Geert Kleinnibbelink

Chapter 3 80 baseline (r=0.52, p=0.03), indicating that individuals with smaller RV cavity size show a smaller elevations in RV systolic function during exercise. In contrast to RVFAC, other measures did not significantly correlate with adaptation to exercise training. A possible explanation for this may be that RVFWS, TAPSE and TDI s’ respond differently to alterations in load compared to RVFAC. 22 These elevations in load may be central as a stimulus for subsequent cardiac adaptation to exercise. Moreover, RVFAC takes into account both radial and longitudinal functional whereas the other systolic functional indices only take the latter into account. The stress received by the RV may therefore better reflected by the augmentation in RVFAC to acute exercise compared to RVFWS, TAPSE and TDI s’. Right ventricular adaptations to hypoxic exercise training After 12 weeks of hypoxic exercise training, the right side of the heart showed structural adaptation concomitant with altered mechanics in the strain-area loop. Our observation of RV remodelling contrasts with others, who report the absence of RV adaption after an increase in training volume. 23, 24 Importantly, the lack of structural RV remodelling observed in these previous studies is mainly observed when examining elite athlete populations, who already had a high level of training at baseline evaluation (e.g. they were not detrained for example during pre-season evaluation). Interestingly, the LV showed no evidence for adaptation after training. This agrees with a study by Arbab-Zadeh et al. 25 where they showed that after 12 months progressive and intensive marathon training in 12 previously sedentary subjects (mean age, 29±6 years), that RV size increased during the initial 3-month training period, but the LV only started to remodel after 6 months of training. The hypoxic exercise stimulus mainly effects RV afterload, and to a lesser extent LV afterload. 8-12 Moreover, it may be that LV afterload is reduced during hypoxic exercise as a result of hypoxic induced peripheral vasodilation. 26, 27 This may have amplified the disproportionate RV remodelling. However, due to the lack of a control group this remains speculative. Based on the lack of structural adaptation in the LV in this study, this may suggest that RV remodelling precedes LV remodelling in relatively untrained individuals. Future work, however, is required to better understand this phenomenon. Previously, we have demonstrated changes in the strain-area loop in acute exercise settings 6, 13 but also marked differences in pulmonary hypertension populations 28-30 likely