Lactic acidosis and diaphragmatic function in vitro

Diaphragm fatigue occurs during heavy exercise. Acidosis leads to skeletal muscle fatigue, yet the diaphragm is not a net producer of either lactic acid or hydrogen ions. We tested the hypothesis that hydrogen ion and lactic acid concentrations similar to those seen in arterial blood at maximal exercise decrease contractility of the in vitro isolated rat diaphragm. Diaphragm strips were exposed to a control solution for 15 min and then to one of the following treatment solutions: control (C, pH = 7.4) or 10 mM lactic acid buffered to pH 7.4 (L74), pH 7.2 (L72), pH 7.1 (L71), or pH 6.8 (L68). After 15 min, the force-frequency relationship of the strip was measured. The strips were then stressed with 75 contractions at 25 Hz (250-ms train duration) at the rate of one per second and the force-frequency curve was measured after 15 min of recovery. The L74, L72, and L71 strips responded similarly to the C strips at all times and frequencies. Decrements in force associated with acidosis were only seen in L68. Within L68, we found decreases in force at stimulation frequencies < 100 Hz. These data suggest that physiologic levels of exogenous hydrogen ions are not a primary cause of in vitro diaphragm fatigue.