Fregosi R F, Dempsey J A
J Appl Physiol Respir Environ Exerc Physiol. 1984 Aug;57(2):396-402. doi: 10.1152/jappl.1984.57.2.396.
For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
我们首次在大鼠中描述了运动对动脉酸碱状态的影响，并研究了化学刺激作为该物种过度通气反应决定因素的作用。在非训练雄性大鼠休息时以及在不同强度的跑步机运动10分钟期间，测量了耗氧量（VO₂）、二氧化碳产生量（VCO₂）、动脉血气、动脉乳酸浓度（[LA⁻]a）和直肠温度（Tre）。在轻度运动期间（VCO₂增加2.5倍），动脉血二氧化碳分压（PaCO₂）下降5.5±0.6托，尽管[LA⁻]a有小幅但显著的增加，但呼吸性碱中毒仍然存在[动脉pH值变化（δpHa）=0.034±0.006]。动脉血氧分压（PaO₂）增加4.1±1.5托，Tre增加0.6±0.1℃。从轻度运动到重度运动，出现了逐渐增强的过度通气。这种反应并非归因于动脉低氧血症或酸中毒，并且不受阻止运动引起的体温升高的影响。在最大运动期间，VO₂增加3.4倍（72±1.50毫升·千克⁻¹·分钟⁻¹），VCO₂增加4.5倍（74±1.90毫升·千克⁻¹·分钟⁻¹），导致[LA⁻]a增加9倍，并出现严重的代谢性酸中毒（pHa 7.31±0.02）。明显的过度通气[动脉血二氧化碳分压（PaCO₂）28.5±1.4托]导致pHa部分代偿，但几乎所有这种过度通气都发生在代谢性酸中毒发作之前，[即，在最大VO₂（VO₂max）的65%以下]，并且随着VO₂进一步升高，[H⁺]a增加并未导致进一步的低碳酸血症。（摘要截断于250字）
