Overbuilt for exercise or not: how do lung structure and distensibility impact exercise capacity?

Abstract

Cardiacoutput,muscleoxygendeliveryand oxygen extraction are hypothesized to limit maximal oxygen consumption ( ˙ VO2max )i n healthy individuals. Much work aiming to address the long-standing question of cardiac output limitation has focused on the capacity of the left ventricle to increase stroke volume with substantially less focus on the importance of the right ventricle. The right ventricle is thin-walled, crescent shaped and generally less resistant to afterload stress than the left ventricle. While the increase in mean pressure encountered by the left ventricle during exercise is ∼25%, the right ventricle encounters a threeto four-fold increase in mean pulmonary vascular pressure. Indeed, elite endurance athletes experience acute right ventricular dysfunction and show evidence of right ventricular fibrosis after a race (3‐11 h) although left ventricular structure and function are unaffected (La Gerche et al. 2012). Within our group, we have frequently discussed how the right ventricle might be limited in its ability to increase cardiac output in the face of hypertensive pulmonary vascular pressures and find the question of whether right ventricular afterload stress impacts exercise capacity in healthy individuals breathing room air to be intriguing. Thus, we were excited to have the opportunity to discuss the recent paper entitled ‘Pulmonary vascular distensibility predicts aerobic capacity in healthy humans’, published (Lalande et al. 2012). Here, Lalande et al. hypothesized that the distensibility of the pulmonary vasculature predicts ˙ VO2max in healthy humans.