Behnke Brad J, Barstow Thomas J, Kindig Casey A, McDonough Paul, Musch Timothy I, Poole David C
Department of Anatomy, Kansas State University, Manhattan, KS 66506-5802, USA.
Respir Physiol Neurobiol. 2002 Nov 19;133(3):229-39. doi: 10.1016/s1569-9048(02)00183-0.
Technical limitations have precluded measurement of the V(O(2)) profile within contracting muscle (mV(O(2))) and hence it is not known to what extent V(O(2)) dynamics measured across limbs in humans or muscles in the dog are influenced by transit delays between the muscle microvasculature and venous effluent. Measurements of capillary red blood cell flux and microvascular P(O(2)) (P(O(2)m)) were combined to resolve the time course of mV(O(2)) across the rest-stimulation transient (1 Hz, twitch contractions). mV(O(2)) began to rise at the onset of contractions in a close to monoexponential fashion (time constant, J = 23.2 +/- 1.0 sec) and reached it's steady-state value at 4.5-fold above baseline. Using computer simulation in healthy and disease conditions (diabetes and chronic heart failure), our findings suggest that: (1) mV(O(2)) increases essentially immediately (< 2 sec) following exercise onset; (2) within healthy muscle the J blood flow (thus O(2) delivery, J Q(O(2)m)) is faster than JmV(O(2)) such that oxygen delivery is not limiting, and 3) a faster P(O(2)m) fall to a P(O(2)m) value below steady-state values within muscle from diseased animals is consistent with a relatively sluggish Q(O(2)m) response compared to that of mV(O(2)).
技术限制使得无法测量收缩肌肉内的VO₂分布（mV O₂），因此，尚不清楚在人体四肢或犬类肌肉中测量的VO₂动力学在多大程度上受肌肉微脉管系统与静脉流出之间传输延迟的影响。结合对毛细血管红细胞通量和微血管PO₂（PO₂m）的测量，以解析在静息-刺激瞬态（1Hz，单收缩）期间mV O₂的时间进程。mV O₂在收缩开始时开始以接近单指数的方式上升（时间常数，J = 23.2±1.0秒），并在比基线高4.5倍时达到其稳态值。通过在健康和疾病状态（糖尿病和慢性心力衰竭）下进行计算机模拟，我们的研究结果表明：（1）运动开始后，mV O₂基本立即增加（<2秒）；（2）在健康肌肉中，J血流量（因此O₂输送，J QO₂m）比JmV O₂快，使得氧气输送不受限制，并且3）与mV O₂相比，患病动物肌肉内PO₂m更快降至低于稳态值的PO₂m值，这与相对缓慢的QO₂m反应一致。
