Peak Inspiratory Activity Research Articles

Interplay Between the Inspiratory and Postural Functions of the Human Parasternal Intercostal Muscles

The parasternal intercostal muscles are obligatory inspiratory muscles. To test the hypothesis that they are also involved in trunk rotation and to assess the effect of any postural role on inspiratory drive to the muscles, intramuscular electromyographic (EMG) recordings were made from the parasternal intercostals on the right side in six healthy subjects during resting breathing in a neutral posture ("neutral breaths"), during an isometric axial rotation effort of the trunk to the right ("ipsilateral rotation") or left ("contralateral rotation"), and during resting breathing with the trunk rotated. The parasternal intercostals were commonly active during ipsilateral rotation but were consistently silent during contralateral rotation. In addition, with ipsilateral rotation, peak parasternal inspiratory activity was 201 +/- 19% (mean +/- SE) of the peak inspiratory activity in neutral breaths (P < 0.001), and activity commenced earlier relative to the onset of inspiratory flow. These changes resulted from an increase in the discharge frequency of motor units (14.3 +/- 0.3 vs. 11.0 +/- 0.3 Hz; P < 0.001) and the recruitment of new motor units. The majority of units that discharged during ipsilateral rotation were also active in inspiration. However, with contralateral rotation, parasternal inspiratory activity was delayed relative to the onset of inspiratory flow, and peak activity was reduced to 72 +/- 4% of that in neutral breaths (P < 0.001). This decrease resulted from a decrease in the inspiratory discharge frequency of units (10.5 +/- 0.2 vs. 12.0 +/- 0.2 Hz; P < 0.001) and the derecruitment of units. These observations confirm that in addition to an inspiratory function, the parasternal intercostal muscles have a postural function. Furthermore the postural and inspiratory drives depolarize the same motoneurons, and the postural contraction of the muscles alters their output during inspiration in a direction-dependent manner.

Respiratory-related control of extrinsic tongue muscle activity

The purpose of this brief report is to introduce new evidence showing that the protrudor and retractor muscles of the tongue are co-activated during inspiration in eupnea and hyperpnea in an anesthetized, tracheotomized rat model. We also review previous work on the respiratory related control of the tongue musculature, and briefly consider the clinical significance of this work. The important new findings are that: (1) Both hypoxia and hypercapnia cause parallel increases in drive to the tongue protrudor and retractor muscles (the genioglossus and hyoglossus muscles, respectively); (2) phasic volume feedback inhibits the peak inspiratory activity of both muscles; and (3) the tongue muscles consistently produce a retraction force when the genioglossus and hyoglossus are co-activated, in both animal and human subjects. This latter observation is consistent with previous work showing that the retractor muscles (hyoglossus and styloglossus) develop up to ten times more force than the genioglossus muscle. The possible mechanical consequences of tongue muscle co-activation are briefly considered.

Histamine induced bronchoconstriction and end tidal inspiratory activity in man.

End tidal inspiratory activity (ETIA) in diaphragm and parasternal intercostal muscles can be evoked in man and in animals by administration of histamine. Exacerbations of asthma and administration of histamine are often accompanied by hyperinflation. The aims of the study were to determine (1) the magnitude of ETIA in response to histamine in man, (2) the relative contributions of chemical and mechanical stimulation of airway receptors to ETIA, and (3) the importance of ETIA to hyperinflation. The effects of inhalation of histamine on the electrical activities of the diaphragm and parasternal intercostal muscles measured with surface electrodes were studied in 21 subjects. The experiments were repeated after inhalation of 600 micrograms of salbutamol to prevent histamine induced bronchoconstriction and concomitant mechanical stimulation of airway receptors. Subjects were connected to a closed breathing circuit to measure the changes in functional residual capacity (FRC) for the different experiments. The mean values of histamine induced ETIA were 60.6% and 46.9% of peak inspiratory activities during control conditions for the diaphragm and intercostal muscles, respectively. After salbutamol histamine induced ETIA was reduced to about one quarter of pre-salbutamol values. FRC increased by 427 ml as a result of inhalation of histamine, but after salbutamol this increase was only 53 ml. The data for ETIA and FRC were interpreted as indicating that the contributions of airflow limitation and ETIA to histamine induced hyperinflation are comparable. Histamine is a forceful stimulus for inducing ETIA. Both chemical and mechanical stimulation of airway receptors contribute to evoke ETIA, of which the contribution of mechanical stimulation is the more important one. ETIA contributes substantially to histamine induced hyperinflation.

Ventilatory effects of high and pulsatile blood flow in the pulmonary circulation

The mechanism of ventilatory stimulation that accompanies increases in cardiac output is unknown. Previous studies addressing this issue have been inconclusive. However, only steady pulmonary blood flow was used. The effect of flow pulsatility merits consideration, because increasing cardiac output raises not only mean pulmonary arterial pressure but also pulse pressure; mechanoreceptors with an important dynamic component to their responses may cause a response to pulsatile, but not steady, flow. Studies were done on anesthetized cats (n = 4) and dogs (n = 4). The right pulmonary artery was cannulated within the pericardium, and systemic blood was pumped from the left atrium to the right pulmonary artery. The right pulmonary circulation was perfused at different levels of flow, which was either steady or pulsatile. Steady-state flow of up to 150 ml.kg-1.min-1 (270 ml.kg-1.min-1 when corrected for the proportion of lung tissue perfused) did not affect breathing pattern. When high pulmonary flow was made pulsatile (pulse pressure approximately 23 mmHg), breath duration decreased from 3.7 +/- 0.72 to 3.4 +/- 0.81 (SD) s (P less than 0.01), representing a change in frequency of only 9%. There was no change in peak inspiratory activity. It was concluded that pulmonary vascular mechanoreceptors are not likely to contribute significantly to the increase in ventilation in association with increases in cardiac output.

Regulation of upper airway maintaining muscles during progressive asphyxia.

The electromyographic activity of an upper airway muscle (genioglossus, GG) and the diaphragm were studied in 10 adult and three young anesthetized rabbits during progressive asphyxia induced by airway occlusion. Results were similar for both age groups. Peak inspiratory activity of GG muscle increased more than that of the diaphragm during both the hyperpnea and gasping (P less than 0.05). The increase in GG activity during gasping was not significantly different from that during hyperpnea even though an important stimulus, arousal, was absent during gasping. During end stage asphyxia, as the strength of gasps grew weaker, the rate of loss of GG muscle activity was greater than that of the diaphragm. However, GG activity remained greater than that of the diaphragm at the time of the last spontaneous gasp. As asphyxia progressed, inspiratory duration and the inspiratory contour of integrated electromyogram activity of both muscles changed. These data indicate differences in the control mechanism of the genioglossus and diaphragm during acute severe asphyxia. Increased upper airway muscle activity seen during gasping should help preserve upper airway patency and facilitate autoresuscitation by gasping. These observations of coordinated changes in timing and activity of two functionally different respiratory muscles support the concept that gasping is a highly organized function of the respiratory centers.

Effects of hypocapnia on respiratory timing and inspiratory activities of the superior laryngeal, hypoglossal, and phrenic nerves in the vagotomized rat.

Effects of acute hypocapnia on respiratory timing (inspiratory and expiratory times (TI, TE) ) and on inspiratory activities of the efferent superior laryngeal (Xs1), hypoglossal (XII), and phrenic (Phr) nerves were studied in artificially ventilated vagotomized, and anesthetized rats. Hyperventilation induced a decrease in respiratory frequency exclusively due to prolongation of TE and resulted in expiratory apnea. Inspiratory activities of three nerves decreased with reduction in CO2 concentration of end-tidal gas (FETCO2), and disappeared simultaneously at a threshold FETCO2 for apnea. The decrease in the peak inspiratory activity by hypocapnia was larger in the XII than in the Phr or Xs1 nerve (XII greater than Phr greater than Xs1). The results suggest that the CO2 stimulus (mainly via a central chemosensor) plays an important role in the process of terminating expiration or of expiratory-inspiratory phase switching and that the responses of the XII or Xs1 motoneurons to variation in CO2 stimulus differ from that of the Phr motoneurons (or of the Phr driving medullary neurons). A possible functional significance of these observations is discussed.

Influence of upper airway pressure changes on genioglossus muscle respiratory activity.

The effects of change in pharyngeal airway pressure on electromyographic (EMG) activity of a pharyngeal dilating muscle (genioglossus) were investigated in 20 anesthetized rabbits. In vagotomized animals, upper airway loading maneuvers (nasal occlusion) increased the peak inspiratory activity of the genioglossus (GG) muscle on the first occluded breath. In contrast, "unloading" maneuvers (switching from nose to tracheostomy breathing) decreased GG activity. To further characterize the GG response, sustained pressure changes were produced within the isolated upper airway. Negative pressure increased GG activity; positive pressure decreased it. A poststimulus effect consisting of increased GG activity compared with control was seen following both negative- and positive-pressure stimuli. Cyclical pressure changes applied to the isolated upper airway increased the GG activity. These observations indicate the presence of reflex pathways that regulate GG muscle activity in response to upper airway pressure loads. This reflex system appears to play a role in regulating GG activity during tidal breathing and could be important in ensuring pharyngeal airway patency.

Roles of vagal afferents on discharge patterns and CO2-responsiveness of efferent superior laryngeal, hypoglossal, and phrenic respiratory activities in anesthetized rats.

Discharge patterns and CO2-responsiveness of the efferent respiratory activities in the superior laryngeal (Xsl), hypoglossal (XII), and phrenic (Phr) nerves were compared between vagi-intact and -denervated rats. Bilateral cervical vagotomy decreased the respiratory frequency (f), minute Phr activity (peak integrated Phr activity X f) and consequently elevated end-tidal PCO2 (PETCO2). Augmentation of the peak inspiratory activity following vagotomy was much larger in the Xsl and XII nerves than that in the Phr nerve. After vagotomy, the time delay from the onset of inspiratory activities in the Xsl or XII nerve to the onset of the Phr bursts was greatly prolonged. While in the vagi-intact rats the peak inspiratory activities of these cranial nerves were not increased in response to elevated PETCO2, the activities, in particular of the XII nerve, were augmented by high PETCO2 in the absence of vagal afferents. These results suggested that the vagal afferents inhibit not only phasic Phr discharges but also inspiratory output neurons in the Xsl or XII motor nuclei being activated in normo- and hypercapnia and that they facilitate temporally the onset and progress of inspiratory activities in various groups of respiratory output neurons.

Diaphragmatic EMG in studies of inspiratory "off-switch" threshold in humans.

Diaphragmatic EMG (EMGdi) analyzed as a moving time average and quantitated as peak inspiratory activity $$\left( {\bar X_p } \right)$$ was used with tidal volume (V T)to assess the changes in inspiratory “of-switch” threshold in six normal subjects during three CO2 rebreathing experiments performed on different days. The qualitative characteristics ofV Tvs inspiratory time (T)Iwere not reproducible andV Tshowed poor linear correlation with 1/T Iduring range 2 (Meanr=0.54±0.24) whereas, the qualitative characteristics of $$\left( {\bar X_p } \right)$$ vsT Irelationship showed good reproducibility and during range 2, $$\left( {\bar X_p } \right)$$ correlated better with 1/T I(Meanr=0.81±0.20) thanV T.In each runV Tresponse to increasing CO2 eventually flattened afterV Treached its maximum in spite of continuing increase in $$\left( {\bar X_p } \right)$$ giving rise to a plateau ofV Tvs $$\left( {\bar X_p } \right)$$ relationship. We suggest that $$\left( {\bar X_p } \right)$$ is a better index of inspiratory “off-switch” threshold thanV Twhich seems to be dependent on mechanical factors in addition to neural modification ofT Iduring CO2 rebreathing in humans.