The abdominal muscles have been shown to fatigue in response to voluntary isocapnic hyperpnea using direct nerve stimulation techniques. We investigated whether the abdominal muscles fatigue in response to dynamic lower limb exercise using such techniques. Eleven male subjects [peak oxygen uptake (VO2 peak) = 50.0 +/- 1.9 (SE) ml.kg(-1).min(-1)] cycled at >90% VO2 peak to exhaustion (14.2 +/- 4.2 min). Abdominal muscle function was assessed before and up to 30 min after exercise by measuring the changes in gastric pressure (Pga) after the nerve roots supplying the abdominal muscles were magnetically stimulated at 1-25 Hz. Immediately after exercise there was a decrease in Pga at all stimulation frequencies (mean -25 +/- 4%; P < 0.001) that persisted up to 30 min postexercise (-12 +/- 4%; P = 0.001). These reductions were unlikely due to changes in membrane excitability because amplitude, duration, and area of the rectus abdominis M wave were unaffected. Declines in the Pga response to maximal voluntary expiratory efforts occurred after exercise (158 +/- 13 before vs. 145 +/- 10 cmH2O after exercise; P = 0.005). Voluntary activation, assessed using twitch interpolation, did not change (67 +/- 6 before vs. 64 +/- 2% after exercise; P = 0.20), and electromyographic activity of the rectus abdominis and external oblique increased during these volitional maneuvers. These data provide new evidence that the abdominal muscles fatigue after sustained, high-intensity exercise and that the fatigue is primarily due to peripheral mechanisms.

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To determine whether expiratory muscle fatigue (EMF) is involved in regulating operating lung volumes during exercise, nine recreationally active subjects cycled at 90% of peak work rate to the limit of tolerance with prior induction of EMF (EMF-ex) and for a time equal to that achieved in EMF-ex without prior induction of EMF (ISO-ex). EMF was assessed by measuring changes in magnetically evoked gastric twitch pressure. Changes in end-expiratory and end-inspiratory lung volume (EELV and EILV) and the degree of expiratory flow limitation (EFL) were quantified using maximal expiratory flow-volume curves and inspiratory capacity maneuvers. Resistive breathing reduced gastric twitch pressure (-24 ± 14%, P = 0.004). During EMF-ex, EELV decreased from rest to the 3rd min of exercise [39 ± 8 vs. 27 ± 7% of forced vital capacity (FVC), P = 0.001] before increasing toward baseline (34 ± 8% of FVC end exercise, P = 0.073 vs. rest). EILV increased from rest to the 3rd min of exercise (54 ± 8 vs. 84 ± 9% of FVC, P = 0.006) and remained elevated to end exercise (88 ± 9% of FVC). Neither EELV (P = 0.18) nor EILV (P = 0.26) was different at any time point during EMF-ex vs. ISO-ex. Four subjects became expiratory flow limited during the final minute of EMF-ex and ISO-ex; the degree of EFL was not different between trials (37 ± 18 vs. 35 ± 16% of tidal volume, P = 0.38). At end exercise in both trials, EELV was greater in subjects without vs. subjects with EFL. These findings suggest that 1) contractile fatigue of the expiratory muscles in healthy humans does not regulate operating lung volumes during high-intensity sustained cycle exercise; and 2) factors other than "frank" EFL cause the terminal increase in EELV.

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