Endogenous Opiates and Exercise-Related Hypoalgesia

Abstract

Endogenous opiates, endorphins and enkephalins, influence processes within the body including pain, cardiac function, blood pressure, cellular growth, immunity, and blood glucose regulation. Opiates discharged inside the CNS stay within this compartment, whereas those in the circulation primarily arise from the anterior pituitary gland, but some are released from immune cells and peripheral nerves. Generally, acute aerobic and resistance exercises of sufficient intensity and volume have been reported to induce a hypoalgesia response. This hypoalgesia response appears to be related to various pathways involved with endorphins and other neurotransmitters that alter perceptions of pain. Alteration of pain thresholds may transiently occur with exercise. Changes within the CNS using new technologies suggest beta-endorphins (βE) influence brain signaling. Furthermore, elevation in βE modifies immune responses that alter blood pressure, pain, and assist with blood glucose regulation during exercise. Limited research on enkephalins and exercise has been conducted, and results are equivocal. A limited number of studies have reported enkephalin increases within certain regions of the brain. However, discrepancies with the enkephalin response to endurance training have occurred. Clearly more research is needed dealing with endogenous opioids and exercise, especially in the CNS compartment, to help elucidate how exercise influences hypoalgesia and immune function.