Key result
Sex differences in acute peripheral vascular responses to hypoxia exist but pathological mechanisms remain unclear.
Why the study?
Mechanisms governing the vascular response to hypoxia in females compared to males have only recently been examined, with most data derived from predominantly male or all-male cohorts.
Understanding sex-specific mechanisms in the vascular response to hypoxia is essential for developing targeted therapeutics for conditions like obstructive sleep apnoea.
Answers are grounded in this paper and cite their sources.
Suggests sex-specific considerations in managing OSA-related CV risk; leaves open mechanisms of differential vascular response to hypoxia.
The incidence and presentation of obstructive sleep apnoea, as well as hypertension and cardiovascular disease, have been reported to differ by sex. It is thus reasonable to propose mechanisms contributing to subsequent pathology differ by sex. This concept is supported from a pre-pathological perspective, as sex differences have been observed in the vascular response to hypoxia both alone and during concomitant hypoxia and sympathetic activation. However, the mechanisms governing the vascular response to hypoxia in females compared to males have only recently been examined, with the preponderance of data in predominantly male or all-male cohorts. Determining the sex-specific mechanisms contributing to the foundational vascular response to hypoxia is essential to the development of targeted therapeutics. Herein we outline literature in support of vascular sex-related differences in the acute response to both intermittent and steady-state hypoxia, with an emphasis on the healthy state. However, questions remain to bridge the gap between preclinical observations to pathological conditions, such as the role of sex hormones and adrenergic receptors, with increasing adiposity, age and chronic disease (e.g., sleep apnoea).
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Jacob et al. (2026) conducted a review in Obstructive sleep apnoea. Sex-related differences in the acute peripheral vascular response to intermittent and steady-state hypoxia are evident in healthy states, but mechanisms linking these to pathology remain unclear.
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