Acidosis stimulates ,8-endorphin release during exercise

Taylor, Derek V., James G. Boyajian, Norman James, Danette Woods, Aleksandra Chicz-Demet, Archie F. Wilson, and Curt A. Sandman. Acidosis stimulates P-endorphin release during exercise. J. Appl. Physiol. 77(4): 1913-1918, 1994.-Elevated blood levels of /3-endorphin have been associated with high-intensity exertion, but the stimulus for P-endorphin release is unknown. Some studies of exercise have associated @-endorphin release with increased exertion levels, but other evidence suggests that acidosis may stimulate the release of /3-endorphin. This study examines acidosis as a possible stimulus for /3-endorphin release by examining the effects of arterial blood gases, whole blood lactate, and respiratory changes on /?3-endorphin levels and by examining the effects of buffering during exercise on these levels. Initially, seven healthy adult males were evaluated during incremental exercise. During incremental exertion, indicators of acidosis correlated with endorphin levels: pH (r = -0.94), PCO~ (r = -0.83, HCO, (r = -O&3), base excess (r = -0.94), and lactate (r = 0.89). A multivariate model showed that P-endorphin levels were predicted best by the change in base excess. A time course analysis showed that /3-endorphin responses peaked postexercise and paralleled blood acid levels. Subsequently, subjects were compared after alkali loading and placebo during constant-intensity exercise at 85% of maximal exertion to determine whether acidosis is necessary for endorphin release. Treatment with a buffer, which effectively maintained pH above 7.40, significantly suppressed endorphin release (F = 3.07; P < 0.0001). The results of this study indicate that acidosis rather than any other physiological change associated with high-intensity exertion is the primary stimulus for /3-endorphin release.