|Title||Substrate-specific Respiration of Isolated Skeletal Muscle Mitochondria after 1 h of Moderate Cycling in Sedentary Adults|
|Publication Type||Journal Article|
|Year of Publication||2021|
|Authors||Newsom, SA, Stierwalt, HD, Ehrlicher, SE, Robinson, MM|
|Journal||Medicine & Science in Sports & Exercise|
|Volume||Publish Ahead of Print|
Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and non-lipid substrates. It is unclear if aerobic exercise stimulates intrinsic oxidative metabolism of mitochondria or varies between substrates.
We studied mitochondrial metabolism in sedentary male and female adults (n=11F/4M) who were free of major medical conditions with mean±SD age of 28±7 years, peak aerobic capacity of 2.0±0.4 L/min, and body mass index of 22.2±2 kg/m2. Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 minutes after exercise (1 hour cycling at 65% peak aerobic capacity). Isolated mitochondria were analyzed using high-resolution respirometry of separate titration protocols for lipid (palmitoyl-carnitine, F-linked) and non-lipid substrates (glutamate-malate, N-linked; succinate S-linked). Titration protocols distinguished between oxidative phosphorylation and leak respiration and included measurement of reactive oxygen species emission (H2O2). Western blotting determined protein abundance of electron transfer flavoprotein (ETF) subunits including inhibitory methylation site on ETF-β.
Aerobic exercise induced modest increases in mitochondrial respiration due to increased coupled respiration across F-linked (+13%, p=0.08), N(S)-linked (+14%, p=0.09) and N-linked substrates (+17%, p=0.08). Prior exercise did not change P:O ratio. Electron leak to H2O2 increased 6% increased after exercise (p=0.06) for lipid substrates but not for non-lipid. Protein abundance of ETFα or β subunit or inhibitory methylation on ETF-β was not different between rest and after exercise.
In sedentary adults, the single bout of moderate intensity cycling induced modest increases for intrinsic mitochondrial oxidative phosphorylation that was consistent across multiple substrates.