Recent work in humans suggests that increasing nitric oxide (NO) bioavailability may induce physiological changes beyond the well known hemodynamic effects (Dejam, Hunter et al. 2004; Webb, Patel et al. 2008). NO plays a key role in the regulation of blood flow, muscle contractility, myocyte differentiation, glucose and calcium homeostasis (Dejam, Hunter et al. 2004). Within the human body, exogenous nitrate (NO3-) which has a half-life of 6-7 hours (h) (Lundberg, Weitzberg et al. 2008) is reduced to bioactive nitrite (NO2-) by facultative anaerobic bacteria in the saliva and further to NO via various pathways (Duncan, Dougall et al. 1995; Zhang, Naughton et al. 1998). Several groups (Larsen, Weitzberg et al. 2007; Bailey, Fulford et al. 2009; Bailey, Winyard et al. 2010; Larsen, Weitzberg et al. 2010; Vanhatalo, Bailey et al. 2010; Lansley, Winyard et al. 2011) have investigated whether dietary nitrate provision affects metabolic or circulatory parameters during exercise in vivo in humans. Oral ingestion of sodium nitrate (0.1 mmol•kg-1•d-1) for 2-3 days (d) has been shown to significantly reduce pulmonary oxygen uptake (VO2) during submaximal cycling exercise in both untrained (Larsen, Weitzberg et al. 2010) and trained men (Larsen, Weitzberg et al. 2007). Since the use of sodium nitrate is regulated in most countries, researchers have started to examine the impact of ingesting nitrate-rich foods, such as beetroot juice, on the physiological response to exercise (Bailey, Fulford et al. 2009; Bailey, Winyard et al. 2010; Vanhatalo, Bailey et al. 2010; Lansley, Winyard et al. 2011).