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Abstract Sub‐acute (e.g., inhalation injury) and/or acute insults sustained during a severe burn injury impairs pulmonary function. However, previous work has not fully characterized pulmonary function in adults with well‐healed burn injuries decades after an injury. Therefore, we tested the hypothesis that adults with well‐healed burn injuries have lower pulmonary function years after recovery. Our cohort of adults with well‐healed burn‐injuries (n = 41) had a lower forced expiratory volume in one second (Burn: 93 ± 16 vs. Control: 103 ± 10%predicted, mean ± SD; d = 0.60, p = 0.04), lower maximal voluntary ventilation (Burn: 84 [71–97] vs. Control: 105 [94–122] %predicted, median [IQR]; d = 0.84, p

Abstract A high sodium (Na+) meal impairs peripheral vascular function. In rodents, chronic high dietary Na+ impairs cerebral vascular function, and in humans, habitual high dietary Na+ is associated with increased stroke risk. However, the effects of acute high dietary Na+ on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na+ impairs cerebrovascular reactivity in healthy adults. Thirty‐seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross‐over study. Participants were given a low Na+ meal (LSM; 138 mg Na+) and a high Na+ meal (HSM; 1,495 mg Na+) separated by ≥ one week. Serum Na+, beat‐to‐beat BP, middle cerebral artery velocity (transcranial Doppler), and end‐tidal carbon dioxide (PETCO2) were measured pre‐ (baseline) and 60 min post‐prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO2, 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow‐mediated dilation (FMD). Changes in serum Na+ were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p

Abstract Older adults have reduced fluid intake and impaired body fluid and electrolyte regulation. Older female adults exhibit exaggerated exercise blood pressure (BP) responses, which is associated with an increased risk of adverse cardiovascular events. However, it is unclear if dysregulated body fluid homeostasis contributes to altered exercise BP responses in older female adults. We tested the hypothesis that short‐term water deprivation (WD) increases exercise BP responses in older female adults. Fifteen female adults (eight young [25 ± 6 years] and seven older [65 ± 6 years]) completed two experimental conditions in random crossover fashion; a euhydration control condition and a stepwise reduction in water intake over three days concluding with a 16‐hr WD period. During both trials, beat‐to‐beat BP (photoplethysmography) and heart rate (electrocardiogram) were continuously assessed during rest, handgrip exercise (30% MVC), and post‐exercise ischemia (metaboreflex isolation). At screening, older compared to young female adults had greater systolic and diastolic BP (p ≤ .02). Accelerometer‐assessed habitual physical activity was not different between groups (p = .65). Following WD, 24‐hr urine flow rate decreased, whereas thirst, urine specific gravity, and plasma osmolality increased (condition: p