Effect of Ammonia on in vitro Diaphragmatic Contractility, Fatigue and Recovery

Abstract

Background: Following strenuous exercise, in vivo diaphragmatic strength has been reported to decrease. This decrease has been suggested to result from an increase in metabolic by-products of intense exercise. Objective: We tested the hypothesis that physiological NH₃ concentrations adversely affect diaphragmatic contractility, fatigability, and recovery. Methods: Rat diaphragm strips were exposed to one of six experimental conditions (n = 6 per condition): Krebs-Ringer control solution, or the control solution with NH₃ added (in mM): 0.11, 2.5, 5.0, 10.0, or 14.0. Initial diaphragmatic contractility was assessed with the force-frequency response in the control solution. Following the first force-frequency response, the solution was replaced with one of the six solutions and a second force-frequency response was measured. Strips were then subjected to a short fatigue protocol and contractility was reassessed with a third force-frequency response. A longer fatigue protocol was then administered, followed by a 20-min recovery assessment period. Results: Ammonia significantly (p < 0.05) reduced diaphragmatic contractility, but only at concentrations of 5 mM or greater. Additionally, ammonia did not alter the rate of fatigue. Conclusions: This study suggests that physiological NH₃ concentrations do not adversely affect in vitro diaphragmatic contractility, fatigue, or recovery. These data are not consistent with diaphragmatic fatigue associated with exercise induced by arterial concentrations of NH₃ seen in humans, although further testing in situ or in vivo is needed.