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Updated: May 13, 2026

Fiber Type and Subcellular-Specific Analysis of Lipid Droplet Content in Skeletal Muscle
Published on: June 8, 2022
Skeletal muscle fat metabolism after exercise in humans: influence of fat availability
Nicholas E Kimber1, David Cameron-Smith, Sean L McGee
1Department of Applied Science and Allied Health, Christchurch Polytechnic Institute of Technology, Christchurch, New Zealand. nick.kimber@cpit.ac.nz
Abstract:
The mechanisms facilitating increased skeletal muscle fat oxidation following prolonged, strenuous exercise remain poorly defined. The aim of this study was to examine the influence of plasma free fatty acid (FFA) availability on intramuscular malonyl-CoA concentration and the regulation of whole-body fat metabolism during a 6-h postexercise recovery period. Eight endurance-trained men performed three trials, consisting of 1.5 h high-intensity and exhaustive exercise, followed by infusion of saline, saline + nicotinic acid (NA; low FFA), or Intralipid and heparin [high FFA (HFA)]. Muscle biopsies were obtained at the end of exercise (0 h) and at 3 and 6 h in recovery. Ingestion of NA suppressed the postexercise plasma FFA concentration throughout recovery (P < 0.01), except at 4 h. The alteration of the availability of plasma FFA during recovery induced a significant increase in whole-body fat oxidation during the 6-h period for HFA (52.2 ± 4.8 g) relative to NA (38.4 ± 3.1 g; P < 0.05); however, this response was unrelated to changes in skeletal muscle malonyl-CoA and acetyl-CoA carboxylase (ACC)β phosphorylation, suggesting mechanisms other than phosphorylation-mediated changes in ACC activity may have a role in regulating fat metabolism in human skeletal muscle during postexercise recovery. Despite marked changes in plasma FFA availability, no significant changes in intramuscular triglyceride concentrations were detected. These data suggest that the regulation of postexercise skeletal muscle fat oxidation in humans involves factors other than the 5'AMP-activated protein kinase-ACCβ-malonyl-CoA signaling pathway, although malonyl-CoA-mediated regulation cannot be excluded completely in the acute recovery period.
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