• R Andrew Shanely and J Richard Coast.
• Department of Exercise Science, Northern Arizona University, Flagstaff, Ariz., USA. shanely@ufl.edu
• Respiration. 2002 Jan 1;69(6):534-41.

BackgroundFollowing 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.ObjectiveWe tested the hypothesis that physiological NH(3) concentrations adversely affect diaphragmatic contractility, fatigability, and recovery.MethodsRat diaphragm strips were exposed to one of six experimental conditions (n = 6 per condition): Krebs-Ringer control solution, or the control solution with NH(3) 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.ResultsAmmonia 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.ConclusionsThis study suggests that physiological NH(3) 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 NH(3) seen in humans, although further testing in situ or in vivo is needed.Copyright 2002 S. Karger AG, Basel

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