Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise

We have recently demonstrated that changes in the work of breathing during maximal exercise affect leg blood flow and leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573-1583, 1997). Our present study examined the effects of changes in the work of breathing on cardiac output (CO) during maximal exercise. Eight male cyclists [maximal O-2 consumption ((V) over dot o(2max)): 62 +/- 5 ml kg-l:min-l] performed repeated 2.5-min bouts of cycle exercise at (V) over dot o(2). Inspiratory muscle work was either 1) at control levels [inspiratory esophageal pressure (Pes): -27.8 +/- 0.6 cmH(2)O], 2) reduced via a proportional-assist ventilator (Pes: -16.3 +/- 0.5 cmH(2)O), or 3) increased via resistive loads (Pes: -35.6 +/- 0.8 cmH(2)O). O-2 contents measured in arterial and mixed venous blood were used to calculate CO via the direct Fick method. Stroke volume, CO, and pulmonary O-2 consumption ((V) over dot o(2)) were not different (P > 0.05) between control and loaded trials at (V) over dot o(2max) but were lower (-8, -9, and -7%, respectively) than control with inspiratory muscle unloading at (V) over dot o(2). The arterial-mixed venous O-2 difference was unchanged with unloading or loading. We combined these findings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effects on the cardiovascular system: 1) up to 14-16% of the CO is directed to the respiratory muscles; and 2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.