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Aim: To test the hypothesis that the maximal inspiratory muscle (IM) performance, as assessed by the maximal IM pressure-flow relationship, is enhanced with the stretch-shortening cycle (SSC)., Methods: Maximal inspiratory flow-pressure curves were measured in 12 healthy volunteers (35 +/- 6 years) during maximal single efforts through a range of graded resistors (4-, 6-, and 8-mm diameter orifices), against an occluded airway, and with a minimal load (wide-open resistor). Maximal inspiratory efforts were initiated at a volume near residual lung volume (RV). The subjects exhaled to RV using slow (S) or fast (F) manoeuvres. With the S manoeuvre, they exhaled slowly to RV and held the breath at RV for about 4 s prior to maximal inspiration. With the F manoeuvre, they exhaled rapidly to RV and immediately inhaled maximally without a post-expiratory hold; a strategy designed to enhance inspiratory pressure via the SSC., Results: The maximal inspiratory pressure-flow relationship was linear with the S and F manoeuvres (r2 = 0.88 for S and r2 = 0.88 for F manoeuvre, P < 0.0005 in all subjects). With the F manoeuvre, the pressure-flow relationship shifted to the right in a parallel fashion and the calculated maximal power increased by approximately 10% (P < 0.05) over that calculated with the S manoeuvre., Conclusion: The maximal inspiratory pressure-flow capacity can be enhanced with SSC manoeuvres in a manner analogous to increases in the force-velocity relationship with SSC reported for skeletal muscles.

We have recently shown (Eur. Respir. J. 1997;10:522-529) that in spontaneously breathing and actively expiring patients, static intrinsic positive end-expiratory pressure (PEEPi,st) can be corrected for expiratory muscle contraction by subtracting the average expiratory rise in gastric pressure (Pga,exp rise), calculated from three breaths just prior to an airway occlusion, from the end-expiratory airway pressure (Paw) of the first occluded inspiratory effort (PEEPi,st avg). However, since in some patients there is substantial variability in the intensity of expiratory muscle activity and hence in Pga,exp rise, this method may be inaccurate because the Pga,exp rise of breaths preceding airway occlusion may differ from that of the first postocclusion breath. In the present study, we introduced a new method consisting of synchronous subtraction of Pga,exp rise from Paw, both occurring during airway occlusion (PEEPi,st sub). PEEPi,st sub and PEEPi,st avg were each compared with the reference PEEPi,st (PEEPi,st ref), which was obtained during muscular paralysis and simulation of the spontaneous breathing pattern by the ventilator. We found that, in 25 critically ill patients, PEEPi,st sub (mean +/- SD, 5.3 +/- 2.6 cm H(2)O) was nearly identical to PEEPi,st ref (5.4 +/- 2.4 cm H(2)O). Their mean difference was -0.06 cm H(2)O with limits of agreement -0.96 to 0.84 cm H(2)O, indicating a strong agreement between these methods. In contrast, mean difference of PEEPi,st avg and PEEPi,st ref was 0.73 cm H(2)O with limits of agreement -3.97 to 5.43 cm H(2)O, indicating lack of agreement. Coefficient of variation of Pga,exp rise was 14.3 +/- 7.2% (range, 5.2 to 28.3%). There was a good correlation between the coefficient of variation of Pga,exp rise and the difference between PEEPi,st avg and PEEPi,st ref (r = 0.909; p < 0.001). We conclude that PEEPi,st can be accurately measured in spontaneously breathing patients by synchronous subtraction of Pga,exp rise from Paw during airway occlusion.

Because the inspiratory rib cage muscles are recruited during inspiratory resistive loaded breathing, we hypothesized that such loading would preferentially fatigue the rib cage muscles. We measured the pressure developed by the inspiratory rib cage muscles during maximal static inspiratory maneuvers (Pinsp) and the pressure developed by the diaphragm during maximal static open-glottis expulsive maneuvers (Pdimax) in four human subjects, both before and after fatigue induced by an inspiratory resistive loaded breathing task. Tasks consisted of maintaining a target esophageal pressure, breathing frequency, and duty cycle for 3-5 min, after which the subjects maintained the highest esophageal pressure possible for an additional 5 min. After loading, Pinsp decreased in all subjects [control, -128 +/- 14 (SD) cmH2O; with fatigue, -102 +/- 18 cmH2O; P less than 0.001, paired t test]. Pdimax was unchanged (control, -192 +/- 23 cmH2O; fatigue, -195 +/- 27 cmH2O). These data suggest that 1) inability to sustain the target during loading resulted from fatigue of the inspiratory rib cage muscles, not diaphragm, and 2) simultaneous measurement of Pinsp and Pdimax may be useful in partitioning muscle fatigue into rib cage and diaphragmatic components.