Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans

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Abstract
1 We tested the hypothesis that reflexes arising from working respiratory muscle can elicit increases in sympathetic vasoconstrictor outflow to limb skeletal muscle, in seven healthy human subjects at rest. 2 We measured muscle sympathetic nerve activity (MSNA) with intraneural electrodes in the peroneal nerve while the subject inspired (primarily with the diaphragm) against resistance, with mouth pressure (PM) equal to 60 % of maximal, a prolonged duty cycle (TI/TTot) of 0.70, breathing frequency (fb) of 15 breaths min−1 and tidal volume (VT) equivalent to twice eupnoea. This protocol was known to reduce diaphragm blood flow and cause fatigue. 3 MSNA was unchanged during the first 1–2 min but then increased over time, to 77 ± 51 % (s.d.) greater than control at exhaustion (mean time, 7 ± 3 min). Mean arterial blood pressure (+12 mmHg) and heart rate (+27 beats min−1) also increased. 4 When the VT, fb and TI/TTot of these trials were mimicked with no added resistance, neither MSNA nor arterial blood pressure increased. 5 MSNA and arterial blood pressure also did not change in response to two types of increased central respiratory motor output that did not produce fatigue: (a) high inspiratory flow rate and fb without added resistance; or (b) high inspiratory effort against resistance with PM of 95 % maximal, TI/TTot of 0.35 and fb of 12 breaths min−1. The heart rate increased by 5–16 beats min−1 during these trials. 6 Thus, in the absence of any effect of increased central respiratory motor output per se on limb MSNA, we attributed the time-dependent increase in MSNA during high resistance, prolonged duty cycle breathing to a reflex arising from a diaphragm that was accumulating metabolic end products in the face of high force output plus compromised blood flow.