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−1, duty cycle 0.5; ERL_Pm] on mean arterial pressure (MAP), leg vascular resistance (LVR), and leg blood flow (Q̇_L). On a separate day, a subset of five male subjects performed ERL targeting 65% of maximal expiratory gastric pressure (ERL_Pga). ERL-induced expiratory muscle fatigue was confirmed by a 17 ± 5% reduction in MEP (P < 0.05) and a 16 ± 12% reduction in the gastric twitch pressure response to magnetic nerve stimulation (P = 0.09) from before to after ERL_Pm and ERL_Pga, respectively. From rest to task failure in ERL_Pm and ERL_Pga, MAP increased (ERL_Pm = 31 ± 10 mmHg, ERL_Pga = 18 ± 9 mmHg, both P < 0.05), but group mean LVR and Q̇_L were unchanged (ERL_Pm: LVR = 0.78 ± 0.21 vs. 0.97 ± 0.36 mmHg·mL⁻¹·min, Q̇_L = 133 ± 34 vs. 152 ± 74 mL·min⁻¹; ERL_Pga: LVR = 0.70 ± 0.21 vs. 0.84 ± 0.33 mmHg·mL⁻¹·min, Q̇_L = 160 ± 48 vs. 179 ± 110 mL·min⁻¹) (all P ≥ 0.05). Interestingly, Q̇_L during ERL_Pga 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 Q̇_L 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. NEW & NOTEWORTHY Fatiguing expiratory muscle work in otherwise resting humans elicits an increase in sympathetic motor outflow; whether limb blood flow (Q̇_L) and leg vascular resistance (LVR) are affected remains unknown. We found that fatiguing expiratory resistive loaded breathing (ERL) did not affect group mean Q̇_L or LVR. However, within-breath oscillations in Q̇_L may reflect a sympathetically mediated vasoconstriction that was counteracted by transient increases in Q̇_L due to the mechanical effects of high intra-abdominal pressure during ERL. [ABSTRACT FROM AUTHOR]