Skeletal muscle proteins involved in fatty acid transport influence fatty acid oxidation rates observed during exercise.
Ed Maunder, Jeffrey A Rothschild, Andreas M Fritzen, Andreas B Jordy, Bente Kiens, Matthew J Brick, Warren B Leigh, Wee-Leong Chang, Andrew E Kilding
Author Information
Ed Maunder: Sports Performance Research Institute New Zealand, Auckland University of Technology, Auckland, New Zealand. ed.maunder@aut.ac.nz. ORCID
Jeffrey A Rothschild: Sports Performance Research Institute New Zealand, Auckland University of Technology, Auckland, New Zealand. ORCID
Andreas M Fritzen: The August Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark. ORCID
Andreas B Jordy: The August Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark. ORCID
Bente Kiens: The August Krogh Section for Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark. ORCID
Matthew J Brick: Orthosports North Harbour, AUT Millennium, Auckland, New Zealand. ORCID
Warren B Leigh: Orthosports North Harbour, AUT Millennium, Auckland, New Zealand. ORCID
Wee-Leong Chang: Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand. ORCID
Andrew E Kilding: Sports Performance Research Institute New Zealand, Auckland University of Technology, Auckland, New Zealand. ORCID
Several proteins are implicated in transmembrane fatty acid transport. The purpose of this study was to quantify the variation in fatty acid oxidation rates during exercise explained by skeletal muscle proteins involved in fatty acid transport. Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to estimate peak whole-body fatty acid oxidation rate (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 2 h of fed-state, moderate-intensity cycling to estimate whole-body fatty acid oxidation during fed-state exercise (FO). Bivariate correlations and stepwise linear regression models of PFO and FO during 0-30 min (early FO) and 90-120 min (late FO) of continuous cycling were constructed using muscle data. To assess the causal role of transmembrane fatty acid transport in fatty acid oxidation rates during exercise, we measured fatty acid oxidation during in vivo exercise and ex vivo contractions in wild-type and CD36 knock-out mice. We observed a novel, positive association between vastus lateralis FATP1 and PFO and replicated work reporting a positive association between FABPpm and PFO. The stepwise linear regression model of PFO retained CD36, FATP1, FATP4, and FABPpm, explaining ~87% of the variation. Models of early and late FO explained ~61 and ~65% of the variation, respectively. FATP1 and FATP4 emerged as contributors to models of PFO and FO. Mice lacking CD36 had impaired whole-body and muscle fatty acid oxidation during exercise and muscle contractions, respectively. These data suggest that substantial variation in fatty acid oxidation rates during exercise can be explained by skeletal muscle proteins involved in fatty acid transport.
