Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude.
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 after 10 days at 5,050 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 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 because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.
Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom; mstembridge@cardiffmet.ac.uk.
Mike
M
Stembridge
Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan Campus, Kelowna, Canada;
Philip N
PN
Ainslie
Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;
Michael G
MG
Hughes
Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;
Eric J
EJ
Stöhr
School of Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand;
James D
JD
Cotter
Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan Campus, Kelowna, Canada; Department of Biology, Mount Royal University, Calgary, Canada; and.
Michael M
MM
Tymko
Department of Biology, Mount Royal University, Calgary, Canada; and.
Trevor A
TA
Day
MIRA Institute, University of Twente, Twente, The Netherlands.
Akke
A
Bakker
Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;
Rob
R
Shave
D000328:Adult; D000531:Altitude; D002302:Cardiac Output / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D012146:Rest / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology*; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000503:physiopathology*
hypoxia; left ventricular mechanics; stroke volume