Respiratory Muscle Work Constrains Locomotor Convective and Diffusive Transport in Heart Failure during Exercise

Abstract

IntroductionHeart failure (HF) patients demonstrate augmented ventilation for a given metabolic demand which results in increased respiratory muscle work and subsequent competition for blood flow between the respiratory and locomotor muscle beds. Unloading the respiratory muscles during submaximal exercise has been shown to increase leg oxygen uptake (VO2) in HF patients due increased leg blood flow via increased cardiac output and redistribution of cardiac output from the respiratory to locomotor muscles. It has been suggested that increased leg VO2 following respiratory muscle unloading in HF during submaximal exercise is due to augmented convective O2 transport in HF; however, it is unclear if diffusive O2 transport also increases with respiratory muscle unloading. We hypothesized that respiratory muscle unloading during submaximal exercise will lead to increased leg VO2 due to combined increases in convective and diffusive O2 transport.MethodsTen HF patients with reduced systolic function (6M/4W; 53±15 yrs; BMI: 29±6 kg/m2) were recruited. Patients performed two submaximal exercise bouts (i.e. with and without respiratory muscle unloading (via mechanical ventilator) (RM unloading and control (CTL), respectively)). During exercise, leg blood flow (QL) was measured via thermodilution. Intrathoracic pressure was measured via esophageal balloon. Radial arterial and femoral venous blood gases were measured. Blood gases were used to calculate arterial and venous oxygen content (CaO2 and CvO2, respectively). Leg VO2 was calculated as QL multiplied by the difference between CaO2‐CvO2. Leg O2 delivery was calculated as QL multiplied by CaO2. Leg diffusion capacity (DO2) was calculated as leg VO2 divided by femoral venous partial pressure of O2.ResultsFrom CTL to RM unloading, leg VO2 increased during submaximal exercise (0.7±0.3 vs. 1.0±0.4 L/min, p<0.01, respectively). From CTL to RM unloading, leg O2 delivery increased during submaximal exercise (0.9±0.4 vs. 1.4±0.5 L/min, p<0.01, respectively), whereas CaO2‐CvO2 was not different (14.1±3.0 vs. 14.2±3.2 mL/dL, p=0.57, respectively). From CTL to RM unloading, leg DO2 increased during submaximal exercise (30.4±10.8 vs. 49.7±18.6 mL/mmHg, p<0.01, respectively). There was a negative relationship between the degree of RM unloading (i.e. percent decrease in mean inspiratory esophageal pressure) and percent increase in leg DO2 with RM unloading (r= −0.77, p<0.01).ConclusionOur results demonstrate that unloading the respiratory muscles leads to increased leg VO2 due to convective and diffusive O2 transport during submaximal exercise in HF patients. These findings suggest that the naturally occurring respiratory muscle work in HF compromises convective and diffusive O2 transport and thus constrains leg VO2 during submaximal exercise in HF.Support or Funding InformationNIH HL126638 AHA 18POST3990251This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.