Exercise Induces Hypoalgesia: Effect of chronic and individualized exercise and evaluation of the involvement of PPAR-³ receptors in this process

Abstract

Muscle pain has an important clinical relevance and regular exercise has been described as a good alternative therapy, not only by reducing pain, but also by the absence of the common side effects of commercially available analgesics. However, it is known that the body adapts to exercise intensity over time and that individuals with chronic pain conditions respond to exercise differently from healthy people. Therefore, a physical exercise protocol tailored to individual conditions appears to be essential in reducing muscle pain. Despite their clinical relevance, the neurobiological mechanisms involved in hypoalgesia exerciseinduced are not entirely clear. It isknown that during an inflammatory process, the body has both proinflammatory and antiinflammatory mechanisms. Specifically, prostaglandin 15dPGJ2 (15deoxy12,14PGJ2) is an endogenous antiinflammatory mediator that has a potent effect in pain modulation and exerts its effects through the activation of PPAR-gamma receptor (Receptor peroxisome proliferatoractivatedGama). Considering that the muscle pain usually have na inflammatory character and consequently endogenous mechanisms of modulation, the aim of this study is to assess whether an individualized aerobic training protocol induces hypoalgesia exerciseinduced, and if so,compare their efficiency with a classic and not individualized protocol of exercise. Moreover, we will evaluate if the exerciseinduced hypoalgesia is modulated by the activation of PPAR-gamma receptors in muscle tissue