Bulbulian R, Girandola R N, Wiswell R A
Eur J Appl Physiol Occup Physiol. 1983;51(1):17-24. doi: 10.1007/BF00952533.
Eleven male and female subjects were randomly assigned to two treatment groups. One experimental ammonium chloride (NH4Cl) group (n = 6) and one calcium carbonate (CaCO3) placebo control group (n = 5) received treatment lasting 10 days. No significant changes were observed in several ventilatory parameters (VE, VE/V2, VE/VO2) during submaximal or maximal exercise. Heart rates and performance times were similarly unaltered. Changes were observed in oxygen consumption (VO2) and plasma lactates (HLa) during submaximal exercise at 40% maximal power output (approximately 48% VO2max). VO2 decreased from 1.12 l X min-1 to 1.04 l X min-1 (t = 2.87, p less than 0.05) and HLa were depressed from 2.3 to 1.9 mM X 1(-1) (t = 3.92, p less than 0.02). HLa and VO2max were not changed during an incremental VO2max test. The evidence suggests that under conditions of experimental renalcompensated, chronic metabolic acidoses (CMA), there are no significant changes in most cardiopulmonary parameters measured during maximal and submaximal exercise. It appears that the decrements in performance reported by previous investigators may be due to pH changes of acidosis rather than accompanying compensatory changes of acid-base control.
11名男性和女性受试者被随机分为两个治疗组。一个实验性氯化铵（NH4Cl）组（n = 6）和一个碳酸钙（CaCO3）安慰剂对照组（n = 5）接受了为期10天的治疗。在次最大或最大运动期间，未观察到几个通气参数（VE、VE/V2、VE/VO2）有显著变化。心率和运动时间同样未改变。在40%最大输出功率（约48%VO2max）的次最大运动期间，观察到耗氧量（VO2）和血浆乳酸（HLa）有变化。VO2从1.12升/分钟降至1.04升/分钟（t = 2.87，p < 0.05），HLa从2.3毫摩尔/升降至1.9毫摩尔/升（t = 3.92，p < 0.02）。在递增的VO2max测试期间，HLa和VO2max没有变化。证据表明，在实验性肾代偿性慢性代谢性酸中毒（CMA）的情况下，在最大和次最大运动期间测量的大多数心肺参数没有显著变化。看来，先前研究人员报告的运动能力下降可能是由于酸中毒的pH值变化，而不是酸碱控制的伴随性代偿变化。
