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Department of Preventive Medicine, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, Wisconsin 53705
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
O2 consumption
(
O2 max):
62 ± 5 ml · kg
1 · min1]
performed repeated 2.5-min bouts of cycle exercise at
O2 max. Inspiratory
muscle work was either 1) at control
levels [inspiratory esophageal pressure (Pes): 
27.8 ± 0.6 cmH2O],
2) reduced via a proportional-assist
ventilator (Pes: 16.3 ± 0.5 cmH2O), or 3) increased via resistive loads
(Pes: 35.6 ± 0.8 cmH2O).
O2 contents measured in arterial
and mixed venous blood were used to calculate CO via the direct Fick
method. Stroke volume, CO, and pulmonary
O2 consumption
(O2) were not different
(P > 0.05) between control and
loaded trials at
O2 max but were lower
(8, 9, and 7%, respectively) than control with
inspiratory muscle unloading at
O2 max. The
arterial-mixed venous O2
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.
blood flow distribution; intrathoracic pressure
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