Increased uncoupling protein 3 content does not affect mitochondrial function in human skeletal muscle in vivo
Matthijs K C Hesselink1, Paul L Greenhaff, Dimitru Constantin-Teodosiu
1Department of Movement Sciences, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. matthijs.hesselink@bw.unimaas.nl
The Journal of Clinical Investigation
|February 18, 2003
Summary
A high-fat diet increased uncoupling protein 3 (UCP3) in skeletal muscle but did not affect phosphocreatine (PCr) resynthesis rates. This suggests UCP3
Area of Science:
- Exercise Physiology
- Mitochondrial Function
- Skeletal Muscle Metabolism
Background:
- Phosphocreatine (PCr) resynthesis post-exercise is a key indicator of mitochondrial function.
- Uncoupling protein 3 (UCP3) is implicated in mitochondrial energy regulation.
Purpose of the Study:
- To investigate the impact of a diet-induced increase in skeletal muscle uncoupling protein 3 (UCP3) expression on post-exercise phosphocreatine (PCr) resynthesis.
- To determine if elevated UCP3 influences mitochondrial coupling during high metabolic demand.
Main Methods:
- Healthy males underwent intense, one-legged, anoxic contractions after 7 days on either a low-fat (LF) or high-fat (HF) diet.
- Muscle PCr resynthesis rates were measured during recovery (20, 60, 120 seconds) following exercise with occluded limb blood flow.
- UCP3 protein content and muscle metabolites (acetylcarnitine, free-creatine, lactate) were analyzed.
Main Results:
- The HF diet significantly increased UCP3 protein content by ~44% compared to the LF diet.
- Despite increased UCP3, there were no significant differences in the rate of PCr resynthesis between LF and HF diet groups.
- Muscle acetylcarnitine, free-creatine, and lactate concentrations during recovery were not affected by the HF diet.
Conclusions:
- Increased skeletal muscle UCP3 expression, induced by a high-fat diet, does not impair the rate of phosphocreatine (PCr) resynthesis.
- These findings suggest that the primary role of UCP3 in humans is unlikely to be mitochondrial uncoupling under conditions of maximal oxidative phosphorylation flux.
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