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Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle
Author(s) -
Fernström Maria,
Tonkonogi Michail,
Sahlin Kent
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.055202
Subject(s) - ucp3 , uncoupling protein , respiration , endurance training , medicine , mitochondrion , oxidative phosphorylation , endocrinology , thermogenesis , basal metabolic rate , skeletal muscle , ant , citrate synthase , biology , atp synthase , chemistry , biochemistry , anatomy , ecology , enzyme , brown adipose tissue , obesity
Mitochondrial proteins such as uncoupling protein 3 (UCP3) and adenine nucleotide translocase (ANT) may mediate back‐leakage of protons and serve as uncouplers of oxidative phosphorylation. We hypothesized that UCP3 and ANT increase after prolonged exercise and/or endurance training, resulting in increased uncoupled respiration (UCR). Subjects were investigated with muscle biopsies before and after acute exercise (75 min of cycling at 70% of ) or 6 weeks endurance training. Mitochondria were isolated and respiration measured in the absence (UCR or state 4) and presence of ADP (coupled respiration or state 3). Protein expression of UCP3 and ANT was measured with Western blotting. After endurance training , citrate synthase activity (CS), state 3 respiration and ANT increased by 24, 47, 40 and 95%, respectively (all P < 0.05 ), whereas UCP3 remained unchanged. When expressed per unit of CS (a marker of mitochondrial volume) UCP3 and UCR decreased by 54% and 18% ( P < 0.05) . CS increased by 43% after acute exercise and remained elevated after 3 h of recovery ( P < 0.05) , whereas the other muscle parameters remained unchanged. An intriguing finding was that acute exercise reversibly enhanced the capacity of mitochondria to accumulate Ca 2+ ( P < 0.05) before opening of permeability transition pores. In conclusion, UCP3 protein and UCR decrease after endurance training when related to mitochondrial volume. These changes may prevent excessive basal thermogenesis. Acute exercise enhances mitochondrial resistance to Ca 2+ overload but does not influence UCR or protein expression of UCP3 and ANT. The increased Ca 2+ resistance may prevent mitochondrial degradation and the mechanism needs to be further explored.