Apelin as a Potential Regulator of Peak Athletic Performance

Abstract

Apelin, as a cardiokine/myokine, is emerging as an important regulator of cardiac and skeletal muscle homeostasis. Loss of apelin signaling results in premature cardiac aging and sarcopenia. However, the contribution of apelin to peak athletic performance remains largely elusive. In this paper, we assessed the impact of maximal cardiorespiratory exercise testing on the plasma apelin levels of 58 male professional soccer players. Circulating apelin-13 and apelin-36, on average, increased transiently after a single bout of treadmill exercise; however, apelin responses (Δapelin = peak - baseline values) showed a striking interindividual variability. Baseline apelin-13 levels were inversely correlated with those of Δapelin-13 and Δapelin-36. Δapelin-13 showed a positive correlation with the maximal metabolic equivalent, relative maximal O₂ consumption, and peak circulatory power, whereas such an association in the case of Δapelin-36 could not be detected. In conclusion, we observed a pronounced individual-to-individual variation in exercise-induced changes in the plasma levels of apelin-13 and apelin-36. Since changes in plasma apelin-13 levels correlated with the indicators of physical performance, whole-body oxygen consumption and pumping capability of the heart, apelin, as a novel exerkine, may be a determinant of peak athletic performance.

Keywords: VO2max; apelin; differential response; exercise; myokine; peak performance.

Figure 1

(A) Violin plots comparing the plasma levels of apelin-13 before (baseline), immediately after (peak), and 30 min after (recovery) the vita maxima treadmill test. Medians and the 75th and 25th percentiles are shown within the violin plots. Data were analyzed by a repeated measures one-way ANOVA followed by Tukey’s multiple comparison test (n = 54), ns: no statistical significance, * p < 0.05, ***p < 0.001. (B) Difference between time point means (baseline, peak, and recovery) of apelin-13 levels with multiplicity-adjusted 95% confidence intervals according to Tukey’s test, *p < 0.05, ***p < 0.001. (C) Spearman correlation of baseline apelin-13 and Δapelin-13 (N = 58). (D) Individual apelin-13 responses to the exercise test. Each point represents the change in a subject’s apelin-13 level from baseline to maximum load. Baseline values are subtracted from peak values and sorted in ascending order (N = 58).

Figure 2

Correlation of Δapelin-13 and baseline systolic BP (A), baseline diastolic BP (B), peak diastolic BP (C), circulatory power (D), maximum MET (E), and relative VO₂max (F) (N = 58). Data were analyzed by Spearman correlation.

Figure 3

Correlation of apelin-13 baseline levels with the maximum MET (A), relative VO₂max (B), circulatory power (C), and circulatory stroke work (D) in the Δapelin-13 low responder group (N = 29). Data were analyzed by Pearson correlation.

Figure 4

(A) Violin plots comparing the plasma levels of apelin-36 before (baseline), immediately after (peak), and 30 min after (recovery) the vita maxima treadmill test. Medians and the 75th and 25th percentiles are shown within the violin. Data were analyzed by a Friedman test followed by a Dunn’s multiple comparisons test (N = 28), * p < 0.05, ** p < 0.01, **** p < 0.001. (B) Individual apelin-36 responses to the exercise test. Each point represents the change in a subject’s apelin-36 level from baseline to maximum load. Baseline values are subtracted from peak values and sorted in ascending order (N = 28).

Figure 5

Correlation between baseline apelin-13 and Δapelin-36 (A), peak apelin-13 and Δapelin-36 (B), and recovery apelin-13 and Δapelin-36 (C). Data were analyzed by Pearson correlation (A,B) or Spearman correlation (C) based on the distribution of the data (N = 28).

Figure 5

Correlation between baseline apelin-13 and Δapelin-36 (A), peak apelin-13 and Δapelin-36 (B), and recovery apelin-13 and Δapelin-36 (C). Data were analyzed by Pearson correlation (A,B) or Spearman correlation (C) based on the distribution of the data (N = 28).