Geert Kleinnibbelink

Acute Cardiac Responses vs. Cardiac Remodelling 3 81 due to variation in loading conditions. We also demonstrated that 24-weeks of endurance exercise induced a modest rightward shift with a somewhat stronger coupling of the LV strain-volume loop. 31 This is the first study, to our knowledge, that assessed RV strain- area loops following an exercise training in humans. We showed that training induced changes in RV mechanics concomitant to right-side structural adaptions. Specifically, lessening of the systolic and diastolic slope of the RV strain-area loop fits with the change in geometry of the RV, where the cavity size became larger. This is challenging to interpret but may be explained by the larger RV having greater unit area of myocardium requiring less deformation/contractility to facilitate the same stroke volume. Furthermore, we observed stronger coupling following training, potentially suggesting the presence of a more dominant longitudinal contribution to area change in diastole compared to systole. This adaptation fits with previous cross-sectional findings, in that we previously observed that athletes with a sports discipline with low-static and high-dynamic components (IIIA Mitchell classification 32 ; e.g. high-intensity exercise as adopted in our study), showed more coupling in RV strain-area loops compared to other Mitchell classifications sports. 6 This could be suggestive for a sport discipline specific adaptation and the significant influence of variable loading conditions across disciplines on RV physiology. Moreover, the resemblance between the improved systolic-diastolic coupling following endurance training in the RV (this study) and LV (study by Oxborough et al . 31 ) with increasing cavity sizes may indicate that a change in cardiac mechanics is not an isolated process but merely a consequence of cardiac structural remodelling due to exercise training. Future work, in larger cohorts assessing both RV and LV, is required to better understand this topic. Perspectives Challenging the cardiac system, e.g. through exercise, may be relevant in better understanding (patho)physiology. Indeed, exercise-induced troponin I elevation, independent from resting troponin I, predicts mortality and cardiovascular morbidity. 33, 34 In the present study, we found that exercise-induced changes in RV function relate to chronic RV adaptation. This concept, i.e. exploring cardiac responses to exercise, may be a potential strategy for future studies aiming to better understand cardiac (patho) physiology.