Skeletal muscles support posture and locomotion, thermoregulation, cardiorespiratory function, metabolic health and other important aspects of life. Muscles generate chemical energy by synthesizing ATP through the creatine kinase reaction, glycolysis, and oxidative phosphorylation (oxphos), the latter of which produces the majority of ATP in the cell. Oxidative phosphorylation occurs in the mitochondrion, which is structured as a reticulum located near the ATPases responsible for powering the cross-bridge cycle, calcium pumps and membrane homeostasis (Glancy et al., 2015). Energy production in mitochondria is accomplished by coupling the oxidation of reducing equivalents (NADH, FADH 2 ) in the electron transport chain (ETC) with the phosphorylation of ADP to create ATP. The importance of mitochondria to muscle function and the plasticity of the mitochondria to chronic stimuli, such as disease or exercise training, has long made it a target of intense focus in the biology of ageing muscle. The focus of this debate is whether there is an obligatory age-related decline in the capacity of human skeletal muscle to produce ATP via oxphos (defined here as ‘oxidative capacity’). We recognize that other mitochondrial duties such as signalling and regulation are likewise essential, but these topics lay beyond the scope of this debate. Note that evaluation of oxphos in vivo requires adequate delivery of oxygen from the lungs to the mitochondria. Ex vivo techniques from muscle biopsies evaluate mitochondrial capacity more directly, with the caveat that the measurements are acquired under non-physiological conditions (Lanza et al., 2011; Picard et al., 2010). The question at hand – whether muscle oxidative capacity necessarily declines in older age – is more than an academic exercise. The answer will inform effective interventions for maintaining the health, mobility and independence of the growing population that is >65 years of age.