Influence of respiratory muscle work on VO2 and leg blood flow during submaximal exercise

The work of breathing (W-b) normally incurred during maximal exercise not only requires substantial cardiac output and O-2 consumption ((V)over dotO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow ((Q)over dot(leg)). We wondered whether the W-b normally incurred during submaximal exercise would also reduce (Q)over dot(leg). Therefore, we investigated the effects of changing the W-b on (Q)over dot(leg) via thermodilution in 10 healthy trained male cyclists [maximal (V)over dotO(2) ((V)over dotO(2max)) = 59 +/- 9 ml.kg(-1).min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of (V)over dotO(2max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W-b during submaximal exercise caused (V)over dotO(2) to increase; decreasing the W-b was associated with lower (V)over dotO(2) (Delta(V)over dotO(2) = 0.12 and 0.21 l/min at 50 and 75% of (V)over dotO(2max), respectively, for similar to 100% change in W-b) There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or (Q)over dot(leg) when W-b was reduced or increased. Why are LVR, norepinephrine spillover, and (Q)over dot(leg) influenced by the W-b at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W-b required makes insufficient demands for (V)over dotO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W-b during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or (Q)over dot(leg).