Effects of augmented respiratory muscle pressure production on locomotor limb venous return during calf contraction exercise.
We determined effects of augmented inspiratory and expiratory intrathoracic pressure or abdominal pressure (Pab) excursions on within-breath changes in steady-state femoral venous blood flow (Qfv) and net Qfv during tightly controlled (total breath time = 4 s, duty cycle = 0.5) accessory muscle/"rib cage" (DeltaPab <2 cmH2O) or diaphragmatic (DeltaPab >5 cmH2O) breathing. Selectively augmenting inspiratory intrathoracic pressure excursion during rib cage breathing augmented inspiratory facilitation of Qfv from the resting limb (69% and 89% of all flow occurred during nonloaded and loaded inspiration, respectively); however, net Qfv in the steady state was not altered because of slight reductions in femoral venous return during the ensuing expiratory phase of the breath. Selectively augmenting inspiratory esophageal pressure excursion during a predominantly diaphragmatic breath at rest did not alter within-breath changes in Qfv relative to nonloaded conditions (net retrograde flow = -9 +/- 12% and -4 +/- 9% during nonloaded and loaded inspiration, respectively), supporting the notion that the inferior vena cava is completely collapsed by relatively small increases in gastric pressure. Addition of inspiratory + expiratory loading to diaphragmatic breathing at rest resulted in reversal of within-breath changes in Qfv, such that >90% of all anterograde Qfv occurred during inspiration. Inspiratory + expiratory loading also reduced steady-state Qfv during mild- and moderate-intensity calf contractions compared with inspiratory loading alone. We conclude that 1) exaggerated inspiratory pressure excursions may augment within-breath changes in femoral venous return but do not increase net Qfv in the steady state and 2) active expiration during diaphragmatic breathing reduces the steady-state hyperemic response to dynamic exercise by mechanically impeding venous return from the locomotor limb, which may contribute to exercise limitation in health and disease.
Miller
Jordan D
JD
John Rankin Laboratory of Pulmonary Medicine, Medical Sciences Center, University of Wisconsin-Madison, Madison, Wisconsin, USA. jordan-miller@uiowa.edu
Pegelow
David F
DF
Jacques
Anthony J
AJ
Dempsey
Jerome A
JA
D000328:Adult; D003964:Diaphragm / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D005263:Femoral Artery / Q000502:physiology; D006801:Humans; D007866:Leg / Q000098:blood supply; D008124:Locomotion / Q000502:physiology; D008297:Male; D008954:Models, Biological; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D011312:Pressure; D015656:Respiratory Mechanics / Q000502:physiology; D012146:Rest / Q000502:physiology; D012272:Ribs / Q000502:physiology; D014680:Veins / Q000502:physiology*