School of Biological and Population Health Sciences, College of Public Health and Human Sciences, Oregon State University, Corvallis, OR.
Med Sci Sports Exerc. 2021 Jul 1;53(7):1375-1384. doi: 10.1249/MSS.0000000000002615.
Skeletal muscle mitochondria have dynamic shifts in oxidative metabolism to meet energy demands of aerobic exercise. Specific complexes oxidize lipid and nonlipid 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 yr, peak aerobic capacity of 2.0 ± 0.4 L·min-1, and body mass index of 22.2 ± 2 kg·m-2. Biopsies were collected from the vastus lateralis muscle on separate study days at rest or 15 min after exercise (1 h cycling at 65% peak aerobic capacity). Isolated mitochondria were analyzed using high-resolution respirometry of separate titration protocols for lipid (palmitoylcarnitine, F-linked) and nonlipid substrates (glutamate-malate, N-linked; succinate S-linked). Titration protocols distinguished between oxidative phosphorylation and leak respiration and included the measurement of reactive oxygen species emission (H2O2). Western blotting determined the protein abundance of electron transfer flavoprotein (ETF) subunits, including inhibitory methylation site on ETF-β.
Aerobic exercise induced modest increases in mitochondrial respiration because of 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 nonlipid. The protein abundance of ETF-α or ETF-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.
骨骼肌线粒体的氧化代谢具有动态变化，以满足有氧运动的能量需求。特定的复合物氧化脂质和非脂质底物。目前尚不清楚有氧运动是否能刺激线粒体的内在氧化代谢，或者是否因底物而异。
我们研究了久坐的男性和女性成年人（n = 11F/4M）的线粒体代谢，这些成年人没有重大疾病，平均年龄为 28 ± 7 岁，最大有氧能力为 2.0 ± 0.4 L·min-1，体重指数为 22.2 ± 2 kg·m-2。在休息或运动后 15 分钟（以 65%最大有氧能力进行 1 小时自行车运动）的不同研究日，从股外侧肌采集活检。使用高分辨率呼吸测定法对分离的线粒体进行分析，采用单独的滴定方案分析脂质（棕榈酰肉碱，F 连接）和非脂质底物（谷氨酸-苹果酸，N 连接；琥珀酸 S 连接）。滴定方案区分了氧化磷酸化和漏呼吸，并包括活性氧物种（H2O2）的测量。Western blot 确定了电子传递黄素蛋白（ETF）亚基的蛋白丰度，包括 ETF-β上的抑制性甲基化位点。
有氧运动导致线粒体呼吸增加，这是由于 F 连接（增加 13%，P = 0.08）、N(S)-连接（增加 14%，P = 0.09）和 N 连接底物（增加 17%，P = 0.08）的偶联呼吸增加所致。运动前不会改变 P:O 比值。运动后脂质底物的电子泄漏到 H2O2 增加了 6%（P = 0.06），而非脂质底物则没有增加。休息和运动后，ETF-α 或 ETF-β 亚基或 ETF-β 上的抑制性甲基化的蛋白丰度没有差异。
在久坐的成年人中，单次中等强度的自行车运动诱导了适度的内在线粒体氧化磷酸化增加，这在多种底物中是一致的。
