Respiratory Muscle Work Constrains Locomotor Convective and Diffusive Transport in Heart Failure during Exercise (2019)

Introduction Heart 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 (VO 2 ) 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 VO 2 following respiratory muscle unloading in HF during submaximal exercise is due to augmented convective O 2 transport in HF; however, it is unclear if diffusive O 2 transport also increases with respiratory muscle unloading. We hypothesized that respiratory muscle unloading during submaximal exercise will lead to increased leg VO 2 due to combined increases in convective and diffusive O 2 transport. Methods Ten HF patients with reduced systolic function (6M/4W; 53±15 yrs; BMI: 29±6 kg/m 2 ) 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 (Q L ) 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 (CaO 2 and CvO 2 , respectively). Leg VO 2 was calculated as Q L multiplied by the difference between CaO 2 ‐CvO 2 . Leg O 2 delivery was calculated as Q L multiplied by CaO 2 . Leg diffusion capacity (DO 2 ) was calculated as leg VO 2 divided by femoral venous partial pressure of O 2 . Results From CTL to RM unloading, leg VO 2 increased during submaximal exercise (0.7±0.3 vs. 1.0±0.4 L/min, p&lt;0.01, respectively). From CTL to RM unloading, leg O 2 delivery increased during submaximal exercise (0.9±0.4 vs. 1.4±0.5 L/min, p&lt;0.01, respectively), whereas CaO 2 ‐CvO 2 was not different (14.1±3.0 vs. 14.2±3.2 mL/dL, p=0.57, respectively). From CTL to RM unloading, leg DO 2 increased during submaximal exercise (30.4±10.8 vs. 49.7±18.6 mL/mmHg, p&lt;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 DO 2 with RM unloading (r= −0.77, p&lt;0.01). Conclusion Our results demonstrate that unloading the respiratory muscles leads to increased leg VO 2 due to convective and diffusive O 2 transport during submaximal exercise in HF patients. These findings suggest that the naturally occurring respiratory muscle work in HF compromises convective and diffusive O 2 transport and thus constrains leg VO 2 during submaximal exercise in HF. Support or Funding Information NIH HL126638 AHA 18POST3990251 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .