Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, C103

Oral Communications

Skeletal muscle deoxygenation during respiratory fatigue in heart failure

A. Nobrega1, A. Moreno1, R. Castro1, P. Guerra1, A. Rezende1, M. Junior1

1. Fluminense Federal University, Niteroi, RJ, Brazil.


Respiratory muscle fatigue is a key factor in the diminished exercise capacity of patients with heart failure (HF) (1,2). In addition to the ventilatory limitation in promoting hematosis, respiratory fatigue activates the respiratory muscle metaboreflex increasing reflex sympathetic outflow, which in turn limits the increase in perfusion to working muscles (2). The metaboreflex is triggered by the accumulation of metabolites within muscle caused by oxygen demand-delivery mismatch, but the effect of respiratory fatigue on respiratory muscle oxygenation in HF has not investigated. We hypothesized that respiratory muscle fatigue in HF occurs with deoxygenation of intercostal muscle leading to reflex peripheral vasoconstriction and tissue deoxygenation. Five subjects with HF and respiratory weakness (age: 66±12 yrs, left ventricle ejection fraction 34±3%; maximal inspiratory pressure <70% predicted) and nine paired healthy controls (age: 65±13 yrs) underwent respiratory fatigue induced by 3 min ventilation against fixed resistance at 60% maximal inspiratory pressure (Threshold Inspiratory Muscle Training, Heathscan Products Inc., NJ, USA) followed by respiratory unloading (3 min with non-invasive ventilation support in continuous positive airway pressure mode CPAP at 20 cmH2O) (3), while muscle oxygenation were monitored by near-infrared spectroscopy (NIRS; Oxiplex TS, ISS, IL, USA) with transducers placed on the seventh left intercostal space and on a resting peripheral muscle group (forearm). The difference in the tissue absorbancy between the 850 nm (oxy-hemoglobin) and 760 nm (desoxy-hemoglobin) wavelengths indicates tissue oxygenation. The responses to respiratory fatigue in controls were discounted from those in HF patients. Values are means±SEM, compared by two-way ANOVA-Bonferroni. Tissue oxygenation in intercostals muscle decreased during fatigue in HF relative to controls (1 min: -1.35±1.6 a.u.; 2 min: -2.23±1.9 a.u.; fatigue: -4.92±2.6 a.u., p<0.05). Forearm tissue oxygenation did not change in controls (p>0.05), but decreased in HF (1 min: -0.61±1.6 a.u.; 2 min: -1.52±1.5 a.u.; fatigue: -4.54±1.5 a.u., p<0.05). All these changes in tissue oxygenation were reversed by CPAP applied on the recovery period. Since the difference between tissue oxy-hemoglobin and deoxy-hemoglobin is considered a proxy of tissue oxygenation, reflecting the balance between oxygen delivery and utilization (4,5), the results suggest that respiratory fatigue in HF causes relative ischemia in intercostal and peripheral muscles. Therefore, these results provide original evidence that respiratory muscle fatigue provokes a local oxygen demand/delivery mismatch and tissue deoxyganation in HF, which is associated to reduction in tissue oxygenation also in peripheral muscles at resting conditions, suggesting the operation of respiratory muscle metaboreflex.

Where applicable, experiments conform with Society ethical requirements