Endogenous opioid effects on motoneuron pool excitability: Potential analgesic effect of acute exercise

Background: Metabolic and thermal stresses of exercise mediate the release of endogenous opioids depressing motoneuron activation (MNA). Although exercise is routinely presented as a coequal treatment for management of acute and chronic low back pain (LBP), it is not clear that exercise-induced endogenous opioid release can play a role in the analgesic and treatment outcomes for patients with LBP. Furthermore, if opioid involvement is present, it is not clear what level of exercise might be beneficial in the suppression of MNA and possibly LBP. Objective: To determine whether exercise-induced endogenous opioid release can play a role in the analgesic and treatment outcomes for patients with LBP and to determine what level of exercise might be beneficial in the suppression of MNA and possibly LBP. Methods: To test this hypothesis, male (n = 3) and female (n = 3) healthy volunteers were tested 6 times over a 4-week period. The 6 trials included high-intensity treadmill exercise at 75% O-2max with placebo or naloxone, low-intensity exercise at 40% O-2max (placebo or naloxone) and no exercise control (placebo or naloxone). The evoked spinal Hoffmann H-reflex (soleus muscle) was measured as the criterion for MNA before and after exercise and expressed with the maximal M-wave as the maximal H-max/M-max percent ratio. Naloxone (10 mg) or isovolumic saline solution was administered double-blind (1 mL bolus) after recovery from exercise and before H-reflex measurement. Results: The results show a significant reduction in the H-max/M-max percent ratio for both exercise conditions (40.0 +/- 7.1 to 33.9 +/- 9.1% for 75% +/- O-2max and 37.4 :+/- 4.8 to 33.0 +/- 5.3% for 40% O-2max; P < .01). Naloxone treatment did not attenuate the exercise-induced H-max/M-max percent ratio suppression. Conclusion: Endogenous opioids do not appear to modulate motoneuron responses to exercise under these experimental conditions.