Ischemic preconditioning (IPC), otherwise known as brief periods of occlusion (~ 5 min) followed by reperfusion, elicits improvements in exercise performance when used prior to exercise (de Groot, Thijssen, Sanchez, Ellenkamp, & Hopman, 2010; Foster, Paresh, Rogers, Larson, & Anholm, 2014; Jean-St-Michel et al., 2011). Whilst the underlying mechanisms remain unclear, researchers have suggested that improved vasodilation may contribute to improvements in exercise performance after an IPC protocol, because relevant modulators are involved in matching the increased metabolic demand of muscles during exercise (de Groot et al., 2010; Keller et al., 2004).
Although vasodilation may enhance maximal exercise-induced blood flow, this does not necessarily improve oxygen consumption, since oxygen extraction can be decreased due to a less efficient flow distribution (Calbert et al., 2006). Thus acute and/or chronic functional changes within the muscles allowing for a greater uptake/use of oxygen, in other words improvements in mitochondrial capacity, have been proposed as alternative mechanisms (de Groot et al., 2010). IPC has been found to have a protective effect on oxygenation in animal skeletal muscle (Pang et al., 1995; Satio, Komiyama, Aramoto, Miyata, & Shigematsu, 2004) however, the effects of IPC on mitochondrial function in humans have yet to be established and if this is connected to IPC-induced improvements in exercise performance.
This study aims to investigate the mitochondrial response to acute and chronic IPC in the quadriceps to determine if skeletal muscle mitochondrial capacity is affected by IPC. Furthermore, the aim is also to evaluate if mitochondrial capacity plays a mechanistic role in IPC-induced improvements in exercise performance.
