Geert Kleinnibbelink

Chapter 1 18 have been proposed as possible mechanisms for EICF, including β -adrenergic receptor desensitization, oxidative stress and altered post-exercise loading. 13, 20-22 Interestingly, the RV appears to be affected to a greater magnitude than the LV. 19, 23 A possible explanation for this observation may be the disproportionately higher wall stress experienced by the RV relative to the LV during exercise. 24 However, no studies have directly examined this concept. Hypoxic exposure induces altered loading conditions for the RV and could therefore be an important substrate to investigate the direct relation between EICF and wall stress experienced during exercise. Specifically, acute exposure to hypoxia induces an increase in PVR and subsequently in PAP. 25 Accordingly, exercise under hypoxia may exaggerate RV wall stress and increase the workload of the RV to maintain CO. Therefore, exercise under hypoxia versus exercise under normoxia provides the possibility to examine the direct relationship between changes in RV afterload as a contributing factor to the magnitude of EICF. In this thesis, we will examine this potential relationship between RV afterload and EICF. Figure 3 . A) Differences between right and left ventricular structure (i.e. cavity size and wall thickness) (source: Betts et al. 3 ) and B) function (source: Bellofiore et al. 9 ). Cardiac plasticity The adult humanheart has an exceptional ability to alter its phenotype to adapt to changes in environmental demand. This response involves metabolic, mechanical, electrical, and