**1. Introduction**

Blood flow to contracting skeletal muscles closely matches their metabolic rate [1, 2]. In humans, it has been robustly demonstrated that there is a positive linear relationship between the rate of oxygen uptake (VO2) in the quadriceps muscles and blood flow through the femoral artery [1], which ensures there is a match between oxygen (O2) supply and demand for the exercising muscles. Blood flow is directed to areas in need by adjusting vasoconstriction in the relatively inactive regions and vasodilatation in the active locomotor muscles [2–4]. During high-intensity and maximal exercise, the accompanying increase in cardiac output is almost exclusively devoted to the working skeletal muscle [5], whereas blood flow to the splanchnic, renal and inactive skeletal muscle tissue beds can fall by ≈70% from resting values [6, 7]. It is likely that multiple biological factors contribute to biological redundancy in the system [8]. However, there does appear to be a limit to systemic vasodilation, a procreative mechanism to maintain arterial blood pressure and ensure adequate

O2 supply to vital organs [4, 9–11]. Additionally, when the metabolic demands of multiple muscle groups are high, and cardiac output is nearing maximal flow rates, competition for available blood flow can arise between muscle groups. One such example is the interplay between limb locomotor musculature and the respiratory muscles.

The respiratory muscles perform work to overcome the elastic recoil of the lungs and chest, resistance from turbulent and viscous airflow through the respiratory tract and tissue deformation [12]. As pulmonary ventilation (VE) rises, there is an exponential increase in the work being performed by the respiratory muscles [12, 13]. This ventilation-induced rise in work of breathing is caused by two factors; (1) dynamic hyperinflation to accommodate greater expiratory flow rates [14], and (2) progressive increase in the contribution of the expiratory muscles to breathing [15]. As the lungs and chest are progressively stretched to accommodate the increasing volume of inhaled air and end-expiratory lung volume is reduced, the contribution of elasticity in these tissues to the work of breathing increases [16, 17]. Accompanying the changes in work of breathing with VE, there is a certain O2 cost of exercise hyperpnoea [13, 18]. By mimicking the ventilation pattern (respiratory frequency and tidal volume) obtained during exercise while at rest, it is possible to estimate the proportion of whole-body VO2 that is devoted to the respiratory muscles. During moderate exercise, the O2 cost of breathing accounts for 3–6% of the total whole-body VO2. During high-intensity exercise, the relative contribution of exercise hyperpnoea to whole-body VO2 is estimated increases to 10–15% and can become a limiting factor of exercise capacity [2, 9, 19–21].
