Rossiter H B, Ward S A, Howe F A, Wood D M, Kowalchuk J M, Griffiths J R, Whipp B J
St George;s Medical School, Department of Physiology, London SW17 ORE, United Kingdom.
J Appl Physiol (1985). 2003 Sep;95(3):1105-15. doi: 10.1152/japplphysiol.00964.2002. Epub 2003 May 16.
Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.
传统的肌肉耗氧量控制理论基于一种通过ATP分解特征（如[ADP]反馈，方括号表示浓度）运行的“惯性”反馈系统。然而，最近有人提出，前馈机制（相对于ATP利用）可能通过控制底物向电子传递链的供应速率发挥重要作用。这是通过在运动前经二氯乙酸（DCA）输注激活丙酮酸脱氢酶复合体来实现的。为了研究这些观点，六名男性在磁共振波谱仪的腔内进行重复的高强度、恒定负荷的股四头肌运动，每次运动前分别进行DCA或生理盐水对照静脉输注。逐次呼吸测量摄氧量（Vo2）（使用涡轮和质谱仪），同时通过31P-MRS测量肌肉内磷酸肌酸（PCr）浓度（[PCr]）、[Pi]、[ATP]和pH值，并进行动脉化静脉血采样。DCA对Vo2增加或PCr分解的时间常数（tau）均无影响[tauVo2 45.5±7.9 vs. 44.3±8.2秒（平均值±标准差；对照vs. DCA）；tauPCr 44.8±6.6 vs. 46.4±7.5秒；95%置信区间平均<±2秒]。然而，DCA导致以下各项显著（P<0.05）降低：1）运动结束时的[乳酸]（-1.0±0.9 mM）、肌肉内酸化（pH，+0.08±0.06单位）和[Pi]（-1.7±2.1 mM）；2）[PCr]（-1.9±1.6 mM）和Vo2（-0.1±0.07 l/min，或8%）的基波成分幅度；3）Vo2慢成分的幅度。因此，尽管DCA输注减少了潜在疲劳代谢产物的积累，并降低了运动期间能量转移的有氧和无氧成分，但它并未提高tauVo2或tau[PCr]，这表明在高强度运动期间，反馈而非前馈控制机制起主导作用。
