G. Citterio

Decay rate of inspiratory muscle pressure during expiration in man.

Decay rate of inspiratory muscle pressure (PmusI) was studied in 4 subjects during post-inspiratory period of zero flow (TEz) occurring under discontinuous inspiratory elastic load (DIL). End-inspiratory pressure (PmuseI) was increased by dead spaces or exercises. Decay rate was related to PmuseI by a power function with exponent greater than 1. It was not directly affected by concomitant changes of PCO2. It did not increase when an expiratory resistive load was added, i.e. when braking action of inspiratory muscles was no longer required. Time course of PmusI during TEz was more straight than exponential. Relative decay rate increased with PmuseI and with decrease of inspiratory or expiratory time. Experiments with resistive loads suggest that relative rate is mainly related to timing factors. During voluntary inspiratory efforts with closed airways, relative decay rate was not related to PmuseI, while decay rate increased linearly with PmuseI.

Decay of inspiratory muscle activity and breath timing in man

Time required by moving average EMG of diaphragm and parasternal intercostal muscle to decay to 25% of its peak (T0.25) decreased of expiratory time (TE). Accordingly, relative decay rate (RDRI) of EMG increased of breathing frequency (f). This confirms conclusions based on decay of inspiratory muscle pressure under discontinuous inspiratory elastic load (DIL). Data were better fitted by power functions: only this combination of T0.25 vs. TE and RDRI vs. f equations provided a relationship fitting corresponding inspiratory time vs. TE data. For each timing, RDRI of EMG was higher under DIL than during unloaded breathing. Under DIL scattering of EMG data increased, coupling between diaphragm and parasternal muscle EMG decreased, and RDRI of EMG was higher than that of pressure, likely because of muscle intrinsic properties. This difference decreased with the increase of f: this could be due to recruitment of fast fibers at high f. Both during loaded and unloaded breathing T0.25 was proportional to time from peak to zero EMG, indicating that decay shape did not change with timing.

Relative decay rate of inspiratory muscle pressure and breath timing in man.

The decay rate of inspiratory muscle pressure (PmusI) was measured during the postinspiratory period of zero flow (TEz) occurring under a discontinuous inspiratory elastic load with the following tests, (a) Voluntary changed breathing frequency (f) at similar end-inspiratory muscle pressure (PmuseI), (b) as above plus dead space, hence greater PmuseI, (c) breathing spontaneously through a dead space or during exercise to obtain different f at similar PmuseI. The decay rate of PmusI relative to PmuseI (RDRI) at increased f was similar to the corresponding relative decay rate of transdiaphragmatic pressure. Hence, the increase of f did not elicit phasic activity of expiratory muscles during TEz. RDRI increased proportionally to f: i.e. for a given f, the decay rate of PmusI was proportional to PmuseI. RDRI increased hyperbolically with decrease of expiratory time and was not directly related to inspiratory time. In each subject these relationships were unique for different tests. These findings show that increase of Pmusel alone does not shorten the persistence of PmusI during expiration, whereas a timing factor, by increasing RDRI, allows shortening of expiration without the intervention of expiratory muscles.

Slow to fast shift in inspiratory muscle fibers during heat tachypnea.

The firing patterns of single diaphragm fibers and electromyographic moving average (M.A.) of diaphragm and parasternal intercostal muscles (P.I.) were studied in rabbits during control and heat tachypnea at nearly constant tidal volume (VT). During tachypnea the percentage of single diaphragm fibers with relatively high values of peak firing rate (fp) increased. Conversely, fibers with relatively low values of fp at control (likely slow) showed little or no increase of this parameter during tachypnea. These findings, similar to those previously found in P.I., suggest a slow to fast shift in diaphragm fibers during tachypnea. Inspiratory flow at half VT control increased significantly during tachypnea, while the corresponding M.A. of diaphragm did not change. Moreover, during tachypnea mean inspiratory flow increased significantly, while the mean M.A. over inspiratory time did not change either in diaphragm or in P.I. Since during tachypnea the firing rate of most fibers is greater than at control, a lack of increase of M.A. in spite of an increased mechanical power confirms a shift from slow to fast inspiratory muscle fibers under this condition.

Inspiratory facilitation and inhibition from pulmonary stretch receptors in rabbits

In anesthetized rabbits firing rate (FR) of single fibers of diaphragm and of parasternal intercostal muscles (PIM) was determined at 30, 50 and 70% of control inspiratory time. During first inspiratory effort after airway occlusion at end expiration it increased on the average by 12.1 +/- 0.6 and 43.0 +/- 2.2% relative to control. Under pulmonary stretch receptor (PSR) block with SO2 this increase disappeared in diaphragm and fell to 28.3 +/- 1.8% in PIM. During first inspiratory efforts under PSR block FR decreased by 11.3 +/- 2.2% in diaphragm and 18.3 +/- 1.6 in PIM relative to unblocked efforts. In open inspirations FR under block did not decrease significantly either in diaphragm or PIM relative to unblocked inspirations. Moving average electromyography of diaphragm and of PIM showed similar trends. These results suggest that PSR discharge at FRC activates a mechanism facilitating inspiratory activity while during inspiration it also activates a mechanism inhibiting this activity since early inspiration. Both effects are greater on PIM.

Reflex effects on breathing of laryngeal denervation, negative pressure and SO2 in upper airways

Respiratory reflex effects of laryngeal denervation, negative pressure and SO2 in upper airways were studied in anesthetized rabbits. Inspiratory efforts with nasal occlusion had longer duration (TIo) and smaller diaphragm activity (Adi) than with tracheal occlusion. After section of superior laryngeal nerves (SLN) these differences disappeared: values with tracheal occlusion became similar to those with nasal occlusion before denervation. This suggests that laryngeal pressure receptors, firing at zero pressure and decreasing their discharge with negative pressures, increase central inspiratory activity. After SO2 TIo, both with tracheal and nasal occlusion, increased even after laryngeal denervation, provided SO2 flowed through nasal pathway. Hence, nose and/or rhinopharynx contain receptors affected by SO2. After laryngeal denervation and SO2 TIo was shorter with nasal than with tracheal occlusion, despite equal Adi. This, combined with the above findings, suggests two groups of pressure receptors in nose and/or rhinopharynx with opposite effects on inspiratory off-switch: one unaffected and the other probably blocked by SO2. During nose breathing section of SLN produced only a slight decrease in mean inspiratory flow.

Reflex partitioning of inputs from stretch receptors of bronchi and thoracic trachea

A selective block of slowly adapting stretch receptors in anesthetized rabbits was induced by exposing to SO2 all thoracic airways (T) or the carina and bronchi alone (B). Increment of inspiratory time (TI) relative to control was 61% greater under B than T. The reverse would have happened if input responsible for Breuer-Hering inflation reflex originated from both bronchi and trachea. Hence, bronchial input activates inspiratory off-switch, while tracheal input delays its activation. During single inspiratory efforts with airways closed at end expiration diaphragm activity (Adi) decreased and TI0 increased relative to control equally under B and T. Hence, the input facilitating central inspiratory activity at end expiratory volume does not stem from trachea. At end of inspiratory ramp Adi stopped within 43 msec at control and 57 msec under B and T. Hence, bronchial input speeds up off-switching of inspiration. Postinspiratory Adi was greater under B than T, and nearly nil at control. Hence, bronchial input inhibits postinspiratory Adi, while tracheal input facilitates it. Inspiratory and expiratory flows were more damped under B than T, and under T than at control.

Selective activation of parasternal muscle fibers according to breathing rate

The activity of single parasternal intercostal muscle fibers of rabbits was recorded during control breathing and during heat tachypnea at near-constant tidal volume. In order to identify with high probability the type of fibers on the basis of available knowledge, differences in firing pattern were enhanced by occluding the airways during an inspiration or adding dead space. Under both conditions the percentage of fibers with relatively high values of peak firing rate (fp) and rising rate of firing frequency (delta f/delta t) was greater during tachypnea. Fibers with relatively low values of fp and delta f/delta t during control breathing showed little or no increase of these parameters during tachypnea. Fibers with low fp and delta f/delta t should be slow, and others fast. Hence, the greater percentage of fibers with high fp and delta f/delta t during tachypnea indicates a recruitment of fast fibers. these findings support our previous hypothesis of selective activation of inspiratory muscle fibers according to the speed of movements.

Breathing pattern and diaphragm EMG after SO2 in rabbit intra- or extrathoracic airways

In anesthetized rabbits under SO2 block of slowly adapting stretch receptors (SAR) in intrathoracic airways TI increased by 49.7 +/- 6.9% and VT by 19.5 +/- 3.7%. TE decreased for small increases of TI and vice versa. Slope of moving average of diaphragm EMG (M.A.) decreased by 16.7 +/- 4.1% from 0 to 30% TI control, and increased by 26.3 +/- 8.1% from 30 to 70%. Considering that discharge from intrathoracic SAR increases during inspiration, these changes of M.A. indicate that their input facilitates inspiration at its beginning, but inhibits it later on, in line with previous conclusions based on SAR block which included 2/3 of extrathoracic trachea (ETT). Neither SO2 nor pressures from -40 to +40 cm H2O in ETT changed breathing pattern or M.A.. Hence, SAR of ETT do not affect parameters studied in rabbits. When extrathoracic airways were exposed to SO2 TI increased by 30.5 +/- 8.2%, TE by 37.9 +/- 5.1%, VT did not change. Hence, some receptors rostral to trachea, involved in respiratory control, are affected by SO2.

Discontinuity between inspiratory and postinspiratory diaphragm activity in man and rabbit

Diaphragm activity (Edi, 20 Hz low cutoff) was recorded with great time resolution to ascertain whether there is a discontinuity between its inspiratory and postinspiratory periods in humans. We first determined in anesthetized rabbits that gaps or notches in Edi occurred within 80 msec before and after the end of mechanical inspiration in 70% of the analysable breaths in the esophageal lead and in 77% in direct leads. We then determined from the esophageal lead of 4 conscious subjects that gaps or notches in Edi occurred during the above-defined period in 45% of 682 analysable breaths. In each subject mean of moving average Edi (12 msec averaging interval) was computed out of 14-24 breaths, free of ECG artifacts within 200-250 msec before and after end inspiration. A deep indentation occurred near end-inspiration despite the lack of gaps or notches in 1/2 to 4/5 of these breaths. These results suggest that also in humans postinspiratory diaphragm activity does not represent the decay of inspiratory ramp.