Geert Kleinnibbelink
General Discussion 10 207 10.3.2 – Cardiac remodelling to exercise training Based on the disproportionate end-systolic wall stress experienced by the RV during exercise 21 , it has been hypothesized that chronic exercise-induced remodelling may also disproportionally affect the RV. In Chapter 3 , we studied the effect of a 12 weeks hypoxic high-intensity running exercise programme on cardiac remodelling in healthy individuals. Indeed, we observed RV structural remodelling (increase in RV dimensions) but no LV remodelling, that supports previous data and theory. Another prospective study by Arbab-Zadeh et al . showed that after 12 months progressive and intensive marathon training in 12 previously sedentary subjects (mean age, 29±6 years), the RV increased in size during the initial 3-month training period. 48 The LV, however, only started to remodel after 6 months of training. In contrast to these observations, in less trained individuals, an increase in training volume in already highly-trained Olympic rowers induced LV but not RV structural remodelling ( Chapter 4 ). These findings contrast with other studies performed in elite athletes. 49, 50 D’Ascenzi et al. reported seasonal variation in RV size in a cohort of top-level basketball and volleyball players where RV remodelling occurred from pre- to mid-season but plateaued towards the end of the season. 50 Across three consecutive Olympic Games, Aengevaeren et al. noted that RV remodelling occurred between the first two Olympics Games, followed by a plateau during the subsequent 4 years in a heterogeneous group of athletes (n=50, 17 different sports). 49 Data from these two studies suggests that once these athletes reach a specific level of training, the RV does not continue to remodel having potentially reached a plateau. This may explain why we did not find RV remodelling despite a gradual increase of training volume over 9 months in the cohort with Olympic rowers ( Chapter 4 ). In combination, these data suggest that when an untrained individual starts to exercise, the primary cardiac response will be RV remodelling, with LV remodelling occurring later in the training exposure. Once the individual reaches a higher level of training changes in the RV will slow or stop but the LV may continue to adapt or remodel. This hypothesis of structural cardiac remodelling pattern suggests that the RV and LV do not mirror each other and remodel differently to chronic exercise. This hypothesis is outlined in Figure 4 .
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