Hormonal and metabolic responses to opioid antagonism during dynamic exercise : influence of exercise intensity
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Abstract
In an attempt to investigate the role of the endogenous opioid peptides in substrate utilization and hormonal responses to exercise, eight trained cyclists completed two exercise trials at each of two distinct intensity/duration combinations. Briefly, cyclists completed two trials at 70% VO2max for 90 minutes and two trials at 90% VO2max until exhaustion. Trials were conducted following the administration of the opiate antagonist naloxone (NAL) (0.1 mg-kg-1 bolus + 0.1 mg-kg-1-·hr-1) or volume matched saline (SAL). Serum glucose was maintained at significantly higher levels at 60 and 90 minutes of exercise in 70% NAL vs 70% SAL. Serum glucose was significantly higher at all points during exercise and at 30 and 60 minutes of recovery in 90% NAL vs 90% SAL. Serum insulin was not altered by naloxone administration at either 70% or 90% trials. Serum Cpeptide was significantly higher at 60 and 90 minutes in 70%-NAL vs 70% SAL, and was significantly lower during exercise in 90%-NAL vs 90% SAL. Plasma glucagon was not different during exercise in the 70% trials, but was significantly higher during exercise in 90%-NAL vs 90%-SAL. The glucagon:insulin molar ration was not significantly altered by naloxone administration in any trial. Rating of peceived exertion was significantly higher during exercise in 70%-NAL, but was not different during exercise in the 90% trials. However, time to exhaustion was significantly (18%) reduced in 90%-NAL vs 90%-SAL. No systematic differences were observed in the cardiorespiratory responses to exercise at either intensity, although pulmonary ventilation was modestly (7%) elevated in 90%-NAL. Thus, opiate antagonism prevents the decline in serum glucose seen in prolonged exercise without altering substrate oxidation, and with minimal influence on the pancreatic hormone response. In contrast, opiate antagonism potentiates the hyperglycemic response to high intensity exercise at least in part by altering pancreatic hormone responses which may contribute to the hyperglycemia.