title: Respiratory muscle work compromises leg blood flow during maximal exercise.
abstract: We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max 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, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) 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 Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; 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, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max 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 and VO2.
authors.affiliation: John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison 53705, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Harms
authors.forename: M A
authors.initials: MA
authors.lastname: Babcock
authors.forename: S R
authors.initials: SR
authors.lastname: McClaran
authors.forename: D F
authors.initials: DF
authors.lastname: Pegelow
authors.forename: G A
authors.initials: GA
authors.lastname: Nickele
authors.forename: W B
authors.initials: WB
authors.lastname: Nelson
authors.forename: J A
authors.initials: JA
authors.lastname: Dempsey
mesh_terms: D000328:Adult; D001794:Blood Pressure; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate; D006801:Humans; D007866:Leg / Q000098:blood supply; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation / Q000502:physiology; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D015203:Reproducibility of Results; D012119:Respiration / Q000502:physiology; D012132:Respiratory Muscles / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000378:metabolism; D014939:Work of Breathing / Q000502:physiology
chemical_list: D014662:Vasoconstrictor Agents; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine