Phrenic afferent contribution to reflexes elicited by changes in diaphragm length

1990 ◽  
Vol 69 (2) ◽  
pp. 640-647 ◽  
Author(s):  
M. Cheeseman ◽  
W. R. Revelette

Recent evidence from several laboratories suggests that activation of afferents in the diaphragm can reflexly affect inspiratory muscle activation. This study determined whether afferents in the diaphragm contribute to compensatory changes in phrenic motor drive when the operating length of the diaphragm is suddenly increased. Experiments were performed in six closed-chest pentothal-anesthetized cats. Length changes were measured using a pair of piezoelectric crystals implanted in the left crural diaphragm. The crural electromyogram (EMGdi) was measured by electrodes fixed to each crystal. The animal was suspended in a spinal frame, and a Plexiglas tube was fitted around the cat's abdomen. A balloon placed inside the tube was inflated during the expiratory phase to produce a mean increase of 17% in diaphragm length at functional residual capacity. Ten trials were performed in succession under the following conditions: intact, after bilateral vagotomy, after spinal section at C7, and after cervical dorsal rhizotomy. Peak integrated EMGdi (integral of EMGdi) and neural inspiratory time (nTI) were measured for the last control inspiration and the first after inflation. There was a significant reduction in the peak integral of EMGdi when the length of the diaphragm was increased for all conditions except after rhizotomy. Although not measured, it is likely that the tension developed by the diaphragm was also increased during abdominal compression. Results suggest that afferents sensitive to changes in the operating length and/or tension in the diaphragm contribute to compensatory alterations in phrenic motor drive.

1987 ◽  
Vol 62 (6) ◽  
pp. 2436-2441 ◽  
Author(s):  
D. L. Fryman ◽  
D. T. Frazier

Experiments were performed in eight lightly anesthetized thiopental sodium (Pentothal) cats to examine whether diaphragmatic afferents can significantly alter the neural drive to the diaphragm when the animal is exposed to lower body negative pressure. Moving-time-averaged diaphragmatic electromyograms (EMGma) were recorded and compared before and during exposure to lower body negative pressure in each of three consecutive conditions: C7 spinalization, bilateral vagotomy, and cervical dorsal rhizotomy. Application of lower body negative pressure in C7-spinalized animals resulted in a decrease in inspiratory time and peak diaphragmatic activity compared with control levels. After bilateral vagotomy, EMGma activity was prolonged with the application of lower body negative pressure. However, there was no increase in peak EMGma activity. After transection of the cervical dorsal roots subserving the phrenic nerve, the prolongation of diaphragmatic activity negative was eliminated. Therefore, we conclude that the significant increase in duration of inspiration in response to application of lower body negative pressure in the C7-spinalized, bilaterally vagotomized cat is mediated by phrenic nerve afferents.


1989 ◽  
Vol 66 (1) ◽  
pp. 392-399 ◽  
Author(s):  
C. A. Smith ◽  
D. M. Ainsworth ◽  
K. S. Henderson ◽  
J. A. Dempsey

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.


1993 ◽  
Vol 75 (2) ◽  
pp. 682-687 ◽  
Author(s):  
D. T. Frazier ◽  
F. Xu ◽  
L. Y. Lee ◽  
R. F. Taylor

In a previous study, we reported that inspiratory tracheal occlusion (TO) significantly inhibited the motor drive to the diaphragm in a decerebellated bilaterally vagotomized preparation (J. Appl. Physiol. 75:675–681, 1993). The hypothesis to be tested in the present study was that respiratory muscle afferents activated by inspiratory TO provided the inputs responsible for the observed inhibition. Adult cats were anesthetized, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. The cerebellum, vagi, and dorsal spinal cord (C2-T2) were surgically exposed. Inspiratory TO was applied before and after cold blockade of the dorsal cord (C6) or dorsal root (C3–6) transection in the intact and decerebellated vagotomized cat. Respiratory timing (inspiratory and expiratory duration) was determined from the EMGdi record, and the peak integrated EMGdi (integral of EMGdi) response was used as an index of respiratory motor drive. Our results showed that 1) cold blockade at the dorsal C6 level in an intact preparation significantly increased the peak of the integral of EMGdi response to TO and was reversible upon rewarming; 2) as previously reported, decerebellation coupled with bilateral vagotomy significantly decreased the peak integral of EMGdi response to TO with no effect on timing; 3) cold blockade (-1 degree C) of the dorsal cord at C6 significantly attenuated this inhibition, and subsequent dorsal rhizotomy at C3–6 completely abolished this inhibition; and 4) decerebellation, cold blockade of the dorsal cord (C6), and dorsal rhizotomy (C3–6) did not significantly affect baseline values in bilaterally vagotomized cats.(ABSTRACT TRUNCATED AT 250 WORDS)


2017 ◽  
Vol 312 (3) ◽  
pp. R443-R450
Author(s):  
Brooke Greybeck ◽  
Raymond Lu ◽  
Arvind Ramanujam ◽  
Mary Adeyeye ◽  
Matthew Wettergreen ◽  
...  

Muscle shortening and volume displacement (VD) are critical determinants of the pressure-generating capacity of the diaphragm. The present study was designed to test the hypothesis that diaphragm VD is heterogeneous and that distribution of VD is dependent on regional muscle shortening, posture, and the level of muscle activation. Radioopaque markers were sutured along muscle bundles of the peritoneal surface of the crural, dorsal costal, midcostal, and ventral costal regions of the left hemidiaphragm in four dogs. The markers were followed by biplanar video fluoroscopy during quiet spontaneous breathing, passive inflation to total lung capacity (TLC), and inspiratory efforts against an occluded airway at three lung volumes spanning the vital capacity [functional residual capacity, functional residual capacity + ½ inspiratory capacity, and TLC in both the prone and supine postures]. Our data show the ventral costal diaphragm had the largest VD and contributed nearly two times to the total diaphragm VD compared with the dorsal costal portion. In addition, the ventral costal diaphragm contributed nearly half of the total VD in the prone position, whereas it only contributed a quarter of the total VD in the supine postition. During efforts against an occluded airway and during passive inflation to TLC in the supine position, the crural diaphragm displaced volume equivalent to that of the midcostal portion. Regional muscle shortening closely matched regional VD. We conclude that the primary force generator of the diaphragm is primarily dominated by the contribution of the ventral costal region to its VD.


Author(s):  
Fabio Giuseppe Laginestra ◽  
Markus Amann ◽  
Emine Kirmizi ◽  
Gaia Giuriato ◽  
Chiara Barbi ◽  
...  

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, non-fatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically-induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), while on the other day, the same KE exercise was repeated following electrically-induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to post-exercise changes in potentiated twitch force (ΔQtw,pot; peripheral-fatigue), and voluntary muscle activation (ΔVA; central-fatigue). As reflected by the 57±11% reduction in electrically-evoked pulse force, the electrically-induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared to No-PreF (4.6±1.2 vs 7.7±2.4 min; p<0.01). While ΔQtw,pot was significantly larger in No-PreF compared to PreF (-60% vs -52%, p<0.05), ΔVA was greater in PreF (-14% vs -10%, p<0.05). Taken together, electrically-induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover-effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon.


2019 ◽  
Vol 126 (2) ◽  
pp. 376-385 ◽  
Author(s):  
Ole Emil Andersen ◽  
Ole Bækgaard Nielsen ◽  
Kristian Overgaard

Muscle-damaging eccentric exercise impairs muscle glucose uptake several hours to days after exercise. Little, however, is known about the acute effects of eccentric exercise on contraction- and insulin-induced glucose uptake. This study compares glucose uptake rates in the first hours following eccentric, concentric, and isometric contractions with and without insulin present. Isolated rat extensor digitorum longus muscles were exposed to either an eccentric, concentric, or isometric contraction protocol, and muscle contractions were induced by electric stimulation that was identical between contraction protocols. In eccentric and concentric modes, length changes of 0.6 or 1.2 mm were used during contractions. Both contraction- and insulin-induced glucose uptake were assessed immediately and 2 h after contractions. Glucose uptake increased significantly following all modes of contraction and was higher after eccentric contractions with a stretch of 1.2 mm compared with the remaining contraction groups when assessed immediately after contractions [eccentric (1.2 mm) > eccentric (0.6 mm), concentric (1.2 mm), concentric (0.6 mm), isometric > rest; P < 0.05]. After 2 h, contraction-induced glucose uptake was still higher than noncontracting levels, but with no difference between contraction modes. The presence of insulin increased glucose uptake markedly, but this response was blunted by, respectively, 39–51% and 29–36% ( P < 0.05) immediately and 2 h after eccentric contractions stretched 1.2 mm compared with concentric and isometric contractions. The contrasting early effects of eccentric contractions on contraction- and insulin-induced glucose uptake suggest that glucose uptake is impaired acutely following eccentric exercise because of reduced insulin responsiveness.NEW & NOTEWORTHY This study shows that, in isolated rat muscle, muscle-damaging eccentric contractions result in a transient increase in contraction-induced glucose uptake compared with isometric and concentric contractions induced by identical muscle activation protocols. Furthermore, our results demonstrate that, in contrast, the insulin-stimulated glucose uptake is impaired immediately following muscle-damaging eccentric contractions.


1988 ◽  
Vol 65 (3) ◽  
pp. 1033-1039 ◽  
Author(s):  
L. Fedorko ◽  
E. N. Kelly ◽  
S. J. England

We studied the effect of acute bilateral vagotomy on ventilation and ventilatory pattern in rats. In 1- to 6-day-old unanesthetized rats, vagotomy resulted in a substantial decrease (38%) in ventilation during air breathing. After vagotomy there was a threefold increase in tidal volume (VT), inspiratory time (TI) doubled, and expiratory time (TE) was six times longer. When studied under isoflurane anesthesia, newborn rats showed decreases in ventilation similar to that observed without anesthesia, whereas anesthetized adult rats had no consistent changes in ventilation. Adult and newborn rats had nearly identical proportionate increases in VT and TI after vagotomy, but TE lengthened to a greater extent in the newborns. Additionally, we demonstrated a significant decrease in ventilation when 100% O2 rather than air was supplied to nonvagotomized unanesthetized newborn rats. Ventilation decreased by 19% after vagotomy under hyperoxic conditions. We conclude that vagal afferent input, probably of pulmonary mechanoreceptor origin, provides positive feedback to respiration in newborn rats and that newborn rats greater than 24 h old also have a degree of peripheral chemoreceptor drive during air breathing.


1992 ◽  
Vol 72 (2) ◽  
pp. 447-454 ◽  
Author(s):  
J. S. Teitelbaum ◽  
S. A. Magder ◽  
C. Roussos ◽  
S. N. Hussain

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.


1990 ◽  
Vol 68 (6) ◽  
pp. 2296-2304 ◽  
Author(s):  
D. R. Hillman ◽  
J. Markos ◽  
K. E. Finucane

Transdiaphragmatic pressure (Pdi) is lower during maximum inspiratory effort with the diaphragm alone than when maximum inspiratory and expulsive efforts are combined. The increase in Pdi with expulsive effort has been attributed to increased neural activation of the diaphragm. Alternatively, the increase could be due to stretching of the contracted diaphragm. If this were so, Pdi measured during a combined maximum effort would overestimate the capacity of the diaphragm to generate inspiratory force. This study determined the likely contribution of stretching of the contracted diaphragm to estimates of maximum Pdi (Pdimax) obtained during combined inspiratory and expulsive effort. Three healthy trained subjects were studied standing. Diaphragmatic Mueller maneuvers were performed at functional residual capacity and sustained during subsequent abdominal compression by either abdominal muscle expulsive effort or externally applied pressure. Measurements were made of changes in abdominal (Pab) and pleural (Ppl) pressure, Pdi, rib cage and abdominal dimensions and respiratory electromyograms. Three reproducible performances of each maneuver from each subject were analyzed. When expulsive effort was added to maximum diaphragmatic inspiratory effort, Pdimax increased from 86 +/- 12 to 148 +/- 14 (SD) cmH2O within the 1st s and was 128 +/- 14 cmH2O 2 s later. When external compression was added to maximum diaphragmatic inspiratory effort, Pdimax increased from 87 +/- 16 to 171 +/- 19 cmH2O within the 1st s and was 152 +/- 16 cmH2O 2 s later.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 73 (4) ◽  
pp. 1402-1412 ◽  
Author(s):  
S. U. Hasan ◽  
A. Rigaux

To investigate the effects of bilateral cervical vagotomy on arousal and breathing responses, we studied eight sham-operated and eight chronically instrumented unanesthetized vagotomized sheep fetuses between 136 and 144 days of gestation (term approximately 147 days). Each fetus was instrumented to record sleep states, diaphragmatic electromyogram, blood pressure, pH, and blood gas tensions. In a randomized order, fetal lungs were distended with four different O2 concentrations: 0 (100% N2), 21, 50, and 100% at a continuous positive airway pressure of 30 cmH2O via an in situ Y-endotracheal tube. Under control conditions, inspiratory time and the duration of the single longest breathing episode decreased from 598 +/- 99 (SD) ms and 24 +/- 10 min in sham group to 393 +/- 162 ms and 11.0 +/- 3.0 min in vagotomized group (P = 0.04 and 0.033), respectively. In response to lung distension with 100% N2, breathing time decreased from 44 +/- 17 to 20 +/- 18% (P = 0.045) in sham-operated fetuses, whereas it remained unchanged in the vagotomized group. In response to 100% O2, fetal arterial PO2 increased in five of eight fetuses sham-operated from 18.2 +/- 5.1 to 227 +/- 45 Torr (P = 0.0001) and in six of eight vagotomized fetuses from 18.5 +/- 4.4 to 172 +/- 39 Torr (P < 0.001). Although arousal was observed in all oxygenated fetuses at the onset of breathing, the duration of arousal was markedly attenuated in vagotomized fetuses (14 +/- 10 vs. 46 +/- 29 min in sham group; P = 0.024). Frequency and amplitude of breathing and respiratory output (frequency x amplitude) increased only in sham group (P = 0.02, 0.004, and 0.0002, respectively). We conclude that in response to lung distension and oxygenation, arousal and stimulation of breathing during active and quite sleep are critically dependent on intact vagal nerves.


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