Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise.
Level 4 - case-series / case-control
Uncontrolled pre-post human physiological study with in vitro tissue analysis
PubMed 16357012 · doi:10.1113/jphysiol.2005.102178
What was done
Participants completed 120 minutes of cycling at approximately 60% VO2peak. Skeletal muscle samples and isolated mitochondria were analyzed to measure whole-body fat oxidation, palmitate oxidation rates, carnitine palmitoyltransferase I (CPTI) kinetics in response to malonyl-CoA (M-CoA), and mitochondrial fatty acid translocase (FAT)/CD36 protein content. The functional role of FAT/CD36 was tested by adding the specific inhibitor sulfo-N-succimidyloleate (SSO) to isolated mitochondria.
What was found
Whole-body fat oxidation and mitochondrial palmitate oxidation progressively increased during exercise (P < 0.05) and were positively correlated (r = 0.78). Exercise progressively attenuated M-CoA inhibition of CPTI: relative to rest, 120 minutes of cycling decreased inhibition by 16%, 21%, 30%, and 34% at 0.7, 2, 5, and 10 µM M-CoA, respectively (P < 0.05). Mitochondrial FAT/CD36 protein increased by 63% during exercise (P < 0.05) and correlated with mitochondrial palmitate oxidation across all time points (r = 0.41, P < 0.05), peaking after 120 minutes (r = 0.63, P < 0.05). Addition of SSO reduced mitochondrial palmitate oxidation to approximately 20%.
Why it matters
This study provides direct human evidence that exercise-induced increases in muscle fatty acid oxidation rely on both reduced CPTI sensitivity to M-CoA and translocation or functional presence of FAT/CD36 in mitochondria.
Limits
The abstract does not state the sample size or participant characteristics (such as age, sex, or training status). The study used an uncontrolled pre-post design without a non-exercise control group, and in vitro isolated mitochondrial measurements may not fully reflect in vivo transport kinetics.
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- supports Increasing lipolysis and plasma fatty acid availability through supplementation does not necessarily increase fat oxidation because muscle CPT limits oxidation.