Geert Kleinnibbelink

Acute Cardiac Responses vs. Cardiac Remodelling 3 79 DISCUSSION The aim of our study was to relate pre-training changes in cardiac function during acute hypoxic exercise to subsequent adaptations to a 12-week hypoxic endurance exercise training program on RV cardiac structure, function and mechanics in healthy individuals. We present the following findings. First, hypoxic exercise training increased RV size, including diameter and area. Whereas measures of RV function remained largely unchanged, exercise training resulted inadaptations inRVmechanics, with less uncoupling and lessening of the systolic and diastolic slopes of the RV strain-area loop. Second, no adaptation in LV structure, function or mechanics were observed. Third, pre-training augmentation in RV fractional area change to acute hypoxic exercise was inversely related to cardiac remodelling of the RV following 12 weeks of hypoxic endurance training in healthy individuals. Taken together, our results demonstrate that acute cardiac responses of the RV to hypoxic exercise are related to subsequent RV remodelling upon 12-weeks of hypoxic exercise training in healthy, relatively untrained individuals. Acute exercise-induced changes in cardiac responses versus structural adaptation In this study, we tested the assumption that any potential disproportionate ventricular wall stress contributes to RV remodelling. Since assessment of cardiac wall stress during exercise is highly challenging and invasive, we examined cardiac (systolic) function during hypoxic exercise and explored whether these changes related to structural adaptation post-training. We found that augmentation in RV fractional area change to acute exercise is inversely related to RV size following exercise training. In other words, small-to-modest (but not moderate-to-large) increases in RV systolic function during acute exercise relate to subsequent increases in RV structure post-training. One potential explanation for this observation may be that those individuals who had a blunted exercise-induced increase in RV fractional area change, were working at a higher afterload and hence received a greater stimulus for cardiac adaptation. Another potential explanation for this observation may relate to the structure of the RV. A smaller sized RV is less able to elevate measures of systolic RV function during exercise, and are therefore more susceptible for subsequent adaptation. Somewhat in line with this assumption, additional analysis revealed a positive relation between exercise-induced increases in RV fractional area change and RV size at