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Progesterone and its analogues are known to influence ventilation. Therefore, the purpose of this study was to investigate the role of endogenous and pharmaceutical female sex hormones in ventilatory control during the activation of the metaboreflex, mechanoreflex, and CO2 chemoreflex. Women aged 18–30 taking (n = 14) or not taking (n = 12) oral contraceptives (OC and NOC, respectively) were tested in the low hormone (LH) and high hormone (HH) conditions corresponding to the early follicular and mid‐luteal phases (NOC) or placebo and high‐dose pills (OC). Women underwent three randomized trials: (a) 3 min of passive leg movement (PLM), (b) 2 min of 40% maximal voluntary handgrip exercise followed by 2 min of post‐exercise circulatory occlusion (PECO), and (c) 5 min of breathing 5% CO2. We primarily measured hemodynamics and ventilation. During PLM, the OC group had a smaller pressor response (p = .012). During PECO, the OC group similarly exhibited a smaller pressor response (p = .043) and also exhibited a greater ventilatory response (p = .024). Lastly, in response to breathing 5% CO2, women in the HH phase had a greater ventilatory response (p = .022). We found that OC use attenuates the pressor response to both the metaboreflex and mechanoreflex while increasing the ventilatory response to metaboreflex activation. We also found evidence of an enhanced CO2 chemoreflex in the HH phase. We hypothesize that OC effects are from the chronic upregulation of pulmonary and vascular β‐adrenergic receptors. We further suggest that the increased cyclic progesterone in the HH phase enhances the chemoreflex., We have shown that natural and pharmaceutical female sex hormones can influence the metaboreflex, mechanoreflex, and CO2 chemoreflex. Oral contraceptives users have attenuated pressor responses to both metaboreflex and mechanoreflex activation concurrent with augmented ventilatory responses to metaboreflex activation. Women in the high hormone phase of the menstrual cycle have a greater ventilatory response to CO2 compared to the low hormone phase.

After exposure to microgravity, or head‐down bed rest (HDBR), fluid loading is often used with the intent of increasing plasma volume and maintaining mean arterial pressure during orthostatic stress. Nine men (aged 18–32 years) underwent three randomized trials with lower body negative pressure (LBNP) before and after: (1) 4‐h of sitting with fluid loading (1 g sodium chloride/125 mL of water starting 2.5‐h before LBNP), (2) 28‐h of 6‐degree HDBR without fluid loading, and (3) 28‐h of 6‐degree HDBR with fluid loading. LBNP was progressive from 0 to −40 mmHg. After 28‐h HDBR, fluid loading did not protect against the loss of plasma volume (−280 ± 64 mL without fluid loading, −207 ± 86 with fluid loading, P = 0.472) nor did it protect against a drop of mean arterial pressure (P = 0.017) during LBNP (Post‐28 h HDBR response from 0 to −40 mmHg LBNP: 88 ± 4 to 85 ± 4 mmHg without fluid loading and 93 ± 4 to 88 ± 5 mmHg with fluid loading, P = 0.557 between trials). However, fluid loading did protect against the loss of stroke volume index and central venous pressure observed after 28‐h HDBR. Fluid loading also attenuated the increase of angiotensin II seen after 28‐h HDBR and throughout the LBNP protocol (Post‐28 h HDBR response from 0 to −40 mmHg LBNP: 16.6 ± 3.4 to 23.7 ± 5.0 pg/mL without fluid loading and 6.1 ± 0.8 to 12.2 ± 2.3 pg/mL with fluid loading, P

Orthostatic intolerance is more common in women than men, and some studies have found that women in the early follicular (EF) phase of the menstrual cycle experience the greatest feelings of lightheadedness. Chemoreflex function while supine or upright was investigated to determine the potential contribution of ventilatory control to these phenomena. Men (n = 13) and women (n = 14) were tested while supine and 70° upright (head‐up tilt [HUT]) and given: (1) normoxia or (2) hypercapnia (5% CO2). Women were tested during the EF phase (days 2–5) and the midluteal phase (ML; days 18–24). During HUT, all groups reduced cerebrovascular resistance index (men: 1.45 ± 0.08 to 1.42 ± 0.07 mmHg/(cm·sec), EF: 1.38 ± 0.11 to 1.26 ± 0.10 mmHg/(cm·sec), ML: 1.25 ± 0.07 to 1.09 ± 0.07 mmHg/(cm·sec); P ≤ 0.019); however, only men increased ventilation (men: 11.99 ± 0.65 to 13.24 ± 0.83 L/min; P