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The purpose of this study was to examine the effect of prolonged exercise on plasma lipid and lipoprotein concentrations and to identify caloric time-points where changes occurred. Eleven active male subjects ran on a treadmill at 70% of maximal fitness (VO2max) and expended 6278.7 kilojoules (Kj) energy (1500 kcal). Blood samples were obtained at the 4185.8 Kj (1000 kcal) timepoint during exercise and at each additional 418.6 Kj (100 kcal) expenditure until 6278.7 Kj was expended. After correcting for plasma volume changes, decreases in low-density lipoprotein cholesterol (LDL-C) were observed during exercise at time-points corresponding to 4604.4 and 5441.5 Kj (1100 and 1300 kcal) of energy expenditure, and immediately after exercise. Total cholesterol concentrations decreased significantly at exercise kilojoule expenditures of 4604.4, 5441.5 and 5860.1 (1100, 1300 and 1400 kcal). There were also exercise induced increases in high-density lipoprotein cholesterol (HDL-C) and HDL2-C concentrations immediately after exercise. Although acute lipid and lipoprotein changes are typically reported in the days following exercise, the current data indicate that some lipoprotein concentrations change during acute exercise. Our data suggest that a threshold of exercise may be necessary to change lipoproteins during exercise. Future work should identify potential mechanisms (lipoprotein lipase, cholesterol ester transport protein, LDL uptake) that alter lipoprotein concentrations during prolonged exercise.

Purpose: Most studies that use either a single exercise session, exercise training, or a cross-sectional design have failed to find a relationship between exercise and plasma lipoprotein(a) [Lp(a)] concentrations. However, a few studies investigating the effects of longer and/or more strenuous exercise have shown elevated Lp(a) concentrations, possibly as an acute-phase reactant to muscle damage. Based on the assumption that greater muscle damage would occur with exercise of longer duration, the purpose of the present study was to determine whether exercise of longer duration would increase Lp(a) concentration and creatine kinase. (CK) activity more than exercise of shorter duration. Methods: Ten endurance-trained men (mean +/- SD: age, 27 +/- 6 yr; maximal oxygen consumption [(V)over dotO(2max)], 57 +/- 7 mL(.)kg(-1) min(-1)) completed two separate exercise sessions at 70% (V)over dotO(2max). One session required 900 kcal of energy expenditure (60 +/- 6 min), and the other required 1500 kcal (112 +/- 12 min). Fasted blood samples were taken immediately before (0-pre), immediately after (0-post), 1 d after (1-post), and 2 d after (2-post) each exercise session. Results: CK activity increased after both exercise sessions (mean +/- SE; 800 kcal: 0-pre 55 +/- 11, 1-post 168 +/- 64 U(.)L(-1.)min(-1); 1500 kcal: 0-pre 51 +/- 5, 1-post 187 +/- 30, 2-post 123 +/- 19 U(.)L(-1.)min(-1); P < 0.05). However, median Lp(a) concentrations were not altered by either exercise session (800 kcal: 0-pre 5.0 mg(.)dL(-1), 0-post 3.2 mg(.)dL(-1), 1-post 4.0 mg(.)dL(-1), 2-post 3.4 mg(.)dL(-1); 1500 kcal: 0-pre 5.8 mg(.)dL(-1), 0-post 4.3 mg(.)dL(-1), 1-post 3.2 mg(.)dL(-1), 2-post 5.3 mg(.)dL(-1)). In addition, no relationship existed between exercise-induced changes in CK activity and Lp(a) concentration (800 kcal: r = -0.26; 1500 kcal: r = -0.02). Conclusion: These results suggest that plasma Lp(a) concentration will not increase in response to minor exercise-induced muscle damage in endurance-trained runners.

Lipoprotein(a) (Lp(a)) is bound to apolipoprotein B-100 by disulfide linkage and is associated in the upper density range of low density lipoprotein cholesterol. Persons with elevated concentrations of Lp(a) are regarded as having an increased risk for premature coronary artery disease. Although many studies exist evaluating the effects of a single session of exercise on lipids and lipoproteins, little information is available concerning the effects of exercise on Lp(a). Therefore, the purpose of this study was to determine the effects of a single exercise session on plasma Lp(a). Twelve physically active men completed two 30-min submaximal treadmill exercise sessions: low intensity (LI, 50% VO2max) and high intensity (HI, 80% VO2max). Blood samples were obtained immediately before and after exercise. Total cholesterol (LI: before 4.22 +/- 0.26, after 4.24 +/- 0.28; HI: before 4.24 +/- 0.31, after 4.11 +/- 0.28 mmol.l-1, mean +/- SE) and triglyceride (LI: before 1.14 +/- 0.16, after 1.06 +/- 0.16; HI: before 1.12 +/- 0.19, after 1.21 +/- 0.19 mmol.l-1) concentrations did not differ immediately after either exercise session, nor did Lp(a) concentrations differ immediately after either exercise session (LI: before 4.1 +/- 2.2, after 4.0 +/- 2.1: HI: before 3.9 +/- 2.2, after 3.7 +/- 2.0 mg.dl-1). These results suggest that neither a low nor a high intensity exercise session lasting 30 min in duration has an immediate effect on plasma Lp(a).

The purpose of this study was to determine the effects of exercise intensity on lipid and lipoprotein metabolism. Concentrations of triglyceride, cholesterol, high-density lipoprotein cholesterol (HDL-C) and its subfractions (HDL2-C and HDL3-C), low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, and apolipoproteins A-I, A-II, and B were measured. Ten well-trained runners completed treadmill exercise on two different occasions: a high-intensity session at 75% maximal oxygen consumption lasting 60 min and a low-intensity session at 50% maximal oxygen consumption lasting 90 min. Energy expenditure for each session was equal. Fasted blood samples were obtained 24 h before, immediately before, immediately after, and 1, 24, 48, and 72 h after each exercise session. No significant differences were found for the blood variables across time or between treatments. However, HDL-C and HDL2-C were slightly elevated on the days after each treatment. These results suggest that acute exercise sessions lasting less than 90 min, regardless of intensity, do not elicit plasma lipid, lipoprotein, and apolipoprotein changes in men who are habitually physically active and have high initial concentrations of HDL-C.

The metabolic cost of producing submaximal cycling power has been reported to vary with pedaling rate. Pedaling rate, however, governs two physiological phenomena known to influence metabolic cost and efficiency: muscle shortening velocity and the frequency of muscle activation and relaxation. The purpose of this investigation was to determine the relative influence of those two phenomena on metabolic cost during submaximal cycling. Nine trained male cyclists performed submaximal cycling at power outputs intended to elicit 30, 60, and 90% of their individual lactate threshold at four pedaling rates (40, 60, 80, 100 rpm) with three different crank lengths (145, 170, and 195 mm). The combination of four pedaling rates and three crank lengths produced 12 pedal speeds ranging from 0.61 to 2.04 m/s. Metabolic cost was determined by indirect calorimetery, and power output and pedaling rate were recorded. A stepwise multiple linear regression procedure selected mechanical power output, pedal speed, and pedal speed squared as the main determinants of metabolic cost ( R 2 = 0.99 ± 0.01). Neither pedaling rate nor crank length significantly contributed to the regression model. The cost of unloaded cycling and delta efficiency were 150 metabolic watts and 24.7%, respectively, when data from all crank lengths and pedal speeds were included in a regression. Those values increased with increasing pedal speed and ranged from a low of 73 ± 7 metabolic watts and 22.1 ± 0.3% (145-mm cranks, 40 rpm) to a high of 297 ± 23 metabolic watts and 26.6 ± 0.7% (195-mm cranks, 100 rpm). These results suggest that mechanical power output and pedal speed, a marker for muscle shortening velocity, are the main determinants of metabolic cost during submaximal cycling, whereas pedaling rate (i.e., activation-relaxation rate) does not significantly contribute to metabolic cost.

Initial information on the newly discovered hormone leptin suggests a primary role in energy balance and body weight maintenance. Recent published information suggests that leptin has an impact on several physiological systems, including neuroendocrine and immune function, as well as being involved in growth and development. Although the role of leptin in these areas is only partially understood at best, even less is known about the effect of exercise on plasma leptin concentrations. Further, if exercise has an impact on leptin concentration, how then does exercise affect overall leptin function? This article considers leptin function and the impact that exercise has on blood leptin concentrations, and suggests future directions for research on exercise and leptin. Leptin, a hormone synthesized primarily by adipose tissue and secreted into the circulatory system, is a purported satiety factor with receptors in the hypothalamus. Human leptin is a relatively small protein (16 kDa) which shares a high degree of homology with other species such as mice (84%) and rats (83%). Although rare in humans, leptin mutations in mice result in leptin deficiency and lead to early onset obesity, hyperphagia, and hypothalamic hypogonadism. Unlike leptin deficient mice, humans deficient in leptin do not suffer from hyperinsulinaemia, hyperglycaemia, hypercorticism, or hypothermia. Although regulation of leptin synthesis and release is poorly understood, a distinct circadian pattern for plasma leptin concentrations has been observed and is similar to that of prolactin and thyroid stimulating hormone.1 Conflicting …

The purpose of this study was to determine the effects of a single period of swim exercise to exhaustion on the cellular distribution of hexokinase in rat skeletal muscle. The gastrocnemius muscle from male rats exercised (n = 16) to exhaustion or allowed to remain inactive (n = 14) was analyzed for hexokinase activity (HK) in the whole muscle homogenate and the mitochondrial-rich fraction. Although exercise produced a slight, non-significant, increase in HK activity in the whole muscle homogenate (p less than 0.09), HK activity in the mitochondrial-rich fraction was significantly increased in the exercised muscle (p less than 0.02). This shift in the cellular distribution of HK is towards the more active mitochondrial bound form and indicates an enhanced regulation of HK activity during physical exercise.

OBJECTIVE: The purpose of this study was to determine the association between moderate-intensity physical activity (PA) and fasting insulin levels among African-American (n = 47), Native American (n = 46), and Caucasian women (n = 49), aged 40-83 years, enrolled in the Cross-Cultural Activity Participation Study. Associations by race/ethnicity, levels of central obesity, and cardiorespiratory fitness were also examined. RESEARCH DESIGN AND METHODS: Physical activity scores were obtained from detailed PA records that included all PA performed during two consecutive 4-day periods scheduled 1 month apart. Using MET intensity (the associated metabolic rate for a specific activity divided by a standard resting metabolic rate), PA was expressed as MET-min (the product of the minutes for each activity times the MET intensity level) per day of energy expended in moderate (3-6 METs) and moderate/vigorous (> or = 3 METs) PA. Fasting insulin levels were determined by radioimmunoassay. Data were analyzed by multiple linear regression analysis. RESULTS: After adjusting for race/ethnicity, age, educational attainment, and site, an increase of 30 min of moderate-intensity PA was associated with a 6.6% lower fasting insulin level (P < 0.05). The association was similar among races/ethnicities, centrally lean and centrally obese women, and women with low and high cardiorespiratory fitness levels. CONCLUSIONS: These findings lend support to the 1995 Centers for Disease Control and Prevention and American College of Sports Medicine recommendations for an accumulation of 30 min/day in moderate-intensity PA. They also contribute to the growing literature suggesting that moderate amounts of PA have a significant role in reducing the burden of hyperinsulinemia and diabetes among ethnic populations at highest risk for these conditions.

The purposes of this study were to 1) characterize changes in fibrinolytic activity in response to maximal exercise and 5-min venous occlusion and 2) compare responses in men of various habitual physical activity levels. Tissue plasminogen activator (TPA) activity and plasminogen activator inhibitor 1 (PAI-1) activity were measured in 15 inactive, 15 regularly active, and 15 highly active men. Data were analyzed using a three-way analysis of variance with repeated measures. Pretest TPA activity was similar among groups. TPA activity increased postexercise with higher values seen in the active groups (P < 0.001). The highly active group also significantly increased TPA activity postvenous occlusion (P < 0.01). Pretest PAI-1 activity was different among groups, with the inactive group showing the highest activity and the highly active group the lowest (P < 0.05). PAI-1 activity decreased with exercise (P < 0.01) but did not change with venous occlusion. In conclusion, active men exhibited greater changes in fibrinolytic activity with maximal exercise and venous occlusion than inactive men. This enhanced fibrinolytic activity may be an important mechanism mediating the cardioprotective effect provided by regular physical activity.

The purpose of this investigation was to examine the immediate and delayed effects of prolonged strenuous exercise on plasma lipid and lipoprotein concentrations in female runners. Venous blood samples were collected from 12 female runners 24 h before, 10 min after, and 1, 3, and 5 d after running a 42 km marathon. Whole blood was analyzed for hematocrit and hemoglobin to determine plasma volume shifts. Plasma aliquots were assayed for total cholesterol, high-density lipoprotein cholesterol (HDL-C), and triglyceride concentrations, while low-density lipoprotein cholesterol (LDL-C) was estimated. Total cholesterol concentrations were significantly reduced 1 d following the exercise and were still lower 3 and 5 d post-marathon. LDL-C was lower immediately and 1 d after the marathon. HDL-C concentrations, corrected for changes in plasma volume, were elevated 24 h post-exercise. The ratio of HDL/total cholesterol was increased 24 h post-exercise. Triglyceride concentrations were elevated immediately following the marathon but returned to baseline levels by 24 h post-exercise. These results demonstrate that prolonged strenuous exercise in women produces changes in blood lipid profiles that can last for several days.

Systolic blood pressure was determined weekly to assess the development of hypertension in sedentary and active Dahl salt-sensitive (S) rats that were exercised by running at 20 m/min, 60 min/day, 5 days/wk. The marked rise in blood pressure that occurred with feeding 8% NaCl (wt/wt) diet in Dahl S rats could be attenuated by chronically practiced endurance running, but only if exercise at 20 m/min was started at the beginning of salt feeding. Under the same dietary feeding conditions, running at 27 m/min resulted in incomplete attenuation of hypertension. Further, running for 30 min/day was not as beneficial as running 60 min/day at 20 m/min. Delaying the start of exercise for 6 wk after the beginning of salt feeding did not result in reduction of hypertension in the S rat. These experiments indicate that increases in blood pressure can be prevented in Dahl S rats for 12 wk if running is initiated concomitantly with salt feeding. Blood pressure is not reduced if hypertension due to salt feeding has been continued for 6 wk. The results also indicate that there is an optimal exercise intensity, duration, or both, for controlling hypertension in Dahl rats.

Fat cells were isolated from sedentary and exercise trained female Sprague-Dawley rats and cyclic AMP phosphodiesterase (cyclic AMP-PDE) activities were determined from crude homogenates of the fat cells in the whole homogenate, P5, P48, and S48 fractions. Exercise training resulted in a significant increase in the mean specific activity of cyclic AMP-PDE (pmol X min-1 X mg-1) from the whole homogenate and S48 fraction at cyclic AMP concentrations of 4, 8, and 16 microM and in the P48 fraction at 8 and 16 microM cyclic AMP. Cyclic AMP-PDE kinetic plots according to Lineweaver-Burk for the calculation of Michaelis constants (Km) and maximum enzyme velocities (Vmax) were nonlinear, indicating both a low and high enzyme form. The Michaelis constants were significantly lower in trained rats than those of its control for the high Km form of cyclic AMP-PDE in the whole and soluble fractions and for the low Km form of the P5 particulate fraction. The Vmax of the high Km form of the P48 particulate fraction from trained animals was also significantly higher than that found in its control. Phosphodiesterase inhibition by methylxanthines in the various fractions was similar in both trained and sedentary animals. These changes in specific activity, Michaelis constants, and Vmax of cyclic AMP-PDE from crude homogenates of isolated fat cells from exercise trained animals may account for the decreased intracellular levels of cyclic AMP following catecholamine stimulation of isolated fat cells from trained rats.

Previous studies have concluded that exercise training has resulted in increases in cholesterol associated with high-density lipoprotein (HDL). However, data regarding alterations in triglyceride, cholesterol, and the protein associated with the three major lipoproteins in a hyperlipoproteinemic state in response to exercise training are not available. Serum lipoprotein levels from normal and hyperlipoproteinemic Zucker rats were studied following 9 and 18 wk of treadmill running to determine the extent that the three major serum lipoprotein classes were affected. Nine weeks of treadmill running reduced serum triglyceride content in obese rats (sedentary, 294 +/- 19 [SE]; trained, 128 +/- 40 mg X dl-1) but did not affect total serum cholesterol (sedentary, 85 +/- 6; trained, 90 +/- 6 mg X dl-1). Serum very low-density lipoprotein from the trained obese rats contained lower levels of triglyceride (57%), cholesterol (46%), and protein (61%). HDL cholesterol (sedentary, 61 +/- 4; trained, 73 +/- 4 mg X dl-1) was increased by 14% in the obese rat. In the lean rat, HDL cholesterol was the only lipoprotein fraction altered following 9 wk of treadmill running. The data from this study indicate that hypertriglyceridemia can be reduced in the obese rat and that HDL cholesterol can be increased by physical activity requiring about 70% maximal aerobic capacity.