Manual therapy ameliorates delayed‐onset muscle soreness and alters muscle metabolites in rats

Delayed‐onset muscle soreness (DOMS) can be induced by lengthening contraction (LC); it can be characterized by tenderness and movement‐related pain in the exercised muscle. Manual therapy (MT), including compression of exercised muscles, is widely used as physical rehabilitation to reduce pain and promote functional recovery. Although MT is beneficial for reducing musculoskeletal pain (i.e. DOMS), the physiological mechanisms of MT remain unclear. In the present study, we first developed an animal model of MT in DOMS; LC was applied to the rat gastrocnemius muscle under anesthesia, which induced mechanical hyperalgesia 2–4 days after LC. MT (manual compression) ameliorated mechanical hyperalgesia. Then, we used capillary electrophoresis time‐of‐flight mass spectroscopy (CE‐TOFMS) to investigate early effects of MT on the metabolite profiles of the muscle experiencing DOMS. The rats were divided into the following three groups; (1) normal controls, (2) rats with LC application (LC group), and (3) rats undergoing MT after LC (LC + MT group). According to the CE‐TOFMS analysis, a total of 171 metabolites were detected among the three groups, and 19 of these metabolites were significant among the groups. Furthermore, the concentrations of eight metabolites, including branched‐chain amino acids, carnitine, and malic acid, were significantly different between the LC + MT and LC groups. The results suggest that MT significantly altered metabolite profiles in DOMS. According to our findings and previous data regarding metabolites in mitochondrial metabolism, the ameliorative effects of MT might be mediated partly through alterations in metabolites associated with mitochondrial respiration. e12279 This study established an animal model of manual therapy for delayed‐onset muscle soreness (DOMS), and indicated that manual therapy induced significant changes in metabolite profiles. The results suggest that the ameliorative effects of manual therapy might be mediated partly through alterations in metabolites associated with mitochondrial respiration in humans.