Mike Stembridge, Philip N Ainslie, Michael G Hughes, Eric J Stöhr, James D Cotter, Michael M Tymko, Trevor A Day, Akke Bakker, Rob Shave

Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and following 10 days at 5050 m. In contrast to SL, LV end-diastolic volume was ~19% lower at rest (p=0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (~17%; 60±10 vs. 70±8 ml) despite higher LV twist (43%), apical rotation (115%) and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 ml vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely due to the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, whilst hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.