Lipoprotein(a) [Lp(a)] represents a class of lipoproteins with some structural similarity to low density lipoprotein (LDL), but containing a unique apoprotein, apoprotein(a). First reported in 1963, Lp(a) is now considered to have an independent role in the development of atherosclerotic lesions. The level of Lp(a) in the blood is under strong genetic influence and does not appear to be alterable by lifestyle factors known to influence other lipoproteins. Regular moderate exercise has been shown to favorably alter other lipoproteins, and recent attention has focused on whether Lp(a) level can be influenced by physical activity. Current data from cross-sectional and intervention studies show little effect of moderate exercise on serum Lp(a) concentration. One possible exception may be an elevation of serum Lp(a) concentration in adult endurance and power athletes who exercise intensely on a daily basis. However, not all studies have taken into account possible racial or ethnic differences in Lp(a) concentrations and the skewed distribution observed within most populations. Standard dietary intervention such as a low fat diet recommended for weight loss and control of other blood lipids has little effect on serum Lp(a) level. At present, serum Lp(a) concentration does not appear to be significantly altered by realistic dietary changes and moderate physical activity as recommended for health. The synergistic effect on cardiovascular disease risk when both LDL-cholesterol and Lp(a) are elevated highlight the importance of attending to those risk factors that can be modified by exercise and other lifestyle changes.

Lipoprotein(a) [Lp(a)] is a unique lipoprotein complex in the blood. At high levels (> 30 mg/dl), Lp(a) is considered an independent risk factor for cardiovascular diseases. Serum Lp(a) levels are largely genetically determined, remain relatively constant within a given individual, and do not appear to be altered by factors known to influence other lipoproteins (e.g. lipid-lowering drugs, dietary modification and change in body mass). Since regular exercise is associated with favourable changes in lipoproteins in the blood, recent attention has focused on whether serum Lp(a) levels are also influenced by physical activity. Population and cross-sectional studies consistently show a lack of association between serum Lp(a) levels and regular moderate physical activity. Moreover, exercise intervention studies extending from 12 weeks to 4 years indicate that serum Lp(a) levels do not change in response to moderate exercise training, despite improvements in fitness level and other lipoprotein levels in the blood. However, recent studies suggest the possibility that serum Lp(a) levels may increase in response to intense load-bearing exercise training, such as distance running or weight lifting, over several months to years. Cross-sectional studies have reported abnormally high serum Lp(a) levels in experienced distance runners and body builders who train for 2 to 3 hours each day. However, the possible confounding influence of racial or ethnic factors in these studies cannot be discounted. Recent intervention studies also suggest that 9 to 12 months of intense exercise training may elevate serum Lp(a) levels. However, these changes are generally modest (10 to 15%) and, in most individuals, serum Lp(a) levels remain within the recommended range. It is unclear whether increased serum Lp(a) levels after intense exercise training are of clinical relevance, and whether certain Lp(a) isoforms are more sensitive to the effects of exercise training. Since elevation of both low density lipoprotein cholesterol (LDL-C) and Lp(a) levels in the blood exerts a synergistic effect on cardiovascular disease risk, attention should focus on changing lifestyle factors to decrease LDL-C (e.g. dietary intervention) and increase high density lipoprotein cholesterol (e.g. exercise) levels in the blood.

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Serum lipoprotein(a) [Lp(a)] levels were measured before and after a 12-wk program of moderate-intensity endurance training. The training program consisted of walking and/or jogging, at least three sessions.wk-1 of at least 30 min duration, at an intensity producing 60-85% HRmax reserve. Twenty-eight previously sedentary middle-aged Caucasian males matched for age, body mass, and body mass index (BMI) were randomly allocated to either an exercise (N = 17, mean age +/- SEM = 51.57 +/- 1.25 yr) or a control (N = 11, mean age +/- SEM = 50.0 +/- 1.15 yr) group. Pre- and post-training median Lp(a) levels, measured by immunoturbidimetric analysis, were not significantly different in either the exercise (pre 13.0, post 15.0 mg.dl-1) or the control subjects (pre 14.0, post 12.0 mg.dl-1) (P > 0.05). Kendall Rank correlation analysis revealed no significant relationship between the level of Lp(a) and any other variable in either group before or after training. In the exercisers, a significant increase (P < 0.05) was recorded in the estimated mean VO2max (pre 33.39 +/- 1.70, post 37.7 +/- 1.75 ml.kg-1 min-1). These data indicate that the level of Lp(a) was not influenced by a 12-wk program of moderate-intensity endurance training, and are consistent with previous reports suggesting that Lp(a) level is not altered by lifestyle factors.

This investigation examined the acute response of serum lipoprotein(a) (Lp(a)) concentration immediately after, and during several days following, level and downhill motorized treadmill running. Eight males ran for 1 h on a level motorized treadmill at an intensity producing 90% maximum heart rate (MHR). On a separate occasion, three males and three females performed downhill (negative 13.4% incline) treadmill running at an intensity producing 75-80% MHR. For both protocols, serial blood samples were taken pre- and post-exercise and at the same time of day 1, 3, 5, and 7 days following exercise. Levels of Lp(a), creatine kinase (CK), C-reactive protein (CRP), and ferritin were measured. Repeated measures statistical analysis (Friedman ANOVA) showed no significant change in the median level of Lp(a) (level run, 5.0 mg.dl-1; downhill run, 7.45 mg.dl-1) across time following either protocol. After level running, ferritin levels 5 and 7 d post-exercise were significantly (P < 0.05) lower compared with immediately and 1 d post-exercise measures (Friedman ANOVA). Following level running, the Wilcoxon signed rank test showed significant (P < 0.05) elevations in CK levels immediately, 1 and 5 d post-exercise compared with pre-exercise values. Following downhill running. CK level was significantly elevated up to 3 d post-exercise (Wilcoxon signed rank). Calculated plasma volume did not change significantly following either protocol. These data suggest that Lp(a) does not change acutely in response to level or downhill treadmill running up to 60 min duration.