Exercise induced cardioprotection is mediated via delta opioid receptors

Abstract

Acute exercise exposure dramatically reduces cellular death that results during ischemic reperfusion (IR). Existing evidence indicates endogenous opioids are a critical component of this protection; however the specific opioid receptor subtype responsible for these effects is unknown. The role of the delta opioid receptor in exercise induced cardioprotection was examined. Rats were randomly assigned into Sham, Sedentary (S) or Exercise (Ex) groups. A selective delta‐opioid receptor antagonist, Naltrindole, was administered 15 minutes prior to exercise in a subset of animals (ExD), and at a corresponding time in a subset of S animals (SD). 24hr following the final exercise bout animals received surgically induced IR in vivo. Significant between group differences existed for tissue necrosis, p < 0.0001. Compared to Sham, S, SD, and ExD animals exhibited significant tissue necrosis post IR, while Ex hearts were protected. S increased necrosis compared to Ex, but was not different from SD. Significant between group differences existed for tissue apoptosis, p = 0.013 following IR. Apoptosis levels were elevated in S and SD compared to Sham while Ex and ExD were protected. These data provide evidence that the delta opioid receptor mediates exercise induced cardioprotection against necrosis but not apoptotic tissue death. Supported by JCQ Auburn University Intramural Grant Program.