Richardson Russell S, Wary Claire, Wray D Walter, Hoff Jan, Rossiter Harry B, Layec Gwenael, Carlier Pierre G
1Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, UT; 2Department of Exercise and Sport Science, University of Utah, Salt Lake City, UT; 3Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, UT; 4Institute of Myology, Paris, FRANCE; 5CEA, I2BM, MIRcen, IdM NMR Laboratory, Paris, FRANCE; 6Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, NORWAY; and 7Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA.
Med Sci Sports Exerc. 2015 Nov;47(11):2299-307. doi: 10.1249/MSS.0000000000000675.
At exercise onset, intramuscular oxidative energy production responds relatively slowly in comparison with the change in adenosine triphosphate demand. To determine whether the slow kinetics of oxidative adenosine triphosphate production is due to inadequate O2 supply or metabolic inertia, we studied the kinetics of intramyocellular deoxygenation (deoxy-myoglobin (Mb)) and metabolism (phosphocreatine (PCr)) using proton (1H) and phosphorus (31P) magnetic resonance spectroscopy in six healthy subjects (33 ± 5 yr).
Specifically, using dynamic plantarflexion exercise, rest to exercise and recovery were assessed at both 60% of maximum work rate (moderate intensity) and 80% of maximum work rate (heavy intensity).
At exercise onset, [PCr] fell without delay and with a similar time constant (τ) at both exercise intensities (approximately 33 s). In contrast, the increase in deoxy-Mb was delayed at exercise onset by 5-7 s, after which it increased with kinetics (moderate τ = 37 ± 9 s; heavy τ = 29 ± 6 s) that was not different from τPCr (P > 0.05). At cessation, deoxy-Mb recovered without time delay and more rapidly (τ = ∼20 s) than PCr (τ = ∼33 s) (P < 0.05).
Using a unique combination of in vivo magnetic resonance spectroscopy techniques with high time resolution, this study revealed a delay in intramuscular deoxygenation at the onset of exercise and rapid reoxygenation kinetics upon cessation. Together, these data imply that intramuscular substrate-enzyme interactions, and not O2 availability, determine the exercise onset kinetics of oxidative metabolism in healthy human skeletal muscles.
在运动开始时,与三磷酸腺苷需求的变化相比,肌肉内氧化能量产生的反应相对较慢。为了确定氧化型三磷酸腺苷产生的缓慢动力学是由于氧气供应不足还是代谢惰性,我们使用质子(1H)和磷(31P)磁共振波谱研究了六名健康受试者(33±5岁)肌细胞内脱氧(脱氧肌红蛋白(Mb))和代谢(磷酸肌酸(PCr))的动力学。
具体而言,通过动态跖屈运动,在最大工作率的60%(中等强度)和最大工作率的80%(高强度)下评估从休息到运动以及恢复的过程。
在运动开始时,[PCr]立即下降,且在两种运动强度下的时间常数(τ)相似(约33秒)。相比之下,运动开始时脱氧Mb的增加延迟了5 - 7秒,之后其增加的动力学(中等强度τ = 37±9秒;高强度τ = 29±6秒)与τPCr无差异(P>0.05)。在运动停止时,脱氧Mb无延迟地恢复,且比PCr恢复得更快(τ =约20秒)(τ =约33秒)(P<0.05)。
本研究使用具有高时间分辨率的体内磁共振波谱技术的独特组合,揭示了运动开始时肌肉内脱氧延迟以及停止时快速的复氧动力学。总之,这些数据表明,肌肉内底物 - 酶相互作用而非氧气可用性决定了健康人骨骼肌氧化代谢的运动开始动力学。