Fibronectin mRNA in the developing glomerular crescent in rabbit antiglomerular basement membrane disease.

Fibronectin is a multifunctional matrix protein important in wound healing that is markedly increased in glomerular crescents. A previous report established two phases of fibronectin metabolism in crescent formation in an anti-glomerular basement membrane model of crescentic nephritis in the rabbit. Phase I was associated with increased glomerular fibronectin content from plasma. Phase II was associated with increased fibronectin mRNA in glomeruli. To examine the hypothesis that fibronectin is synthesized in the developing crescent, rabbit fibronectin cDNA was cloned, sense and antisense riboprobes were prepared and their specificity under the conditions to be used was validated and in situ hybridization studies were performed in the model. The results showed that the cells in the developing glomerular crescent express an intense fibronectin mRNA signal at Day 7 and that this signal persisted in cells of the crescent at Day 14. This result shows that fibronectin synthesis does indeed take place in cells of the developing crescent in this model and supports the hypothesis that fibronectin may be an important agent regulating crescent formation and fibrosis.

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.

Cardiovascular response to maximal cycle exercise during pregnancy and at two and seven months post partum.

We examined the cardiovascular response at rest and during upright cycle exercise in nine women during pregnancy (25.6 +/- 3.0 weeks' gestation) and at 2 months (8.8 +/- 1.8 weeks) and 7 months (30.0 +/- 2.5 weeks) post partum. Antepartum resting cardiac output, heart rate, and stroke volume were higher, whereas the arterial-venous oxygen difference was lower than both postpartum values. The antepartum resting oxygen uptake did not differ from 2 months post partum but was higher than at 7 months post partum. Cardiac output during submaximal exercise was greater antepartum than at both postpartum tests. Submaximal antepartum oxygen uptake, heart rate, and stroke volume were generally higher, and the arterial-venous oxygen difference was lower than at 7 months post partum. The slope of the antepartum cardiac output versus oxygen uptake relationship did not differ from the value at 2 months post partum, (6.16 +/- 1.38 and 5.84 +/- 1.34, p greater than 0.05) but was higher than at 7 months post partum (5.22 +/- 0.78, p less than 0.05). There were no significant differences in maximal oxygen uptake or heart rate among the three testing periods. Maximal cardiac output and stroke volume were higher antepartum than at 2 and 7 months post partum, whereas the arterial-venous oxygen difference was lower than at 7 months post partum. There were few significant differences in resting, submaximal, or maximal measurements between the two postpartum conditions. These data suggest that the augmented cardiac response to exercise during pregnancy is reduced by 2 months post partum but that additional time may be required for a complete resolution of the cardiovascular changes induced by pregnancy.

Effect of maternal weight gain during pregnancy on exercise performance.

We examined the effect of maternal weight gain during pregnancy on exercise performance. Ten women performed submaximal cycle (up to 60 W) and treadmill (4 km/h, up to 10% grade) exercise tests at 34 +/- 1.5 (SD) wk gestation and 7.6 +/- 1.7 wk postpartum. Postpartum subjects wearing weighted belts designed to equal their body weight during the antepartum tests performed two additional treadmill tests. Absolute O2 uptake (VO2) at the same work load was higher during pregnancy than postpartum during cycle (1.04 +/- 0.08 vs. 0.95 +/- 0.09 l/min, P = 0.014), treadmill (1.45 +/- 0.19 vs. 1.27 +/- 0.20 l/min, P = 0.0002), and weighted treadmill (1.45 +/ 0.19 vs. 1.36 +/- 0.20 l/min, P = 0.04) exercise. None of these differences remained, however, when VO2 was expressed per kilogram of body weight. Maximal VO2 (VO2max) estimated from the individual heart rate-VO2 curves was the same during and after pregnancy during cycling (1.96 +/- 0.37 to 1.98 +/- 0.39 l/min), whereas estimated VO2max increased postpartum during treadmill (2.04 +/- 0.38 to 2.21 +/- 0.36 l/min, P = 0.03) and weighted treadmill (2.04 +/- 0.38 to 2.19 +/- 0.38 l/min, P = 0.03) exercise. We conclude that increased body weight during pregnancy compared with the postpartum period accounts for 75% of the increased VO2 during submaximal weight-bearing exertion in pregnancy and contributes to reduced exercise capacity. The postpartum increase in estimated VO2max during weight-bearing exercise is the result of consistently higher antepartum heart rates during all submaximal work loads.

Effects of Anabolic Steroids on Lipoprotein Profiles of Female Weight Lifters.

In brief The effects of resistance exercise and anabolic steroids on lipoprotein profiles were examined in female weight lifters. Steroid users had significantly depressed levels of HDL-C, HDI-2-C (p <.05), and apolipoprotein (apo) A-I compared with nonusers and controls. Nonusers had significantly higher levels of HDL-C and HDL2-C than the controls. Users had significantly less favorable ratios of total cholesterol (TC) to HDL-C, HDL2-C to HDL3-C, and apo A-I to apo B than nonusers or controls. Women who participate in resistance training apparently have significantly better lipoprotein profiles than their sedentary counterparts, but these changes do not offset the deleterious effects of steroid use.

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.

Aerobic exercise during pregnancy. Special considerations.

Alterations in maternal physiology during pregnancy affect the physiological respect to aerobic exercise. Maternal resting oxygen consumption (VO2) and cardiac output increase during pregnancy. Heart rate (HR) becomes progressively elevated through 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 VO2 during pregnancy are dependent on the mode of exercise. At the same workload, VO2 increases during weight-bearing exercise, but usually does not differ from postpartum values during weight-supported exercise. One study found no change in VO2max during pregnancy compared to postpartum values. Some recent evidence indicates that the cardiac output vs VO2 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.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

Contrasting effects of testosterone and stanozolol on serum lipoprotein levels.

Oral anabolic steroids produce striking reductions in serum concentrations of high-density lipoprotein (HDL) cholesterol. We hypothesized that this effect related to their route of administration and was unrelated to their androgenic potency. We administered oral stanozolol (6 mg/d) or supraphysiological doses of intramuscular testosterone enanthate (200 mg/wk) to 11 male weight lifters for six weeks in a crossover design. Stanozolol reduced HDL-cholesterol and the HDL2 subfraction by 33% and 71%, respectively. In contrast, testosterone decreased HDL-cholesterol concentration by only 9% and the decrease was in the HDL3 subfraction. Apolipoprotein A-I level decreased 40% during stanozolol but only 8% during testosterone treatment. The low-density lipoprotein cholesterol concentration increased 29% with stanozolol and decreased 16% with testosterone treatment. Stanozolol, moreover, increased postheparin hepatic triglyceride lipase activity by 123%, whereas the maximum change during testosterone therapy (+25%) was not significant. Weight gain was similar with both drugs, but testosterone was more effective in suppressing gonadotropic hormones. We conclude that the undesirable lipoprotein effects of 17-alpha-alkylated steroids given orally are different from those of parenteral testosterone and that the latter may be preferable in many clinical situations.

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.

Cardiovascular response to cycle exercise during and after pregnancy.

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(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.

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.

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.

Fetal heart rate response to maternal exertion.

Doppler monitoring of fetal heart rates during maternal exertion has suggested that fetal bradycardia occurs frequently during vigorous exercise, causing concern for fetal safety. Doppler determination of fetal heart rate during vigorous maternal effort is difficult. To avoid motion artifact, we observed fetal heart rate using two-dimensional ultrasound and determined the incidence of fetal bradycardia in 45 pregnant women (age, 29.0 +/- 3.7 years [mean +/- SD]; gestational age, 25.2 +/- 3.0 weeks) during 85 submaximal and 79 maximal cycle ergometer tests. Average fetal heart rate did not change during exercise. A single episode of fetal bradycardia (heart rate less than 110 beats per minute for greater than or equal to 10 s) occurred during submaximal exertion during a maternal vasovagal episode. Sixteen episodes of fetal bradycardia were noted within three minutes after cessation of exercise, 15 of which followed maximal maternal effort. We conclude that brief submaximal maternal exercise up to approximately 70% of maximal aerobic power (maternal heart rate less than or equal to 148 beats per minute) does not affect fetal heart rate. In contrast to submaximal maternal exertion, maximal exertion is commonly followed by fetal bradycardia. This may indicate inadequate fetal gas exchange.

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)

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.

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)

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.

Cardiorespiratory exercise training in children.

Definitive statements concerning the cardiorespiratory effects of exercise training in children cannot be made. Few carefully controlled and well-defined exercise training studies including important cardiorespiratory variables have been conducted. Generally, it appears that the response to training in pubescent and postpubescent children is not different from what is observed in adults.