Preserved muscle oxidative capacity in COPD patients with hypoxemia treated by long term O2 therapy

Long-term oxygen therapy (LTOT) is an established treatment for patients with chronic obstructive pulmonary disease (COPD) diagnosed with hypoxemia at rest or during activity. Chronic hypoxemia is a potential mediator of loss of muscle mass and oxidative capacity in COPD. In this retrospective analysis, we sought to determine whether patients with COPD receiving LTOT have impaired muscle oxidative capacity compared to those without LTOT. Personal characteristics, medical and smoking history, spirometry, diffusing capacity, use of LTOT, 6-min walk distance (6MWD), dyspnea symptoms (mMRC Dyspnea scale) were extracted from medical records. Gastrocnemius muscle oxidative capacity was assessed from the O2 consumption recovery rate constant (k) using near-infrared spectroscopy. Chi2 and t-tests assessed group differences. ANCOVA was used to compare k, after adjusting for known covariates (FEV1%predicted, age, race), in COPD patients with and without LTOT. 23 COPD with LTOT (LTOT) and 29 COPD (non-LTOT) were included in the analysis. The LTOT group tended to be older (p = 0.060), had worse spirometry and diffusing capacity (p < 0.023) and 6MWD (p < 0.001), but similar dyspnea (p > 0.105) compared to the non-LTOT group. After adjusting for covariates, k was not different between groups (LTOT, 1.06 ± 0.07 vs non-LTOT, 1.09 ± 0.26 min−1; p = 0.436). Contrary to our hypothesis, muscle oxidative capacity was not lower in LTOT-treated COPD compared to those without LTOT. Because COPD patients with LTOT had lower FEV1%pred and tended to be older (known correlates of k), our findings suggest that LTOT may protect against loss of muscle oxidative function in COPD patients with chronic hypoxemia.