Abstract

Patients with chronic obstructive pulmonary disease (COPD) and congestive heart failure (CHF) often have dyspnea. Despite differences in primary organ derangement and similarities in secondary skeletal muscle changes, both patient groups have prominent functional impairment. With similar daily exercise performance in patients with CHF and COPD, we hypothesized that patients with CHF would have worse ventilatory muscle oxygenation than patients with COPD. This study aimed to compare differences in tissue oxygenation and blood capacity between ventilatory muscles and leg muscles and between the two patient groups. Demographic data, lung function, and maximal cardiopulmonary exercise tests were performed in 134 subjects without acute illnesses. Muscle oxygenation and blood capacity were measured using frequency-domain near-infrared spectroscopy (fd-NIRS). We enrolled normal subjects and patients with COPD and CHF. The two patient groups were matched by oxygen-cost diagram scores, New York Heart Association functional classification scores, and modified Medical Research Council scores. COPD was defined as forced expired volume in one second and forced expired vital capacity ratio ≤0.7. CHF was defined as stable heart failure with an ejection fraction ≤49%. The healthy subjects were defined as those with no obvious history of chronic disease. Age, body mass index, cigarette consumption, lung function, and exercise capacity were different across the three groups. Muscle oxygenation and blood capacity were adjusted accordingly. Leg muscles had higher deoxygenation (HHb) and oxygenation (HbO2) and lower oxygen saturation (SmO2) than ventilatory muscles in all participants. The SmO2 of leg muscles was lower than that of ventilatory muscles because SmO2 was calculated as HbO2/(HHb+HbO2), and the HHb of leg muscles was relatively higher than the HbO2 of leg muscles. The healthy subjects had higher SmO2, the patients with COPD had higher HHb, and the patients with CHF had lower HbO2 in both muscle groups throughout the tests. The patients with CHF had lower SmO2 of ventilatory muscles than the patients with COPD at peak exercise (p < 0.01). We conclud that fd-NIRS can be used to discriminate tissue oxygenation of different musculatures and disease entities. More studies on interventions on ventilatory muscle oxygenation in patients with CHF and COPD are warranted.

Highlights

  • Exercise intolerance and exertional dyspnea are often encountered in patients with chronic obstructive pulmonary disease (COPD) and cardiovascular diseases, and especially in those with congestive heart failure (CHF) [1]

  • The symptoms are primarily caused by heart and lung pathological changes that lead to physiological limitations, and secondarily by ventilatory and locomotor muscle weakness due to myopathy [1,2,3,4]

  • Even though the mechanisms of myopathy, muscle morphology, muscle fiber type distribution and shifting, and muscle metabolism in the locomotor muscles are similar in patients with COPD and CHF [1,9], exercise-induced hypoxemia, if it occurs, is expected to aggravate hypoxic stress in patients with COPD, as the patterns of muscle cytochrome oxidase gene activation are altered in these patients [8]

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Summary

Introduction

Exercise intolerance and exertional dyspnea are often encountered in patients with chronic obstructive pulmonary disease (COPD) and cardiovascular diseases, and especially in those with congestive heart failure (CHF) [1]. Hypoxemia may cause an increase in myostatin protein expression, which is related to muscle atrophy [10], and patients with COPD can experience vascular dysfunction with a higher extraction of muscle oxygen during exercise even in the early stage [11]. It is not clear whether there are differences in the functions of locomotor and ventilatory muscles between patients with COPD and CHF who have similar daily exercise performance and dyspnea sensation

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