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.

Acute respiratory muscle unloading by normoxic helium–O2 breathing reduces the O2 cost of cycling and perceived exertion in obese adolescents

“…Previous investigations demonstrated that respiratory muscle unloading during high-intensity exercise can prevent respiratory muscle fatigue and the reflex vasoconstriction within active locomotor muscles, and can ultimately lead to increased limb blood flow (Babcock et al 2002;Chiappa et al 2009;Harms et al 1997;Romer et al 2006). Although in normal subjects, this phenomenon may not happen during submaximal exercise (Wetter et al 1999), it could occur in obese patient population characterized by a substantially higher work of breathing and increased metabolic demands.…”

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

“…First, ventilation was reduced by ϳ8% when EIAH was prevented during high-intensity exercise. Decreasing inspiratory muscle work by Ͼ50% via mechanical ventilation during heavy exercise, but not during submaximal exercise, has been shown to increase vascular conductance and blood flow in the working limb (15,51) and to reduce quadriceps muscle fatigue (43). Accordingly, we would expect the relatively small reductions in ventilatory work with EIAH prevention to contribute in a minor way to relief of locomotor muscle fatigue.…”

Effects of high-intensity interval training on pulmonary function

“…It has been suggested that the respiratory muscles can demand as much as 10-15% of the blood flow during heavy exercise (Harms et al, 1998). This results in an earlier onset of respiratory muscle fatigue due to a recruitment of additional respiratory muscles, especially with maximal exercise (Enright et al, 2006;Gibala et al, 2006;Harms et al, 1997;Harms et al, 1998). During these conditions, it has been demonstrated that the respiratory muscles, in a sense, "steal" oxygen and blood flow from the working locomotor muscles to meet the demand placed upon them (Harms et al, 1997;Harms et al, 1998).…”