Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation.
Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation.
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急性高强度运动和骨骼肌线粒体呼吸功能：代谢扰动的作用。
DOI：
10.1152/ajpregu.00158.2021
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Richards
中科院分区：
文献类型：
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作者：
Lewis,MatthewT;Blain,GregoryM;Hart,CoreyR;Layec,Gwenael;Rossman,MatthewJ;Park,Song-Young;Trinity,JoelD;Gifford,JaysonR;Sidhu,SimranjitK;Weavil,JoshuaC;Hureau,ThomasJ;Jessop,JacobE;Bledsoe,AmberD;Amann,Markus;Richards
最近有文献表明，疲劳、高强度的运动导致最大骨骼肌线粒体呼吸能力的显著衰减，这可能是由于这种高强度运动引起的肌内代谢扰动。利用鞘内芬太尼来减弱III/IV组肌肉传入的传入反馈，允许增加肌肉激活和更大的肌内代谢紊乱，本研究旨在更好地阐明代谢紊乱对线粒体呼吸功能的作用。8名年轻健康男性在对照组（CTRL）和芬太尼治疗组（FENT）条件下进行高强度循环运动。采用液相色谱-质谱法和高分辨率呼吸测定法分别评估运动前和运动后股外侧肌肉活检的代谢物和线粒体呼吸功能。与对照组相比，FENT产生了更大的运动诱导代谢扰动（PCr: - 67% vs. - 82%, Pi: 353% vs. 534%, pH: - 0.22 vs. - 0.31，乳酸：820% vs. 1,160%）。令人惊讶的是，尽管与CTRL相比，FENT的代谢扰动更大，但除了呼吸控制率（RCR）（- 3%和- 36%）外，FENT的影响明显更大，但通过复合体I（- 15%和- 33%）、复合体II（- 36%和- 23%）、复合体I + II（- 31%和- 20%）的最大呼吸通量来评估，运动后线粒体呼吸能力的减弱程度在CTRL和FENT之间分别没有差异。状态3CI+CIIcontrol比值（- 24%和- 39%）。虽然不能排除基础效应，但这种增强代谢扰动不能广泛地进一步削弱线粒体功能，这对高强度运动诱导的代谢物积累在这种运动后反应中的直接作用提出了质疑。
Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: −67% vs. −82%, Pi: 353% vs. 534%, pH: −0.22 vs. −0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (−3% and −36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (−15% and −33%), complex II (−36% and −23%), complex I + II (−31% and −20%), and state 3CI+CIIcontrol ratio (−24% and −39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response.