Department of Medicine, University of Utah, Salt Lake City, UT.
Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT.
Med Sci Sports Exerc. 2018 Dec;50(12):2409-2417. doi: 10.1249/MSS.0000000000001735.
The effect of an acute bout of exercise, especially high-intensity exercise, on the function of mitochondrial respiratory complexes is not well understood, with potential implications for both the healthy population and patients undergoing exercise-based rehabilitation. Therefore, this study sought to comprehensively examine respiratory flux through the different complexes of the electron transport chain in skeletal muscle mitochondria before and immediately after high-intensity aerobic exercise.
Muscle biopsies of the vastus lateralis were obtained at baseline and immediately after a 5-km time trial performed on a cycle ergometer. Mitochondrial respiratory flux through the complexes of the electron transport chain was measured in permeabilized skeletal muscle fibers by high-resolution respirometry.
Complex I + II state 3 (state 3CI + CII) respiration, a measure of oxidative phosphorylation capacity, was diminished immediately after the exercise (pre, 27 ± 3 ρm·mg·s; post, 17 ± 2 ρm·mg·s; P < 0.05). This decreased oxidative phosphorylation capacity was predominantly the consequence of attenuated complex II-driven state 3 (state 3CII) respiration (pre, 17 ± 1 ρm·mg·s; post, 9 ± 2 ρm·mg·s; P < 0.05). Although complex I-driven state 3 (3CI) respiration was also lower (pre, 20 ± 2 ρm·mg·s; post, 14 ± 4 ρm·mg·s), this did not reach statistical significance (P = 0.27). In contrast, citrate synthase activity, proton leak (state 2 respiration), and complex IV capacity were not significantly altered immediately after the exercise.
These findings reveal that acute high-intensity aerobic exercise significantly inhibits skeletal muscle state 3CII and oxidative phosphorylation capacity. This, likely transient, mitochondrial defect might amplify the exercise-induced development of fatigue and play an important role in initiating exercise-induced mitochondrial adaptations.
高强度运动特别是急性运动对线粒体呼吸复合物功能的影响尚未完全清楚，这对健康人群和接受运动康复的患者都有潜在影响。因此，本研究旨在全面研究高强度有氧运动前后骨骼肌线粒体中电子传递链不同复合物的呼吸流量。
在固定自行车上进行 5 公里计时赛后，立即从股外侧肌获取肌肉活检。通过高分辨率呼吸测量法，在通透的骨骼肌纤维中测量电子传递链复合物的线粒体呼吸流量。
代表氧化磷酸化能力的复合物 I + II 状态 3（状态 3CI + CII）呼吸在运动后立即下降（运动前，27 ± 3 ρm·mg·s；运动后，17 ± 2 ρm·mg·s；P < 0.05）。这种氧化磷酸化能力的降低主要是由于复合物 II 驱动的状态 3（状态 3CII）呼吸减弱（运动前，17 ± 1 ρm·mg·s；运动后，9 ± 2 ρm·mg·s；P < 0.05）。虽然复合物 I 驱动的状态 3（3CI）呼吸也较低（运动前，20 ± 2 ρm·mg·s；运动后，14 ± 4 ρm·mg·s），但这并没有达到统计学意义（P = 0.27）。相比之下，柠檬酸合酶活性、质子泄漏（状态 2 呼吸）和复合物 IV 能力在运动后即刻没有明显改变。
这些发现表明，急性高强度有氧运动显著抑制了骨骼肌的状态 3CII 和氧化磷酸化能力。这种可能是短暂的线粒体缺陷可能会放大运动引起的疲劳发展，并在启动运动诱导的线粒体适应中发挥重要作用。
