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00005768-199608000-0000400005768_1996_28_962_halle_lipoprotein_8article< 82_0_12_1 >Medicine & Science in Sports & Exercise©1996The American College of Sports MedicineVolume 28(8)August 1996pp 962-966Lipoprotein(a) in endurance athletes, power athletes, and sedentary controls[Clinical Sciences: Clinically Relevant Studies]HALLE, MARTIN; BERG, ALOYS; VON STEIN, THOMAS; BAUMSTARK, MANFRED W.; KÖNIG, DANIEL; KEUL, JOSEPHMedizinische Universitätsklinik, Abt. Rehabilitative und Präventive Sportmedizin, Freiburg, GERMANYSubmitted for publication October 1995.Accepted for publication April 1996.The profound statistical advice of D. Grathwohl is kindly appreciated.M.Halle is a scholar of the German Heart Foundation (Deutsche Herzstiftung, Frankfurt/Main, Germany).Address for correspondence: Dr. med. Martin Halle, Medizinische Universitätsklinik, Abt. Rehabilitative und Präventive Sportmedizin, Hugstetter Str. 55, D-79106 Freiburg, Germany.ABSTRACTElevated concentrations of lipoprotein(a) [Lp(a)] have been shown to be an independent risk factor for atherosclerotic disease. Physical activity and physical fitness have been shown to improve lipoprotein metabolism and reduce the risk of coronary artery disease. Studies on the influence of physical activity and physical fitness on Lp(a) levels including a large number of endurance as well as power athletes have not been performed before. Therefore, we determined parameters of physical fitness (maximal oxygen consumption), physical activity, and lipoproteins in 105 endurance athletes, 57 power athletes, and 87 sedentary young men. As expected, we found that endurance athletes with a good physical fitness had significantly higher concentrations of high-density lipoprotein cholesterol than power athletes and sedentary controls. Regarding mean Lp(a) levels (rocket immunoelectrophoresis), however, there were no significant differences between endurance athletes, power athletes, and sedentary controls. Even when including only those with Lp(a) values >10 mg · dl-1, no differences were observed between the groups. These findings indicate that intensive training over years and good aerobic fitness improve the ratio of low-density lipoprotein to high-density lipoprotein cholesterol but have no or only minor effects on Lp(a) concentrations.In 1963 K. Berg first described a “new” serum lipoprotein that was very similar to the low-density lipoprotein (LDL) but possessed an additional protein coat, the apolipoprotein(a)(5). This lipoprotein was named lipoprotein(a) [Lp(a)]. Because of the similarity between Lp(a) and the LDL particle, a recognized risk factor for coronary heart disease (CHD), several studies investigated the relationship between Lp(a) levels and atherosclerotic disease. These studies revealed that a serum concentration of Lp(a) of over 25-30 mg · dl-1 was associated with a higher incidence of CHD and acute myocardial infarction (1,29). Lp(a) was also shown to be an independent risk factor for CHD, not correlating with other risk factors such as body weight, peripheral insulin resistance, coagulation parameters, and other lipoprotein values (11,12,19).The pathogenicity of the Lp(a) particle has been explained by two mechanisms: the direct deposition of Lp(a) particles in the subendothelial layer of the arterial wall and its effect on the coagulation system(24,28,29). Structural analysis reveals that apolipoprotein(a) is homologous with plasminogen and can therefore compete for the plasminogen receptor (24). With high serum concentrations of Lp(a) the fibrinolytic effect of plasminogen is thereby impaired, resulting in increased coagulability. Thus, Lp(a) can be considered both a lipid and a coagulation-mediated risk factor for CHD.Low levels of daily and leisure time activity and poor physical fitness are recognized risk factors for CHD (6,25). It is also known that the coronary risk profile, particularly the factors related to coagulation and lipid metabolism, can be improved through regular physical activity (3). As there is no association between Lp(a) and other metabolic risk factors for CHD and there has to date been little success in attempts to lower Lp(a) levels pharmacologically (29), it is presumed that Lp(a) concentrations are primarily genetically determined and not amenable to influence by physical activity. There are currently, however, only a few studies involving mostly small numbers of patients that have investigated the influence of physical activity on the Lp(a) profile(7,10,13,15,17,18,21,23,26,30). In order to obtain more detailed information on this association we examined 249 individuals without proven CHD but with differing levels of physical activity and fitness and compared their Lp(a) and other lipoprotein concentrations.METHODSStudy GroupTwo hundred forty-nine healthy men aged between 20 and 40 yr were enrolled in the study. They included 162 male athletes who had attended the Department of Rehabilitation, Prevention, and Sports Medicine of the Freiburg University Hospital for an elective cardiopulmonary assessment. In addition, 87 healthy medical students who did not participate in sport regularly were recruited. All participants consumed a normal Western diet without daily or excessive intake of alcohol. Exclusion criteria were age >40 yr; drug therapy of any kind, particularly of anabolic steroids; diabetes mellitus; a history of gastrointestinal, hepatic, or endocrine disease; symptoms of coronary artery disease; or an abnormal physical examination.The study was approved by an institutional review committee, and all subjects gave informed consent for participation in the study.Anthropometric Data and Exercise TestingWeight, height, blood pressure, and heart rate were measured after blood was drawn. Body mass index (BMI) was calculated as the weight in kilograms divided by the square of the height in meters. Physical fitness (maximum oxygen uptake, ˙VO2max) was assessed by means of a stepwise treadmill or bicycle ergometry test measuring lactate levels(4).QuestionnaireIn addition to this, a questionnaire covering physical activity, type of sport, years of training, and current training hours per week was administered. The athletes were defined on the basis of their training history and physical fitness as either endurance athletes (cross-country skiing, cycling, long-distance running) or power athletes (weight-lifting, wrestling, shot-putting, hammer-throwing), and all were elite athletes involved in regular training and competition. Those athletes not clearly fitting into one of the categories were not included.EchocardiographyTwo-dimensional echocardiography was performed to assess heart size and volume (9). In left parasternal view the following parameters were obtained: end-diastolic left ventricular diameter, total end-diastolic diameter at the papillary muscle and mitral valve level, and end-diastolic septum and posterior wall thickness in the papillary area(8). The end-diastolic left ventricular longitudinal axis was assessed from the apical four-chamber view. Total left ventricular volume(LVV) was calculated according to the modified Simpson's rule(9). The total ventricular heart volume (HV) was determined by the following formula: HV = 2.432 × LVV + 130(9).Chemical AnalysisVenous blood was obtained between 8 and 10 a.m. after a 12-h fast. Lipid parameters such as serum cholesterol and triglycerides were determined by means of enzymatic tests on fresh serum (Boehringer, Mannheim, Germany). Lipoproteins were separated by quantitative electrophoresis(31). The Lp(a) analysis was performed on frozen serum(-25°C) using an electroimmunoassay (20) known as rocket immunoelectrophoresis (monospecific antihuman Lp(a), Immunodiagnostica, Heidelberg, Germany). Values below 10 mg · dl-1 could not be quantified with this method (coefficient of variation >15%).StatisticsLp(a) values were determined for all individuals, and concentrations below 10 mg · dl-1 were recoded as below the detection limit. As all variables were not on an interval but ordinal scale, the nonparametric Mann-Whitney test could be applied for comparison between the groups of endurance athletes, power athletes, and sedentary controls. It was also used for comparison between those individuals with low (<10 mg · dl-1) and higher (>10 mg · dl-1) Lp(a) levels. The Holm correction was applied for multiple testing (16). All values are expressed as mean ± standard deviation.In addition, the Spearman correlation coefficient was used between the ordinal variables Lp(a) and other lipoproteins, as well as training history,˙VO2max, heart volume, and BMI. The Spearman correlation analysis was used instead of the Pearson correlation analysis because of the skewed distribution of Lp(a). P values less than 0.05 were considered significant.The statistical program SPSS/PC+ (SPSS Inc., Chicago, IL) was used for all statistical analyses.RESULTSThe three groups of subjects differed with respect to their training history, weight, maximum oxygen uptake, and heart volume(Table 1). Endurance athletes demonstrated the expected cardiovascular adaptation to training, with significantly higher heart volume and correspondingly higher aerobic capacity (˙VO2max) than sedentary controls. Power athletes had no evidence of cardiovascular adaptation compared to control subjects. They had a similar training history and trained the same amount of hours per week as the endurance athletes(Table 1).TABLE 1. Anthropometric data, training history, maximum oxygen uptake(˙VO2max), echocardiographic heart volume, and cholesterol concentrations of lipoproteins (VLDL, LDL, and HDL), and Lp(a) of endurance athletes, power athletes, and sedentary controls with very low (<10 mg· dl-1) and elevated (>10 mg · dl-1) Lp(a) levels.*Comparison of the lipid profiles of the sedentary group, endurance athletes, and power athletes confirmed that the endurance athletes had the least atherogenic profile. This group had the lowest (P < 0.01) mean LDL cholesterol (108 ± 22 mg · dl-1) and highest(P < 0.01) high-density lipoprotein (HDL) cholesterol levels (46± 12 mg · dl-1) compared to power athletes (LDL, 129± 37 mg · dl-1; HDL, 36 ± 13 mg · dl-1) and sedentary controls (LDL, 128 ± 25 mg · dl-1; HDL, 40 ± 15). Although their LDL to HDL ratio was the most favorable of the three groups, this was not statistically significant when dividing the three groups into individuals with low (<10 mg · dl-1) and higher (>10 mg · dl-1) Lp(a) levels. Only power athletes with low Lp(a) levels had the lowest HDL cholesterol levels(Table 1), giving them the least favorable LDL to HDL cholesterol ratio. Despite the differences in LDL to HDL ratio, no differences in the Lp(a) values of the three groups could be discerned among the three groups. This finding was still present when dividing the groups with respect to their Lp(a) levels (Table 1). Lp(a) values >25 mg/dl were observed in 10% of endurance as well as power athletes and in 8% of the sedentary group. Overall, even in the presence of cardiovascular and metabolic adaptations to training, there was no difference in Lp(a) serum concentrations. This was confirmed by the Spearman analysis, which revealed no significant correlation between Lp(a) levels and current training hours (r = 0.03), training history, ˙VO2max (r = -0.06), BMI (r = 0.08), and lipoproteins such as serum cholesterol (r = 0.10), serum triglycerides (r =-0.06), and LDL cholesterol (r = 0.04). Weak positive correlations were observed only for the correlation between Lp(a) and very low-density lipoprotein cholesterol (r = 0.18; P < 0.05) and HDL cholesterol(r = 0.18; P < 0.05).DISCUSSIONThis study gives additional evidence that Lp(a) levels may not be influenced to the same extent by physical fitness and regular physical activity as other lipoproteins. Neither endurance nor power training had a significant effect on Lp(a) levels, despite the presence of recognized changes in the concentrations of other lipoproteins. Thus, endurance athletes had a significantly better ratio of atherogenic LDL to cardioprotective HDL cholesterol than power athletes or untrained individuals. Because of its structural homology with the LDL particle, one might expect that the Lp(a) particle would be influenced by physical activity in a similar fashion. However, on the basis of our data, there does not appear to be a direct association between LDL and Lp(a) metabolism, since endurance athletes had on average both the lowest LDL cholesterol levels and the highest concentration of Lp(a). Moreover, a significant correlation between the two parameters was not observed. Thus, we conclude that regular physical activity of an endurance nature leading to cardiovascular and metabolic adaptations has no significant effect on Lp(a) concentration in healthy young men. A minor influence of exercise on Lp(a) levels <10 mg · dl-1 cannot be excluded, as with the method applied here these differences cannot be identified. However, from a preventive point of view this is of minor importance, as individuals with low Lp(a) levels (<10 mg · dl-1) are not at an increased cardiovascular risk because of their Lp(a) values.Although these results were obtained by a cross-sectional analysis, the large number of subjects and the lack of any variation in Lp(a) levels between the groups despite clear differences in physical fitness, exercise activity, and other lipoproteins indicate that Lp(a) levels at least above 10 mg· dl-1 may not be improved by physical activity over time. This is supported by a large study by Selby et al. (30), who found no association between leisure time physical activity and Lp(a) levels in women. Also, Israel et al. (18) cross-sectionally investigated 150 men and women and found no difference in Lp(a) concentration with respect to physical fitness levels, even though subjects in the highest fitness quartile had twice the treadmill time of their unfit counterparts in the lowest quartile. Physically fit men in this study, however, had significantly lower serum triglycerides and higher HDL cholesterol levels than unfit men (18). Similar results were obtained in a comparison of 57 male endurance athletes running 61 ± 3 km · wk-1 and sedentary subjects. Despite a significantly more favorable lipoprotein and apolipoprotein profile no significant differences could be observed for median Lp(a) levels (17). Only minor effects of Lp(a) by exercise were also reported by Lobo et al.(21), who found that Lp(a) levels remained relatively stable (-2.5%) during a 6-month exercise program in postmenopausal women. Physical fitness and training seem to have only minor effects on Lp(a) levels, even in individuals with pathologically elevated Lp(a), as a similar distribution of elevated Lp(a) levels was observed among athletes and controls in our study.However, there is evidence that concentrations of Lp(a) may increase by physical exercise. A cross-sectional analysis of 60 men with different training histories showed that endurance athletes had even higher Lp(a) concentrations than bodybuilders or untrained individuals(7). Also, Hubinger et al. (17) found higher Lp(a) serum concentrations in long-distance runners compared to nonathletic controls, although these differences were only minor and not statistically significant. There is also evidence that Lp(a) levels may increase after competitive exercise. Dufaux et al. (10) observed an increase of Lp(a) concentrations on the second day after a 3-h running test in moderately trained young men. Also, a study investigating the long-term effect of an exercise program of running 3-4 times · wk-1 in sedentary individuals demonstrated that Lp(a) levels rose almost twofold over a period of 9 months (26). Indeed, a similar but insignificant trend was also observed in our study. One hypothesis for the higher serum concentration of Lp(a) in endurance athletes is that greater physical demands cause a muscular or systemic stress reaction. This condition may be associated with raised Lp(a) values, as Lp(a) has been shown to share characteristics of inflammatory parameters(22,27). This phenomenon might explain why moderate physical training over 4 wk reduced Lp(a) levels by 25% only in those men additionally taking fish oil but not in those receiving peanut oil(15), as it is known that n-3 polyunsaturated fatty acids have an antiinflammatory effect. The hypothesis is further supported by the fact that a reduction of Lp(a) was associated with a lowering (-13%) of the acute-phase protein fibrinogen (15). Austin et al.(2), showing an inverse correlation between maximum oxygen consumption and serum concentrations of Lp(a) (r = -0.28; P = 0.02) in Type I diabetic children, also observed a positive correlation between Lp(a) and poor glycemic control (HbA1) in children with Lp(a) levels>10 mg · dl-1 (2). These findings may be interpreted in the way that physical fitness improves glycemic control, thereby also reducing the systemic acute-phase reaction and leading indirectly to a reduction of Lp(a) levels in these diabetic children.Reductions of Lp(a) levels by physical exercise might be explained via an impairment of hepatic synthesis of lipoproteins during exercise. Herrmann et al. (15) found that a reduction of Lp(a) by exercise training correlated directly with reductions in serum concentrations of apolipoprotein B. A similar observation was made by Hellsten et al.(13), who found that both cholesterol and Lp(a) may significantly decrease by 22% in well-trained individuals performing prolonged(10 h · d-1) heavy physical exercise over 8 d in a cold environment. During this so-called “igloo tour,” liver synthesis might have been impaired, leading to reduced cholesterol and Lp(a) levels, as suggested by Israel et al. (18). A similar effect was demonstrated in another study showing that detraining in eight long-distance runners caused an increase in Lp(a) (15%) and LDL cholesterol (10%); these changes, however, were not statistically significant(23).Different effects of physical exercise and physical fitness on Lp(a) concentrations may be explained by hormonal mechanisms, since levels of estrogen, androgens, and thyroid hormones are inversely correlated with serum concentrations of Lp(a) (14,30,32). However, whether Lp(a) levels might increase by physical activity in certain individuals due to differences in hormone regulation is unclear. Although a history of medication was obtained in our study, the effects of anabolic steroids on Lp(a) can never be completely excluded in studies including power athletes. Anabolic steroids are known to lower both HDL cholesterol and Lp(a) levels. As HDL cholesterol concentrations were the lowest in power athletes with Lp(a) levels <10 mg · dl-1, it cannot be excluded that some of these power athletes were abusing anabolic steroids. However, the ratio between those athletes with low and elevated Lp(a) values was similar for all groups and ranged from 22% to 28% (Table 1).It is well recognized that the effect of elevated Lp(a) levels in increasing the risk of CHD is potentiated in the presence of additional dyslipoproteinemia, particularly with high LDL values (1). Although regular physical activity does not appear to reduce Lp(a) in those individuals, it can at least reduce the risk indirectly by improving the lipid profile and fibrinolytic pathway (3). Hence, regular exercise and dietary intervention are both ways in which individuals with an Lp(a) serum concentration above 25 mg · dl-1 can reduce their risk of CHD. For those whose LDL cholesterol remains elevated, pharmacological intervention is indicated (29). It remains to be seen whether large prospective epidemiological studies will confirm the lack of association between physical exercise and Lp(a) levels in men as observed here or will even reveal increased or reduced levels. It would be important to clarify whether benefits of exercise on the CHD risk, i.e., a more favorable lipid profile, lowered insulin resistance, and enhanced fibrinolysis, will also be found in individuals with raised Lp(a) levels and whether inflammatory processes contribute to these findings. 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[CrossRef] [Medline Link] [Context Link]EXERCISE; PHYSICAL FITNESS; LIPOPROTEINSovid.com:/bib/ovftdb/00005768-199608000-0000400000898_1986_62_249_armstrong_angiographically_|00005768-199608000-00004#xpointer(id(R1-4))|11065213||ovftdb|SL0000089819866224911065213P47[CrossRef]10.1016%2F0021-9150%2886%2990099-7ovid.com:/bib/ovftdb/00005768-199608000-0000400000898_1986_62_249_armstrong_angiographically_|00005768-199608000-00004#xpointer(id(R1-4))|11065405||ovftdb|SL0000089819866224911065405P47[Medline Link]2948513ovid.com:/bib/ovftdb/00005768-199608000-0000400003458_1993_16_421_austin_relationship_|00005768-199608000-00004#xpointer(id(R2-4))|11065213||ovftdb|SL0000345819931642111065213P48[CrossRef]10.2337%2Fdiacare.16.2.421ovid.com:/bib/ovftdb/00005768-199608000-0000400003458_1993_16_421_austin_relationship_|00005768-199608000-00004#xpointer(id(R2-4))|11065405||ovftdb|SL0000345819931642111065405P48[Medline 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