Background: Determinants of increased sympathetic drive in COPD remain poorly understood. The gold standard of sympathetic drive assesement, available only in a few centers worldwide, is invasive microneurographic measurement of muscle sympathetic activity (MSNA). Burst rate (/min) or incidence (adjusted for heart rate) then express sympathetic activity as the spontaneous discharge rate of sympathetic nerve fascicles measured with microneurographic electrodes.

Methods: In 7 COPD patients without any cardiovascular disease, external and intraneural stimulation was used to locate the peroneal nerve in the leg, and then invasive microneurographic measurement of MSNA was performed via this nerve, and the influence of oxygen therapy in correcting hypoxemia and noninvasive ventilation (NIV) in correcting hypercapnia on sympathetic drive was studied.

Results: In 7 COPD patients (age 65±9 years, GOLD III-IV, with NIV including 4 long-term oxygen therapy. Heart rate decreased with correction of hypoxemia under oxygen therapy (2-3 L/min; increased PaO2 from 53±8 to 63±7 mmHg; p?0.05) (HF 74±9 vs. 68±7 bpm, p=0.05). Burst rate decreased under oxygen therapy (32±6 vs. 25±5 bursts/min, p=0.04) as did burst incidence (44±8 vs. 37±8 bursts/100bpm, p=0.047). Burst rate was decreased with correction of hypercapnia (decreased PaCO2 51±3 vs. 43±2 mmHg; p?0.05) by NIV (31±7 vs. 24±6 bursts/min, p=0.02). Burst incidence was also decreased with correction of hypercapnia by NIV (41±6 vs. 36±4 bursts/min, p=0.017).

Conclusion: Both oxygen and NIV therapies lead to a decrease in MSNA in COPD by correcting hypoxemia and hypercapnia, respectively. This could explain the prognostic value of both forms of therapy.