Harms, Craig A., Mark A. Babcock, Steven R. McClaran, David F. Pegelow, Glenn A. Nickele, William B. Nelson, and Jerome A. Dempsey.Respiratory muscle work compromises leg blood flow during maximal exercise. J. Appl. Physiol.82(5): 1573–1583, 1997.—We hypothesized that during exercise at maximal O2 consumption (V˙o 2 max), high demand for respiratory muscle blood flow (Q˙) would elicit locomotor muscle vasoconstriction and compromise limb Q˙. Seven male cyclists (V˙o 2 max 64 ± 6 ml ⋅ kg−1 ⋅ min−1) each completed 14 exercise bouts of 2.5-min duration atV˙o 2 max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q˙ (Q˙legs; thermodilution), esophageal pressure, and O2 consumption (V˙o 2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74–0.90;P < 0.05) between work of breathing (Wb) and Q˙legs (inverse), leg vascular resistance (LVR), and leg V˙o 2(V˙o 2 legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a ±50% change from control in Wb,Q˙legs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2extraction did not change; thusV˙o 2 legschanged 0.4 l/min or 10% of control. TotalV˙o 2 max was unchanged with loading but fell 9.3% with unloading; thusV˙o 2 legsas a percentage of totalV˙o 2 max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion andV˙o 2.
- vascular resistance
- blood flow
- work of breathing
- maximal exercise
- sympathetic vasoconstriction
- autonomic reflexes
Address for reprint requests: C. A. Harms, Dept. of Preventive Medicine, 504 N. Walnut St., Madison, WI 53705.
This research was supported by National Heart, Lung, and Blood Institute (NHLBI) Grant RO1 HL-15469. C. A. Harms and S. R. McClaran were supported by an NHLBI Training Grant, and M. A. Babcock was supported by a Parker B. Francis Foundation Fellowship.
- Copyright © 1997 the American Physiological Society