Lipoprotein(a) response to intensive exercise: implications for cardiovascular risk assessment in athletes

Abstract Background Lipoprotein(a) Lp(a) is a genetically determined, independent risk factor for atherosclerotic cardiovascular disease (1). Recent evidence shows that Lp(a) even predicts subclinical coronary atherosclerosis in ageing endurance athletes despite low conventional cardiovascular risk (2). Although generally stable throughout life, Lp(a) may act as an acute-phase protein in certain inflammatory conditions (3). Intensive exercise triggers a transient inflammatory response (4), but its effect on Lp(a) remains inconclusive. Purpose To investigate whether Lp(a) levels change following high-intensity exercise, assessing its reliability for cardiovascular risk evaluation in athletes. Methods Twelve recreational endurance athletes (mean age 34 ± 6 years; 58% men) completed a 3-hour high-intensity interval race on a cycling ergometer. Cardiorespiratory fitness (VO2max) and anaerobic threshold (AnT) were determined via cardiopulmonary exercise testing a priori. The race was individualized to their AnT, alternating between long-duration submaximal (55–65% AnT), threshold (88–95% AnT), and short high-intensity intervals (107% AnT). Blood samples were collected 1 hour pre-exercise (T0), immediately post-exercise (T1), 2.5 hours (T2), 5 hours (T3), and 24 hours post-exercise (T4) to assess Lp(a) and C-reactive protein (CRP) responses. Non-parametric Friedman tests were used to evaluate changes over time, as Lp(a) and CRP values were not normally distributed. Values below the lower detection limit of the assay (1 mg/L for CRP, 6 nmol/L for Lp(a)) were assigned the detection limit, which is acceptable for non-parametric tests. Perceived intensity was evaluated by the Borg scale. Results Athletes had a mean VO2max of 63 ± 10 mL/kg/min and rated the exercise as hard to very hard (Borg 16 ± 1). The Friedman test revealed statistically significant changes over time for both Lp(a) (p=0.011) and CRP (p0.001). Individual Lp(a) and CRP values per athlete at each timepoint are shown in Figures 1 and 2. Median percentage changes in Lp(a) relative to T0 were minimal: T1: −8.6% (IQR 13.50), T2: −3.0% (11.00), T3: −8.5% (7.90), and T4: −2.3% (14.3). 2 athletes with elevated Lp(a) values (105 nmol/L, according to updated ESC guidelines (5)) remained in the high-risk category, while the remaining ten stayed in the low-risk category. For CRP, median values from T0 to T3 were below the detection limit (1 mg/L), with a small increase at T4 observed in 8 of 12 athletes (median 1.8 mg/L, IQR 2.15); the other 4 athletes remained below the detection limit at T4. Conclusion As expected, CRP was slightly elevated at 24 hours, reflecting mild inflammation. Changes in Lp(a) were minimal and clinically irrelevant. These results confirm that Lp(a) remains a reliable marker for cardiovascular risk assessment in athletes, even after intensive training.For image description, please refer to the figure legend and surrounding text. For image description, please refer to the figure legend and surrounding text.