Such increased rib-cage contribution can reduce diaphragmatic sho

Such increased rib-cage contribution can reduce diaphragmatic shortening (Druz and Sharp, 1981), and contribute to improved diaphragmatic coupling (Druz and Sharp, 1981). The increase in ΔPga/ΔPes ratio during loading together with the postexpiratory expiratory muscle recruitment – supported by our results (Fig. 6) and by previous investigations (Loring and Mead, 1982 and Strohl et al., 1981) – suggests that loading triggered a coordinated action of extra-diaphragmatic muscles, which, in turn, improved the mechanical advantage of the diaphragm. In addition, co-activation of (inspiratory) rib-cage muscles facilitates the action of the diaphragm by reducing

the muscle’s velocity of shortening during contraction – a functional synergism (De Troyer, 2005). Diaphragmatic coupling while subjects sustained Etoposide cost the small, constant threshold load recorded 5 and 15 min after loading was similar to the coupling

recorded before loading. During these three time periods, the values of EELV, end-expiratory Pga and ΔPga/ΔPes remained constant (data not shown). These results further support the possibility that improvements in the mechanical advantage of the diaphragm were indeed responsible for the improvement in coupling during incremental loading. The proximate cause of task failure was the intolerable discomfort required to breathe. Upstream processes responsible for this intolerable discomfort could include peripheral mechanisms, central mechanisms or Selleckchem MI-773 both. Peripheral processes include impaired neuromuscular Montelukast Sodium transmission and contractile fatigue (Hill, 2000), while central processes include hypercapnia-induced dyspnea (Morelot-Panzini et al., 2007), dyspnea triggered by stimulation of intrathoracic

C-fibers and intramuscular C-fibers (Morelot-Panzini et al., 2007), and dyspnea triggered by decreased output form pulmonary stretch receptors (Killian, 2006). Two considerations suggest that peripheral mechanisms were not primarily responsible for the unbearable discomfort at task failure. Diaphragmatic CMAPs (elicited by stimulation of the phrenic nerves) at task failure and 20 and 40 min later had similar amplitudes to the amplitudes recorded before loading. That is, neuromuscular transmission at task failure and after task failure was not affected by the preceding loading. Moreover, the presence of contractile fatigue after loading was an inconsistent finding (Fig. 7). On this basis, we reason that upstream processes responsible for the intolerable breathing discomfort at task failure were central in origin. One mechanism was alveolar hypoventilation consequent to load-induced inhibition of central activation (Gandevia, 2001). The presence of inadequate central activation in our subjects is inconsistent with the results of Eastwood and collaborators (Eastwood et al., 1994) who reported near maximal recruitment of the diaphragm at maximum load.

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