Influence of posture and breathing route on neural drive to upper airway dilator muscles during exercise

2000 ◽  
Vol 89 (2) ◽  
pp. 590-598 ◽  
Author(s):  
J. S. Williams ◽  
P. L. Janssen ◽  
D. D. Fuller ◽  
R. F. Fregosi

Our purpose was to determine the influence of posture and breathing route on electromyographic (EMG) activities of nasal dilator (NDM) and genioglossus (GG) muscles during exercise. Nasal and oral airflow rates and EMG activities of the NDM and GG were recorded in 10 subjects at rest and during upright and supine incremental cycling exercise to exhaustion. EMG activities immediately before and after the switch from nasal to oronasal breathing were also determined for those subjects who demonstrated a clear switch point ( n = 7). NDM and GG EMG activities were significantly correlated with increases in nasal, oral, and total ventilatory rates during exercise, and these relationships were not altered by posture. In both upright and supine exercise, NDM activity rose more sharply as a function of nasal inspired ventilation compared with total or oral inspired ventilation ( P < 0.01), but GG activity showed no significant breathing-route dependence. Peak NDM integrated EMG activity decreased ( P = 0.008), and peak GG integrated EMG activity increased ( P = 0.032) coincident with the switch from nasal to oronasal breathing. In conclusion, 1) neural drive to NDM and GG increases as a function of exercise intensity, but the increase is unaltered by posture; 2) NDM activity is breathing-route dependent in steady-state exercise, but GG activity is not; and 3) drive to both muscles changes significantly at the switch point, but the change in GG activity is more variable and is often transient. This suggests that factors other than the breathing route dominate drive to the GG soon after the initial changes in the configuration of the oronasal airway are made.

2003 ◽  
Vol 95 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Pierre-Hugues Fortier ◽  
Philippe Reix ◽  
Julie Arsenault ◽  
Dominique Dorion ◽  
Jean-Paul Praud

We tested the hypotheses that active upper airway closure during induced central apneas in nonsedated lambs 1) is complete and occurs at the laryngeal level and 2) is not due to stimulation of the superior laryngeal nerves (SLN). Five newborn lambs were surgically instrumented to record thyroarytenoid (TA) muscle (glottal constrictor) electromyographic (EMG) activity with supra- and subglottal pressures. Hypocapnic and nonhypocapnic central apneas were induced before and after SLN sectioning in the five lambs. A total of 174 apneas were induced, 116 before and 58 after sectioning of the internal branch of the SLN (iSLN). Continuous TA EMG activity was observed in 88% of apneas before iSLN section and in 87% of apneas after iSLN section. A transglottal pressure different from zero was observed in all apneas with TA EMG activity, with a mean subglottal pressure of 4.3 ± 0.8 cmH2O before and 4.7 ± 0.7 cmH2O after iSLN section. Supraglottal pressure was consistently atmospheric. Sectioning of both iSLNs had no effects on the results. We conclude that upper airway closure during induced central apneas in lambs is active, complete, and occurs at the glottal level only. Consequently, a positive subglottal pressure is maintained throughout the apnea. Finally, this complete active glottal closure is independent from laryngeal afferent innervation.


1987 ◽  
Vol 62 (1) ◽  
pp. 15-26 ◽  
Author(s):  
K. Sasaki ◽  
J. A. Nadel ◽  
H. L. Hahn

We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.


1996 ◽  
Vol 80 (5) ◽  
pp. 1520-1527 ◽  
Author(s):  
J. Sullivan ◽  
D. Fuller ◽  
R. F. Fregosi

Our primary aim was to determine whether reducing the activity of nasal airway receptors would influence drive to the nasal dilator muscles (NDMs) during exercise. We used lidocaine (2%) or nasal splints to diminish afferent airway receptor activity and measured the electromyogram (EMG) activity of the NDMs during incremental bicycle exercise in subjects who breathed nasally. NDM EMG activities increased as a function of exercise intensity but were not changed by lidocaine and were only slightly reduced by splinting. Similarly, neither intervention altered the normal decrease in NDM EMG activity associated with reductions in airway resistance evoked by He-O2 breathing. We also compared the NDM EMG response to exercise with that evoked by CO2 rebreathing at rest to determine whether the nature of the ventilatory stimulus influences drive to the NDMs; comparisons were made at constant levels of nasal inspired ventilation and, therefore, constant total ventilatory output. The increase in EMG activity was much higher during exercise compared with hyperoxic hypercapnia. In conclusion, 1) desensitizing the nasal airway does not alter NDM activity significantly during exercise and 2) exercise results in much greater increases in NDM activity compared with hypercapnia, indicating that different ventilatory stimuli can evoke more or less activation of upper airway motoneurons, even when comparisons are made at constant levels of total ventilatory output.


1987 ◽  
Vol 63 (1) ◽  
pp. 368-374 ◽  
Author(s):  
S. Redline ◽  
K. P. Strohl

We reasoned that neural information from upper airway (UA) sensory receptors could influence the relationship between UA and diaphragmatic neuromuscular responses to hypercapnia. In this study, the electromyographic (EMG) activities of the alae nasi (AN), genioglossus (GG), and chest wall (CW) or diaphragm (Di) to ventilatory loading were assessed in six laryngectomized, tracheostomized human subjects and in six subjects breathing with an intact UA before and after topical UA anesthesia. The EMG activities of the UA and thoracic muscles increased at similar rates with increasing hypercapnia in normal subjects, in subjects whose upper airways were anesthetized, and in laryngectomized subjects breathing with a cervical tracheostomy. Furthermore, in the laryngectomized subjects, respiratory muscle EMG activation increased with resistive inspiratory loading (15 cmH2O X l–1 X s) applied at the level of a cervical tracheostomy. At an average expired CO2 fraction of 7.0%, resistive loading resulted in a 93 +/- 26.3% (SE) increase in peak AN EMG activity, a 39 +/- 2.0% increase in peak GG EMG activity, and a 43.2 +/- 16.5% increase in peak CW (Di) EMG activity compared with control values. We conclude that the ventilatory responses of the UA and thoracic muscles to ventilatory loading are not substantially influenced by laryngectomy or UA anesthesia.


1996 ◽  
Vol 81 (1) ◽  
pp. 470-479 ◽  
Author(s):  
P. C. Deegan ◽  
P. Nolan ◽  
M. Carey ◽  
W. T. McNicholas

To determine upper airway (UA) and ventilatory responses to nasal continuous positive airway pressure (CPAP) and expiratory positive airway pressure (EPAP), we quantitated changes in alae nasi (AN) and genioglossus (GG) electromyographic (EMG) activity, ventilatory timing, and end-expiratory lung volume (EELV) at various levels of CPAP and EPAP in six normal subjects during wakefulness and in seven during sleep. The same measurements were also made before and after UA anesthesia in six normal subjects during wakefulness. During both wakefulness and sleep, CPAP application significantly increased EELV and decreased AN and GG EMG activities. In contrast, EPAP significantly increased EMG activities of both muscles while also increasing EELV during wakefulness. The EMG responses were less marked during sleep. Anesthesia of the UA abolished the EMG responses to CPAP but not to EPAP. These results suggest that, in normal subjects, CPAP application causes a reflex reduction in UA dilator muscle activity mediated by UA sensory receptors. In contrast, EPAP increases UA dilator muscle activity, with the response mediated by conscious influences or reflexes arising outside of the UA.


1997 ◽  
Vol 77 (6) ◽  
pp. 3168-3179 ◽  
Author(s):  
O. Hidaka ◽  
T. Morimoto ◽  
Y. Masuda ◽  
T. Kato ◽  
R. Matsuo ◽  
...  

Hidaka, O., T. Morimoto, Y. Masuda, T. Kato, R. Matsuo, T. Inoue, M. Kobayashi, and K. Takada. Regulation of masticatory force during cortically induced rhythmic jaw movements in the anesthetized rabbit. J. Neurophysiol. 77: 3168–3179, 1997. To examine the relationships between masticatory force, electromyogram (EMG) of masticatory muscles, and jaw movement pattern, we quantitatively evaluated the effects of changing hardness of a chewing substance on these three variables. Cortically induced rhythmic jaw movements of a crescent-shaped pattern were induced by electrical stimulation of the cerebral cortical masticatory area in the anesthetized rabbit. The axially directed masticatory force was recorded with a small force-displacement transducer mounted on the ground surface of the lower molars. EMGs were recorded from the masseter and digastric muscles simultaneously with jaw movements. Five test strips of polyurethane foam of different hardness were prepared and inserted between the upper molar and the transducer during the movements. The peak, impulse, and buildup speed of the masticatory force increased with strip hardness, whereas duration of the exerted force did not vary with strip hardness. The integrated activity and duration of the masseteric EMG bursts also increased with strip hardness. The integrated EMG activity of the digastric bursts was weakly related to strip hardness, whereas the duration was not. The minimum gape increased with strip hardness, but the maximum gape did not. The horizontal excursion of the jaw did not vary in a hardness-dependent manner, although it was greater in the cycles with strip application than in the cycles without strip application. Deprivation of periodontal sensation by cutting the nerves to the teeth reduced the buildup speed of the force, maximum gape, net gape, and horizontal jaw movements. The denervation also elongated the force duration and that of masseteric EMG bursts. However, the rate of the hardness-dependent changes in the above parameters did not alter after denervation. The latency of the masseteric EMG response to strip application was evaluated before and after denervation. In both conditions, it was ⩾6 ms in ∼70% of the cycles and <6 ms in the remaining ∼30%, which cannot be explained by a simple reflex mechanism. On the basis of the analysis of correlation coefficients, the masseteric integrated EMG seemed to be a good indicator of the peak and impulse of the masticatory force both before and after denervation. We conclude that periodontal afferents would be responsible for a quick buildup of masticatory force and that afferents other than those from periodontal tissue would contribute to the hardness-dependent change of masticatory force during cortically induced rhythmic jaw movements.


1995 ◽  
Vol 79 (1) ◽  
pp. 270-278 ◽  
Author(s):  
D. Fuller ◽  
J. Sullivan ◽  
E. Essif ◽  
K. Personius ◽  
R. F. Fregosi

The upper airway muscles play an important role in breathing, swallowing, and speaking, but little is known about the electromyogram (EMG)-force relationship of these muscles. We have measured the peak integrated EMG activity (iEMG) and force of human nasal dilator muscles (NDM) with a custom-designed headpiece that was attached via the forehead and upper lip. The headpiece contains a micromanipulator that holds a rod with a load cell mounted on its tip. The reproducibility of the force measurements was examined by measuring the lateral or “flaring” force of the NDM in multiple trials on two separate occasions in 13 subjects. For these studies the subjects were instructed to perform maximal voluntary contractions (MVCs). Test-retest reproducibility averaged 8.3% (coefficient of variation) for within-day comparisons and 13.7% between days. We also measured iEMG and NDM force during an incremental exercise test in nine of the subjects; they were instructed to breathe nasally throughout one 30-s epoch at rest and at each workload. The iEMG and force during peak exercise (175–275 W) averaged 81 +/- 26% (SD) MVC and 235 +/- 127 mN (approximately 75% MVC), respectively. The iEMG during incremental exercise was linearly related to the peak force (r = 0.90, P < 0.001). Contractile properties were measured in seven of the subjects by application of single supramaximal shocks (0.1-ms pulse) to the facial nerve. Twitch force averaged 9 +/- 6% MVC, and the time to peak force was 62 +/- 13 ms, which is considerably faster than that in human diaphragm or elbow flexors.


2021 ◽  
Vol 7 (1) ◽  
pp. e000907
Author(s):  
Giovanni Polsinelli ◽  
Angelo Rodio ◽  
Bruno Federico

IntroductionThe measurement of heart rate is commonly used to estimate exercise intensity. However, during endurance performance, the relationship between heart rate and oxygen consumption may be compromised by cardiovascular drift. This physiological phenomenon mainly consists of a time-dependent increase in heart rate and decrease in systolic volume and may lead to overestimate absolute exercise intensity in prediction models based on heart rate. Previous research has established that cardiovascular drift is correlated to the increase in core body temperature during prolonged exercise. Therefore, monitoring body temperature during exercise may allow to quantify the increase in heart rate attributable to cardiovascular drift and to improve the estimate of absolute exercise intensity. Monitoring core body temperature during exercise may be invasive or inappropriate, but the external auditory canal is an easily accessible alternative site for temperature measurement.Methods and analysisThis study aims to assess the degree of correlation between trends in heart rate and in ear temperature during 120 min of steady-state cycling with intensity of 59% of heart rate reserve in a thermally neutral indoor environment. Ear temperature will be monitored both at the external auditory canal level with a contact probe and at the tympanic level with a professional infrared thermometer.Ethics and disseminationThe study protocol was approved by an independent ethics committee. The results will be submitted for publication in academic journals and disseminated to stakeholders through summary documents and information meetings.


2005 ◽  
Vol 288 (3) ◽  
pp. R591-R599 ◽  
Author(s):  
Mitsuharu Okutsu ◽  
Kenji Ishii ◽  
Kai Jun Niu ◽  
Ryoichi Nagatomi

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1α/CXCL12. Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.


1996 ◽  
Vol 80 (5) ◽  
pp. 1475-1484 ◽  
Author(s):  
M. C. Khoo ◽  
S. S. Koh ◽  
J. J. Shin ◽  
P. R. Westbrook ◽  
R. B. Berry

The polysomnographic and ventilatory patterns of nine normal adults were measured during non-rapid-eye-movement (NREM) stage 2 sleep before and after repeated administrations of a tone (40-72 dB) lasting 5 s. The ventilatory response to arousal (VRA) was determined in data sections showing electrocortical arousal following the start of the tone. Mean inspiratory flow and tidal volume increased significantly above control levels in the first seven breaths after the start of arousal, with peak increases (64.2% > control) occurring on the second breath. Breath-to-breath occlusion pressure 100 ms after the start of inspiration showed significant increases only on the second and third postarousal breaths, whereas upper airway resistance declined immediately and remained below control for > or = 7 consecutive breaths. These results suggest that the first breath and latter portion of the VRA are determined more by upper airway dynamics than by changes in the neural drive to breathe. Computer model simulations comparing different VRA time courses show that sustained periodic apnea is more likely to occur when the fall in the postarousal increase in ventilation is more abrupt.


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