Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle.
Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.
D000138:Acidosis / Q000503:physiopathology*; D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001834:Body Water / Q000032:analysis; D002245:Carbon Dioxide / Q000494:pharmacology*; D004573:Electrolytes / Q000032:analysis; D005221:Fatigue / Q000503:physiopathology*; D009119:Muscle Contraction / Q000187:drug effects*; D009132:Muscles / Q000378:metabolism / Q000503:physiopathology*; D010725:Phosphocreatine / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D000227:Adenine Nucleotides; D004573:Electrolytes; D010725:Phosphocreatine; D002245:Carbon Dioxide