Sex differences in the vascular response to sympathetic activation during acute hypoxaemia

Abstract

Activation of the sympathetic nervous system causes vasoconstriction and a reduction in peripheral blood flow. Sympathetically mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically mediated vasoconstriction is preserved or even enhanced during hypoxaemia. Given the potential for sex-specific differences in hypoxic vascular control, prior results are limited in application. We tested the hypothesis that young women attenuate sympathetically mediated vasoconstriction during steady-state hypoxaemia, whereas men do not. Healthy young men (n = 13, 25 ± 4 years) and women (n = 11, 24 ± 4 years) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxaemia. Beat-to-beat blood pressure (finger photoplethysmography) and forearm blood flow (venous occlusion plethysmography) were measured continuously. Total and forearm vascular conductance (TVC and FVC, respectfully) were calculated. A change (Δ) in TVC and FVC from steady-state during the last 1 min of CPT was calculated and differences between normoxia and systemic hypoxia were assessed. In men, the reduction in TVC during CPT was greater during hypoxia compared to normoxia (ΔTVC, P = 0.02), whereas ΔTVC did not differ between conditions in women (P = 0.49). In men, ΔFVC did not differ between normoxia and hypoxia (P = 0.92). In women, the reduction in FVC during CPT was attenuated during hypoxia (ΔFVC, P < 0.01). We confirm sympathetically mediated vasoconstriction is preserved or enhanced during hypoxaemia in young men, whereas peripheral vascular responsiveness to sympathetic activation during hypoxaemia is attenuated in young women. The results advance our understanding of sex-related differences in hypoxic vascular control.

On the haemodynamic consequence of the chemoreflex and muscle mechanoreflex interaction in women and men: two tales, one story

“…In fact, there is compelling evidence of an upregulated β‐adrenergic responsiveness of the peripheral vasculature to sympathetic outflow in premenopausal women (Hart et al., 2011; Kneale et al., 2000) and, as such, the vasodilatory response to hypoxic exercise is higher in women compared to men (Casey et al., 2014). Moreover, Jacob and colleagues (2021) recently reported that acute hypoxia increases the vasoconstrictor response to other sympathoexcitatory stressors (e.g. cold pressor test) in men, but attenuates the response in women, a finding which further substantiates the current conclusion of the sex difference in the MMR:O 2 ‐CR interaction.…”

Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans

“…As a result, males may have greater vasodilatory reserve when faced with a potent local vasodilatory stimulus (i.e., local tissue hypoxia, explaining the twofold increase in vascular conductance when exposed to hypoxia we observed in males compared females ( than females, despite matched microvascular function (Kobayashi et al, 2015). Additionally, the forearm vascular response to hypoxia has been observed to be greater in males (Jacob et al, 2021), but this is not a finding shared by all studies (Casey et al, 2014).…”

Hemodynamic changes in the temporalis and masseter muscles during acute stress in healthy humans

“…This latter study was the first to directly compare hemodynamic stress responses in head muscles and included an extensive review of the recent literature, although head muscles were limited to the masseter muscle (Rashid and Roatta 2022 ). Limb muscles were no longer examined in the present study but sympathetic constrictory responses or increases in muscle sympathetic nerve activity in these muscles have consistently been reported in response to several stressors, including cold pressor test (Wray et al 2007 ; Jacob et al 2021 ; Coovadia et al 2022 ), post-exercise muscle ischemia (Saito et al 2000 ; Tokizawa et al 2006 ), and acute pain stimuli (Burton et al 2016 ).…”