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

Hsuan-Yu Wan; Jonathon L Stickford; Koichi Kitano; Wesley J Manz; David M Koceja; Robert F Chapman; Joel M Stager

doi:10.1016/j.resp.2018.05.012

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

Respir Physiol Neurobiol. 2018 Dec:258:60-68. doi: 10.1016/j.resp.2018.05.012. Epub 2018 May 30.

Authors

Hsuan-Yu Wan¹, Jonathon L Stickford², Koichi Kitano³, Wesley J Manz⁴, David M Koceja⁵, Robert F Chapman⁶, Joel M Stager⁷

Affiliations

¹ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: hsuan-yu.wan@hsc.utah.edu.
² Exercise & Respiratory Physiology Laboratory, Department of Health and Exercise Science, Appalachian State University, 111 Rivers Street, Boone, NC 28608, USA. Electronic address: stickfordjl@appstate.edu.
³ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: kkitano@indiana.edu.
⁴ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: manzwesleyj@gmail.com.
⁵ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: koceja@indiana.edu.
⁶ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: rfchapma@indiana.edu.
⁷ Human Performance Laboratory, Department of Kinesiology, Indiana University, 1025 E 7th Street, Bloomington, IN 47405, USA. Electronic address: stagerj@indiana.edu.

PMID: 29859322
DOI: 10.1016/j.resp.2018.05.012

Abstract

Although systemic hypercapnia is a common outcome of pulmonary disease, the relationship between hypercapnia and voluntary diaphragmatic activation (VA_di) 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 VA_di during the three trials. Although P_ETCO₂ was elevated during HH compared with NN and NH (52 vs 36 mmHg), VA_di 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.

Keywords: Carbon dioxide; Diaphragmatic voluntary activation; Group III/IV afferents; Respiratory acidosis; Respiratory muscles.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Action Potentials / physiology
Adolescent
Adult
Analysis of Variance
Diaphragm / physiopathology*
Female
Healthy Volunteers
Humans
Hypercapnia*
Hyperventilation / physiopathology
Magnetics / methods
Male
Muscle Contraction / physiology*
Phrenic Nerve / physiology
Respiratory Mechanics / physiology*
Young Adult