Exercise and Inflammation

Exercise and inflammation induce multi-faceted physiological responses in their own right, let alone when considered together [...].

glucose-6-phosphate dehydrogenase-deficient individuals. Such deficiency subjects the individuals to compromised glutathione levels and increased susceptibility to oxidative stress; thus, such repercussions were investigated systemically from blood, in response to an acute exercise insult performed before and after the supplementation period. Resting markers of oxidative defense from total antioxidant capacity and bilirubin concentrations were increased after four weeks of supplementation, but such effects were absent post-exercise.
Implementing a chronic supplementation regime alongside exercise training is a popular approach aimed at promoting adaptation in a number of contexts. Given the identification of leucine as a nutrient 'trigger' for muscle anabolism in recent years [25], it is unsurprising that its metabolite, HMB, is receiving much attention as a potential promoter of adaptation to resistance training. Arazi and colleagues [16] examined the effects of HMB free acid supplementation on resting systemic oxidative stress markers following six weeks of resistance training. Strength training induced reductions in oxidative stress, as identified by reductions in malondialdehyde concentrations, and a marker of protein carbonylation. However, no differences were identified following HMB supplementation.
A multiple (low and high) dose-response investigation in to the effects of an extended (7 day) dose of a daily plant-based nutraceutical, barley-wheat grass juice was conducted by Williamson and colleagues [22]. Acute resting peripheral cell mononuclear DNA damage was subsequently examined in response to the supplementation period, and post-exercise, after an acute bout of high-intensity exercise that followed each supplementation period. DNA damage increased in response to each exercise bout, irrespective of the preceding supplementation dose. Another study that investigated the acute multiple (low and high) dose-response effects of nutrient ingestion was conducted by Tanisawa and colleagues [23]. In this instance, the temporal responses of neutrophil activation and circulating cytokines were compared between low and high doses of carbohydrate consumption, after an endurance exercise task. Herein, they identified favorable conditions for exercise recovery following supplementation that were not associated with elevations in inflammatory responses.
Hydrogen baths are frequently used post-exercise, supported by anecdotal evidence of enhanced perceptions of recovery and wellbeing. Empirical evidence regarding this approach is lacking, however. Kawamura and colleagues [24] examined the influences of a hydrogen bath on muscle soreness and function, alongside neutrophil dynamics after muscle damage induced by a bout of downhill-running. Whilst circulating interleukin-6 concentrations were identified as being associated with neutrophil numbers and additional markers of muscle damage, there was no detectable effect of the hydrogen bath on physiological parameters or recovery. As such, the hydrogen bath did not offer any additional benefits over and above a placebo bath. An in vitro muscle cell damage model was utilized by Yano and colleagues [20], to investigate the cellular underpinnings of macrophage chemotaxis. By manipulating culture medium in the presence or absence of lipopolysaccharide combined with the phosphoinositide 3-kinase (PI3K) inhibitor, Ly294002, the role of PI3K in macrophage chemotaxis was investigated. Following the induction of muscle cell damage by liquid nitrogen and heat exposure, macrophage chemotaxis was identified as being dependent on PI3K/Protein Kinase B pathway activation.
Collectively, the use of exercise to promote health and prevent and improve disease states has become known as "Exercise is Medicine", and is considered as a valuable non-pharmacological therapy in many international societies. However, exercise has the capacity to induce muscle damage and fatigue that may become stressors to the body, thus inducing acute inflammation and increasing susceptibility to infection [15,26]. As such, a better understanding of current biomarkers, and the identification and understanding of new candidate biomarkers are required to help reveal the effects of exercise from a pathological point of view, or to develop early prognostic markers [26][27][28]. However, future examination of the implementation and optimization of exercise approaches alone, and in combination with other efficacious influences such as diet and lifestyle factors are warranted, and are anticipated to become more actively promoted and highlighted in the future [29].

Conflicts of Interest:
The authors declare no conflict of interest.