Wüst Rob C I, McDonald James R, Sun Yi, Ferguson Brian S, Rogatzki Matthew J, Spires Jessica, Kowalchuk John M, Gladden L Bruce, Rossiter Harry B
Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 W. Carson Street, CDCRC Building, Torrance, CA 90502, USA.
J Physiol. 2014 Apr 15;592(8):1857-71. doi: 10.1113/jphysiol.2013.267476. Epub 2014 Jan 27.
Oxygen uptake kinetics (τVO2) are slowed when exercise is initiated from a raised metabolic rate. Whether this reflects the recruitment of muscle fibres differing in oxidative capacity, or slowed blood flow (Q) kinetics is unclear. This study determined τVO2 in canine muscle in situ, with experimental control over muscle activation and Q during contractions initiated from rest and a raised metabolic rate. The gastrocnemius complex of nine anaesthetised, ventilated dogs was isolated and attached to a force transducer. Isometric tetanic contractions (50 Hz; 200 ms duration) via supramaximal sciatic nerve stimulation were used to manipulate metabolic rate: 3 min stimulation at 0.33 Hz (S1), followed by 3 min at 0.67 Hz (S2). Circulation was initially intact (SPON), and subsequently isolated for pump-perfusion (PUMP) above the greatest value in SPON. Muscle VO2 was determined contraction-by-contraction using an ultrasonic flowmeter and venous oximeter, and normalised to tension-time integral (TTI). τVO2/TTI and τQ were less in S1SPON (mean ± s.d.: 13 ± 3 s and 12 ± 4 s, respectively) than in S2SPON (29 ± 19 s and 31 ± 13 s, respectively; P < 0.05). τVO2/TTI was unchanged by pump-perfusion (S1PUMP, 12 ± 4 s; S2PUMP, 24 ± 6 s; P < 0.001) despite increased O2 delivery; at S2 onset, venous O2 saturation was 21 ± 4% and 65 ± 5% in SPON and PUMP, respectively. VO2 kinetics remained slowed when contractions were initiated from a raised metabolic rate despite uniform muscle stimulation and increased O2 delivery. The intracellular mechanism may relate to a falling energy state, approaching saturating ADP concentration, and/or slowed mitochondrial activation; but further study is required. These data add to the evidence that muscle VO2 control is more complex than previously suggested.
当运动从升高的代谢率开始时，摄氧动力学（τVO2）会减慢。这是否反映了具有不同氧化能力的肌纤维的募集，还是血流（Q）动力学减慢尚不清楚。本研究在犬类肌肉原位测定了τVO2，在从静息状态和升高的代谢率开始的收缩过程中，对肌肉激活和Q进行了实验控制。将9只麻醉、通气的犬的腓肠肌复合体分离并连接到力传感器上。通过超最大坐骨神经刺激进行等长强直收缩（50Hz；持续200ms）以操纵代谢率：0.33Hz刺激3分钟（S1），然后0.67Hz刺激3分钟（S2）。循环最初完整（SPON），随后分离以进行高于SPON中最大值的泵灌注（PUMP）。使用超声波流量计和静脉血氧计逐次收缩测定肌肉VO2，并将其标准化为张力 - 时间积分（TTI）。S1SPON中的τVO2/TTI和τQ（分别为平均值±标准差：13±3秒和12±4秒）低于S2SPON（分别为29±19秒和31±13秒；P<0.05）。尽管氧气输送增加，但泵灌注（S1PUMP，12±4秒；S2PUMP，24±6秒；P<0.001）时τVO2/TTI未改变；在S2开始时，SPON和PUMP中的静脉血氧饱和度分别为21±4%和65±5%。尽管肌肉刺激均匀且氧气输送增加，但当收缩从升高的代谢率开始时，VO2动力学仍然减慢。细胞内机制可能与能量状态下降、接近饱和的ADP浓度和/或线粒体激活减慢有关；但需要进一步研究。这些数据进一步证明肌肉VO2控制比以前认为的更复杂。
