The effects of acute intermittent hypercapnia on cardiovascular and ventilatory control

Acute intermittent blood-gas perturbations elicit cardiorespiratory neuroplasticity, with intermittent hypercapnic hypoxia resulting in well-characterized and persistent increases in ventilation, sympathetic activity, and blood pressure. However, the effects of intermittent hypercapnia (IHc) independent of hypoxia remain unknown in humans. We investigated the long-lasting effects of acute IHc on ventilation, blood pressure, and limb vascular conductance. Twenty-four healthy participants (age: 23 ± 3 yr; body mass index: 22 ± 2 kg/m²) underwent a 10-min baseline, 40 min of either IHc (n = 17; 60-s intervals: 40-s +5 mmHg end-tidal Pco₂, 20-s normocapnia) or room-air control (n = 7), both delivered using end-tidal forcing, followed by 30 min of room-air recovery. Minute ventilation (V̇e) and mean arterial pressure (MAP) were measured continuously, whereas arm and leg blood flow were measured via strain-gauge plethysmography at baseline and every 10 min of recovery. Limb vascular conductance (LVC) was calculated as the sum of arm and leg blood flow multiplied by two and divided by MAP. The change in ventilation from baseline was not different across 30 min of recovery (P = 0.09) or between groups (P = 0.08). MAP was elevated at 10 ([Formula: see text] 6.1 mmHg, CI_95%: 3.8-8.4, P < 0.001), 20 ([Formula: see text] 6.7 mmHg, CI_95%: 4.3-9.0, P < 0.001), and 30 ([Formula: see text] 7.7 mmHg, CI_95%: 5.4-10.0, P < 0.001) min of recovery and was 4.4 mmHg (CI_95%: 0.4-8.4, P = 0.03) greater than control throughout recovery. LVC was reduced across recovery in both groups (P < 0.001). These findings suggest that IHc elicits long-term facilitation of MAP with minimal effect on V̇e. These results further our understanding of intermittent hypercapnia in the regulation of the cardiorespiratory system.NEW & NOTEWORTHY Our findings show that in humans, intermittent hypercapnia independent of hypoxia does not appreciably affect ventilation but increases mean arterial pressure for upward of 30 min. These results help further our understanding of how repeated arterial blood gas fluctuations contribute to persistent changes in cardiovascular control.