Effects of static lung inflation on sympathetic activity in human muscle nerves at rest and during asphyxia.

Muscle sympathetic activity is inhibited during the second half of phasic lung inflation associated with normal (negative pressure) breathing or artificial ventilation with intermittent positive-pressure, and this inspiratory inhibition appears unrelated to the associated changes in arterial pressure. In this present study we tested the hypothesis that a static inflation of the lungs would cause a sustained inhibition of muscle sympathetic activity. Microneurographic techniques were used to record muscle sympathetic activity from the peroneal nerve, and arterial pressure was monitored continuously by finger-pulse photoplethysmography (Finapres). In nine subjects static lung inflation, brought about either actively or passively, caused a pronounced and sustained increase in sympathetic activity (not the predicted decrease) that could not be explained by changes in arterial pressure. When delivered at the end of a voluntary end-expiratory apnoea, static lung inflation caused an initial inhibition of the large chemoreceptor-induced sympathetic bursts and a subsequent excitation that was sustained for the duration of the lung inflation. These observations indicate that respiration can affect muscle sympathetic activity in humans in two opposing ways: inhibition during phasic increases in lung volume, and excitation during large static increases in lung volume. Neither phenomenon depends on changes in arterial pressure, and hence influences of carotid arterial and aortic (high-pressure) baroreceptors can be excluded. We suggest that the initial inhibition is evoked from lung or chest-wall receptors and the static exitation from unloading of cardiopulmonary (low pressure) baroreceptors.