首页> 外文期刊>The Journal of Physiology >Kinetic control of oxygen consumption during contractions in self-perfused skeletal muscle.
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Kinetic control of oxygen consumption during contractions in self-perfused skeletal muscle.

机译:自我控制的骨骼肌收缩过程中耗氧量的动力学控制。

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Fast kinetics of muscle oxygen consumption (VO2) is characteristic of effective physiological systems integration. The mechanism of VO2 kinetic control in vivo is equivocal as measurements are complicated by the twin difficulties of making high-frequency direct measurements of VO2 and intramuscular metabolites, and in attaining high [ADP]; complexities that can be overcome utilising highly aerobic canine muscle for the investigation of the transition from rest to contractions at maximal VO2. Isometric tetanic contractions of the gastrocnemius complex of six anaesthetised, ventilated dogs were elicited via sciatic nerve stimulation (50 Hz; 200 ms duration; 1 contraction s(-1)). Muscle VO2 and lactate efflux were determined from direct Fick measurements. Muscle biopsies were taken at rest and every approximately 10 s during the transient and analysed for [phosphates], [lactate] and pH. The temporal VO2 vs. [PCr] and [ADP] relationships were not well fitted by linear or classical hyperbolic models (respectively), due to the high sensitivity of VO2 to metabolic perturbations early in the transient. The time course of this apparent sensitisation was closely aligned to that of ATP turnover, which was lower in the first approximately 25 s of contractions compared to the steady state. These findings provide the first direct measurements of skeletal muscle VO2 and [PCr] in the non-steady state, and suggest that simple phosphate feedback models (which are adequate for steady-state observations in vitro) are not sufficient to explain the dynamic control of VO2 in situ. Rather an allosteric or 'parallel activation' mechanism of energy consuming and producing processes is required to explain the kinetic control of VO2 in mammalian skeletal muscle.
机译:肌肉耗氧量(VO2)的快速动力学是有效生理系统整合的特征。体内VO2动力学控制的机制是模棱两可的,因为难以进行高频直接测量VO2和肌内代谢产物以及获得高[ADP]的双重困难使测量变得复杂。可以利用高度有氧的犬肌肉克服最大的VO2下从静止到收缩的过渡过程中可以克服的复杂性。通过坐骨神经刺激(50 Hz;持续时间200 ms; 1次收缩s(-1))引起六只麻醉,通气的狗的腓肠肌复合体的等长强直收缩。从直接Fick测量确定肌肉VO2和乳酸外排。休息时每隔10 s进行一次肌肉活检,并分析[磷酸盐],[乳酸]和pH。线性或经典双曲线模型不能分别很好地拟合时间VO2与[PCr]和[ADP]的关系,这是因为VO2对瞬态早期的代谢扰动具有很高的敏感性。这种表观敏化的时间过程与ATP转换的时间过程紧密相关,与稳态相比,它在收缩的前约25 s较低。这些发现提供了对非稳态骨骼肌VO2和[PCr]的首次直接测量,并表明简单的磷酸盐反馈模型(足以进行体外稳态观察)不足以解释对D2的动态控制。 VO2原位。而是需要能量消耗和产生过程的变构或“平行激活”机制来解释哺乳动物骨骼肌中VO2的动力学控制。

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