Intermittent hypobaric hypoxia exposure does not cause sustained alterations in autonomic control of blood pressure in young athletes

Abstract

Intermittent hypoxia (IH), which refers to the discontinuous use of hypoxia to reproduce some key features of altitude acclimatization, is commonly used in athletes to improve their performance. However, variations of IH are also used as a model for sleep apnea, causing sustained sympathoexcitation and hypertension in animals and, thus, raising concerns over the safety of this model. We tested the hypothesis that chronic IH at rest alters autonomic control of arterial pressure in healthy trained individuals. Twenty-two young athletes (11 men and 11 women) were randomly assigned to hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normoxia (500 m) in a double-blind and placebo-controlled design. Both groups rested in a hypobaric chamber for 3 h/day, 5 days/wk for 4 wk. In the sitting position, resting hemodynamics, including heart rate (HR), blood pressure (BP), cardiac output (Q(c), C(2)H(2) rebreathing), stroke volume (SV = Q(c)/HR), and total peripheral resistance (TPR = mean BP/Q(c)), were measured, dynamic cardiovascular regulation was assessed by spectral and transfer function analysis of cardiovascular variability, and cardiac-vagal baroreflex function was evaluated by a Valsalva maneuver, twice before and 3 days after the last chamber exposure. We found no significant differences in HR, BP, Q(c), SV, TPR, cardiovascular variability, or cardiac-vagal baroreflex function between the groups at any time. These results suggest that exposure to intermittent hypobaric hypoxia for 4 wk does not cause sustained alterations in autonomic control of BP in young athletes. In contrast to animal studies, we found no secondary evidence for sustained physiologically significant sympathoexcitation in this model.

Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

“…Consistent with previous reports, following exposure to IH of similar duration (8,22,27), baseline cardiorespiratory and cerebrovascular variables were unchanged. The lack of change in cardiovascular measurements (BP, heart rate, cardiac output) at rest is consistent with recent reports (10,27), indicating an absence of change to autonomic control. During hypoxic but not normoxic exercise, following both IH and CH, there was a greater elevation in Fig.…”

“…The chronic (i.e., years) repetitive and brief "apneas" associated with obstructive sleep apnea cause hypoxia, hypercapnia, and asphyxia, all of which contribute to sympathoexcitation (6), which seem critical to evoke adverse vascular changes. It should be acknowledged that comparable hypoxiato-reoxygenation cycles do not occur during the "typical" IH protocols used for athletic training [e.g., 5:5-min hypoxia-tonormoxia for 60 -90 min/day (2,8), or 30 min to 3 h continued hypoxia/day (10)] or by researchers as interventions to examine the potential consequences on systemic and cerebrovascular function (8,10,27,44). For example, during a typical 5:5-min hypoxia-to-normoxia session for 60 min or during a 1-h hypoxic exposure, the episodes of hypoxia to normoxia will be 6/h and 1/h, respectively; this represents very different conditions to Ͼ50 apneic events/h in a patient with moderate to severe obstructive sleep apnea.…”

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

“…Whilst comparison between studies is difficult, the comparable decrease in cerebral oxygenation at maximal exercise in the current study was more likely a consequence of the related hypocapnic-induced lower cerebral perfusion, rather than an intrinsic alteration in cerebrovascular function. Moreover, the unchanged heart rate response throughout the IHE are consistent with a recent report which also showed that autonomic control is unaltered following exposure to intermittent hypoxia (Fu et al 2007). …”

Preacclimatization in simulated altitudes

“…The degree of hypoxia was about 12% or equivalent to about 4,000 m at least when starting exposures [3][4][5][6][7]. Most studies exposed subjects at rest to hypoxia [8][9][10][11][12][13][14][15][16][17][18][19]. Those comparing the effects when exposures were at rest or with exercise did not find any differences [5,6].…”