We commend Baranauskas et al. (1) for their attempt to compare the effectiveness of hypoxic versus heat stressors for enhancing endurance performance in normoxic (sea level) and thermoneutral (temperate) conditions. Based on the available evidence, the authors conclude that “physiological adaptations acquired through conventional altitude training practices are superior for temperate sea-level endurance exercise performance of well-trained athletes compared to those gained with heat training.” Whereas we concur with the authors' view that heat training is erroneously spread as the “new altitude training,” we would advise caution regarding such a general statement.
We recognize that comparing hypoxia and heat is challenging as physiological challenges and consequences imposed by these two environmental stressors do not necessarily match. In addition, different protocols (e.g., exercise type, exposure duration, stressor severity, test timings) add further confusion. Importantly, any environmental stressor–induced adaptation is a function of its duration, intensity, frequency, and variability (2), which inherently generate different adaptation kinetics and outcomes. Furthermore, given that numerous factors underlie endurance performance (e.g., maximal oxygen consumption, thresholds, critical power, mechanical efficiency, economy), it seems even more complicated to elucidate the independent effect of a particular environmental stressor. In this regard, differentiating specific environmental training effect from chronic exposure does not seem so obvious as adding environmental stress during training also quickly elicits tolerance and acclimatization/acclimation (3).
Baranauskas et al. (1) mostly focused on the opposing physiological responses related to hemoglobin mass (hypoxia) or plasma volume (heat) expansion, although such environmental-induced mechanisms, potentially explaining some of the beneficial normoxic and thermoneutral endurance performance adaptations remain to be fully elucidated. Looking beyond cardiovascular and hemodynamics adaptation, current literature provides evidence that repeated exposures to both hypoxia and heat provoke both similar and distinct central (e.g., autonomic nervous system) and peripheral (e.g., molecular transcription) adaptations (4,5). The overview of the physiological adaptations proposed by Baranauskas et al. (see Fig. 2 in ) does not account for the hypoxia-inducible factor-1α (HIF-1α) and the heat shock protein (HSP) (5) upregulation — common key contributors that serve as molecular chaperones for a myriad of cellular pathways. Specifically, in hypoxia, HSP expression is increased and contributes to HIF-1α stabilization (5), which is well known to be time dependent (6). In the heat, HSP-70 and HSP-90 expression also amplifies the HIF-1α pathway with similar downstream effects than after hypoxic exposure (e.g., increased vascular endothelial growth factor, erythropoietin and its receptors, mitochondria enzymes, and GLUT-1 transporters) (5). Therefore, to fully substantiate the ergogenic benefits of these environmental stressors on endurance performance, “cross-tolerance” or “cross-adaptation” through the combination (e.g., larger transcriptional responses when combining chronic hypoxic exposure and repeated maximal-intensity hypoxic exercise (4); larger hemoglobin mass and plasma volume expansion when adding heat training during a “living high–training low” camp ) or sequential succession of these environmental stressors (8) seems warranted.
To conclude, we believe that exact matching (and thereby comparing) of hypoxia and heat stressors in the context of endurance training process seems unfeasible. We, thereby, argue that assessing the additive and/or combined effects of environmental stressors would provide more physiological insights and, even more importantly, practical value for endurance athletes.
Expertise and Performance (EA 7370)
French Institute of Sport
Faculty of Sport
University of Ljubljana
and Department of Automation
Biocybernetics and Robotics
Jozef Stefan Institute
Grégoire P. Millet
Institute of Sport Sciences
University of Lausanne
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