Influence of respiratory muscle work onV˙o2and leg blood flow during submaximal exercise

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Abstract
The work of breathing (Wb) normally incurred during maximal exercise not only requires substantial cardiac output and O2consumption (V˙o2) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q˙leg). We wondered whether the Wbnormally incurred during submaximal exercise would also reduceQ˙leg. Therefore, we investigated the effects of changing the WbonQ˙legvia thermodilution in 10 healthy trained male cyclists [maximalV˙o2(V˙o2 max) = 59 ± 9 ml ⋅ kg−1⋅ min−1] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% ofV˙o2 max. 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 Wbduring submaximal exercise caused V˙o2to increase; decreasing the Wbwas associated with lowerV˙o2(ΔV˙o2= 0.12 and 0.21 l/min at 50 and 75% ofV˙o2 max, respectively, for ∼100% change in Wb). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, orQ˙legwhen Wbwas reduced or increased. Why are LVR, norepinephrine spillover, andQ˙leginfluenced by the Wbat maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal Wbrequired makes insufficient demands forV˙o2and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50–70% increase in Wbduring 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 orQ˙leg.

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