Geniohyoid muscle function in awake canines.

The geniohyoid (Genio) upper airway muscle shows phasic, inspiratory electrical activity in awake humans but no activity and lengthening in anesthetized cats. There is no information about the mechanical action of the Genio, including length and shortening, in any awake, nonanesthetized mammal during respiration (or swallowing). Therefore, we studied four canines, mean weight 28.8 kg, 1.5 days after Genio implantation with sonomicrometry transducers and bipolar electromyogram (EMG) electrodes. Awake recordings of breathing pattern, muscle length and shortening, and EMG activity were made with the animal in the right lateral decubitus position during quiet resting, CO2-stimulated breathing, inspiratory-resisted breathing (80 cmH2O. l-1. s), and airway occlusion. Genio length and activity were also measured during swallowing, when it shortened, showing a 9.31% change from resting length, and its EMG activity increased 6.44 V. During resting breathing, there was no phasic Genio EMG activity at all, and Genio showed virtually no movement during inspiration. During CO2-stimulated breathing, Genio showed minimal lengthening of only 0.07% change from resting length, whereas phasic EMG activity was still absent. During inspiratory-resisted breathing and airway occlusion, Genio showed phasic EMG activity but still lengthened. We conclude that the Genio in awake, nonanesthetized canines shows active contraction and EMG activity only during swallowing. During quiet or stimulated breathing, Genio is electrically inactive with passive lengthening. Even against resistance, Genio is electrically active but still lengthens during inspiration.     

Respiratory muscle electromyogram responses to acute hypoxia in awake ponies

We determined the effect of acute hypoxia on the ventilatory (VE) and electromyogram (EMG) responses of inspiratory (diaphragm) and expiratory (transversus abdominis) muscles in awake spontaneously breathing ponies. Eleven carotid body-intact (CBI) and six chronic carotid body-denervated (CBD) ponies were studied during normoxia (fractional inspired O2 concn [FIO2] = 0.21) and two levels of hypoxia (FIO2 approximately 0.15 and 0.12; 6-10 min/period). Four CBI and five CBD ponies were also hilar nerve (pulmonary vagal) denervated. Mean VE responses to hypoxia were greater in CBI ponies (delta arterial PCO2 = -4 and -7 Torr in CBI during hypoxic periods; -1 and -2 Torr in CBD). Hypoxia increased the rate of rise and mean activity of integrated diaphragm EMG in CBI (P less than 0.05) and CBD (P greater than 0.05) ponies relative to normoxia. Duration of diaphragm activity was reduced in CBI (P less than 0.05) but unchanged in CBD ponies. During hypoxia in both groups of ponies, total and mean activities per breath of transversus abdominis were reduced (P less than 0.05) without a decrease in rate of rise in activity. Time to peak and total duration of transversus abdominis activity were markedly reduced by hypoxia in CBI and CBD ponies (P less than 0.05). Hilar nerve denervation did not alter the EMG responses to hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyroarytenoid muscle activity during hypoxia in awake lambs

It is generally accepted that hypoxia in early life results in active laryngeal braking of expiratory airflow via the recruitment of glottic adductor muscles. We examined the electromyogram expiratory activity of the thyroarytenoid muscle in seven 11- to 18-day-old awake nonsedated lambs exposed to an inspired O2 fraction of 0.08 for 18 min. The lambs breathed through a face mask and a pneumotachograph. During baseline prehypoxic breathing, the thyroarytenoid muscle was largely inactive in each awake lamb. Unexpectedly, no recruitment of the thyroarytenoid muscle was recorded during hypoxia in any of the seven lambs; simultaneous examination of the flow-volume curves revealed an absence of expiratory airflow braking. Also unexpectedly, marked expiratory activity of the thyroarytenoid muscle was recorded, with each expiration occurring within less than 10 s after the return to room air. The resulting delay of expiration was apparent in the flow-volume loops. Thus, in awake 11- to 18-day-old lambs, 1) active expiratory glottic adduction is absent during hypoxia and 2) a return from hypoxia to room air results in prolonged expiration as well as active glottic adduction that controls end-expiratory lung volume.     

Respiratory muscle function during CO2 rebreathing with inspiratory flow-resistive loading

We investigated the respiratory muscle contribution to inspiratory load compensation by measuring diaphragmatic and intercostal electromyograms (EMGdi and EMGic), transdiaphragmatic pressure (Pdi), and thoracoabdominal motion during CO2 rebreathing with and without 15 cmH2O X l-1 X s inspiratory flow resistance (IRL) in normal sitting volunteers. During IRL compared with control, Pdi measured during airflow and during airway occlusion increased for a given change in CO2 partial pressure and EMGdi, and there was a greater decrease in abdominal (AB) end expiratory anteroposterior dimensions with increased expiratory gastric pressure (Pga), this leading to an inspiratory decline in Pga with outward AB movement, indicating a passive component to the descent of the abdomen-diaphragm. The response of EMGic to IRL was similar to that of EMGdi, though rib cage (RC)-Pga plots did infer intercostal muscle contribution. We conclude that during CO2 rebreathing with IRL there is improved diaphragmatic neuromuscular coupling, the prolongation of inspiration promoting a force-velocity advantage, and increased AB action serving to optimize diaphragm length and configuration, as well as to provide its own passive inspiratory action. Intercostal action provides increased assistance also. Therefore, compensation for inspiratory resistive loads results from the combined and integrated effort of all respiratory muscle groups.     

Respiratory muscle control during vomiting

The changes in thoracic and abdominal pressure that generate vomiting are produced by coordinated action of the major respiratory muscles. During vomiting, the diaphragm and external intercostal (inspiratory) muscles co-contract with abdominal (expiratory) muscles in a series of bursts of activity that culminates in expulsion. Internal intercostal (expiratory) muscles contract out of phase with these muscles during retching and are inactive during expulsion. The periesophageal portion of the diaphragm relaxes during expulsion, presumably facilitating rostral movement of gastric contents. Recent studies have begun to examine to what extent medullary respiratory neurons are involved in the control of these muscles during vomiting. Bulbospinal expiratory neurons in the ventral respiratory group caudal to the obex discharge at the appropriate time during (fictive) vomiting to activate either abdominal or internal intercostal motoneurons. The pathways that drive phrenic and external intercostal motoneurons during vomiting have yet to be identified. Most bulbospinal inspiratory neurons in the dorsal and ventral respiratory groups do not have the appropriate response pattern to initiate activation of these motoneurons during (fictive) vomiting. Relaxation of the periesophageal diaphragm during vomiting could be brought about, at least in part, by reduced firing of bulbospinal inspiratory neurons.     

Respiratory changes in thoracic muscle length during bronchoconstriction

The purpose of the present study was to assess the effects of bronchoconstriction on respiratory changes in length of the costal diaphragm and the parasternal intercostal muscles. Ten dogs were anesthetized with pentobarbital sodium and tracheostomized. Respiratory changes in muscle length were measured using sonomicrometry, and electromyograms were recorded with bipolar fine-wire electrodes. Administration of histamine aerosols increased pulmonary resistance from 6.4 to 14.5 cmH2O X l-1 X s, caused reductions in inspiratory and expiratory times, and decreased tidal volume. The peak and rate of rise of respiratory muscle electromyogram (EMG) activity increased significantly after histamine administration. Despite these increases, bronchoconstriction reduced diaphragm inspiratory shortening in 9 of 10 dogs and reduced intercostal muscle inspiratory shortening in 7 of 10 animals. The decreases in respiratory muscle tidal shortening were less than the reductions in tidal volume. The mean velocity of diaphragm and intercostal muscle inspiratory shortening increased after histamine administration but to a smaller extent than the rate of rise of EMG activity. This resulted in significant reductions in the ratio of respiratory muscle velocity of shortening to the rate of rise of EMG activity after bronchoconstriction for both the costal diaphragm and the parasternal intercostal muscles. Bronchoconstriction changed muscle end-expiratory length in most animals, but for the group of animals this was statistically significant only for the diaphragm. These results suggest that impairments of diaphragm and parasternal intercostal inspiratory shortening occur after bronchoconstriction; the mechanisms involved include an increased load, a shortening of inspiratory time, and for the diaphragm possibly a reduction in resting length.     

Respiratory muscle reserve in rats during heavy exercise

Gosselin, Luc E., David Megirian, Joshua Rodman, DonnaMueller, and Gaspar A. Farkas. Respiratory muscle reserve in ratsduring heavy exercise. J. Appl.Physiol. 83(4): 1405-1409, 1997.The extent towhich the respiratory pump muscles limit maximal aerobic capacity inquadrupeds is not entirely clear. To examine the effect of reducedrespiratory muscle reserve on aerobic capacity, whole bodypeak oxygen consumption(O_{2 peak}) wasmeasured in healthy Sprague-Dawley rats before and after Sham,unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery.O_{2 peak} wasdetermined by using a graded treadmill running test.Hemidiaphragm paralysis was verified after testing byrecording the absence of electromyographic activity duringinspiration. Before surgery, O_{2 peak} averaged 86, 87, and 92 ml · kg¹ · min¹for the Sham, unilateral, and bilateral Dnv groups, respectively. Twoweeks after surgery, there was no significant change inO_{2 peak} foreither the Sham or unilateral Dnv group. However,O_{2 peak} decreased~19% in the bilateral Dnv group 2 wk after surgery. These findingsstrongly suggest that the pulmonary system in rats is designed suchthat during heavy exercise, the remaining respiratory pump muscles areable to compensate for the loss of one hemidiaphragm, but not of both.

     

Respiratory muscle activity during repeated airflow interruption

We observed striking differences in respiratory muscle electromyogram activity when active expirations were interrupted in rapid succession, depending on the mode of interruption. When the interruptions were produced at the level of the glottis (utterances, uh-uh-uh-uh, at 5-8 Hz) there were synchronous bursts of activity from expiratory muscles in all three subjects during the periods of no flow and rapid bursts of diaphragmatic activity during the flow phases in one subject. In contrast, when similarly rapid interruptions of active expirations were produced with the tongue on a mouthpiece (utterance, te-te-te-te) or with an external valve, no synchronous bursts were observed. Since all interruptions would have been mechanically similar at expiratory muscular and pulmonary levels, we reasoned that the bursts with glottic interruptions were either programmed centrally or driven reflexly at the laryngeal level.     

Postinspiratory activity of the parasternal and external intercostal muscles in awake canines.

Previous studies have shown in awake dogs that activity in the crural diaphragm, but not in the costal diaphragm, usually persists after the end of inspiratory airflow. It has been suggested that this difference in postinspiratory activity results from greater muscle spindle content in the crural diaphragm. To evaluate the relationship between muscle spindles and postinspiratory activity, we have studied the pattern of activation of the parasternal and external intercostal muscles in the second to fourth interspaces in eight chronically implanted animals. Recordings were made on 2 or 3 successive days with the animals breathing quietly in the lateral decubitus position. The two muscles discharged in phase with inspiration, but parasternal intercostal activity usually terminated with the cessation of inspiratory flow, whereas external intercostal activity persisted for 24.7 +/- 12.3% of inspiratory time (P < 0.05). Forelimb elevation in six animals did not affect postinspiratory activity in the parasternal but prolonged postinspiratory activity in the external intercostal to 45.4 +/- 16.3% of inspiratory time (P < 0.05); in two animals, activity was still present at the onset of the next inspiratory burst. These observations support the concept that muscle spindles are an important determinant of postinspiratory activity. The absence of such activity in the parasternal intercostals and costal diaphragm also suggests that the mechanical impact of postinspiratory activity on the respiratory system is smaller than conventionally thought.