Behnke Brad J, Ferreira Leonardo F, McDonough P J, Musch Timothy I, Poole David C
Department of Applied Physiology & Kinesiology, University of Florida, Gainesville, FL 32611, USA.
Respir Physiol Neurobiol. 2009 Sep 30;168(3):254-60. doi: 10.1016/j.resp.2009.07.013. Epub 2009 Jul 18.
The time course of muscle .V(O2) recovery from contractions (i.e., muscle .V(O2) off-kinetics), measured directly at the site of O(2) exchange, i.e., in the microcirculation, is unknown. Whereas biochemical models based upon creatine kinase flux rates predict slower .V(O2) off- than on-transients [Kushmerick, M.J., 1998. Comp. Biochem. Physiol. B: Biochem. Mol. Biol.], whole muscle .V(O2) data [Krustrup, et al. J. Physiol.] suggest on-off symmetry.
We tested the hypothesis that the slowed recovery blood flow (Qm) kinetics profile in the spinotrapezius muscle [Ferreira et al., 2006. J. Physiol.] was associated with a slowed muscle .V(O2) recovery compared with that seen at the onset of contractions (time constant, tau approximately 23s, Behnke et al., 2002. Resp. Physiol.), i.e., on-off asymmetry.
Measurements of capillary red blood cell flux and microvascular pressure of O(2) (P(O2) mv) were combined to resolve the temporal profile of muscle .V(O2) across the moderate intensity contractions-to-rest transition.
Muscle .V(O2) decreased from an end-contracting value of 7.7+/-0.2 ml/100 g/min to 1.7+/-0.1 ml/100g/min at the end of the 3 min recovery period, which was not different from pre-stimulation .V(O2). Contrary to our hypothesis, muscle .V(O2) in recovery began to decrease immediately (i.e., time delay <2s) and demonstrated rapid first-order kinetics (tau, 25.5+/-2.6s) not different (i.e., symmetrical to) to those during the on-transient. This resulted in a systematic increase in microvascular P(O2) during the recovery from contractions.
The slowed Qm kinetics in recovery serves to elevate the Qm/.V(O2) ratio and thus microvascular P(O2) . Whether this Qm response is obligatory to the rapid muscle .V(O2) kinetics and hence speeds the repletion of high-energy phosphates by maximizing conductive and diffusive O(2) flux is an important question that awaits resolution.
肌肉从收缩中恢复时的耗氧量（即肌肉耗氧量的下降动力学），直接在氧气交换部位（即微循环）测量，目前尚不清楚。基于肌酸激酶通量率的生化模型预测，耗氧量下降的瞬变比上升的瞬变更慢[库什梅里克，M.J.，1998年。《比较生物化学与生理学B：生物化学与分子生物学》]，但全肌肉耗氧量数据[克鲁斯特鲁普等人，《生理学杂志》]表明上升和下降是对称的。
我们检验了以下假设：与收缩开始时相比，斜方肌中恢复血流（Qm）动力学曲线减慢[费雷拉等人，2006年。《生理学杂志》]与肌肉耗氧量恢复减慢有关（时间常数，τ约为23秒，本克等人，2002年。《呼吸生理学》），即上升和下降不对称。
结合测量毛细血管红细胞通量和微血管氧气压力（P（O2）mv），以解析中等强度收缩至休息过渡期间肌肉耗氧量的时间曲线。
肌肉耗氧量从收缩末期的7.7±0.2毫升/100克/分钟降至3分钟恢复期结束时的1.7±0.1毫升/100克/分钟，与刺激前的耗氧量无差异。与我们的假设相反，恢复过程中的肌肉耗氧量立即开始下降（即时间延迟<2秒），并表现出快速的一级动力学（τ，25.5±2.6秒），与上升瞬变期间的动力学无差异（即对称）。这导致收缩恢复期间微血管P（O2）系统性增加。
恢复过程中Qm动力学减慢有助于提高Qm/耗氧量比值，从而提高微血管P（O2）。这种Qm反应是否对快速的肌肉耗氧量动力学是必需的，从而通过最大化传导性和扩散性氧气通量来加速高能磷酸盐的补充，这是一个有待解决的重要问题。
