在逐步收缩方案中，人股外侧肌的氧化 ATP 合成速率不会超过 pH 阈值而增加。

Muscle Physiology Laboratory, Department of Kinesiology, University of Massachusetts, Amherst, MA, 01003, USA.

J Physiol. 2021 Apr;599(7):1997-2013. doi: 10.1113/JP280851. Epub 2021 Mar 3.

KEY POINTS

The oxygen cost of high-intensity exercise at power outputs above an individual's lactate threshold (LT) is greater than would be predicted by the linear oxygen consumption-power relationship observed below the LT. However, whether these augmentations are caused by an increased ATP cost of force generation (ATP ) or an increased oxygen cost of ATP synthesis is unclear. We used P-MRS to measure changes in cytosolic [ADP] (intramyocellular marker of oxidative metabolism), oxidative ATP synthesis (ATP ) and ATP during a 6-stage, stepwise knee extension protocol. ATP was unchanged across stages. The relationship between [ADP] and muscle power output was augmented at workloads above the pH threshold (pH ; proxy for LT), whereas increases in ATP were attenuated. These results suggest the greater oxygen cost of contractions at workloads beyond the pH is not caused by mechanisms that increase ATP , but rather mechanisms that alter intrinsic mitochondrial function or capacity.

ABSTRACT

Increases in skeletal muscle metabolism and oxygen consumption are linearly related to muscle power output for workloads below the lactate threshold (LT), but are augmented (i.e. greater rate of increase relative to workload) thereafter. Presently, it is unclear whether these metabolic augmentations are caused by increases in the ATP cost of force generation (ATP ) or changes in the efficiency of mitochondrial oxygen consumption and oxidative ATP synthesis (ATP ). To partition these two hypotheses in vivo, we used P-MRS to calculate slopes relating step-changes in muscle work to concurrent changes in cytosolic phosphates and ATP before and after the pH threshold (pH ; used here as a proxy for LT) within the vastus lateralis muscle of eight young adults during a stepwise knee extension test. Changes in muscle phosphates and ATP were linearly related to workload below the pH . However, slopes above the pH were greater for muscle phosphates (P < 0.05) and lower for ATP (P < 0.05) than were the slopes observed below the pH . The maximal capacity for ATP ( ) and ADP-specific ATP also declined beyond the pH (P < 0.05), whereas ATP was unchanged (P = 0.10). These results oppose the hypothesis that high-intensity contractions increase ATP and suggest that greater oxidative metabolism at workloads beyond the pH is caused by mechanisms that affect intrinsic mitochondrial function or capacity, such as alterations in substrate selection or electron entry into the electron transport chain, temperature-mediated changes in mitochondrial permeability to protons, or stimulation of mitochondrial uncoupling by reactive oxygen species generation.

要点

高于个体乳酸阈（LT）的高强度运动的耗氧量大于 LT 以下线性氧耗与功率关系所预测的耗氧量。然而，这些增加是由于力产生的 ATP 成本增加（ATP）还是由于 ATP 合成的耗氧量增加尚不清楚。我们使用 P-MRS 在 6 个阶段的逐步膝关节伸展方案中测量细胞溶胶[ADP]（氧化代谢的细胞内标志物）、氧化型 ATP 合成（ATP）和 ATP 的变化。在整个阶段，ATP 保持不变。在 pH 阈值（pH；LT 的代理）以上的工作负荷下，[ADP]与肌肉功率输出之间的关系增强，而 ATP 的增加则减弱。这些结果表明，超过 pH 时收缩的耗氧量增加不是由于增加 ATP 的机制引起的，而是由于改变内在线粒体功能或容量的机制引起的。

摘要

在乳酸阈（LT）以下，骨骼肌代谢和耗氧量与肌肉功率输出呈线性关系，但此后则会增加（即相对于工作负荷的增加率增加）。目前，尚不清楚这些代谢增加是由于力产生的 ATP 成本增加（ATP）还是线粒体耗氧和氧化型 ATP 合成（ATP）效率的变化引起的。为了在体内分离这两个假设，我们使用 P-MRS 在 8 名年轻人的股外侧肌中，在逐步膝关节伸展测试期间，在 pH 阈值（此处用作 LT 的代理）之前和之后，计算肌肉工作的阶跃变化与细胞溶胶磷酸盐和 ATP 同时变化之间的斜率。在 pH 以下，肌肉磷酸盐和 ATP 的变化与工作负荷呈线性关系。然而，pH 以上的斜率对于肌肉磷酸盐（P<0.05）和 ATP（P<0.05）大于 pH 以下观察到的斜率。ATP 的最大容量（）和 ADP 特异性 ATP 也在 pH 以上下降（P<0.05），而 ATP 保持不变（P=0.10）。这些结果与高强度收缩增加 ATP 的假设相矛盾，表明超过 pH 时的氧化代谢增加是由于影响内在线粒体功能或容量的机制引起的，例如底物选择或电子进入电子传递链的改变、质子跨线粒体通透性的温度介导变化，或活性氧生成刺激线粒体解偶联。