The cardiovascular consequences of fatiguing expiratory muscle work in otherwise resting healthy humans.

In 11 healthy adults (25 ± 4 yr; 2 female, 9 male subjects), we investigated the effect of expiratory resistive loaded breathing [65% maximal expiratory mouth pressure (MEP), 15 breaths·min, duty cycle 0.5; ERL] on mean arterial pressure (MAP), leg vascular resistance (LVR), and leg blood flow ([Formula: see text]). On a separate day, a subset of five male subjects performed ERL targeting 65% of maximal expiratory gastric pressure (ERL). ERL-induced expiratory muscle fatigue was confirmed by a 17 ± 5% reduction in MEP ( < 0.05) and a 16 ± 12% reduction in the gastric twitch pressure response to magnetic nerve stimulation ( = 0.09) from before to after ERL and ERL, respectively. From rest to task failure in ERL and ERL, MAP increased (ERL = 31 ± 10 mmHg, ERL = 18 ± 9 mmHg, both < 0.05), but group mean LVR and [Formula: see text] were unchanged (ERL: LVR = 0.78 ± 0.21 vs. 0.97 ± 0.36 mmHg·mL·min, [Formula: see text] = 133 ± 34 vs. 152 ± 74 mL·min; ERL: LVR = 0.70 ± 0.21 vs. 0.84 ± 0.33 mmHg·mL·min, [Formula: see text] = 160 ± 48 vs. 179 ± 110 mL·min) (all ≥ 0.05). Interestingly, [Formula: see text] during ERL oscillated within each breath, increasing (∼66%) and decreasing (∼50%) relative to resting values during resisted expirations and unresisted inspirations, respectively. In conclusion, fatiguing expiratory muscle work did not affect group mean LVR or [Formula: see text] in otherwise resting humans. We speculate that any sympathetically mediated peripheral vasoconstriction was counteracted by transient mechanical effects of high intra-abdominal pressures during ERL. Fatiguing expiratory muscle work in otherwise resting humans elicits an increase in sympathetic motor outflow; whether limb blood flow ([Formula: see text]) and leg vascular resistance (LVR) are affected remains unknown. We found that fatiguing expiratory resistive loaded breathing (ERL) did not affect group mean [Formula: see text] or LVR. However, within-breath oscillations in [Formula: see text] may reflect a sympathetically mediated vasoconstriction that was counteracted by transient increases in [Formula: see text] due to the mechanical effects of high intra-abdominal pressure during ERL.