The impact of exercise modality and menstrual cycle phase on circulating cardiac troponin T

Abstract

Objectives: It is unclear whether exercise modality (moderate-intensity continuous [MCE]; high-intensity interval [HIE]) and menstrual cycle phase (follicular [FP]; luteal [LP]), individually or in combination, mediate the commonly observed exercise-induced elevation in cardiac troponin T (cTnT). This study examines cTnT responses to MCE and HIE during both the FP and LP. Design: Randomised crossover study. Methods: Seventeen healthy, eumenorrheic women completed four trials including MCE (60% VO 2max steady-state cycling until 300 kJ) and work-equivalent HIE (repeated 4-min cycling at 90% VO 2max interspersed with 3-min rest) during both the FP and LP. The FP and LP were verified based on ovarian hormones. Serum cTnT was assessed using a high-sensitivity assay before, immediately after, and 1 (1HR), 3 (3HR) and 4 (4HR) hours after exercise. cTnT values were corrected for plasma volume changes. Results: cTnT was significantly elevated (p < 0.05) post-exercise in both MCE (at 3HR and 4HR) and HIE (at 1HR, 3HR and 4HR). No statistically significant difference (p > 0.05) in peak post-exercise cTnT, which mostly occurred at 3HR, was seen among the four trials (median [range], ng l −1 : 5.2 [1.7-18.1] after MCE during FP; 4.8 [1.7-24.9] after MCE during LP, 8.2 [3.9-24.8] after HIE during FP and 6.9 [1.7-23.1] after HIE during LP). Conclusions: A single 300 kJ bout of both MCE or HIE resulted in a significant post-exercise increase in cTnT, with no differences in peak cTnT response between menstrual cycle phases or between exercise modes, but the cTnT elevation occurs slightly earlier after HIE.

Left Cardiac Remodelling assessed by Echocardiography is Associated with Rho-kinase Activation in Long-distance Runners

“…A meta-analysis in athletes with high training regime showed that acute and prolonged exercise was associated with larger LV volumes and a relative lower LV ejection fraction post intensive exercise [21]. In this study, the HT group showed a greater left cardiac remodelling process, which potentially gives athletes a better performance in a highly demanding race [11]; however, these changes could be related to a theoretically excessive and deleterious remodelling process [13], which is in keeping with other reports showing inflammatory and cell remodelling biomarkers elevation in athletes whose final significance are not fully clarified [22][23].…”

Cardiac Troponin-T Release After Sport and Differences by Age, Sex, Training Type, Volume, and Intensity: A Critical Review

“…5,22 Results of a recent (2019) metanalysis, 5 including 22 studies on adults analyzing different sports, showed that postexercise cTn release was positively correlated with exercise intensity (evaluated by the mean HR). Average 13,17 and peak HR 13 and race time 26,44 were positively associated with cTn postexercise rise, 14 regardless of the biomarker used. However, data are not univocal.…”

Left Cardiac Remodelling Assessed by Echocardiography Is Associated with Rho-Kinase Activation in Long-Distance Runners

“…The ROCK signaling pathway participates in cell survival and cardiac hypertrophy, cardiac fibrosis, and cell apoptosis [15]. Some athletes may develop an extreme cardiac remodelling process, including atrial structure and function changes [12,13,26], worse ventricular performance post-effort [6], and appearance of arrhythmias in long-term followup [27,28]. Regarding the physiopathology of previous processes, the ROCK signaling pathway could play an important role in electrical property changes in atrial tissue (connexin expression), as Chen et al (2018) showed while studying the LA appendage in patients with and without atrial fibrillation [29].…”

“…A recent meta-analysis of animal models of myocardial ischemia/reperfusion injury showed that fasudil, a Rho kinase inhibitor, exerts a cardioprotective effect including lowering of troponin-I elevation [31]. Multiple protocols have assessed troponin levels post-different intensities of exercise, but the results have different results and there have been different interpretations on the mechanism of troponin release, which probably depends on multiple individual mechanisms of adaptation to exercise [26,27,32]. In our protocol we did not find troponin-I elevation post-marathon race (troponin-I < 0.156 ng•mL −1 in all subjects).…”