Excitatory lung reflex may stress inspiratory muscle by suppressing expiratory muscle activity

2001 ◽  
Vol 90 (3) ◽  
pp. 857-864 ◽  
Author(s):  
J. Yu ◽  
Y. Wang ◽  
G. Soukhova ◽  
L. C. Collins ◽  
J. C. Falcone
Keyword(s):  
Duty Cycle ◽  
Muscle Activity ◽  
Breathing Pattern ◽  
Lung Parenchyma ◽  
Abdominal Muscle ◽  
Inspiratory Muscle ◽  
Nerve Activity ◽  
Expiratory Muscle ◽  
Inspiratory Activity ◽  
Inspiratory Muscle Fatigue

Recently, a vagally mediated excitatory lung reflex (ELR) causing neural hyperpnea and tachypnea was identified. Because ventilation is regulated through both inspiratory and expiratory processes, we investigated the effects of the ELR on these two processes simultaneously. In anesthetized, open-chest, and artificially ventilated rabbits, we recorded phrenic nerve activity and abdominal muscle activity to assess the breathing pattern when the ELR was evoked by directly injecting hypertonic saline (8.1%, 0.1 ml) into lung parenchyma. Activation of the ELR stimulated inspiratory activity, which was exhibited by increasing amplitude, burst rate, and duty cycle of the phrenic activity (by 22 ± 4, 33 ± 9, and 57 ± 11%, respectively; n = 13; P < 0.001), but suppressed expiratory muscle activity. The expiratory muscle became silent in most cases. On average, the amplitude of expiratory muscle activity decreased by 88 ± 5% ( P < 0.002). The suppression reached the peak at 6.9 ± 1 s and lasted for 200 s (median). Injection of H2O2 into the lung parenchyma produced similar responses. By suppressing expiration, the ELR produces a shift in the workload from expiratory muscle to inspiratory muscle. Therefore, we conclude that the ELR may contribute to inspiratory muscle fatigue, not only by directly increasing the inspiratory activity but also by suppressing expiratory activity.

Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia

1992 ◽  
Vol 72 (3) ◽  
pp. 881-887 ◽  
Author(s):  
Y. Wakai ◽  
M. M. Welsh ◽  
A. M. Leevers ◽  
J. D. Road
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Ventilatory Threshold ◽  
Minute Ventilation ◽  
Abdominal Muscle ◽  
Transversus Abdominis ◽  
Abdominal Muscles ◽  
Lung Inflation ◽  
Expiratory Muscle ◽  
Intramuscular Electrodes

Expiratory muscle activity has been shown to occur in awake humans during lung inflation; however, whether this activity is dependent on consciousness is unclear. Therefore we measured abdominal muscle electromyograms (intramuscular electrodes) in 13 subjects studied in the supine position during wakefulness and non-rapid-eye-movement sleep. Lung inflation was produced by nasal continuous positive airway pressure (CPAP). CPAP at 10–15 cmH2O produced phasic expiratory activity in two subjects during wakefulness but produced no activity in any subject during sleep. During sleep, CPAP to 15 cmH2O increased lung volume by 1,260 +/- 215 (SE) ml, but there was no change in minute ventilation. The ventilatory threshold at which phasic abdominal muscle activity was first recorded during hypercapnia was 10.3 +/- 1.1 l/min while awake and 13.8 +/- 1 l/min while asleep (P less than 0.05). Higher lung volumes reduced the threshold for abdominal muscle recruitment during hypercapnia. We conclude that lung inflation alone over the range that we studied does not alter ventilation or produce recruitment of the abdominal muscles in sleeping humans. The internal oblique and transversus abdominis are activated at a lower ventilatory threshold during hypercapnia, and this activation is influenced by state and lung volume.

Differential timing of respiratory muscles in response to chemical stimuli in awake dogs

1989 ◽  
Vol 66 (1) ◽  
pp. 392-399 ◽  
Author(s):  
C. A. Smith ◽  
D. M. Ainsworth ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Muscle Activation ◽  
Respiratory Muscles ◽  
Abdominal Muscle ◽  
Transversus Abdominis ◽  
Inspiratory Time ◽  
Expiratory Muscle ◽  
Inspiratory Activity ◽  
Chemical Stimuli ◽  
Crural Diaphragm ◽  
Differential Timing

We assessed changes in respiratory muscle timing in response to hyperpnea and shortened inspiratory and expiratory times caused by chemoreceptor stimuli in six awake dogs. Durations of postinspiratory inspiratory activity of costal and crural diaphragm (PIIA), the delay in diaphragm electromyogram (EMG) after the initiation of inspiratory airflow, postexpiratory expiratory activity of the transversus abdominis (PEEA), and the delay of abdominal expiratory muscle activity after the initiation of expiratory airflow were measured. In control, four out of six dogs showed PIIA [8–10% of expiratory time (TE)]; all showed delay of diaphragm [19% of inspiratory time (TI)], delay of abdominal muscle activation (21% of TE), and PEEA (24% of TI). Hypercapnia decreased PIIA (4–9% of TE), maintained diaphragm delay at near control values (23% of TI), increased PEEA (36% of TI), eliminated delay of abdominal muscle activation (4% of TE), and decreased end-expiratory lung volume (EELV). Hypocapnic hypoxia increased PIIA (24–25% of TE), eliminated diaphragm delay (3% of TI), eliminated PEEA (3% of TI), reduced delay of abdominal muscle activation (14% of TE), and increased EELV. Most of these effects of hypoxic hypocapnia vs. hypercapnia on the within-breath EMG timing parameters corresponded to differences in the magnitude of expiratory muscle activation. These changes exerted significant influences on flow rates and EELV.

Inspiratory muscle activity and breathing pattern during different intensity inspiratory muscle training

2016 ◽  
Author(s):  
Tsuyoshi Ichikawa ◽  
Masanori Yokoba ◽  
Masahiko Kimura ◽  
Shinichiro Ryuge ◽  
Ken Katono ◽  
...  
Keyword(s):  
Muscle Activity ◽  
Breathing Pattern ◽  
Inspiratory Muscle ◽  
Inspiratory Muscle Training ◽  
Muscle Training

Physiological Determinants of Inspiratory Effort Sensation during CO2 Rebreathing in Normal Subjects

1993 ◽  
Vol 85 (5) ◽  
pp. 637-642 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Partial Pressure ◽  
Muscle Fatigue ◽  
Breathing Pattern ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Inspiratory Muscle ◽  
Time Index ◽  
Partial Pressure Of Co2 ◽  
Tension Time ◽  
Inspiratory Muscle Fatigue

1. The physiological basis of inspiratory effort sensation remains uncertain. Previous studies have suggested that pleural pressure, rather than inspiratory muscle fatigue, is the principal determinant of inspiratory effort sensation. However, only a limited range of inspiratory flows and breathing patterns have been examined. We suspected that inspiratory effort sensation was related to the inspiratory muscle tension-time index developed whatever the breathing pattern or load, and that this might explain the additional rise in sensation seen with hypercapnia. 2. To investigate this we measured hypercapnic re-breathing responses in seven normal subjects (six males, age range 21–38 years) with and without an inspiratory resistive load of 10 cm H2O. Pleural and transdiaphragmatic pressures, mouth occlusion pressure and breathing pattern were measured. Diaphragmatic and ribcage tension-time indices were calculated from these data. Inspiratory effort sensation was recorded using a Borg scale at 30s intervals during each rebreathing run. 3. Breathing pattern and inspiratory pressure partitioning were unrelated to changes in inspiratory effort sensation during hypercapnia. Tension-time indices reached pre-fatiguing levels during both free breathing and inspiratory resistive loading. 4. Stepwise multiple regression analysis using pooled mechanical, chemical and breathing pattern variables showed that pleural pressure was more closely related to inspiratory effort sensation than was transdiaphragmatic pressure. When converted to tension-time indices, ribcage tension-time index was the major determinant of inspiratory effort sensation during loaded rebreathing, but partial pressure of CO2 was an important independent variable, whereas during unloaded rebreathing partial pressure of CO2 was the most important determinant of inspiratory effort sensation. 5. These results suggest that the pattern of inspiratory pressure partitioning and inspiratory flow rate have little influence on inspiratory effort sensation during CO2 stimulated breathing. The close association between inspiratory effort sensation and ribcage tension-time index, an index of inspiratory muscle work, suggests that inspiratory effort sensation may forewarn of potential inspiratory muscle fatigue. Changes in PaCO2 have a small independent effect on respiratory perception.

Neuromechanical regulation of respiratory motor output in ventilator-dependent C1-C3 quadriplegics

1995 ◽  
Vol 79 (1) ◽  
pp. 312-323 ◽  
Author(s):  
P. M. Simon ◽  
A. M. Leevers ◽  
J. L. Murty ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Mechanical Ventilation ◽  
Muscle Activity ◽  
Normal Subjects ◽  
Inspiratory Muscle ◽  
Phasic Activity ◽  
Cord Injury ◽  
Inhibitory Feedback ◽  
Dependent Inhibition ◽  
Inspiratory Activity ◽  
End Tidal

To evaluate the role of phrenic and sternocleidomastoid afferents as alternate sources of inhibitory feedback during mechanical ventilation, we studied five C2-C3 quadriplegics with sensory denervation of the rib cage and diaphragm, six C1-C2 quadriplegics with additional loss of sensory feedback from the neck muscles, and seven normal subjects. We compared the return of inspiratory muscle activity [the recruitment threshold (PCO2RT)] during mechanical ventilation between subject groups after stepwise increases in end-tidal PCO2 (PETCO2) either by increasing the inspired fraction of CO2 (FICO2), decreasing tidal volume (VT; 50 ml/min), or decreasing frequency (f; 1 breath/2 min). Normal subjects were mechanically hyperventilated via a nasal mask until inspiratory activity was undetectable. Efferent input to the sternocleidomastoid was intact at both levels of spinal cord injury, but phasic activity was not evident at the quadriplegics' baseline resting ventilation. The PCO2RT was defined as the level of PETCO2 at which phasic activity of the diaphragm in normal subjects and of the sternocleidomastoid in C1-C2 and C2-C3 quadriplegics recurred. The mean PCO2RT (in response to raising PETCO2 via increased FICO2 while maintaining a high VT and f) was not significantly different (P = 0.6) between normal subjects (43 +/- 3 Torr) and C2-C3 quadriplegics (38 +/- 5 Torr). Both subject groups demonstrated a frequency- and volume-related inhibition, as evidenced by a substantially lower PCO2RT when PETCO2 was raised by reducing either VT or f. In contrast to the C2-C3 quadriplegics, the C1-C2 quadriplegics responded with a similar PCO2RT among the three different mechanical ventilation trials, independent of whether PETCO2 was raised with high VT and f, with reduced VT, or with reduced f. We conclude that feedback from at least some part of the chest wall is required to produce a volume- and frequency-dependent inhibition of inspiratory muscle activity observed during mechanical ventilation.

Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading

1991 ◽  
Vol 70 (4) ◽  
pp. 1627-1632 ◽  
Author(s):  
M. J. Mador ◽  
F. A. Acevedo
Keyword(s):  
Muscle Fatigue ◽  
Breathing Pattern ◽  
Inspiratory Muscle ◽  
Transdiaphragmatic Pressure ◽  
Inspiratory Muscles ◽  
Resistive Loading ◽  
Diaphragmatic Fatigue ◽  
Shallow Breathing ◽  
Resistive Loads ◽  
Inspiratory Muscle Fatigue

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.

Tonic respiratory drive in the absence of rhythm generation in the conscious dog

1994 ◽  
Vol 76 (2) ◽  
pp. 671-680 ◽  
Author(s):  
R. L. Horner ◽  
L. F. Kozar ◽  
E. A. Phillipson
Keyword(s):  
Muscle Activity ◽  
Spontaneous Breathing ◽  
Respiratory Activity ◽  
Reciprocal Inhibition ◽  
Response Threshold ◽  
Respiratory Drive ◽  
Vagus Nerves ◽  
Arterial Pco2 ◽  
Expiratory Muscle ◽  
Inspiratory Activity

This study was designed to determine whether a chemoreceptor-mediated tonic respiratory drive exists below the apneic threshold. Expiratory (triangularis sterni) and inspiratory (diaphragm and parasternal intercostal) electromyographic activities were recorded in three awake relaxed dogs breathing through an endotracheal tube inserted into a permanent tracheostomy. The cervical vagus nerves were cold blocked to avoid the complicating effects of vagal inputs on respiratory activity. During hypocapnia produced by mechanical hyperventilation, expiratory muscle activity converted from rhythmic to tonic discharge when inspiratory muscle activity and spontaneous breathing movements were abolished. In hypocapnia, changes in arterial PCO2 (in hyperoxia) were produced by changing the ventilator rate for steady-state (> 6 min) CO2 stimuli and by disconnecting the ventilator for transient CO2 stimuli. By use of either method, a CO2-mediated drive to the expiratory muscle was consistently observed during hypocapnic apnea. At a constant level of hypocapnia, inhalation of 5% O2 consistently caused the onset of spontaneous breathing; the onset of phasic inspiratory activity was associated with reciprocal inhibition of the tonic expiratory activity. However, inhalation of 10 and 15% O2 caused an inhibition of the tonic expiratory activity, even without the onset of breathing. These results suggest that the response threshold of the respiratory chemoreceptors is lower than the apneic threshold and that a chemoreceptor-mediated tonic respiratory drive persists during apnea.

Breathing in Singing

2014 ◽  
pp. 86-108
Author(s):  
Alan Watson
Keyword(s):  
Abdominal Wall ◽  
Muscle Activity ◽  
Abdominal Muscle ◽  
Inspiratory Muscle ◽  
Lung Volumes ◽  
Inspiratory Muscles

Accounts of breathing in methodological books on singing are often confusing or inaccurate rather than helpful. This chapter provides an overview of the principles ofrespiration and how this is modified for singing. Inspiration results from an increase inthoracic dimensions caused by activity in the diaphragm and external intercostal muscles.At high lung volumes the sternocleidomastoids and scalenes also aid chest expansion.Subglottic pressure is created during expiration by the contraction of the abdominal wall,predominantly as a result of lateral abdominal muscle activity, which drives the relaxeddiaphragm upwards while simultaneously the internal intercostals pull the ribsdownwards. When the lungs are full and the inspiratory muscles release, elastic recoilforces alone can drive out the air and in order to regulate subglottic pressure theseforces must be resisted by gradually reducing inspiratory muscle activity. How different patterns of activity in these and other muscles contribute to singing is described and theway in which similar ends can be achieved by different means in different singers isexplained.

Bradykinin stimulates respiratory drive by activating pulmonary sympathetic afferents in the rabbit

2003 ◽  
Vol 95 (1) ◽  
pp. 241-249 ◽  
Author(s):  
G. Soukhova ◽  
Y. Wang ◽  
M. Ahmed ◽  
J. F. Walker ◽  
J. Yu
Keyword(s):  
Hypertonic Saline ◽  
Muscle Activity ◽  
Lung Parenchyma ◽  
Respiratory Drive ◽  
Breathing Patterns ◽  
Afferent Pathways ◽  
Expiratory Muscle ◽  
Shallow Breathing ◽  
External Oblique ◽  
Respiratory Reflexes

We recently identified a vagally mediated excitatory lung reflex by injecting hypertonic saline into the lung parenchyma (Yu J, Zhang JF, and Fletcher EC. J Appl Physiol 85: 1485–1492, 1998). This reflex increased amplitude and burst rate of phrenic (inspiratory) nerve activity and suppressed external oblique abdominal (expiratory) muscle activity. In the present study, we tested the hypothesis that bradykinin may activate extravagal pathways to stimulate breathing by assessing its reflex effects on respiratory drive. Bradykinin (1 μg/kg in 0.1 ml) was injected into the lung parenchyma of anesthetized, open-chest and artificially ventilated rabbits. In most cases, bradykinin increased phrenic amplitude, phrenic burst rate, and expiratory muscle activity. However, a variety of breathing patterns resulted, ranging from hyperpnea and tachypnea to rapid shallow breathing and apnea. Bradykinin acts like hypertonic saline in producing hyperpnea and tachypnea, yet the two agents clearly differ. Bradykinin produced a higher ratio of phrenic amplitude to inspiratory time and had longer latency than hypertonic saline. Although attenuated, bradykinin-induced respiratory responses persisted after vagotomy. We conclude that bradykinin activates multiple afferent pathways in the lung; portions of its respiratory reflexes are extravagal and arise from sympathetic afferents.

Sign in / Sign up

Export Citation Format

Share Document