Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia.

P>Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33 center dot 2 +/- 11 center dot 5 years; FEV1 108 center dot 3 +/- 16 center dot 2% predicted), 14 asthma patients (5 male; age 48 center dot 1 +/- 16 center dot 1 years; FEV1 101 center dot 6 +/- 15 center dot 3% predicted), and 15 moderate to severe COPD patients (9 male; age 62 center dot 8 +/- 6 center dot 8 years; FEV1 50 center dot 0 +/- 11 center dot 8% predicted). An acute metabolic acidemia of BE -3 center dot 1 mmol.L-1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference -0 center dot 1 kPa.sec.L-1 [95%-CI: -0 center dot 1 --0 center dot 02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference -1 center dot 73 mmHg [-3 center dot 0 --0 center dot 08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure.