HDL-C) increased 2 +/- 4 mg/dL in T (P less than 0.05) and 1 +/- 2 mg/dL in UT subjects beginning 48 hours after exercise. This increase was magnified by adjusting for the 5% to 8% postexercise expansion of PV. The increase in HDL in the T subjects was produced by increases in the HDL2-C subfraction (+3 +/- 4 mg/dL, P less than 0.05) whereas HDL3 increased in the UT men (+2 +/- 3 mg/dL, P less than 0.05). LPLA did not change in either subject group when estimated PV changes were ignored but increased 11% (P less than 0.05) at 24 hours after exercise when PV was considered. HTGLA was 11% below baseline in the UT men 24 to 72 hours after exercise (P less than 0.05) but showed no change in either subject group after adjustment for PV. These results demonstrate that exercise acutely increases HDL levels by raising the HDL2 subfraction in T and the HDL3 subfraction in UT men.(ABSTRACT TRUNCATED AT 250 WORDS)

Variations in plasma volume affect total and low-density lipoprotein cholesterol concentrations during the menstrual cycle.

Serum lipids are known to vary during the menstrual cycle. To determine if changes in plasma volume contribute to this effect, we determined serum lipids, lipoproteins, and estimated changes in plasma volume in 18 premenopausal women at the start of and at 5-day intervals after menstruation. Eleven men served as a comparison group. Changes in plasma volume were estimated from changes in hemoglobin and hematocrit. Total and low-density lipoprotein (LDL) cholesterol (mean +/- SD) increased 15 +/- 14 mg/dL (9% +/- 10%) and 11 +/- 13 (11% +/- 14%) within 10 days after the start of menstruation (P < .05) and then decreased toward baseline during the rest of the cycle. High-density lipoprotein (HDL) cholesterol increased 3 mg/dL, or 5%, (P < .05) on days 10 and 15 after menstruation. Plasma volume decreased 4% +/- 9% (P < .06) 10 days after the start of menstruation, and this maximum decrease in plasma volume coincided with peak increases in total, LDL, and HDL cholesterol. Except for an 8-mg/dL increase in LDL cholesterol at day 5, lipid changes were no longer significant after adjusting for changes in plasma volume. We conclude that alterations in plasma volume account for approximately half of the increase in total and LDL cholesterol during the menstrual cycle.

Postheparin plasma lipolytic activities in physically active and sedentary men after varying and repeated doses of intravenous heparin.

We sought to determine the optimal dose of heparin for evaluating the activities of lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase (HTGLA) in postheparin plasma. Nine physically active and ten sedentary men (age 30 +/- 5 yr, mean +/- SD) received 30, 50, 75, and 100 IU/kg of heparin in random order during a 2-week period. Based on all the samples, the average LPLA in the athletes was 43% higher (P less than 0.001) and HTGLA was 19% lower than in the untrained subjects (NS). The greatest LPLA was obtained after a heparin dose of 75 IU/kg, but LPLA after the three highest doses were not significantly different. There was also a dose effect on HTGLA (P less than 0.001) with greatest activities following doses of 75 and 100 IU/kg. Despite these dose effects, subjects maintained their rank order for both postheparin lipase activities regardless of the heparin dose. The only exception was for LPLA in the sedentary men probably because of lower LPLA and a smaller range of values. We also examined the effect of repeated daily injections of 75 IU/kg heparin on LPLA, HTGLA, and serum lipids. Repeated heparin administration on three consecutive days produced no significant effects on the apparent lipase activities. When all subjects were combined, HDL-cholesterol was increased over time (P less than 0.05) due to increases in both the HDL2 (P less than 0.05) and HDL3-cholesterol (NS) subfractions. Infusion of heparin or saline on three consecutive days into 18 additional men, however, had no effect on any lipid parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Prediction of VO2max during cycle exercise in pregnant women.

We measured maximal O2 uptake (VO2max) during stationary cycling in 40 pregnant women [aged 29.2 +/- 3.9 (SD) yr, gestational age 25.9 +/- 3.3 wk]. Data from 30 of these women were used to develop an equation to predict the percent VO2max from submaximal heart rates. This equation and the submaximal VO2 were used to predict VO2max in the remaining 10 women. The accuracy of VO2max values estimated by this procedure was compared with values predicted by two popular methods: the Astrand nomogram and the VO2 vs. heart rate (VO2-HR) curve. VO2max values estimated by the derived equation method in the 10 validation subjects were only 3.7 +/- 12.2% higher than actual values (P greater than 0.05). The Astrand method overestimated VO2max by 9.0 +/- 19.4% (P greater than 0.05), whereas the VO2-HR curve method underestimated VO2max by only 1.6 +/- 10.3% in the same 10 subjects (P greater than 0.05). Both the Astrand and the VO2-HR curve methods correlated well with the actual values when all 40 subjects were considered (r = 0.77 and 0.85, respectively), but the VO2-HR curve method had a lower SE of prediction than the Astrand method (8.7 vs. 10.4%). In a comparison group of 10 nonpregnant sedentary women (29.9 +/- 4.5 yr), an equation relating %VO2max to HR nearly identical to that obtained in the pregnant women was found, suggesting that pregnancy does not alter this relationship. We conclude that extrapolating the VO2-HR curve to an estimated maximal HR is the most accurate method of predicting VO2max in pregnant women.

Physiological factors associated with the lower maximal oxygen consumption of master runners.

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.

Assessing VO2max in epidemiologic studies: modification of the Astrand-Rhyming test.

Direct measurement of maximum oxygen uptake (VO2max) is the standard index of cardiorespiratory fitness, but is practical only in a laboratory setting. Current cycle ergometer tests to estimate VO2max are difficult for inactive adults because most of these tests are lengthy and require a high initial exercise rate. We modified an existing test, the Astrand-Rhyming test, to avoid these problems. Maximum oxygen uptake was measured directly and estimated by means of our protocol in a test group of 50 men and women, ten for each decade between 20 and 70 yr, to develop multiple regression equations to correct for variations due to age. Equations for each sex were computed with directly measured VO2max as the dependent variable and with the estimated VO2max and age as independent variables. The validity of these equations was tested by deriving data from an additional 63 subjects (validity group). No significant differences were found between the directly measured VO2max and the VO2max estimated by our protocol and equations. For each group, the mean difference between the two values was less than 120 ml X min-1. Correlations between the measured and estimated VO2max ranged from 0.92-0.93 for the age groups. Our modification of the Astrand-Rhyming protocol accurately estimates VO2max and is safe and suitable for assessing cardiovascular fitness in epidemiologic studies of people between the ages of 20-70 yr.

Cardiac size and VO2max do not decrease after short-term exercise cessation.

We measured maximum oxygen uptake, estimated changes in plasma volume, and the cardiac dimensions of 15 male competitive distance runners (28.2 +/- 5.6 yr of age, mean +/- SD) before and after 10 days of exercise cessation. Subjects were habitually active but adjusted their training to run 16 km daily for 2 wk before the study. Subjects were maintained on defined diets for the week before and during the detraining period. Average body weight decreased 1.0 +/- 0.5 kg (P less than 0.001) within 2 days of exercise cessation and was accompanied by a 5.0 +/- 5.9% (P less than 0.01) decrease in estimated plasma volume. No additional changes in body weight and plasma volume occurred during the study, and estimated percent body fat did not change. Resting heart rate, blood pressure, and cardiac dimensions were also unchanged with physical inactivity. In addition, maximum oxygen uptake was not altered although peak exercise heart rate was an average of 9 +/- 5 beats X min-1 (P less than 0.01) or 5% higher after detraining. We conclude that short periods of exercise cessation decrease estimated plasma volume and increase the maximum exercise heart rate of endurance athletes but do not alter their cardiac dimensions or maximum oxygen uptake.

Teaching behavioral medicine using individual coronary heart disease risk factors.

Two hundred twenty-one first-year medical students participated in a voluntary coronary heart disease risk factor self-change project designed to teach the principles of behavioral change. Blood pressure, serum lipids, percentage body fat, cardiovascular fitness, and smoking status were measured prior to the project. Students designed their own programs of behavior modification and, after 8 weeks, repeat measurements were obtained in students whose projects related to coronary heart disease risk (56% of entire group). Despite generally low initial coronary heart disease risk factors, most risk factor groups successfully altered the targeted risk factors. The subgroup attempting to lower serum cholesterol (n = 49) reduced total cholesterol 15 +/- 24 mg/dl (mean +/- SD) and low-density lipoprotein cholesterol 11 +/- 20 mg/dl (P less than 0.001 for both). The blood pressure group (n = 9) decreased systolic blood pressure 8 +/- 10 mm Hg (P less than 0.05), and the weight-loss group (n = 33) lost 3.0 +/- 2.9 kg (P less than 0.001), reducing estimated percentage body fat 1.7 +/- 1.8 (P less than 0.001). The self-change project was well received by the students and appears to be a useful technique for introducing the principles of behavioral medicine to first-year medical students.

High-density lipoprotein metabolism in runners and sedentary men.

We studied the high-density lipoprotein (HDL) metabolism of five trained men who ran 16 km daily and five inactive men. Runners were leaner and their aerobic exercise capacity was much greater. The mean HDL cholesterol level was 65 mg/dL in the runners and 41 mg/dL in the controls. The lipid-rich HDL2 species accounted for a much higher proportion of the HDL in runners (49% v 29%). Tracer studies of radioiodinated autologous HDL demonstrated that runners did not produce more HDL protein but rather catabolized less. The mean biologic half-life of HDL proteins was 6.2 days in the runners compared with 3.8 days in the sedentary men. The activity of lipoprotein lipase was 80% higher in the postheparin plasma of the runners, whereas the activity of hepatic triglyceride hydrolase was 38% lower. Thus, the prolonged survival of plasma HDL proteins in runners may result from augmented lipid transfer to HDL by lipoprotein lipase or diminished HDL clearance by hepatic lipase.

High density lipoprotein metabolism in endurance athletes and sedentary men.

BACKGROUND: Endurance athletes have higher high density lipoprotein (HDL) concentrations than sedentary controls. To examine the mechanism for this effect, we compared HDL apoprotein metabolism in 10 endurance athletes aged 34 +/- 6 years (mean +/- SD) and 10 sedentary men aged 36 +/- 8 years. METHODS AND RESULTS: Subjects were maintained on controlled diets for 4 weeks, and metabolic studies using autologously labeled 125I HDL were performed during the final 2 weeks. Lipids and lipoproteins were measured daily during these 2 weeks, and the average of 14 values was used in the analysis. HDL cholesterol (58 +/- 14 versus 41 +/- 10 mg/dl), HDL2 cholesterol (26 +/- 10 versus 12 +/- 8 mg/dl), and apolipoprotein A-I (apo A-I) (144 +/- 18 versus 115 +/- 22 mg/dl) were higher in the athletes, whereas triglyceride concentrations (60 +/- 18 versus 110 +/- 48 mg/dl) were lower (p less than 0.01 for all). Postheparin lipoprotein lipase activity was not different, but hepatic triglyceride lipase activity was 27% lower (p less than 0.06) in the athletes. The athletes' mean clearance rate of triglycerides after an infusion of Travamulsion (1 ml/kg) was nearly twofold that of the inactive men (5.8 +/- 1.5 versus 3.2 +/- 0.9%/min, p less than 0.001). There was no differences in HDL apoprotein synthetic rates, whereas the catabolic rates of both apo A-I (0.15 +/- 0.02 versus 0.22 +/- 0.05 pools per day, p less than 0.01) and apolipoprotein A-II (apo A-II) (0.15 +/- 0.02 versus 0.20 +/- 0.04 pools per day, p less than 0.05) were reduced in the trained men. Apo A-I and apo A-II half-lives correlated with HDL cholesterol in each group (r greater than 0.76, p less than 0.05 for all) but not consistently with lipase activities or fat clearance rates. This relation between apoprotein catabolism and HDL cholesterol was strongest at HDL cholesterol concentrations of less than 60 mg/dl. CONCLUSIONS: We conclude that higher HDL levels in active men are associated with increased HDL protein survival. The mechanisms mediating this effect require better definition, and other factors appear to contribute to HDL cholesterol and protein concentrations among individual subjects.

Prolonged exercise augments plasma triglyceride clearance.

We studied ten male distance runners before and after a marathon to determine the effects of prolonged exercise on serum lipoprotein values and the capacity to clear plasma triglycerides. Serum lipid and lipoprotein concentrations, intravenous fat clearance, and postheparin plasma lipolytic activities were measured 24 hours before and 18 hours after the race. The clearance rate of exogenous fat increased 76% +/- 64%, postheparin lipoprotein lipase activity increased 46% +/- 35%, and fasting triglyceride levels decreased 26% +/- 13% after the race. High-density lipoprotein (HDL) cholesterol level increased 10% +/- 8%, primarily due to a 19% +/- 17% increase in the HDL2 subfraction. Changes in the clearance rate of exogenous fat were directly related to changes in HDL cholesterol level and the HDL2 subfraction. Thus, the rise in HDL cholesterol concentrations after prolonged exercise may be a consequence of enhanced fat clearance.

Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training.

High-density lipoprotein (HDL) metabolism was studied in eight sedentary men before and after 14 and 32-48 weeks of exercise training. Subjects rode stationary bicycles 1 hour daily, 5 days each week for 14 weeks (n = 8), and 4 days each week thereafter for a total of 32-48 weeks (n = 7) of training. HDL metabolism was assessed with 125I-radiolabeled autologous HDL while subjects consumed defined diets. Maximal oxygen uptake increased 26 +/- 7% (p less than 0.001) after 14 weeks but did not increase further with more prolonged training. Body weight and estimated body fat did not change. HDL cholesterol increased 5 +/- 3 mg/dl, and triglycerides decreased 19 +/- 23 mg/dl after 14 weeks (p less than 0.025 for both), but there were no additional changes with continued training. Postheparin plasma lipoprotein lipase activity was 22% higher than baseline activity after both 14 (p less than 0.025) and 32 or more weeks of exercise. In contrast, hepatic triglyceride lipase activity was 16 +/- 8% and 15 +/- 8% lower than baseline at each measurement (p less than 0.005 for both). The disappearance rate of triglycerides after an intravenously administered fat solution was 24 +/- 24% higher at 14 weeks and 49 +/- 18% (p less than 0.005) higher after more prolonged training. Total and low-density lipoprotein cholesterol and apolipoprotein A-I and A-II concentrations at the end of study were not different from initial values. Plasma volume was 8% above initial values at both post-training measurements. The biological half-life of apolipoprotein A-I was unchanged at 14 weeks but was 10 +/- 13% longer (p = 0.07) and increased in all but one subject at the end of the study. Half-life for apolipoprotein A-II was 8 +/- 8% (p = 0.031) and 11 +/- 14% (p = 0.06) above baseline at 14 and 32 or more weeks, respectively. The synthetic rates for apolipoproteins A-I and A-II were not different from baseline values at 32-48 weeks. We conclude that 8-11 months of exercise training in previously sedentary men enhances fat tolerance and increases HDL cholesterol concentrations by prolonging HDL survival. The changes in HDL apolipoprotein survival, however, do not approximate the differences previously noted between elite endurance athletes and sedentary men. Changes in HDL cholesterol concentration were not large and suggest that the potential for exercise-related changes in HDL may be modest in many subjects.