Cerebrovascular and ventilatory responses to acute normobaric hypoxia in girls and women

Abstract

Physiological responses to hypoxia in children are incompletely understood. We aimed to characterize cerebrovascular and ventilatory responses to normobaric hypoxia in girls and women. Ten healthy girls (9.9 ± 1.7 years; mean ± SD; Tanner stage 1 and 2) and their mothers (43.9 ± 3.5 years) participated. Internal carotid (ICA) and vertebral artery (VA) velocity, diameter and flow (Duplex ultrasound) was recorded pre- and post-1 h of hypoxic exposure (FIO₂ = 0.126;~4000 m) in a normobaric chamber. Ventilation (V˙E) and respiratory drive (V_T/T_I) expressed as delta change from baseline (∆%), and end-tidal carbon-dioxide (P_ETCO₂) were collected at baseline (BL) and 5, 30 and 60 min of hypoxia (5/30/60 HYP). Heart rate (HR) and oxygen saturation (SpO₂) were also collected at these time-points. SpO₂ declined similarly in girls (BL-97%; 60HYP-80%, P < 0.05) and women (BL-97%; 60HYP-83%, P < 0.05). Global cerebral blood flow (gCBF) increased in both girls (BL-687; 60HYP-912 mL·min^-1, P < 0.05) and women (BL-472; 60HYP-651 mL·min^-1, P < 0.01), though the ratio of ICA:VA (%) contribution to gCBF differed significantly (girls, 75:25%; women, 61:39%). The relative increase in V˙E peaked at 30HYP in both girls (27%, P < 0.05) and women (19%, P < 0.05), as did ∆%V_T/T_I (girls, 41%; women, 27%, P's < 0.05). Tidal volume (V_T) increased in both girls and women at 5HYP, remaining elevated above baseline in girls at 30 and 60 HYP, but declined back toward baseline in women. Girls elicit similar increases in gCBF and ventilatory parameters in response to acute hypoxia as women, though the pattern and contributions mediating these responses appear developmentally divergent.

Keywords: Cerebral perfusion; children; hypoxia; respiratory drive; ventilation.

Figure 1

Heart rate (panel A) and oxygen saturation (panel B) at baseline and following 5 (5 HYP), 30 (30 HYP) and 60 (60 HYP) minutes of hypoxia in girls (white circles) and women (black squares); *within subject change from baseline in girls, P < 0.05; ≠within subject change from baseline in women, P < 0.05; #child‐adult difference, P < 0.05.

Figure 2

Relative change from baseline in ventilation (Δ%; panel A), tidal volume (Δ%; panel B), breathing frequency (Δ%; panel C) and respiratory drive (Δ%; panel D) following 5 (5 HYP), 30 (30 HYP) and 60 (60 HYP) minutes of hypoxia in girls (white circles) and women (black squares); *within subject change from baseline in girls, P < 0.05; ≠ within subject change from baseline in women, P < 0.05; # child‐adult difference, P < 0.05.

Figure 3

Relative change from baseline to 60 min of hypoxia in internal carotid artery blood flow (Δ%; panel A) and vertebral artery blood flow (Δ%; panel B) in girls (white circles) and women (black squares); *within subject change from baseline, P < 0.05.

Figure 4

Global cerebral blood flow distribution at baseline and after 60 min of hypoxia in girls (A) and women (B). The gray bars represent vertebral artery contribution and the white bars represent internal carotid artery contribution; *within subject change from baseline, P < 0.05.