Abstract
PurposeTo investigate whether there is a differential response at rest and following exercise to conditions of genuine high altitude (GHA), normobaric hypoxia (NH), hypobaric hypoxia (HH), and normobaric normoxia (NN).MethodMarkers of sympathoadrenal and adrenocortical function [plasma normetanephrine (PNORMET), metanephrine (PMET), cortisol], myocardial injury [highly sensitive cardiac troponin T (hscTnT)], and function [N-terminal brain natriuretic peptide (NT-proBNP)] were evaluated at rest and with exercise under NN, at 3375 m in the Alps (GHA) and at equivalent simulated altitude under NH and HH. Participants cycled for 2 h [15-min warm-up, 105 min at 55% Wmax (maximal workload)] with venous blood samples taken prior (T0), immediately following (T120) and 2-h post-exercise (T240).ResultsExercise in the three hypoxic environments produced a similar pattern of response with the only difference between environments being in relation to PNORMET. Exercise in NN only induced a rise in PNORMET and PMET.ConclusionBiochemical markers that reflect sympathoadrenal, adrenocortical, and myocardial responses to physiological stress demonstrate significant differences in the response to exercise under conditions of normoxia versus hypoxia, while NH and HH appear to induce broadly similar responses to GHA and may, therefore, be reasonable surrogates.
Highlights
Performing field research at high altitude (HA) is challenging and is often compounded by an austere environment and confounders such as variable environmental temperature, sleep, and exercise intensity
normobaric normoxia (NN) differed from the three hypoxic environments in that only plasma normetanephrine (PNORMET) and PMET showed a significant rise with exercise
PNORMET, PMET, highly sensitive cardiac troponin T (hscTnT), and cortisol had returned to baseline 22-h post-exercise, but NTproBNP was significantly elevated compared to baseline (36.75 ± 39 vs. 48.2 ± 61, pg/ml, p < 0.01)
Summary
Performing field research at high altitude (HA) is challenging and is often compounded by an austere environment and confounders such as variable environmental temperature, sleep, and exercise intensity To mitigate these factors, the hypoxia of HA may be simulated. There remains little direct comparison between the effects of NH, HH, and a “real-world” equivalent altitude, in relation to the physiological stress induced. This was emphasized again when a recent review of studies utilizing NH and HH reiterated the limitations of the existing literature (Coppel et al 2015)
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