CENTRAL MODULATION OF EXERCISE-INDUCED MUSCLE PAIN

Abstract

The purpose of the current study was to determine if exercise- induced muscle pain is modulated by central neural mechanisms (i.e., higher brain systems). Ratings of muscle pain perception (MPP) and perceived exertion (RPE), muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were measured during fatiguing isometric handgrip (IHG) at 30% of maximum voluntary contraction and postexercise muscle ischemia (PEMI). The exercise trial was performed twice, before (control) and after administration of naloxone (16 mg iv; n = 9) and codeine (60 mg oral; n = 7). All measured variables increased with exercise duration. During the control trial in all subjects (n = 16), MPP significantly increased during PEMI above ratings reported during exercise (6.6 ± 0.8 to 9.5 ± 1.0 for IHG and PEMI, respectively). MSNA did not significantly change (3.0 ± 0.5 to 4.0 ± 0.4 bursts/15 s) whereas mean arterial pressure (104 ± 4 to 100 ± 3 mmHg; P < 0.05) and heart rate (83 ± 3 to 67 ± 2 beats/min; P < 0.01) decreased from exercise to PEMI. These responses were not significantly altered by the administration of naloxone or codeine. There was no significant relationship between arterial pressure and MSNA with MPP during PEMI. These findings suggest that “central command” has a modulating effect on perception of muscle pain during exercise and reinforces the concept that endogenous opioids and sympathetic activity do not modulate exercise-induced muscle pain. Supported by NIH HL58503 & NASA NAG 9-1034