Abstract
Background: A reduction in the inspired oxygen fraction (FiO2) induces a decline in arterial oxygen saturation (SpO2) and changes of heart rate variability (HRV). It has been shown that SpO2 and HRV responses to similar levels of acute normobaric hypoxia are inter-individual variable. Variable response may be influenced by normoxia reached maximal oxygen uptake (VO2max) value. Objective: The primary aim was to assess HRV and the SpO2 response to hypoxia, and examine the association with normoxic VO2max. Methods: Supine HRV and SpO2 were monitored during normobaric hypoxia (FiO2 = 9.6%) for 10 minutes in 28 subjects, aged 23.7 ± 1.7 years. HRV was evaluated by using both spectral and time domain HRV analysis. Low frequency (LF, 0.05-0.15 Hz) and high frequency (HF, 0.15-0.50 Hz) power together with square root of the mean of the squares of the successive differences (rMSSD) were calculated and transformed by natural logarithm (Ln). Based on the SpO2 in hypoxia, subjects were divided into Resistant (RG, SpO2 ≥ 70.9%, n = 14) and Sensitive (SG, SpO2 < 70.9%, n = 14) groups. Perceived hypoxia tolerance was self-scored on a 4-level scale. Results: VO2max was higher in SG (62.4 ± 7.2 ml ⋅ kg-1 ⋅ min-1) compared with RG (55.5 ± 7.1 ml ⋅ kg-1 ⋅ min-1, p = .017, d = 0.97). A significant relationship (r = -.45, p = .017) between hypoxic-normoxic difference in SpO2 and normoxic VO2max level was found. Vagal activity (Ln rMSSD) was significantly decreased (SG: p < .001, d = 2.64; RG: p < .001, d = 1.22), while sympathetic activity (Ln LF/HF) was relatively increased (p < .001, d = -1.40) in only the SG during hypoxia. Conclusions: Results show that subjects with a higher aerobic capacity exhibited a greater decline in SpO2, accompanied by greater autonomic cardiac disturbances during hypoxia. The SpO2 reduction was associated with perceived hypoxia comfort/discomfort. The hypoxia discomfort state was accompanied by a greater withdrawal in cardiac vagal activity.
Highlights
A reduction in the inspired oxygen fraction (FiO2) induces a decline in oxygen saturation (SpO2) (Iwasaki et al, 2006; Pighin et al, 2012) and causes homeostatic impairment due to systemic hypoxia (Mizuno et al, 1990; Ventura et al, 2003)
Some studies have revealed that a similar level of short-term acute normobaric hypoxia induces individual differences in the magnitude of SpO2 response that are related to variable changes in autonomic cardiac regulation (Bobyleva & Glazachev, 2007; Botek, Krejčí, De Smet, Gába, & McKune, 2015)
The main findings of the study were a) during hypoxia, significantly decreased (SG) showed a greater decline in vagal activity compared with RG, with a relative increase in sympathetic activity apparent in SG only; b) there was a negative correlation (r = –.45, p = .017) between normoxic VO2max level and ΔSpO2 in hypoxia; c) HDG demonstrated a greater reduction in SpO2 with a relative increase in sympathetic activity in hypoxia compared with HCG; d) Ln rMSSD exhibited a stronger association (r = .64; p < .001) with SpO2 during hypoxia compared with Ln High frequency power (HF) (r = .54; p = .003)
Summary
A reduction in the inspired oxygen fraction (FiO2) induces a decline in oxygen saturation (SpO2) (Iwasaki et al, 2006; Pighin et al, 2012) and causes homeostatic impairment due to systemic hypoxia (Mizuno et al, 1990; Ventura et al, 2003). Some studies have revealed that a similar level of short-term acute normobaric hypoxia induces individual differences in the magnitude of SpO2 response that are related to variable changes in autonomic cardiac regulation (Bobyleva & Glazachev, 2007; Botek, Krejčí, De Smet, Gába, & McKune, 2015). Considering the above mentioned findings, we propose that differences in normoxic VO2max may contribute to the individual variation in SpO2 during hypoxic exposure, and in the autonomic cardiac response to acute normobaric hypoxia at rest. The primary aim of this study was to assess the SpO2 response to hypoxia (FiO2 = 9.6%) and the concomitant changes in autonomic cardiac regulation during resting conditions. Conclusions: Results show that subjects with a higher aerobic capacity exhibited a greater decline in SpO2, accompanied by greater autonomic cardiac disturbances during hypoxia. The hypoxia discomfort state was accompanied by a greater withdrawal in cardiac vagal activity
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