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Complex regional pain syndrome type I (CRPS-I) is a condition that responds poorly to treatments. The role of omega-3 fatty acids in the treatment of inflammatory disorders is well described in the literature; however, few studies have evaluated its therapeutic benefits in different types of pain. We evaluated the potential antihyperalgesic and anti-inflammatory effects of preventive omega-3 supplementation in an animal model of CRPS-I. In experiment 1, Swiss female mice were supplemented for 30 days with omega-3 before the induction of the CRPS-I model and 14 days after. Mechanical hyperalgesia was evaluated at baseline and from the 4th to the 14th day after CPRS-I induction along with open field locomotor activity after 30 days of supplementation. In experiment 2, Swiss female mice were supplemented for 30 days with omega-3 and then subjected to the CRPS-I model. Twenty-four hours later the animals were euthanized, and tissue samples of the spinal cord and right posterior paw muscle were taken to measure pro-inflammatory cytokine TNF and IL-1β concentrations. Omega-3 supplementation produced antihyperalgesic and anti-inflammatory effects, as well as reducing pro-inflammatory cytokine concentrations, without altering the animals' locomotion. No open field locomotor changes were found. The 30-day supplementation at the tested dose was effective in the CRPS-I model., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 de Oliveira Galassi, Fernandes, Salgado, Cidral-Filho, Piovezan, Lüdtke, Mack, Weber, Reed, Bobinski and Martins.)

The present study was undertaken to evaluate whether the muscle atrophy associated with glucocorticoid excess results in a reduction in maximal oxygen uptake (VO2max) and endurance during exercise. Female rats were administered single subcutaneous injections of cortisone acetate (CA) (100 mg X kg-1 b.w.) or the vehicle (1% carboxymethyl cellulose) for 14 consecutive days. The weights of plantaris muscles (which were used as a marker of the atrophy) of CA-treated rats were 27% less than those of plantaris muscles in the vehicle-treated rats. This condition also produced a 12-fold increase in free serum glucocorticoid concentrations (cortisol) but did not alter serum androgen (testosterone) levels. Peak VO2 (ml X kg-1 X min-1) and endurance were greater in CA-treated vs vehicle-treated animals; however, these effects were shown to be a function of body weight loss. Homogenate oxygen uptakes in the presence of pyruvate or palmitate were also similar in slow-twitch soleus, fast-twitch red vastus, and fast-twitch white vastus lateralis muscles between CA- and vehicle-treated groups. These data provide no evidence to demonstrate that the catabolic actions of glucocorticoids in skeletal muscle result in a decrement in work capacity through at least 14 d of treatment.