Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation

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 f...

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Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2021-11, Vol.321 (5), p.R687-R698
Main Authors: Lewis, Matthew T., Blain, Gregory M., Hart, Corey R., Layec, Gwenael, Rossman, Matthew J., Park, Song-Young, Trinity, Joel D., Gifford, Jayson R., Sidhu, Simranjit K., Weavil, Joshua C., Hureau, Thomas J., Jessop, Jacob E., Bledsoe, Amber D., Amann, Markus, Richardson, Russell S.
Format: Article
Language:English
Subjects:
Adult
Analgesics, Opioid
Attenuation
Bicycling
Biopsy
Cell Respiration
Electron transport chain
Energy Metabolism
Exercise
Fentanyl
Healthy Volunteers
Human health and pathology
Humans
Injections, Spinal
Lactic acid
Life Sciences
Liquid chromatography
Male
Mass spectrometry
Mass spectroscopy
Metabolic rate
Metabolism
Metabolites
Mitochondria
Mitochondria, Muscle
Muscle Contraction
Muscles
Musculoskeletal system
Neurons, Afferent
Perturbation
Quadriceps Muscle
Random Allocation
Respiration
Respiratory function
Respirometry
Sensory neurons
Skeletal muscle
Tissues and Organs
Young Adult
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Summary: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 3 CI+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.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00158.2021