A high prevalence of risk factors for cardiovascular diseases, such as physical inactivity, obesity, and poor diet, has been observed among young adults living in developed countries [23]. Consistently, many studies suggested that cardiovascular disease is less common in physically active individuals; this may be due to improved endothelial function, decreased inflammation, decreased plasma TGs and LDL-C, and increased HDL-C [24]. Furthermore, it has also been shown an increased risk of cardiovascular diseases and death associated with an increase in BMI [25].
Among professional soccer players, a lower BMI is associated with a more favorable lipid-lipoprotein profile [21]. There are also studies reporting changes in anthropometric characteristics and body composition during periods of soccer training and their significant impact on player performance [26, 27]. During the season we noted a constant decrease in weight, BMI, and percentage of fat mass together with an increase in lean mass, thus confirming the significant decrement in adipose tissue content during the training period reported by other studies [28,29]. However, our results are in contrast with those reported by Oliver et al., [30] who showed a BMI increment in soccer players during the soccer season along with no effect on plasma lipids and cardiovascular disease risk [30]. Many studies have shown that aerobic and resistance training decrease dyslipidemia [11,31]. However, the different exercise interventions, the experimental protocols, and the characteristics of the participants in the longitudinal investigations make it very difficult to quantify the dose of exercise necessary to modify the levels of lipids and lipoproteins. Additionally, HDL-C and TG, are more amenable to exercise than others [32, 33]. It should be kept in mind that dose-response relationships between training volume of exercise and changes in blood lipids suggest that even low training volumes may benefit the plasma lipid profile although effects may not be observable if certain exercise thresholds are not met [34]. Previous studies have evaluated the effects of a soccer match on the plasma lipid profile with conflicting results. Sotiropoulos et al., [19] showed that HDL levels increased, while TG and total cholesterol decreased after the game. Conversely, Rahnama et al., [35] showed that soccer matches do not have particularly favorable effects on lipid profiles but, nevertheless, lower levels of LDL, cholesterol and TG and higher levels of HDL are measured in soccer players thus suggesting a beneficial effect of regular training on lipid profiles. In light of these results, we can hypothesize that long-lasting intermittent exercise occurring throughout the soccer season, may modify the antiatherogenic lipid profile, probably due to high aerobic energy expenditure. Indeed, our results demonstrate that HDL concentration significantly increased during the soccer season whilst LDL levels decreased. Given the antiatherogenic role of HDL-C, its increase is an important result, as is the ratio between TC and HDL-C in the risk and progression of CHD [36]. LDL transports cholesterol into peripheral tissue cells where it can be oxidized thus reaching excessive amounts that accumulate within the walls of the arteries [5]. On the contrary, HDL is important in the removal of cholesterol from peripheral cells, and also from atheroma of the arterial wall to the liver (reverse cholesterol transport); thus, cholesterol contained within HDL is sometimes labeled as “good”. Finally, HDL-C blood concentration above 60 mg/dL seem to have a protective effect against atherosclerosis and is related to the decrease in the incidence of CHD [37].
There have been conflicting data concerning the effect of exercise on HDL-C, mostly depending on the type of sport. For example, aerobic exercise performed for 12–24 weeks improves HDL-C by approximately 3.8–15.4 mg/dL from the initial level whilst resistance exercise does not [38]. The exercise effect on HDL-C and LDL-C concentrations is probably mediated by modifications in the concentration and activity of enzymes such as lipoprotein lipase, lecithin/cholesterol acyl transferase, and hepatic triglyceride lipase implicated in the synthesis, transport, and catabolism of lipoproteins [8]. Likely, exercise-induced lipid utilization is influenced by adipose tissue and intramuscular TG lipolysis, delivery of fatty acid to the exercising muscle, regulation of fatty acid transmembrane transport in muscle cells and mitochondrial metabolism [18]. Our results obtained over long periods of intervention are consistent with previous reports showing decreases in TC, TG and LDL-C and increases in HDL-C in basketball and soccer players [39-42]. Furthermore, soccer players have 18% higher baseline HDL-C values, and 15% lower TC/HDL-C ratio than non-athletes, presumably because they have significantly higher energy expenditure than sedentary people [20]. However, LDL levels increased significantly after the soccer match, although it was still in the advisable range (<130 mg/dl) [19]. This may be due to the fact that the increased free radical production associated with aerobic exercise can influence the oxidative activity status of circulating LDL particles immediately after the match [43]. Since the TC/HDL-C ratio has been proposed as another risk indicator for CHD [44], our results show that long periods of soccer training can cause significant changes in this ratio, consistent with previous studies performed on 12-week intervention periods of soccer training that caused a LDL and LDL/HDL decrement in untrained men [42, 45]. On the other hand, improvements in these lipid variables appear to be associated with a reduction in body mass and body fat percentage [46, 47]. Our findings are consistent with those previously observed when the recreational soccer intervention period longer than 12 weeks caused significant decrement in lean body mass and body fat percentage [45,48].
Conflicting results have been reported regarding TG levels assayed in soccer players, with studies reporting lower values [49-51] and other higher values than in control groups [52-54]. For example, baseball players have lower TG values than soccer players [55], for whom, however and consistently with previously reported studies, significant decreases occur during the season [39-42]. Although exercise is known to affect intramuscular TG lipolysis [8], sedentary individuals show no change in TG levels after a single session of exercise [11]. Thus, a longer period of intervention would appear to be necessary to produce significant effects on lipid profile. Furthermore, the aforementioned variations appear to be related to the training program and to variations in VO2max [56]. Consistently, it must be considered that fatty acids derived from adipose tissue, muscle lipid droplets, and diet represent the main energy supply during exercise at intensities between 45% and 65% VO2max [18]. Thus, at low to moderate intensity and during sustained exercise, many skeletal muscle energy needs can be met predominantly by fatty acid oxidation, with a small contribution from glucose oxidation.