The effects of eccentric exercise on delayed onset muscle soreness, muscle function and free radical production

Abstract

Delayed onset muscle soreness (DOMS) is a muscle strain injury that presents as tender or aching muscles, often felt during palpation or movement. DOMS is associated with unaccustomed, high-force muscular work and is most pronounced if the work involves a significant eccentric component. Despite substantial research into DOMS its aetiology is still unresolved. There have been recent suggestions that reactive oxygen species (ROS) may be involved in the aetiology of DOMS, however the evidence for this association is equivocal. Therefore, the aims of this thesis were to investigate the effects of unaccustomed exercise (downhill running) on DOMS, specifically investigating the role of ROS in its aetiology. Once this had been established, the effects of dietary intervention and antioxidant supplementation on DOMS and ROS were also investigated. Study 1 demonstrated that downhill running, which resulted in DOMS, also induced the production of ROS, detected by ESR spectroscopy as well as an increases in serum malondialdehyde (MDA) concentration. It was noted that this increase in ROS occurred -72 h post exercise and was therefore likely to be a result of increased phagocyte activity. Furthermore, the increase in ROS occurred after peak DOMS and when muscle function (as determined by losses of muscle torque assessed by isokinetic dynamometry) was returning to pre-exercise levels, suggesting a temporal dissociation between ROS production and DOMS following downhill running. Circulating levels of ROS were still increasing 72 h post exercise so this study was unable to map the full time-course of ROS production following downhill running. Study 2 investigated the effects of dietary CHO intake on DOMS, ROS and muscle function. It was found that pre-exercise CHO status had no effect on ROS production, DOMS or losses of muscle function following downhill running. The study demonstrated a bi-phasic increase in creatine kinase (CK), with the second increase corresponding with the post-exercise ROS production. The study extended the postexercise sampling period to 96 h, however, ROS were still increasing at this time and therefore this study was also unable to conclude a definitive tune course of ROS production following downhill running. Study 3 demonstrated that prolonged ascorbic acid supplementation attenuated the post-exercise increase in ROS production compared to placebo. This attenuation in ROS prevented the secondary peak in CK activity, however it had no effect on DOMS. Interestingly, supplementation with ascorbic acid resulted in more prolonged losses of muscle function. ROS peaked at 96 h post exercise and therefore the time course ofROS production following downhill running was established. From these studies it was concluded that downhill running did result in post-exercise ROS production. This post-exercise ROS production was associated with secondary muscle damage as measured by plasma CK activity although it had no effect on DOMS. Since supplementation with ascorbic acid attenuated ROS production and prolonged the losses of muscle function, it was suggested that ROS produced by phagocytes m the days following muscle-damaging exercise have a positive role in assisting in the recovery from the trauma