Exercise and inflammation induce multi-faceted physiological responses in their own right, let alone when considered together. For example, it is widely accepted that aerobic exercise augments numerous key regulatory parameters associated with health and disease. Clinically important transient increases in insulin sensitivity and glucose transporter translocation are observed in healthy individuals across the lifespan [1–3], and within diabetic individuals [4], whilst emerging evidence also supports such responses after resistance-type training [5]. Subsequently, a combined endurance and resistance approach to improve the control of glycemic and lipid profiles in diabetic individuals is promoted [6]. This example has led to a growing onus being paced upon exercise as a cornerstone for the prevention and treatment of lifestyle-related diseases such as diabetes. The development, existence, and function of inflammation, on the other hand, have been considered paradoxical in recent times related to wide-ranging pathological conditions from coronary artery diseases [7] to upper respiratory tract infections [8] and chronic obstructive pulmonary disease [9], and more inherently with ageing [10]. Further, on a fundamental level, our understanding is increasing regarding how inflammation contributes to regulating muscle homeostasis and myogenesis [11]. In an exercise context, this understanding is crucial, given the likely hermetic association with regulating adaptations to chronic exercise, and the association with ageing. Intriguingly, the suppression of inflammation via exogenous supplementation of cyclooxygenase inhibitors seems to attenuate adaptations in the young [12] but not the old [13]. Therefore, it is crucial for us to develop a greater understanding of how these factors are independently influenced by exercise, as well as how exercise regulates the interrelationship between the two, for example, by means of oxidative stress and redox control [12].