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

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.

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.

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.

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.

Endogenous opioids do not appear to modulate motoneuron responses to exercise under these experimental conditions.