Parasternal Intercostal Muscles Research Articles

Effect of acute inflation on the mechanics of the inspiratory muscles

When the lung is inflated acutely, the capacity of the diaphragm to generate pressure, in particular pleural pressure (Ppl), is impaired because the muscle during contraction is shorter and generates less force. At very high lung volumes, the pressure-generating capacity of the diaphragm may be further reduced by an increase in the muscle radius of curvature. Lung inflation similarly impairs the pressure-generating capacity of the inspiratory intercostal muscles, both the parasternal intercostals and the external intercostals. In contrast to the diaphragm, however, this adverse effect is largely related to the orientation and motion of the ribs, rather than the ability of the muscles to generate force. During combined activation of the two sets of muscles, the change in Ppl is larger than during isolated diaphragm activation, and this added load on the diaphragm reduces the shortening of the muscle and increases muscle force. In addition, activation of the diaphragm suppresses the cranial displacement of the passive diaphragm that occurs during isolated intercostal contraction and increases the respiratory effect of the intercostals. As a result, the change in Ppl generated during combined diaphragm-intercostal activation is greater than the sum of the pressures generated during separate muscle activation. Although this synergistic interaction becomes particularly prominent at high lung volumes, lung inflation, either bilateral or unilateral, places a substantial stress on the inspiratory muscle pump.

Effect of salbutamol on respiratory muscle function and ventilation in awake canines

The effect of the beta-agonist bronchodilator salbutamol on respiratory muscles and ventilation is uncertain. The presence of beta2 receptors on skeletal muscles and increased diaphragm contractility in vitro with salbutamol predict a significant effect that has not been confirmed, in vivo in non-fatigued diaphragm or in clinical studies using standard bronchodilator dosages. Therefore, we infused salbutamol at a higher dosage (23.3 microg/min) used clinically for treatment of respiratory emergencies, while measuring directly the length, shortening and EMG activation of costal and crural diaphragm, parasternal intercostal and transversus abdominis muscles, in 10 awake canines. At this salbutamol dosage, ventilation and tidal volume increased significantly during both resting and CO2-stimulated breathing. Salbutamol elicited significant increases in respiratory muscle shortening with much smaller increases in EMG activity, so the proportionally greater muscle shortening per unit EMG showed increased muscle contractility. The effects of salbutamol were not extinguished by inspiratory flow resistance or fluid challenge but were reversed specifically by the beta-blocker, propranolol. This study demonstrates that, in sufficient intravenous dosage, the beta-agonist salbutamol elicits increased ventilation and a beta2 receptor-mediated increase in contractility of respiratory muscles.

The output from human inspiratory motoneurone pools

Survival requires adequate pulmonary ventilation which, in turn, depends on adequate contraction of muscles acting on the chest wall in the presence of a patent upper airway. Bulbospinal outputs projecting directly and indirectly to 'obligatory' respiratory motoneurone pools generate the required muscle contractions. Recent studies of the phasic inspiratory output of populations of single motor units to five muscles acting on the chest wall (including the diaphragm) reveal that the time of onset, the progressive recruitment, and the amount of motoneuronal drive (expressed as firing frequency) differ among the muscles. Tonic firing with an inspiratory modulation of firing rate is common in low intercostal spaces of the parasternal and external intercostal muscles but rare in the diaphragm. A new time and frequency plot has been developed to depict the behaviour of the motoneurone populations. The magnitude of inspiratory firing of motor unit populations is linearly correlated to the mechanical advantage of the intercostal muscle region at which the motor unit activity is recorded. This represents a 'neuromechanical' principle by which the CNS controls motoneuronal output according to mechanical advantage, presumably in addition to the Henneman's size principle of motoneurone recruitment. Studies of the genioglossus, an obligatory upper airway muscle that helps maintain airway patency, reveal that it receives simultaneous inspiratory, expiratory and tonic drives even during quiet breathing. There is much to be learned about the neural drive to pools of human inspiratory and expiratory muscles, not only during respiratory tasks but also in automatic and volitional tasks, and in diseases that alter the required drive.

Aminophylline increases parasternal intercostal muscle activity during hypoxia in humans

To clarify the mechanism of action of aminophylline on the hypoxic ventilatory response in humans, we analyzed the effects of aminophylline on respiratory neural output. To evaluate the respiratory neural output, we analyzed the electromyogram (EMG) of the parasternal intercostal muscle, one of the major inspiratory muscles, in eight healthy subjects. Both before and during aminophylline administration, measurements of ventilatory parameters with EMG recordings were conducted in room air, mild hypoxia (F(I)(o)(2) 0.15), and severe hypoxia (F(I)(o)(2) 0.11). Before administering aminophylline, hypoxic stimulation elicited ventilatory augmentation in a hypoxia-intensity dependent manner. Administration of aminophylline caused significant increases in ventilation (V (I)), tidal volume (V(T)), respiratory frequency (f(R)), and the respiration-related phasic moving averaged EMG amplitude (tidal EMG), at corresponding levels of hypoxia compared to before aminophylline. Augmentation patterns of hypoxia-induced increases in V(T) and tidal EMG showed close similarity. These results indicate that augmentation of hypoxic ventilatory response by aminophylline is mainly mediated by an increase in the respiratory neural drive in healthy humans.

Role of pleural pressure in the coupling between the intercostal muscles and the ribs

The inspiratory intercostal muscles elevate the ribs and thereby elicit a fall in pleural pressure (DeltaPpl) when they contract. In the present study, we initially tested the hypothesis that this DeltaPpl does, in turn, oppose the rib elevation. The cranial rib displacement (Xr) produced by selective activation of the parasternal intercostal muscle in the fourth interspace was measured in dogs, first with the rib cage intact and then after DeltaPpl was eliminated by bilateral pneumothorax. For a given parasternal contraction, Xr was greater after pneumothorax; the increase in Xr per unit decrease in DeltaPpl was 0.98+/-0.11 mm/cmH2O. Because this relation was similar to that obtained during isolated diaphragmatic contraction, we subsequently tested the hypothesis that the increase in Xr observed during breathing after diaphragmatic paralysis was, in part, the result of the decrease in DeltaPpl, and the contribution of the difference in DeltaPpl to the difference in Xr was determined by using the relation between Xr and DeltaPpl during passive inflation. With diaphragmatic paralysis, Xr during inspiration increased approximately threefold, and 47+/-8% of this increase was accounted for by the decrease in DeltaPpl. These observations indicate that 1) DeltaPpl is a primary determinant of rib motion during intercostal muscle contraction and 2) the decrease in DeltaPpl and the increase in intercostal muscle activity contribute equally to the increase in inspiratory cranial displacement of the ribs after diaphragm paralysis.

Dysfunction of the canine respiratory muscle pump in ascites

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial PCO2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.

To breathe or not to breathe: the respiratory muscles and COPD

The respiratory muscles are unique among skeletal muscles in that they are required to work without sustained rest throughout life. It is not surprising, therefore, that the ventilatory pump has been the subject of intense investigation over the past 30 years, with particular interest in the ability

Differential activation among five human inspiratory motoneuron pools during tidal breathing

Neural drive to inspiratory pump muscles is increased under many pathological conditions. This study determined for the first time how neural drive is distributed to five different human inspiratory pump muscles during tidal breathing. The discharge of single motor units (n = 280) from five healthy subjects in the diaphragm, scalene, second parasternal intercostal, third dorsal external intercostal, and fifth dorsal external intercostal was recorded with needle electrodes. All units increased their discharge during inspiration, but 41 (15%) discharged tonically throughout expiration. Motor unit populations from each muscle differed in the timing of their activation and in the discharge rates of their motor units. Relative to the onset of inspiratory flow, the earliest recruited muscles were the diaphragm and third dorsal external intercostal (mean onset for the population after 26 and 29% of inspiratory time). The fifth dorsal external intercostal muscle was recruited later (43% of inspiratory time; P < 0.05). Compared with the other inspiratory muscles, units in the diaphragm and third dorsal external intercostal had the highest onset (7.7 and 7.1 Hz, respectively) and peak firing frequencies (12.6 and 11.9 Hz, respectively; both P < 0.05). There was a unimodal distribution of recruitment times of motor units in all muscles. Neural drive to human inspiratory pump muscles differs in timing, strength, and distribution, presumably to achieve efficient ventilation.

Effect of diaphragmatic contraction on the action of the canine parasternal intercostals

The inspiratory intercostal muscles enhance the force generated by the diaphragm during lung expansion. However, whether the diaphragm also alters the force developed by the inspiratory intercostals is unknown. Two experiments were performed in dogs to answer the question. In the first experiment, external, cranially oriented forces were applied to the different rib pairs to assess the effect of diaphragmatic contraction on the coupling between the ribs and the lung. The fall in airway opening pressure (deltaPa(O)) produced by a given force on the ribs was invariably greater during phrenic nerve stimulation than with the diaphragm relaxed. The cranial rib displacement (Xr), however, was 40-50% smaller, thus indicating that the increase in deltaPa(O) was exclusively the result of the increase in diaphragmatic elastance. In the second experiment, the parasternal intercostal muscle in the fourth interspace was selectively activated, and the effects of diaphragmatic contraction on the deltaPa(O) and Xr caused by parasternal activation were compared with those observed during the application of external loads on the ribs. Stimulating the phrenic nerves increased the deltaPa(O) and reduced the Xr produced by the parasternal intercostal, and the magnitudes of the changes were identical to those observed during external rib loading. It is concluded, therefore, that the diaphragm has no significant synergistic or antagonistic effect on the force developed by the parasternal intercostals during breathing. This lack of effect is probably related to the constraint imposed on intercostal muscle length by the ribs and sternum.

Parasternal intercostal muscle remodeling in severe chronic obstructive pulmonary disease

Studies in experimental animals indicate that chronic increases in neural drive to limb muscles elicit a fast-to-slow transformation of fiber-type proportions and myofibrillar proteins. Since neural drive to the parasternal intercostal muscles (parasternals) is chronically increased in patients with severe chronic obstructive pulmonary diseases (COPDs), we carried out the present study to test the hypothesis that the parasternals of COPD patients exhibit an increase in the proportions of both slow fibers and slow myosin heavy chains (MHCs). Accordingly, we obtained full thickness parasternal muscle biopsies from the third interspace of seven COPD patients (mean +/- SE age: 59 +/- 4 yr) and seven age-matched controls (AMCs). Fiber typing was done by immunohistochemistry, and MHC proportions were determined by SDS-PAGE followed by densitometry. COPD patients exhibited higher proportions of slow fibers than AMCs (73 +/- 4 vs. 51 +/- 3%; P < 0.01). Additionally, COPD patients exhibited higher proportions of slow MHC than AMCs (56 +/- 4 vs. 46 +/- 4%, P < 0.04). We conclude that the parasternal muscles of patients with severe COPD exhibit a fast-to-slow transformation in both fiber-type and MHC proportions. Previous workers have demonstrated that remodeling of the external intercostals, another rib cage inspiratory muscle, elicited by severe COPD is characterized by a slow-to-fast transformation in both fiber types and MHC isoform proportions. The physiological significance of this difference in remodeling between these two inspiratory rib cage muscles remains to be elucidated.

Spatial distribution of inspiratory drive to the parasternal intercostal muscles in humans

The human parasternal intercostal muscles are obligatory inspiratory muscles with a diminishing mechanical advantage from cranial to caudal interspaces. This study determined whether inspiratory neural drive to these muscles is graded, and whether this distribution matches regional differences in inspiratory mechanical advantage. To determine the neural drive, intramuscular EMG was recorded from the first to the fifth parasternal intercostals during resting breathing in six subjects. All interspaces showed phasic inspiratory activity but the onset of activity relative to inspiratory flow in the fourth and fifth spaces was delayed compared with that in cranial interspaces. Activity in the first, second and third interspaces commenced, on average, within the first 10% of inspiratory time, and sometimes preceded inspiratory airflow. In contrast, activity in the fourth and fifth interspaces began after an average 33% of inspiratory time. The peak inspiratory discharge frequency of motor units in the first interspace averaged 13.4 +/- 1.0 Hz (mean +/- s.e.m.) and was significantly greater than in all other interspaces, in particular in the fifth space (8.0 +/- 1.0 Hz). Phasic inspiratory activity was sometimes superimposed on tonic activity. In the first interspace, only 3% of units had tonic firing, but this proportion increased to 34% in the fifth space. In five subjects, recordings were also made from the medial and lateral extent of the second parasternal intercostal. Both portions showed phasic inspiratory activity which began within the first 6% of inspiratory time. Motor units from the lateral and medial portions fired at the same peak discharge rate (10.4 +/- 0.7 versus 10.7 +/- 0.6 Hz). These observations indicate that the distribution of neural drive to the parasternal intercostals in humans has a rostrocaudal gradient, but that the drive is uniform along the mediolateral extent of the second interspace. The distribution of inspiratory neural drive to the parasternal intercostals parallels the spatial distribution of inspiratory mechanical advantage, while tonic activity was higher where mechanical advantage was lower.

Brief Airway Occlusion Produces Prolonged Reflex Inhibition of Inspiratory Muscles in Obstructive Sleep Apnea

The human inspiratory muscles respond to a brief occlusion of the upper airway during inspiration with a profound short-latency reflex inhibition. This inhibition contrasts with the excitatory stretch reflex of limb muscles and may protect the airway from aspiration. It was postulated that this reflex would be altered in subjects with obstructive sleep apnea (OSA) who have repetitive upper airway occlusion. Subjects underwent overnight polysomnography, as well as muscle reflex studies. For the reflex studies (performed during wakefulness), occlusions lasting 250 milliseconds were delivered during inspiration. Surface electromyogram was recorded over the scalenes, parasternal intercostals, and chest wall (overlying diaphragm). Research and sleep laboratories. Nineteen subjects with untreated OSA (9 moderate and 10 severe) and 9 healthy control subjects. In the subjects with severe OSA, the duration of the inhibition was prolonged by at least 25% compared with control subjects. The peak of the inhibitory response for scalenes occurred significantly later for subjects with severe OSA than for control subjects (by 76 +/- 5 ms vs 60 +/- 3 ms [mean +/- SEM], respectively). Onset latencies of the later excitatory response were delayed for scalenes, parasternal intercostals, and chest wall recordings (eg, scalenes: 105 +/- 9 ms for subjects with severe OSA vs 83 +/- 5 ms for control subjects). The latency of peak inhibition and duration of inhibition were positively correlated with the respiratory disturbance index for all muscle groups. These changes may reflect adaptation in central respiratory paths due to repetitive loading during sleep.

Respiratory activity in scalene muscle of the rabbit. An artefact?

Unlike in the human, it has been shown in the dog that inspiratory EMG activity in scalene arise from underlying muscle layers. We tested here the origin of the activity recorded from this muscle in rabbit, hypothesizing that the presence of an EMG activity could reflect a higher mechanical advantage in that species. In 6 anaesthetized NewZeeland rabbits, EMG activity was obtained from anterior (ASc) and posterior (PSc) parts of the scalene, from the sternomastoïd (SM) and from the parasternal intercostal (PS). These activities were recorded during resting breathing and against increased inspiratory resistive loads: in control, after denervation of scalene and after an additional insulation from underlying layers. At rest, PS, ASc and 4 of 6 PSc showed an activity; with mechanical loads, a huge increase in EMG integrated signal was observed in every muscles except SM that remained invariably silent. After denervation, EMG activity decreased consistently in ASc (residual activity: 34 ± 9 % with the highest load). In PSc, the activity decreased to 19 ± 8 % in 3 animals but remained stable in the others. After insulation, the residual signal was very limited (4 % in ASc and 2% in PSc). Based on pictures taken at FRC and after a passive inflation of the chest, fractional changes in length of the different muscles were measured to evaluate their mechanical advantage. In mean, the change in length was 8.4 ± 0.7 %, 8.0 ± 0.8 %, 5.3 ± 0.6 % and 3.2 ± 0.2 % of the length at FRC for PS, ASc, PSc and SM, respectively. This suggests that from species to species, a given portion of a muscle maintains an activity during breathing according to its mechanical advantage.

The effect of lung inflation on the inspiratory action of the canine parasternal intercostals

Inflation induces a marked decrease in the lung-expanding ability of the diaphragm, but its effect on the parasternal intercostal muscles is uncertain. To assess this effect, the phrenic nerves and the external intercostals were severed in anesthetized, vagotomized dogs, such that the parasternal intercostals were the only muscles active during inspiration, and the endotracheal tube was occluded at different lung volumes. Although the inspiratory electromyographic activity recorded from the muscles was constant, the change in airway opening pressure decreased with inflation from -7.2+/-0.6 cmH2O at functional residual capacity to -2.2+/-0.2 cmH2O at 20-cmH2O transrespiratory pressure (P<0.001). The inspiratory cranial displacement of the ribs remained virtually unchanged, and the inspiratory caudal displacement of the sternum decreased moderately. However, the inspiratory outward rib displacement decreased markedly and continuously; at 20 cmH2O, this displacement was only 23+/-2% of the value at functional residual capacity. Calculations based on this alteration yielded substantial decreases in the change in airway opening pressure. It is concluded that, in the dog, 1) inflation affects adversely the lung-expanding actions of both the parasternal intercostals and the diaphragm; and 2) the adverse effect of inflation on the parasternal intercostals is primarily related to the alteration in the kinematics of the ribs. As a corollary, it is likely that hyperinflation also has a negative impact on the parasternal intercostals in patients with chronic obstructive pulmonary disease.

Respiratory Action of the Intercostal Muscles

The mechanical advantages of the external and internal intercostals depend partly on the orientation of the muscle but mostly on interspace number and the position of the muscle within each interspace. Thus the external intercostals in the dorsal portion of the rostral interspaces have a large inspiratory mechanical advantage, but this advantage decreases ventrally and caudally such that in the ventral portion of the caudal interspaces, it is reversed into an expiratory mechanical advantage. The internal interosseous intercostals in the caudal interspaces also have a large expiratory mechanical advantage, but this advantage decreases cranially and, for the upper interspaces, ventrally as well. The intercartilaginous portion of the internal intercostals (the so-called parasternal intercostals), therefore, has an inspiratory mechanical advantage, whereas the triangularis sterni has a large expiratory mechanical advantage. These rostrocaudal gradients result from the nonuniform coupling between rib displacement and lung expansion, and the dorsoventral gradients result from the three-dimensional configuration of the rib cage. Such topographic differences in mechanical advantage imply that the functions of the muscles during breathing are largely determined by the topographic distributions of neural drive. The distributions of inspiratory and expiratory activity among the muscles are strikingly similar to the distributions of inspiratory and expiratory mechanical advantages, respectively. As a result, the external intercostals and the parasternal intercostals have an inspiratory function during breathing, whereas the internal interosseous intercostals and the triangularis sterni have an expiratory function.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis.

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (DeltaPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate DeltaPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to DeltaPpl and the force generated by the intact hemidiaphragm.

Reflex inhibition of human inspiratory muscles in response to contralateral phrenic nerve stimulation

In animals, high-intensity unilateral stimulation of the phrenic nerve results in short-latency inhibition of phrenic and intercostal nerve activity bilaterally. This study provides the first demonstration in human subjects of a short-latency inhibitory response in the contralateral scalene, parasternal intercostal and diaphragm muscles to single stimuli delivered at cervical level to the phrenic nerve. Electromyographic (EMG) responses were recorded with intramuscular and surface electrodes. An inhibitory response with an onset latency of approximately 35 ms followed by a long-latency excitatory response at approximately 100 ms were observed in the three inspiratory muscles. The inhibition was evident in single trials, averaged EMG, histograms of the discharge of single motor units, and even when the phrenic nerve stimulus intensity was relatively low. Thus, the inhibition may be mediated by large-diameter muscle afferents. The latency of this potent inhibitory response to contralateral phrenic nerve stimulation is too long to be mediated via a simple spinal circuit and may involve a brainstem projection.

Respiratory effects of the scalene and sternomastoid muscles in humans.

Previous studies have shown that in normal humans the change in airway opening pressure (DeltaPao) produced by all the parasternal and external intercostal muscles during a maximal contraction is approximately -18 cmH(2)O. This value is substantially less negative than DeltaPao values recorded during maximal static inspiratory efforts in subjects with complete diaphragmatic paralysis. In the present study, therefore, the respiratory effects of the two prominent inspiratory muscles of the neck, the sternomastoids and the scalenes, were evaluated by application of the Maxwell reciprocity theorem. Seven healthy subjects were placed in a computed tomographic scanner to determine the fractional changes in muscle length during inflation from functional residual capacity to total lung capacity and the masses of the muscles. Inflation induced greater shortening of the scalenes than the sternomastoids in every subject. The inspiratory mechanical advantage of the scalenes thus averaged (mean +/- SE) 3.4 +/- 0.4%/l, whereas that of the sternomastoids was 2.0 +/- 0.3%/l (P < 0.001). However, sternomastoid muscle mass was much larger than scalene muscle mass. As a result, DeltaPao generated by a maximal contraction of either muscle would be 3-4 cmH(2)O, which is about the same as DeltaPao generated by the parasternal intercostals in all interspaces.

Mechanical effect of muscle spindles in the canine external intercostal muscles

High-frequency mechanical vibration of the ribcage increases afferent activity from external intercostal muscle spindles, but the effect of this procedure on the mechanical behaviour of the respiratory system is unknown. In the present study, we have measured the changes in external intercostal muscle length and the craniocaudal displacement of the ribs during ribcage vibration (40 Hz) in anaesthetized dogs. With vibration, external intercostal inspiratory activity increased by approximately 50 %, but the respiratory changes in muscle length and rib displacement were unaltered. A similar response was obtained after the muscles in the caudal segments of the ribcage were sectioned and the caudally oriented force exerted by these muscles on the rib was removed, thus suggesting that activation of external intercostal muscle spindles by vibration generates little tension. Prompted by this observation, we also examined the role played by the external intercostal muscle spindles in determining the respiratory displacement of the ribs during breathing against high inspiratory airflow resistances. Although resistances consistently elicited prominent reflex increases in external intercostal inspiratory activity, the normal inspiratory cranial displacement of the ribs was reversed into an inspiratory caudal displacement. Also, this caudal rib displacement was essentially unchanged after section of the external intercostal muscles, whereas it was clearly enhanced after denervation of the parasternal intercostals. These findings indicate that stretch reflexes in external intercostal muscles confer insufficient tension on the muscles to significantly modify the mechanical behaviour of the respiratory system.

Mechanical effect of muscle spindles in the canine external intercostal muscles.

High-frequency mechanical vibration of the ribcage increases afferent activity from external intercostal muscle spindles, but the effect of this procedure on the mechanical behaviour of the respiratory system is unknown. In the present study, we have measured the changes in external intercostal muscle length and the craniocaudal displacement of the ribs during ribcage vibration (40 Hz) in anaesthetized dogs. With vibration, external intercostal inspiratory activity increased by approximately 50 %, but the respiratory changes in muscle length and rib displacement were unaltered. A similar response was obtained after the muscles in the caudal segments of the ribcage were sectioned and the caudally oriented force exerted by these muscles on the rib was removed, thus suggesting that activation of external intercostal muscle spindles by vibration generates little tension. Prompted by this observation, we also examined the role played by the external intercostal muscle spindles in determining the respiratory displacement of the ribs during breathing against high inspiratory airflow resistances. Although resistances consistently elicited prominent reflex increases in external intercostal inspiratory activity, the normal inspiratory cranial displacement of the ribs was reversed into an inspiratory caudal displacement. Also, this caudal rib displacement was essentially unchanged after section of the external intercostal muscles, whereas it was clearly enhanced after denervation of the parasternal intercostals. These findings indicate that stretch reflexes in external intercostal muscles confer insufficient tension on the muscles to significantly modify the mechanical behaviour of the respiratory system.