Inspiratory muscle training attenuates the human respiratory muscle metaboreflex.

We hypothesized that inspiratory muscle training (IMT) would attenuate the sympathetically mediated heart rate (HR) and mean arterial pressure (MAP) increases normally observed during fatiguing inspiratory muscle work. An experimental group (Exp, n = 8) performed IMT 6 days per week for 5 weeks at 50% of maximal inspiratory pressure (MIP), while a control group (Sham, n = 8) performed IMT at 10% MIP. Pre- and post-training, subjects underwent a eucapnic resistive breathing task (RBT) (breathing frequency = 15 breaths min(-1), duty cycle = 0.70) while HR and MAP were continuously monitored. Following IMT, MIP increased significantly (P < 0.05) in the Exp group (-125 +/- 10 to -146 +/- 12 cmH(2)O; mean +/- s.e.m.) but not in the Sham group (-141 +/- 11 to -148 +/- 11 cmH(2)O). Prior to IMT, the RBT resulted in significant increases in HR (Sham: 59 +/- 2 to 83 +/- 4 beats min(-1); Exp: 62 +/- 3 to 83 +/- 4 beats min(-1)) and MAP (Sham: 88 +/- 2 to 106 +/- 3 mmHg; Exp: 84 +/- 1 to 99 +/- 3 mmHg) in both groups relative to rest. Following IMT, the Sham group observed similar HR and MAP responses to the RBT while the Exp group failed to increase HR and MAP to the same extent as before (HR: 59 +/- 3 to 74 +/- 2 beats min(-1); MAP: 84 +/- 1 to 89 +/- 2 mmHg). This attenuated cardiovascular response suggests a blunted sympatho-excitation to resistive inspiratory work. We attribute our findings to a reduced activity of chemosensitive afferents within the inspiratory muscles and may provide a mechanism for some of the whole-body exercise endurance improvements associated with IMT.