Resistance training protects against the development of muscle pain through activation of androgen receptors

Exercise is an effective and recommended treatment for chronic pain conditions. In the rehabilitation setting, both aerobic and resistance training (RT) exercise programs are recommended for various chronic pain conditions. However, animal research has focused on the utilization of aerobic based exercise programs. Therefore, the purpose of this project was to determine if RT can protect against the development of activity-induced muscle pain and to elucidate the analgesic mechanism. We hypothesized that RT would produce analgesia in an activity-induced pain model through activation of androgen receptors. Either sedentary or 8 week RT male and female mice were subjected to 2 pH 5.0 injections into the gastrocnemius muscle combined with fatiguing muscle contractions. In this model, muscle withdrawal thresholds (MWT), assessed by withdrawal to pressure applied to the gastrocnemius, are significantly decreased in sedentary mice; this decrease in MWT did not occur in mice that performed RT (p=0.001; repeated measures ANOVA). Strength, measured by maximal lifting load and grip force, significantly increased after RT. Since RT increases testosterone and lactate in humans, we examined if lactate and testosterone were elevated following RT by measuring serum concentrations using either an ELISA kit or a lactate meter, respectively. Five minutes after RT, both lactate and testosterone values were significantly higher compared with sedentary animals in both male and female mice (p=0.03-0.05; one-way ANOVA)). To test if androgen receptors mediate the analgesia produced by exercise, slow release flutamide (200mg) or control pellets were implanted subcutaneously prior to initiation of training. Animals that received flutamide pellets did not see the analgesic effects of exercise when compared to animals who received control pellets (p<0.01; repeated measured ANOVA) despite similar increases in strength. Thus, RT protects against the development of activity-induced muscle pain through activation of androgen receptors in both male and female mice. NIH AR061371 and AR061371-SI, AR073187, GM067795, Foundation for Physical Therapy Research Promotion of Doctoral Studies (PODS I) and the Helen C. Levitt Visiting Fellowship from the Carver College of Medicine at the University of Iowa.