Author ORCID Identifier
Park - https://orcid.org/0000-0001-8576-7531
Layec - https://orcid.org/0000-0002-5029-2457
Trinity - https://orcid.org/0000-0001-8271-6536
Sidhu - https://orcid.org/0000-0002-4797-8298
Weavil - https://orcid.org/0000-0002-2032-8498
Document Type
Article
Publication Date
10-15-2021
Publication Title
American Journal of Physiology Regulatory, Integrative and Comparative physiology
Volume
321
Issue
5
First Page
R687
Last Page
R698
Abstract
Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: −67% vs. −82%, Pi: 353% vs. 534%, pH: −0.22 vs. −0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (−3% and −36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (−15% and −33%), complex II (−36% and −23%), complex I + II (−31% and −20%), and state 3CI+CII control ratio (−24% and −39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response.
Recommended Citation
Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation Matthew T. Lewis, Gregory M. Blain, Corey R. Hart, Gwenael Layec, Matthew J. Rossman, Song-Young Park, Joel D. Trinity, Jayson R. Gifford, Simranjit K. Sidhu, Joshua C. Weavil, Thomas J. Hureau, Jacob E. Jessop, Amber D. Bledsoe, Markus Amann, and Russell S. Richardson American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 2021 321:5, R687-R698
Comments
This is the accepted manuscript of an article published in the American Journal of Physiology - Regulatory, Integrative and Comparative physiology on October 15, 2021 and can be accessed at https://doi.org/10.1152/ajpregu.00158.2021