Stanley P. Sady

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)

High density lipoprotein metabolism in endurance athletes and sedentary men.

BackgroundEndurance 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 ResultsSubjects 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), HDIL cholesterol (26 ± f10 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 < 0.01 for all). Postheparin lipoprotein lipase activity was not different, but hepatic triglyceride lipase activity was 27% lower (p < 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 (5.8t1.5 versus 3.2 ± 0.9%o/min, p < 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 < 0.01) and apolipoprotein A-TI (apo A-Il) (0.15 ± 0.02 versus 0.20 ± 0.04 pools per day, p < 0.05) were reduced in the trained men. Apo A-I and apo A-Il half-lives correlated with HDL cholesterol in each group (r > 0.76, p < 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. ConclswionsWe 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. (Circulation 1991;84:140–152)

Androgens reduce HDL2-cholesterol and increase hepatic triglyceride lipase activity

We quantified serum lipids and postheparin plasma lipolytic activities in 5 weightlifters presently self-administering androgenic steroids (users) and an equal number not currently using these drugs (non-users). Mean (+/- SD) age (23 +/- 2 vs 25 +/- 4 yr), body weight (102.7 +/- 11.4 vs 86.8 +/- 13.6 kg), and percent body fat (8.6 +/- 2.5 vs 7.8 +/- 6.0%) were not different in users and non-users, respectively. Similarly, there were no differences in total cholesterol (183 +/- 27 vs 176 +/- 32 mg.dl-1) low-density lipoprotein-cholesterol (138 +/- 25 vs 108 +/- 32 mg.dl-1), or triglyceride (93 +/- 26 vs 93 +/- 41 mg.dl-1) levels in the two groups. High-density lipoprotein (HDL)-cholesterol concentrations, however, were significantly lower in the users (26 +/- 10 vs 50 +/- 13 mg.dl-1; P less than 0.05), and most of the difference was due to lower HDL2-cholesterol concentrations (6 +/- 4 vs 22 +/- 9 mg.dl-1; P less than 0.05). Postheparin plasma lipoprotein lipase activity was only slightly lower in the users (3.49 +/- 2.23 vs 5.36 +/- 1.73 mumol FFA.ml-hr-1; P= NS). but hepatic triglyceride lipase activity was significantly higher in this group (27.99 +/- 6.89 vs 11.15 +/- 2.76, mumol FFA.ml-hr-1: P less than 0.001) and correlated inversely with HDL2-cholesterol concentrations (r = -0.81; P less than 0.01). We conclude that androgenic hormones reduce HDL-cholesterol concentrations and the HDL2-cholesterol subfraction, possibly by enhancing hepatic triglyceride lipase activity.

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)

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 < 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 < 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 < 0.05) due to increases in both the HDL2 (P < 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. We conclude that 75 IU/kg is as effective as 100 IU/kg of heparin for releasing LPLA and HTGLA and that the relative rank for lipase activities among subjects with a wide range of values is not affected by the heparin dose. Repeated heparin injections do not alter postheparin plasma lipase activities or lipid and lipoprotein concentrations measured on subsequent days.

Aerobic Exercise During Pregnancy: Special Considerations

SummaryAlterations in maternal physiology during pregnancy affect the physiological response to aerobic exercise. Maternal resting oxygen consumption (V̇O2) and cardiac output (Q̇) increase during pregnancy. Heart rate (HR) becomes progressively elevated throughout gestation, whereas stroke volume (SV) increases until the third trimester and then declines until term, probably because of diminished venous return. Plasma volume increases earlier and to a greater magnitude than red cell volume, resulting in the ‘haemodilutional anaemia’ of pregnancy and a decline in the oxygen-carrying capacity. Ventilation is greater during pregnancy because of elevated tidal volume and unchanged rate of breathing.The acute and chronic (training) responses to aerobic exercise during pregnancy have not been thoroughly investigated. Specifically, the effect of gestational age, maternal activity status, and type, duration and intensity of exercise on maternal cardiovascular response have only recently begun to be explored.During pregnancy cardiac output during submaximal exertion increases above values in non-pregnant women, except perhaps late in gestation. Both heart rate and stroke volume contribute to the elevated cardiac output. Changes in submaximal exercise V̇O2 during pregnancy are dependent on the mode of exercise. At the same workload, V̇O2 increases during weight-bearing exercise, but usually does not differ from postpartum values during weight-supported exercise. One study found no change in V̇02max during pregnancy compared to postpartum values. Some recent evidence indicates that the cardiac output vs V̇O2 relationship for pregnant women is within the range of average values reported for non-pregnant individuals. Exercise arterial-venous oxygen difference is lower during pregnancy, suggesting that the higher cardiac output is distributed to non-exercising vascular beds. The data are limited but suggest that the perfusion of exercising muscle is unchanged during pregnancy and that the major haemodynamic change is an augmented cardiac output so that blood flow to the uterus and fetus is not compromised.Only one study has measured blood flow during exercise in pregnant women. The reported 25% decrease in uterine blood flow during supine cycle exercise in women late in gestation must be interpreted cautiously because the uterus may obstruct the vena cava in the supine position. Studies of exercising pregnant animals usually indicate a decreased uterine blood flow but an enhanced oxygen extraction; the lower blood flow may be limited to non-placental areas. The applicability of these results to humans is unknown.Fetal heart rate has been reported to increase, decrease or remain unchanged during and after maternal exercise. Some of the discrepancies among studies may be because the measurement techniques do not account for artifact related to maternal movement. Fetal bradycardia is not uncommon following maximal maternal exertion.The few training studies of pregnant women are limited in value by the inclusion of several exercise modes, inadequately defined intensity and duration of exercise, or omission of important cardiovascular variables. Nevertheless, these studies generally indicate increased performance or physiological fitness with training during pregnancy. The literature suggests normal or improved parturition and fetal outcome for women who exercise during pregnancy, although large well-designed prospective studies are lacking. Recommendations for exercising during pregnancy are provided.

Time course of serum amyloid A response in myocardial infarction

Plasma concentrations of serum amyloid A (SAA), high density lipoprotein (HDL) cholesterol, non-HDL cholesterol, and apolipoproteins (Apo) A-I and B were measured daily for 6 days in 10 patients following myocardial infarction (MI) and in 10 secular controls admitted to a coronary care unit. SAA concentrations peaked 3 days following MI (mean 47 mg/dl) and correlated with creatine kinase (CK) (r = 0.67, P less than 0.001). Non-HDL cholesterol and Apo B fell 15 and 18%, respectively, reached nadirs 3-4 days after MI and were inversely related to CK concentrations (P less than 0.01 for both). HDL cholesterol levels, in contrast, increased 15% and were significantly higher than baseline by day 3 when SAA concentrations were maximum. HDL cholesterol subsequently fell in parallel with SAA and had returned to baseline by day 6. Apo A-I declined throughout the 6 days of observation and was 13% lower than initial values on day 6 (P less than 0.05). The Apo A-I reduction was inversely related to both CK and SAA concentrations. There were no significant changes in any of the analytes in control subjects. We conclude that Apo A-I and possibly Apo B containing lipoproteins are negative acute phase reactants. HDL cholesterol is transiently elevated after MI despite decreasing Apo A-I levels and this may relate to incorporation of SAA into HDL particles.

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.

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)