Volume 4 Supplement 1

15th International Conference on Environmental Ergonomics (ICEE XV)

Open Access

Neuromuscular fatigue during hypoxia is mediated by the hypoxic ventilatory response

  • Geoffrey Hartley1,
  • Cody Watson1,
  • Philip Ainslie2,
  • Matthew Greenway3 and
  • Stephen Cheung1Email author
Extreme Physiology & Medicine20154(Suppl 1):A41

https://doi.org/10.1186/2046-7648-4-S1-A41

Published: 14 September 2015

Introduction

Neurons of the corticospinal tract are inherently sensitive to oxygen availability and, in response to hypoxia, reduce their metabolic requirements and activity [1]. Consequently, hypoxia is associated with neuromuscular fatigue, attributed in part to central (i.e., CNS) mechanisms [2]. Although changes in cerebral blood flow (CBF), mediated by the ratio of hypoxia induced vasodilation to hypoxic ventilatory response (HVR) induced hypocapnia (i.e., PETCO2) [3], may be implicated in the development of central fatigue, the contribution from the chemoreflex control of HVR and CBF vs. reductions in CBF per se has yet to be isolated.

Methods

Neuromuscular function, indicated by voluntary torque production, motor evoked potentials (MEP), M-waves and cortical voluntary activation (cVA) of the flexor carpal radialis muscle during isometric wrist flexion was assessed (n = 8; 27 ± 8 y) during 3 separate conditions: 1) poikilocapnic hypoxia (Poikilo); 2) isocapnic hypoxia (Iso); and 3) isocapnic hypoxia and cyclooxygenase inhibition using Indomethacin (Indo) to selectively reduce CBF (estimated using transcranial Doppler ultrasound). End-tidal forcing was used to control PETO2 (51.5 ± 5.1 mmHg) during all conditions and PETCO2 at eucapnia during Iso (43.4 ± 4.0 mmHg) and Indo (41.6 ± 3.8 mmHg). Measurements were taken during baseline and upon steady-state response (i.e., stable SaO2) to hypoxia (approximately 5 minutes).

Results

The experimental conditions successfully isolated CBF and PETCO2. Iso and Indo were associated with a pronounced HVR (0.93 ± 0.60 L·min-1.SaO2-1 and 1.15 ± 0.72 L·min-1.SaO2-1) vs. Poikilo (0.26 ± 0.15 L·min-1·SaO2-1, p < 0.05). Torque was reduced from baseline in all conditions (-10.9 ± 13.7 Nm, p = 0.03). MEP amplitude (% M-wave) decreased in Poikilo (-4.5 ± 3.5%, p = 0.02) and Indo (-4.5 ± 4.8%, p = 0.02) vs. Iso (0.8 ± 2.8%; p = 0.9). No changes were observed in M-wave (p = 0.81). cVA decreased in all conditions (p < 0.01); however, reductions were greater during Iso (-11.5 ± 9.3%, p = 0.01) and Indo (-12.5 ± 9.1%, p = 0.04) vs. Poikilo (-3.8 ± 11.5%, p = 0.77).

Discussion

Consistent with previous research [2], hypoxia resulted in impaired neuromuscular function (i.e., reduced torque) in all conditions. These reductions were mediated by the CNS, as cVA decreased in the absence of changes in M-wave. Reductions in cVA were greater during Iso and Indo, suggesting an association with the magnitude of the HVR. Reduced CBF during Poikilo and Indo was associated with decreased motor cortex excitability; however, was not associated with decrements in torque or cVA.

Conclusion

This study demonstrates that the severity of CNS-mediated neuromuscular fatigue during hypoxia is dependent on the magnitude of the HVR, independent of changes in CBF.

Authors’ Affiliations

(1)
Environmental Ergonomics Laboratory, Department of Kinesiology, Brock University, St. Catharines
(2)
University of British Columbia Okanagan, Okanagan
(3)
McMaster University

References

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Copyright

© Hartley et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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