M. A. Ferguson

Blood Lipid and Lipoprotein Adaptations to Exercise A Quantitative Analysis

Dose-response relationships between exercise training volume and blood lipid changes suggest that exercise can favourably alter blood lipids at low training volumes, although the effects may not be observable until certain exercise thresholds are met. The thresholds established from cross-sectional literature occur at training volumes of 24 to 32km (15 to 20 miles) per week of brisk walking or jogging and elicit between 1200 to 2200 kcal/wk. This range of weekly energy expenditure is associated with 2 to 3 mg/dl increases in high-density lipoprotein- cholestrol (HDL-C) and triglyceride (TG) reductions of 8 to 20 mg/dl. Evidence from cross-sectional studies indicates that greater changes in HDL-C levels can be expected with additional increases in exercise training volume. HDL-C and TG changes are often observed after training regimens requiring energy expenditures similar to those characterised from cross-sectional data. Training programmes that elicit 1200 to 2200 kcal/wk in exercise are often effective at elevating HDL-C levels from 2 to 8 mg/dl, and lowering TG levels by 5 to 38 mg/dl. Exercise training seldom alters total cholesterol (TC) and low-density lipoprotein-cholesterol (LDLC). However, this range of weekly exercise energy expenditure is also associated with TC andLDL-C reductions when they are reported. The frequency and extent to which most of these lipid changes are reported are similar in both genders, with the exception of TG. Thus, for most individuals, the positive effects of regular exercise are exerted on blood lipids at low training volumes and accrue so that noticeable differences frequently occur with weekly energy expenditures of 1200 to 2200 kcal/wk. It appears that weekly exercise caloric expenditures that meet or exceed the higher end of this range are more likely to produce the desired lipid changes. This amount of physical activity, performed at moderate intensities, is reasonable and attainable for most individuals and is within the American College of Sports Medicine’s currently recommended range for healthy adults.

Delayed effects of exercise on the plasma leptin concentration

Recent studies have concluded that a single exercise session has no immediate effect on the plasma concentration of leptin, a putative satiety factor. We tested the hypothesis that an increase in energy expenditure would decrease the leptin concentration but the effects would be manifest in a 48-hour period following exercise. Eleven active males completed two treadmill exercise sessions with different energy expenditure (800 or 1,500 kcal) at 70% maximal O2 consumption (Vo2max). Subjects maintained constant energy intake on the day before, the day of, and 2 days after exercise, as verified by dietary recall. Compared with preexercise in either exercise session, there were no differences in plasma leptin concentrations following exercise (0 and 24 hours postexercise) except at 48 hours postexercise, where an approximately 30% decrease (P < .05) was observed. With either duration of exercise, plasma glucose increased about 10% (P < .05), insulin decreased 35% to 46% (P < .05), and cortisol increased 41% to 50% (P < .05, 1,500 kcal only) immediately following exercise, but returned to preexercise values at 24 and 48 hours postexercise. A statistically significant correlation was observed between the changes in leptin and insulin (r = .49, P < .0001). Single exercise sessions of varying energy expenditure decreased the plasma leptin concentration after 48 hours in association with a preceding decrease in insulin.

Effects of short-duration and long-duration exercise on lipoprotein(a)

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 [VO(2max)], 57 +/- 7 mL x kg(-1) x min(-1)) completed two separate exercise sessions at 70% VO(2max). One session required 800 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 x L(-1) x min(-1); 1500 kcal: 0-pre 51 +/- 5, 1-post 187 +/- 30, 2-post 123 +/- 19 U x L(-1) x min(-1); P < 0.05). However, median Lp(a) concentrations were not altered by either exercise session (800 kcal: 0-pre 5.0 mg x dL(-1), 0-post 3.2 mg x dL(-1), 1-post 4.0 mg x dL(-1), 2-post 3.4 mg x dL(-1); 1500 kcal: 0-pre 5.8 mg x dL(-1), 0-post 4.3 mg x dL(-1), 1-post 3.2 mg x dL(-1), 2-post 5.3 mg x 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.

Effect of a single session of exercise on lipoprotein(a)

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).

EFFECT OF EXERCISE DURATION ON PLASMA ENDOTHELIN-1

AIM Endothelin-1 (ET-1) is a potent vasoconstricting peptide released mostly from vascular endothelial cells. Isolated exercise sessions of relatively long duration (=or>30 min) have produced increases in plasma ET-1 concentration while shorter exercise sessions usually have not. The purpose of the present study was to verify an effect of exercise duration at a steady work rate on plasma ET-1 concentration. METHODS Eleven endurance-trained males (age 27+/-6 years; maximal oxygen consumption--VO2max--56+/-7 mLxkg-1xmin-1, body fat 11+/-5%; mean+/-SD) exercised on a treadmill at 70% VO2max on 2 occasions separated by at least 2 weeks. During a short-duration session, subjects expended approximately 3,360 kJ (60+/-2 min). During a long-duration session, subjects expended approximately 6,300 kJ (112+/-4 min). Six of the subjects performed the 3,360 kJ session before the 6,300 kJ session while the other 5 subjects performed the 6,300 kJ session first. RESULTS The short-duration session did not cause plasma ET-1 concentration to change immediately after exercise (0.23+/-0.01 pmolxL-1 before exercise, 0.22+/-0.02 pmolxL-1 after exercise, mean+/-SE). However, 10 of 11 subjects had increased ET-1 after the long-duration session (0.28+/-0.02 pmolxL-1 before exercise, 0.32+/-0.02 pmolxL-1 after exercise, P=0.0004). A treatment-by-time effect was present (P=0.003). CONCLUSION These results demonstrate an effect of exercise duration on plasma ET-1 concentration. Exercise duration is, therefore, an essential consideration when investigating exercises effect on ET-1.