The effect of NH4Cl induced chronic metabolic acidosis on work capacity in man.
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.
D000138:Acidosis / Q000139:chemically induced / Q000503:physiopathology*; D000328:Adult; D000643:Ammonium Chloride; D002908:Chronic Disease; D004185:Disability Evaluation; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007773:Lactates / Q000097:blood; D008297:Male; D010101:Oxygen Consumption; D012137:Respiratory System / Q000503:physiopathology; D014938:Work Capacity Evaluation
D007773:Lactates; D000643:Ammonium Chloride