ACIDOSIS STIMULATES BETA-ENDORPHIN RELEASE DURING EXERCISE

Elevated blood levels of beta-endorphin have been asso ciated with hig h-intensity exertion, but the stimulus far beta-endorphin release is u nknown. Some studies of exercise have associated beta-endorphin releas e with increased exertion levels, but other evidence suggests that aci dosis may stimulate the release of beta-endorphin. This study examines acidosis as a possible stimulus for beta-endorphin release by examini ng the effects of arterial blood gases, whole blood lactate, and respi ratory changes on beta-endorphin levels and by examining the effects o f buffering during exercise on these levels. Initially, seven healthy adult males were evaluated during incremental exercise. During increme ntal exertion, indicators of acidosis correlated with endorphin levels : pH (r = -0.94), PCO2 (r = -0.85), HCO3- (r = -0.88), base excess (r = -0.94), and lactate (r = 0.89). A multivariate model showed that bet a-endorphin levels were predicted best by the change in base excess. A time course analysis showed that beta-endorphin responses peaked post exercise and paralleled blood acid levels. Subsequently, subjects were compared after alkali loading and placebo during constant-intensity e xercise at 85% of maximal exertion to determine whether acidosis is ne cessary for endorphin release. Treatment with a buffer, which effectiv ely maintained pH above 7.40, significantly suppressed endorphin relea se (F = 3.07; P < 0.0001). The results of this study indicate that aci dosis rather than any other physiological change associated with high- intensity exertion is the primary stimulus for beta-endorphin release.