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Acute hypercapnia does not alter voluntary drive to the diaphragm in healthy humans.

Hsuan-Yu Wan,Jonathon L. Stickford,K. Kitano,Wesley J. Manz,D. Koceja,R. Chapman,J. Stager

Published 2018 in Respiratory Physiology & Neurobiology

ABSTRACT

Although systemic hypercapnia is a common outcome of pulmonary disease, the relationship between hypercapnia and voluntary diaphragmatic activation (VAdi) is unclear. To examine whether hypercapnia independent of ventilatory work contributes to reduced central motor drive to the diaphragm in healthy humans, 14 subjects spontaneously breathed room air (NN) or a hypercapnic gas mixture (HH; 7% CO2 with air) while at rest. Thereafter, subjects volitionally hyperventilated room air (NH) matching the minute ventilation recorded during HH while maintained at eucapnic levels. Twitch interpolation with bilateral magnetic stimulation of phrenic nerves at functional residual capacity was used to assess VAdi during the three trials. Although PETCO2 was elevated during HH compared with NN and NH (52 vs 36 mmHg), VAdi was not altered across the trials (HH = 93.3 ± 7.0%, NN = 94.4 ± 5.0%, NH = 94.9 ± 4.6%, p = 0.48). Our findings indicate that the magnitude of hypercapnia acutely imposed may not be effective in inhibiting voluntary neural drives to the diaphragm in normal resting individuals.

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