Exercise-induced cell signalling. High intensity or high duration exercise induces metabolic stress and increases reactive oxygen species (ROS) production at the mitochondria of skeletal muscle, which contributes to lipid peroxidation and structural cell damage, as well as alters the redox status of the cell. Several transcription factors (TFs), such as nuclear factor kappa B (NFκB), Map Kinase (MapK), activator protein-1 (AP-1), heat shock factor protein-1 (HSF-1), and peroxisome proliferator-activated receptor-γ coactivator (PCG)-1α, are redox sensitive; thus, their function may be altered by the change in redox status. Some of these TFs are involved in muscle adaptation pathways, while others are involved in the production and secretion of cell signalling molecules such as interleukin-6 (IL-6) and interleukin-8 (IL-8). These cytokines are involved in the trafficking of leukocytes, which are attracted to the cell to clear away damaged tissue, but they may also contribute to ROS production at the muscle cell, contributing to structural damage and propagating the positive feedback pattern of the inflammatory response. Similarly, mechanical stress, such as that induced by high force contraction or highly eccentric exercise, may directly cause structural damage, initiating a similar positive feedback mechanism, but attracting leukocytes, which produce ROS and compound structural damage incurred. Lastly, high temperatures induced by exercise may increase the production of ROS from NADPH oxidase (NOX), contributing to the structural damage, change in redox status, nuclear signalling and positive feedback signalling associated with the other forms of exercise stress.