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1
Hoogkamer, Wouter, Frank Van Calenbergh, Stephan P. Swinnen, and Jacques Duysens. "Cutaneous reflex modulation and self-induced reflex attenuation in cerebellar patients." Journal of Neurophysiology 113, no. 3 (February 1, 2015): 915–24. http://dx.doi.org/10.1152/jn.00381.2014.
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Modulation of cutaneous reflexes is important in the neural control of walking, yet knowledge about underlying neural pathways is still incomplete. Recent studies have suggested that the cerebellum is involved. Here we evaluated the possible roles of the cerebellum in cutaneous reflex modulation and in attenuation of self-induced reflexes. First we checked whether leg muscle activity during walking was similar in patients with focal cerebellar lesions and in healthy control subjects. We then recorded cutaneous reflex activity in leg muscles during walking. Additionally, we compared reflexes after standard (computer triggered) stimuli with reflexes after self-induced stimuli for both groups. Biceps femoris and gastrocnemius medialis muscle activity was increased in the patient group compared with the control subjects, suggesting a coactivation strategy to reduce instability of gait. Cutaneous reflex modulation was similar between healthy control subjects and cerebellar patients, but the latter appeared less able to attenuate reflexes to self-induced stimuli. This suggests that the cerebellum is not primarily involved in cutaneous reflex modulation but that it could act in attenuation of self-induced reflex responses. The latter role in locomotion would be consistent with the common view that the cerebellum predicts sensory consequences of movement.
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Gandevia, S. C., S. Miller, A. M. Aniss, and D. Burke. "Reflex influences on muscle spindle activity in relaxed human leg muscles." Journal of Neurophysiology 56, no. 1 (July 1, 1986): 159–70. http://dx.doi.org/10.1152/jn.1986.56.1.159.
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The study was designed to determine whether low-threshold cutaneous and muscle afferents from the foot reflexly activate gamma-motoneurons innervating relaxed muscles of the leg. In 15 experiments multiunit recordings were made from 21 nerve fascicles innervating triceps surae or tibialis anterior. In a further nine experiments the activity of 19 identified single muscle spindle afferents was recorded, 13 from triceps surae, 5 from tibialis anterior, and 1 from extensor digitorum longus. Trains of electrical stimuli (5 stimuli, 300 Hz) were delivered to the sural nerve at the ankle (intensity, twice sensory threshold) and the posterior tibial nerve at the ankle (intensity, 1.1 times motor threshold for the small muscles of the foot). In addition, a tap on the appropriate tendon at varying times after the stimuli was used to assess the dynamic responsiveness of the afferents under study. The conditioning electrical stimuli did not change the discharge of single spindle afferents. Recordings of rectified and averaged multiunit activity also revealed no change in the overall level of background neural activity following the electrical stimuli. The afferent responses to tendon taps did not differ significantly whether or not they were preceded by stimulation of the sural or posterior tibial nerves. These results suggest that low-threshold afferents from the foot do not produce significant activation of fusimotor neurons in relaxed leg muscles, at least as judged by their ability to alter the discharge of muscle spindle afferents. As there may be no effective background activity in fusimotor neurons innervating relaxed human muscles, it is possible that these inputs from the foot could influence the fusimotor system during voluntary contractions when the fusimotor neurons have been brought to firing threshold. In one subject trains of stimuli were delivered to the posterior tibial nerve at painful levels (30 times motor threshold). They produced an acceleration of the discharge of a spindle in soleus at a latency of approximately 125 ms, in advance of detectable activity in skeletomotor neurons and before an increase in muscle length was noted. It presumably resulted from activation of gamma-motoneurons innervating soleus by small myelinated afferents (A-delta range).
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Avela, Janne, Heikki Kyröläinen, and Paavo V. Komi. "Altered reflex sensitivity after repeated and prolonged passive muscle stretching." Journal of Applied Physiology 86, no. 4 (April 1, 1999): 1283–91. http://dx.doi.org/10.1152/jappl.1999.86.4.1283.
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Experiments were carried out to test the effect of prolonged and repeated passive stretching (RPS) of the triceps surae muscle on reflex sensitivity. The results demonstrated a clear deterioration of muscle function immediately after RPS. Maximal voluntary contraction, average electromyographic activity of the gastrocnemius and soleus muscles, and zero crossing rate of the soleus muscle (recorded from 50% maximal voluntary contraction) decreased on average by 23.2, 19.9, 16.5, and 12.2%, respectively. These changes were associated with a clear immediate reduction in the reflex sensitivity; stretch reflex peak-to-peak amplitude decreased by 84.8%, and the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential decreased by 43.8%. Interestingly, a significant ( P < 0.01) reduction in the stretch-resisting force of the measured muscles was observed. Serum creatine kinase activity stayed unaltered. This study presents evidence that the mechanism that decreases the sensitivity of short-latency reflexes can be activated because of RPS. The origin of this system seems to be a reduction in the activity of the large-diameter afferents, resulting from the reduced sensitivity of the muscle spindles to repeated stretch.
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Cidem, Muharrem, Ilhan Karacan, Halil Ibrahim Cakar, Mehmet Cidem, Oguz Sebik, Gizem Yilmaz, Kemal Sitki Turker, and Safak Sahir Karamehmetoglu. "Vibration parameters affecting vibration-induced reflex muscle activity." Somatosensory & Motor Research 34, no. 1 (January 2, 2017): 47–51. http://dx.doi.org/10.1080/08990220.2017.1281115.
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Aminoff, Michael J., Douglas S. Goodin, and Rosemary S. Chequer. "FUNCTIONAL ROLES OF THE LATE REFLEX MUSCLE ACTIVITY." Journal of Clinical Neurophysiology 10, no. 2 (April 1993): 240. http://dx.doi.org/10.1097/00004691-199304000-00014.
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Windhorst, Uwe, Thomas M. Hamm, and Douglas G. Stuart. "On the function of muscle and reflex partitioning." Behavioral and Brain Sciences 12, no. 4 (December 1989): 629–45. http://dx.doi.org/10.1017/s0140525x00024985.
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AbstractStudies have shown that in the mammalian neuromuscular system stretch reflexes are localized within individual muscles. Neuromuscular compartmentalization, the partitioning of sensory output from muscles, and the partitioning of segmental pathways to motor nuclei have also been demonstrated. This evidence indicates that individual motor nuclei and the muscles they innervate are not homogeneous functional units. An analysis of the functional significance of reflex localization and partitioning suggests that segmental control mechanisms are based on subdivisions of motor nuclei–muscle complexes. A partitioned organization of segmental control mechanisms could utilize (1) the potential functional diversity of muscle fiber types, (2) the variety of mechanical actions of individual muscles arising from their distributed origins and insertions, and (3) diverse architectural features such as intramuscular variations in pinnation and complex in-series and in-parallel arrangements of muscle fibers. The differentiated activity observed in some muscles during natural movements also calls for localized segmental control mechanisms. Partitioning may also play a role in mechanical interactions between contracting motor units and in increasing the stability of neuromuscular systems. The functional advantages of reflex localization and partitioning suggest they are probably common features of segmental systems, whose organization reflects the structure and function of their associated neuromuscular systems.
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Oliven, A., M. Haxhiu, and S. G. Kelsen. "Reflex effect of esophageal distension on respiratory muscle activity and pressure." Journal of Applied Physiology 66, no. 2 (February 1, 1989): 536–41. http://dx.doi.org/10.1152/jappl.1989.66.2.536.
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The electrical activity of the respiratory skeletal muscles is altered in response to reflexes originating in the gastrointestinal tract. The present study evaluated the reflex effects of esophageal distension (ED) on the distribution of motor activity to both inspiratory and expiratory muscles of the rib cage and abdomen and the resultant changes in thoracic and abdominal pressure during breathing. Studies were performed in 21 anesthetized spontaneously breathing dogs. ED was produced by inflating a balloon in the distal esophagus. ED decreased the activity of the costal and crural diaphragm and external intercostals and abolished all preexisting electrical activity in the expiratory muscles of the abdominal wall. On the other hand, ED increased the activity of the parasternal intercostals and expiratory muscles located in the rib cage (i.e., triangularis sterni and internal intercostal). All effects of ED were graded, with increasing distension exerting greater effects, and were eliminated by vagotomy. The effect of increases in chemical drive and lung inflation reflex activity on the response to ED was examined by performing ED while animals breathed either 6.5% CO2 or against graded levels of positive end-expiratory pressure (PEEP), respectively. Changes in respiratory muscle electrical activity induced by ED were similar (during 6.5% CO2 and PEEP) to those observed under control conditions. We conclude that activation of mechanoreceptors in the esophagus reflexly alters the distribution of motor activity to the respiratory muscles, inhibiting the muscles surrounding the abdominal cavity and augmenting the parasternals and expiratory muscles of the chest wall.
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Yu, J., Y. Wang, G. Soukhova, L. C. Collins, and J. C. Falcone. "Excitatory lung reflex may stress inspiratory muscle by suppressing expiratory muscle activity." Journal of Applied Physiology 90, no. 3 (March 1, 2001): 857–64. http://dx.doi.org/10.1152/jappl.2001.90.3.857.
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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.
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Luu, Billy L., Rachel A. McBain, Janet L. Taylor, Simon C. Gandevia, and Jane E. Butler. "Reflex response to airway occlusion in human inspiratory muscles when recruited for breathing and posture." Journal of Applied Physiology 126, no. 1 (January 1, 2019): 132–40. http://dx.doi.org/10.1152/japplphysiol.00841.2018.
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Briefly occluding the airway during inspiration produces a short-latency reflex inhibition in human inspiratory muscles. This occlusion reflex seems specific to respiratory muscles; however, it is not known whether the reflex inhibition has a uniform effect across a motoneuron pool when a muscle is recruited concurrently for breathing and posture. In this study, participants were seated and breathed through a mouthpiece that occluded inspiratory airflow for 250 ms at a volume threshold of 0.2 liters. The reflex response was measured in the scalene and sternocleidomastoid muscles during 1) a control condition with the head supported in space and the muscles recruited for breathing only, 2) a postural condition with the head unsupported and the neck flexors recruited for both breathing and to maintain head posture, and 3) a large-breath condition with the head supported and the volume threshold raised to between 0.8 and 1.0 liters to increase inspiratory muscle activity. When normalized to its preocclusion mean, the reflex response in the scalene muscles was not significantly different between the large-breath and control conditions, whereas concomitant recruitment of these muscles for posture control reduced the reflex response by half compared with the control condition. A reflex response occurred in sternocleidomastoid when it contracted phasically as an accessory muscle for inspiration during the large-breath condition. These results indicate that the occlusion reflex does not produce a uniform effect across the motoneuron pool and that afferent inputs for this reflex most likely act via intersegmental networks of premotoneurons rather than at a motoneuronal level. NEW & NOTEWORTHY In this study, we investigated the effect of nonrespiratory activity on the reflex response to brief sudden airway occlusions in human inspiratory muscles. We show that the reflex inhibition in the scalene muscles was not uniform across the motoneuron pool when the muscle was recruited concurrently for breathing and postural control. The reflex had a larger effect on respiratory-driven motoneurons than those recruited to maintain head posture.
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Gregory, J. E., A. K. Wise, S. A. Wood, A. Prochazka, and U. Proske. "Muscle history, fusimotor activity and the human stretch reflex." Journal of Physiology 513, no. 3 (December 1998): 927–34. http://dx.doi.org/10.1111/j.1469-7793.1998.927ba.x.
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Coast, J. R., G. S. Thompson, and S. S. Cassidy. "Inhibition of skeletal muscle activity by lung expansion in the dog." Journal of Applied Physiology 62, no. 5 (May 1, 1987): 2058–65. http://dx.doi.org/10.1152/jappl.1987.62.5.2058.
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The ability of lung expansion to reflexly decrease skeletal muscle activity was tested in anesthetized dogs. In animals whose left lung was vascularly isolated but neurally intact, the left lung was inflated statically to 40 cmH2O pressure or cyclically with tidal volumes of 10, 20, or 30 ml/kg. Responses to these stimuli were compared with those of injecting 120 or 240 micrograms capsaicin into the left pulmonary artery. Skeletal muscle activity was assessed from the electromyogram (EMG) response of the left hindlimb muscles and from the monosynaptic reflex response to a periodic patellar tendon tap of the right leg (knee jerk). Static inflation and cyclic inflations above 10 ml/kg resulted in significant decreases in both EMG and knee jerk responses. The results indicate that lung expansion is capable of initiating a reflex decrease in skeletal muscle activity. Capsaicin injections caused responses that were similar to those caused by lung inflation, suggesting that at least part of this skeletal muscle reflex response to lung inflation can be attributed to the stimulation of pulmonary C-fibers that could be caused by stretch of the lung.
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Oliven, A., M. Haxhiu, and S. G. Kelsen. "Expiratory muscle activity during pulmonary edema in the anesthetized dog." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 2062–68. http://dx.doi.org/10.1152/jappl.1992.73.5.2062.
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The present study evaluated the reflex response of the expiratory muscles to pulmonary congestion and edema. The electromyograms of two thoracic and four abdominal expiratory muscles were recorded in 12 anesthetized dogs. Pulmonary edema was induced by rapid saline infusion in six dogs and injection of oleic acid into the pulmonary circulation in the remaining six dogs. Both forms of pulmonary edema reduced pulmonary compliance, interfered with gas exchange, and induced a rapid and shallow breathing pattern. The electrical activity of all abdominal muscles was suppressed during both forms of pulmonary edema. In contrast, the electromyogram activity of the thoracic expiratory muscles was not significantly affected by pulmonary edema. Acute pulmonary arterial hypertension produced in two dogs by inflating a balloon in the left atrium had no effect on ventilation or expiratory muscle electrical activity. In two vagotomized dogs, pulmonary edema did not inhibit the expiratory muscles. We conclude that pulmonary edema suppresses abdominal but not thoracic expiratory muscle activity by vagal reflex pathway(s). Extravasation of fluid into the lung appears to be more important than an increase in pulmonary vascular pressure in eliciting this response.
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Grider, J. R. "Reciprocal activity of longitudinal and circular muscle during intestinal peristaltic reflex." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 5 (May 1, 2003): G768—G775. http://dx.doi.org/10.1152/ajpgi.00384.1998.
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A two-compartment, flat-sheet preparation of rat colon was devised, which enabled exclusive measurement of longitudinal muscle activity during the ascending and descending phases of the peristaltic reflex. A previous study using longitudinal muscle strips revealed the operation of an integrated neuronal circuit consisting of somatostatin, opioid, and VIP/pituitary adenylate cyclase-activating peptide (PACAP)/nitric oxide synthase (NOS) interneurons coupled to cholinergic/tachykinin motor neurons innervating longitudinal muscle strips that could lead to descending contraction and ascending relaxation of this muscle layer. Previous studies in peristaltic preparations have also shown that an increase in somatostatin release during the descending phase causes a decrease in Met-enkephalin release and suppression of the inhibitory effect of Met-enkephalin on VIP/PACAP/NOS motor neurons innervating circular muscle and a distinct set of VIP/PACAP/NOS interneurons. The present study showed that in contrast to circular muscle, longitudinal muscle contracted during the descending phase and relaxed during the ascending phase. Somatostatin antiserum inhibited descending contraction and augmented ascending relaxation of longitudinal muscle, whereas naloxone had the opposite effect. VIP and PACAP antagonists inhibited descending contraction of longitudinal muscle and augmented ascending relaxation. Atropine and tachykinin antagonists inhibited descending contraction of longitudinal muscle. As shown in earlier studies, the same antagonists and antisera produced opposite effects on circular muscle. We conclude that longitudinal muscle contracts and relaxes in reverse fashion to circular muscle during the peristaltic reflex. Longitudinal muscle activity is regulated by excitatory VIP/PACAP/NOS interneurons coupled to cholinergic/tachykinin motor neurons innervating longitudinal muscle.
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de Souza, Chris, Dilip Karnad, Rosemarie de Souza, A. Raje, K. Mansukhani, and G. H. Tilve. "The stapedial reflex in cephalic tetanus." Journal of Laryngology & Otology 108, no. 9 (September 1994): 736–42. http://dx.doi.org/10.1017/s0022215100127999.
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AbstractThree patients are presented with cephalic tetanus following injuries to the face. Two were adults and one a child. All three had bilateral VIIth cranial nerve involvement and one patient also presented with involvement of the IIIrd, IVth and VIth cranial nerves. The patients initially an ipsilateral VIIth cranial nerve weakness which later in the course of the illness developed into hyperactivity of the VIIth cranial nerve. The contralateral VIIth cranial nerve demonstrated a similar pattern. The stapedial reflex was tested serially. The stapedius muscle activity preceded that of the muscles of the face thus serving as an indicator of improvement or impending deterioration. Deflections measuring more than 1 cm, on stapedial reflex threshold testing, were indicative of stapedial reflex spasm. In the stapedial reflex decay test, both ill-sustained (intermittent) and sustained spasms of the stapedius muscle were seen.
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Deomidov, E. S. "Neurophysiologic laws of wink reflex in patients with facial neupopathy." Kazan medical journal 80, no. 4 (April 7, 1999): 266–67. http://dx.doi.org/10.17816/kazmj70117.
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Electroneuromyographic examination of 120 patients with the Bell paralysis, in the clinical picture of which facial muscle paresis of various gravity dominates, is performed. On the basis of the results obtained the bioelectric activity of facial muscles with the aim of early diagnosis and prevention of secondary contracture of facial muscles is studied.
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Pingel, Jessica, Jacob Wienecke, Jakob Lorentzen, and Jens Bo Nielsen. "Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat." Journal of Neurophysiology 116, no. 6 (December 1, 2016): 2615–23. http://dx.doi.org/10.1152/jn.00452.2016.
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Botulinum toxin is used with the intention of diminishing spasticity and reducing the risk of development of contractures. Here, we investigated changes in muscle stiffness caused by reflex activity or elastic muscle properties following botulinum toxin injection in the triceps surae muscle in rats. Forty-four rats received injection of botulinum toxin in the left triceps surae muscle. Control measurements were performed on the noninjected contralateral side in all rats. Acute experiments were performed, 1, 2, 4, and 8 wk following injection. The triceps surae muscle was dissected free, and the Achilles tendon was cut and attached to a muscle puller. The resistance of the muscle to stretches of different amplitudes and velocities was systematically investigated. Reflex-mediated torque was normalized to the maximal muscle force evoked by supramaximal stimulation of the tibial nerve. Botulinum toxin injection caused severe atrophy of the triceps surae muscle at all time points. The force generated by stretch reflex activity was also strongly diminished but not to the same extent as the maximal muscle force at 2 and 4 wk, signifying a relative reflex hyperexcitability. Passive muscle stiffness was unaltered at 1 wk but increased at 2, 4, and 8 wk ( P < 0.01). These data demonstrate that botulinum toxin causes a relative increase in reflex stiffness, which is likely caused by compensatory neuroplastic changes. The stiffness of elastic elements in the muscles also increased. The data are not consistent with the ideas that botulinum toxin is an efficient antispastic medication or that it may prevent development of contractures.
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Sinkjaer, T., and J. A. Hoffer. "Factors determining segmental reflex action in normal and decerebrate cats." Journal of Neurophysiology 64, no. 5 (November 1, 1990): 1625–35. http://dx.doi.org/10.1152/jn.1990.64.5.1625.
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1. In the companion paper the gain of the stretch reflex in the ankle extensor muscles of normal cats was shown to increase after decerebration. The objectives of this study were 1) to identify the origin of the increased reflex and 2) to evaluate the contribution from afferents other than ankle extensor muscle afferents to the short-latency reflex. 2. Six cats were trained to stand unaided on four pedestals. Three cats were also trained to control the force exerted with the left hindlimb. The left soleus (SOL) and lateral gastrocnemius (LG) electromyogram (EMG), length, force, and temperature were recorded by chronically implanted electrodes and transducers. Measurements were taken before and after decerebration at the premammillary level. After decerebration limb temperature was returned to its normal range by the use of radiant heat. 3. Reproducible ramp-and-hold stretches and releases of the ankle extensor muscles were produced by a servo-controlled motor that rotated the left rear pedestal about the ankle joint. The length of the ankle extensor muscles changed by 2-3 mm within 30-35 ms after the onset of a ramp perturbation. Reflex responses before and after decerebration were compared at matched background values of muscle length and force. 4. In both the SOL and LG muscles, a short-latency EMG burst appeared 8-12 ms after stretch onset and lasted approximately 20 ms. After decerebration the onset of the rectified and smoothed EMG burst remained unchanged, but its area was increased by 36-89%. 5. The lateral gastrocnemius-soleus (LG-S) electroneurogram (ENG) was chronically recorded in two cats with a nerve cuff recording electrode implanted on the LG-S nerve. LG-S ENG activity started to increase soon after stretch onset and remained high during the entire ramp phase. The stretch-evoked LG-S ENG burst started approximately 8 ms earlier than the short-latency SOL and LG EMG bursts. It was interpreted to reflect mainly an increase in the activity of Group Ia and Ib muscle afferents, caused by increases in both muscle length and muscle force during the stretch. After the cats were decerebrated, for matched postural conditions, the area of the stretch-evoked LG-S ENG burst was increased by 29-35%. Because the length and force changes sensed by the muscle receptors before and after decerebration were similar, this suggests that the sensitivity of muscle spindles was increased as a consequence of altered activity in fusimotor neurons after decerebration.(ABSTRACT TRUNCATED AT 400 WORDS)
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Abbink, J. H., A. van der Bilt, F. Bosman, H. W. van der Glas, C. J. Erkelens, and M. F. H. Klaassen. "Comparison of External Load Compensation During Rhythmic Arm Movements and Rhythmic Jaw Movements in Humans." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1209–17. http://dx.doi.org/10.1152/jn.1999.82.3.1209.
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Experiments were performed on human elbow flexor and extensor muscles and jaw-opening and -closing muscles to observe the effect on rhythmic movements of sudden loading. The load was provided by an electromagnetic device, which simulated the appearance of a smoothly increasing spring-like load. The responses to this loading were compared in jaw and elbow movements and between expected and unexpected disturbances. All muscles showed electromyographic responses to unexpected perturbations, with latencies of ∼65 ms in the arm muscles and 25 ms in the jaw. When loading was predictable, anticipatory responses started in arm muscles ∼200 ms before and in jaw muscles 100 ms before the onset of loading. The reflex responses relative to the anticipatory responses were smaller for the arm muscles than for the jaw muscles. The reflex responses in the arm muscles were the same with unexpected and expected perturbations, whereas anticipation increased the reflex responses in the jaw muscles. Biceps brachii and triceps brachii showed similar sensory-induced responses and similar anticipatory responses. Jaw muscles differed, however, in that the reflex response was stronger in masseter than in digastric. It was concluded that reflex responses in the arm muscles cannot overcome the loading of the arm adequately, which is compensated by a large centrally programmed response when loading is predictable. The jaw muscles, particularly the jaw-closing muscles, tend to respond mainly through reflex loops, even when loading of the jaw is anticipated. The differences between the responses of the arm and the jaw muscles may be related to physical differences. For example, the jaw was decelerated more strongly by the load than the heavier arm. The jaw was decelerated strongly but briefly, <30 ms during jaw closing, indicating that muscle force increased before the onset of reflex activity. Apparently, the force-velocity properties of the jaw muscles have a stabilizing effect on the jaw and have this effect before sensory induced responses occur. The symmetrical responses in biceps and triceps indicate similar motor control of both arm muscles. The differences in reflex activity between masseter and digastric muscle indicate fundamental differences in sensory feedback to the jaw-closing muscle and jaw-opening muscle.
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Canning, Brendan J. "Reflex regulation of airway smooth muscle tone." Journal of Applied Physiology 101, no. 3 (September 2006): 971–85. http://dx.doi.org/10.1152/japplphysiol.00313.2006.
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Autonomic nerves in most mammalian species mediate both contractions and relaxations of airway smooth muscle. Cholinergic-parasympathetic nerves mediate contractions, whereas adrenergic-sympathetic and/or noncholinergic parasympathetic nerves mediate relaxations. Sympathetic-adrenergic innervation of human airway smooth muscle is sparse or nonexistent based on histological analyses and plays little or no role in regulating airway caliber. Rather, in humans and in many other species, postganglionic noncholinergic parasympathetic nerves provide the only relaxant innervation of airway smooth muscle. These noncholinergic nerves are anatomically and physiologically distinct from the postganglionic cholinergic parasympathetic nerves and differentially regulated by reflexes. Although bronchopulmonary vagal afferent nerves provide the primary afferent input regulating airway autonomic nerve activity, extrapulmonary afferent nerves, both vagal and nonvagal, can also reflexively regulate autonomic tone in airway smooth muscle. Reflexes result in either an enhanced activity in one or more of the autonomic efferent pathways, or a withdrawal of baseline cholinergic tone. These parallel excitatory and inhibitory afferent and efferent pathways add complexity to autonomic control of airway caliber. Dysfunction or dysregulation of these afferent and efferent nerves likely contributes to the pathogenesis of obstructive airways diseases and may account for the pulmonary symptoms associated with extrapulmonary disorders, including gastroesophageal reflux disease, cardiovascular disease, and rhinosinusitis.
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Caria, Marcello A., Claudio Tavera, Francesco Melis, and Ombretta Mameli. "The Vestibulospinal Reflex in Humans: Effects on Paraspinal Muscle Activity." Acta Oto-Laryngologica 123, no. 7 (July 2003): 817–25. http://dx.doi.org/10.1080/00016480310002483.
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Weber, Christine M., and Anne Smith. "Reflex Responses in Human Jaw, Lip, and Tongue Muscles Elicited by Mechanical Stimulation." Journal of Speech, Language, and Hearing Research 30, no. 1 (March 1987): 70–79. http://dx.doi.org/10.1044/jshr.3001.70.
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Reflex responses in human jaw, lip, and tongue muscles were elicited with brief, innocuous mechanical stimuli. Stimuli were applied to the masseter (and overlying tissue), the lower lip vermilion, and the tongue dorsum. Reflex responses occurred in masseter, orbicularis oris inferior, and genioglossus muscles upon direct stimulation of the sites associated with each of these muscles. In contrast, reflex responses to stimulation of "distant" sites occurred almost exclusively in masseter; that is, stimulation of the lip and tongue produced responses in masseter, but, stimulation of jaw muscle spindle afferents and overlying cutaneous receptors had no observable effect on activity in genioglossus or orbicularis oris inferior muscles. It could be hypothesized that the motoneuron pools controlling jaw muscles are more sensitive to synaptic inputs generated by reflex pathways originating in other structures. The sensitivity of the masseter muscle to inputs from the lip and tongue may serve to link these structures functionally.
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Koba, Satoshi, Shawn G. Hayes, and Lawrence I. Sinoway. "Transient receptor potential A1 channel contributes to activation of the muscle reflex." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 1 (January 2011): H201—H213. http://dx.doi.org/10.1152/ajpheart.00547.2009.
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This study was undertaken to elucidate the role played by transient receptor potential A1 channels (TRPA1) in activating the muscle reflex, a sympathoexcitatory drive originating in contracting muscle. First, we tested the hypothesis that stimulation of the TRPA1 located on muscle afferents reflexly increases sympathetic nerve activity. In decerebrate rats, allyl isothiocyanate, a TRPA1 agonist, was injected intra-arterially into the hindlimb muscle circulation. This led to a 33% increase in renal sympathetic nerve activity (RSNA). The effect of allyl isothiocyanate was a reflex because the response was prevented by sectioning the sciatic nerve. Second, we tested the hypothesis that blockade of TRPA1 reduces RSNA response to contraction. Thirty-second continuous static contraction of the hindlimb muscles, induced by electrical stimulation of the peripheral cut ends of L4 and L5 ventral roots, increased RSNA and blood pressure. The integrated RSNA during contraction was reduced by HC-030031, a TRPA1 antagonist, injected intra-arterially (163 ± 24 vs. 95 ± 21 arbitrary units, before vs. after HC-030031, P < 0.05). Third, we attempted to identify potential endogenous stimulants of TRPA1, responsible for activating the muscle reflex. Increases in RSNA in response to injection into the muscle circulation of arachidonic acid, bradykinin, and diprotonated phosphate, which are metabolic by-products of contraction and stimulants of muscle afferents during contraction, were reduced by HC-030031. These observations suggest that the TRPA1 located on muscle afferents is part of the muscle reflex and further support the notion that arachidonic acid metabolites, bradykinin, and diprotonated phosphate are candidates for endogenous agonists of TRPA1.
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Brown, D. A., and C. G. Kukulka. "Human flexor reflex modulation during cycling." Journal of Neurophysiology 69, no. 4 (April 1, 1993): 1212–24. http://dx.doi.org/10.1152/jn.1993.69.4.1212.
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1. Human flexor reflex (HFR) responses were elicited during ergometer cycling in neurologically intact humans with the objective of understanding the influence of lower limb muscle activity on phase-dependent reflex modulation during movement. The experimental setup permitted control over background muscle activity and stimulus intensity without significantly interfering with the cycling motion. 2. All experiments involved cycling on an ergometer at a set rate and workload. A 333-Hz, 15-ms pulse train of electrical stimulation was randomly delivered to the skin over the tibial nerve at the ankle at selected lower limb positions. In the first group of experiments, subjects were stimulated at six cycling phases while pedaling with normal, phasic ankle activity (free-form cycling). The second and third group of experiments involved stimulation under static limb positioning conditions and during active pedaling while subjects were asked to maintain a consistent background level of isolated tibialis anterior (TA) or soleus (SOL) electromyographic (EMG) activity. 3. Control criteria were established to assure similar isolated muscle EMG levels and sensory stimulation intensities throughout the experiments. With the aid of the application of a lower extremity brace and visual EMG feedback, SOL and TA activity were confined by the subject to a narrow range during the task of cycling. Stimulus consistency was achieved through maintenance of flexor hallucis brevis M-waves to within an envelope encompassing the mean value +/- 5% of the maximum M-wave amplitude in all experimental conditions. 4. When the subject's limb was statically positioned, the HFR responses in the SOL muscle showed no significant changes in pattern when compared at various limb positions. During cycling with consistent SOL activity, a response waveform pattern of early-latency-long-duration depression was followed by a later-latency facilitation response in all positions except the initial power phase. The initial power phase was characterized by an additional early-latency facilitation in all but one subject. 5. In the TA muscle response, no change in onset latency (57.5 +/- 0.8 ms, mean +/- SD), waveform pattern, or response amplitude (7.9 +/- 1.1% maximal voluntary contraction, mean +/- SD) was observed during static limb positioning. Significant increases in response amplitude (P < 0.05) coupled with significant increases (9.2 ms, P < 0.05) in onset latency were seen during the transition from the recovery phase to the power phase during cycling. In addition, there was no correlation between the prestimulation baseline level and the onset latency during controlled TA cycling activity conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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Zajac, F. E. "Thigh muscle activity during maximum-height jumps by cats." Journal of Neurophysiology 53, no. 4 (April 1, 1985): 979–94. http://dx.doi.org/10.1152/jn.1985.53.4.979.
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Cats were trained to jump from a force plate and touch a cotton ball suspended as high as 1.6 m. Force-plate reaction forces and double-joint hamstring muscle activity observed early in propulsion varied from one maximal jump to another. This variability is consistent with theory (31, 32, 42); that is, different coordination strategies can be implemented prior to the heels losing contact with the force plate (heel-off). Single-joint hip extensor and double-joint posterior thigh (hip extensor-knee flexor) muscles were coactivated prior to heel-off. This coactivation is probably partially responsible for the observed backward rotation of the trunk. Forepaws, observed to contact the force plate prior to heel-off, probably assist the hindlimbs in generating trunk rotation. Both single-joint knee extensor and hip extensor muscles exhibited greatest activation between heel-off and body lift-off. Single-joint flexor muscles were inactive throughout propulsion. Double-joint posterior thigh muscles were deactivated at heel-off and remained inactivated until lift-off. These observations agree with the theoretical notion that muscles should be either fully activated, inactivated, or switched from one extreme to the other (i.e., bang-bang control) between heel-off and body lift-off (31, 32, 42, 44). All seven muscles studied shortened while activated. Using computations based on muscle geometry, fiber architecture, and joint angle trajectories, I propose that sarcomeres shorten along the flat and ascending regions of the force-length curve. De- and inactivation of double-joint posterior thigh muscles between heel-off and lift-off coincided with muscle stretch. The reason for inactivation of these muscles is that the negative work that would have been generated had these muscles stayed activated would have hindered propulsion. Contractions preceded by active stretch were not observed. Enhancement of positive work by previous storage of energy in elastic musculotendinous structures is thus not used by cat thigh musculature in jumps starting from the squat. Adductor femoris, semimembranosus anterior, and biceps femoris anterior muscles were activated synergistically as one group yet differently from the synergistic activation of gracilis, semitendinosus, and biceps femoris posterior muscles. The separation of these muscles into two groups based on their activation patterns during jumping is compatible with the classification of these muscles into hip extensor and knee flexor muscle groups, respectively, based on their reflex patterns (37), spinal cord reflex connectivity (18, 30), and firing patterns during locomotion (20).(ABSTRACT TRUNCATED AT 400 WORDS)
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Carter, Allyson M., Stephen J. Kinzey, Linda F. Chitwood, and Judith L. Cole. "Proprioceptive Neuromuscular Facilitation Decreases Muscle Activity during the Stretch Reflex in Selected Posterior Thigh Muscles." Journal of Sport Rehabilitation 9, no. 4 (November 2000): 269–78. http://dx.doi.org/10.1123/jsr.9.4.269.
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Context:Proprioceptive neuromuscular facilitation (PNF) is commonly used before competition to increase range of motion. It is not known how it changes muscle response to rapid length changes.Objective:To determine whether PNF alters hamstring muscle activity during response to rapid elongation.Design:2 X 2 factorial.Setting:Laboratory.Participants:Twenty-four women; means: 167.27 cm, 58.92 kg, 21.42 y, 18.41% body fat, 21.06 kg/m2BMI.intervention:Measurements before and after either rest or PNF were compared.Main Outcome Measures:Average muscle activity immediately after a rapid and unexpected stretch, 3 times pretreatment and posttreatment, averaged into 2 pre-and post- measures.Results:PNF caused decreased activity in the biceps femoris during response to a sudden stretch (P= .04). No differences were found in semitendinosus activity (P= .35).Conclusions:Decreased muscle activity likely results from acute desensitization of the muscle spindle, which might increase risk of muscle and tendon injury.
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Johansson, Anders S., J. Andrew Pruszynski, Benoni B. Edin, and Karl-Gunnar Westberg. "Biting intentions modulate digastric reflex responses to sudden unloading of the jaw." Journal of Neurophysiology 112, no. 5 (September 1, 2014): 1067–73. http://dx.doi.org/10.1152/jn.00133.2014.
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Reflex responses in jaw-opening muscles can be evoked when a brittle object cracks between the teeth and suddenly unloads the jaw. We hypothesized that this reflex response is flexible and, as such, is modulated according to the instructed goal of biting through an object. Study participants performed two different biting tasks when holding a peanut half stacked on a chocolate piece between their incisors. In one task, they were asked to split the peanut half only (single-split task), and in the other task, they were asked to split both the peanut and the chocolate in one action (double-split task). In both tasks, the peanut split evoked a jaw-opening muscle response, quantified from electromyogram (EMG) recordings of the digastric muscle in a window 20–60 ms following peanut split. Consistent with our hypothesis, we found that the jaw-opening muscle response in the single-split trials was about twice the size of the jaw-opening muscle response in the double-split trials. A linear model that predicted the jaw-opening muscle response on a single-trial basis indicated that task settings played a significant role in this modulation but also that the presplit digastric muscle activity contributed to the modulation. These findings demonstrate that, like reflex responses to mechanical perturbations in limb muscles, reflex responses in jaw muscles not only show gain-scaling but also are modulated by subject intent.
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Tsuchimochi, Hirotsugu, Shawn G. Hayes, Jennifer L. McCord, and Marc P. Kaufman. "Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H1157—H1163. http://dx.doi.org/10.1152/ajpheart.01219.2008.
Full textAbstract:
Both static and dynamic exercise are known to increase cardiac pump function as well as arterial blood pressure. Feedforward control by central command and feedback control by the exercise pressor reflex are thought to be the neural mechanisms causing these effects during exercise. It remains unknown as to how each mechanism activates cardiac sympathetic nerve activity (CSNA) during exercise, especially at its onset. Thus we examined the response of CSNA to stimulation of the mesencephalic locomotor region (MLR, i.e., central command) and to static muscle contraction of the triceps surae muscles or stretch of the calcaneal tendon in decerebrate cats. We found that MLR stimulation immediately increased CSNA, which was followed by a gradual increase in heart rate, mean arterial pressure, and ventral root activity in a stimulus intensity-dependent manner. The latency of the increase in CSNA from the onset of MLR stimulation ranged from 67 to 387 ms. Both static contraction and tendon stretch also rapidly increased CSNA. Their latency from the development of tension in response to ventral root stimulation ranged from 78 to 670 ms. These findings suggest that both central command and the muscle mechanoreflex play a role in controlling cardiac sympathetic outflow at the onset of exercise.
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Hansen, J., G. D. Thomas, T. N. Jacobsen, and R. G. Victor. "Muscle metaboreflex triggers parallel sympathetic activation in exercising and resting human skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 6 (June 1, 1994): H2508—H2514. http://dx.doi.org/10.1152/ajpheart.1994.266.6.h2508.
Full textAbstract:
Activation of a metabolically generated reflex in exercising skeletal muscle (muscle metaboreflex) in humans is known to trigger increases in sympathetic nerve activity (SNA) to resting skeletal muscles. In seven healthy human subjects, to determine whether this reflex mechanism also increases SNA to the exercising muscles, we recorded muscle SNA with microelectrodes in the right peroneal nerve and in fascicles of the left peroneal nerve selectively innervating the exercising muscles of the left foot. Subjects performed static toe extension at 20% maximal voluntary contraction alone or in combination with foot ischemia. Only static toe extension at 20% MVC during ischemia activated the muscle metaboreflex. This paradigm caused increases in SNA to exercising muscle that paralleled those to the resting muscles: during the first minute of exercise SNA was unchanged, but during the second minute SNA increased from 29 +/- 2 to 38 +/- 2 bursts/min (P < 0.05) to the exercising muscles and from 30 +/- 3 to 40 +/- 2 bursts/min (P < 0.05) to the resting muscles. These bilateral increases in SNA were maintained when metaboreflex activation was sustained by postexercise foot ischemia. In conclusion, these data provide neurophysiological evidence that the muscle metaboreflex evokes parallel sympathetic activation in exercising and resting human skeletal muscle.
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Murphy, Megan N., Masaki Mizuno, Jere H. Mitchell, and Scott A. Smith. "Cardiovascular regulation by skeletal muscle reflexes in health and disease." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1191—H1204. http://dx.doi.org/10.1152/ajpheart.00208.2011.
Full textAbstract:
Heart rate and blood pressure are elevated at the onset and throughout the duration of dynamic or static exercise. These neurally mediated cardiovascular adjustments to physical activity are regulated, in part, by a peripheral reflex originating in contracting skeletal muscle termed the exercise pressor reflex. Mechanically sensitive and metabolically sensitive receptors activating the exercise pressor reflex are located on the unencapsulated nerve terminals of group III and group IV afferent sensory neurons, respectively. Mechanoreceptors are stimulated by the physical distortion of their receptive fields during muscle contraction and can be sensitized by the production of metabolites generated by working skeletal myocytes. The chemical by-products of muscle contraction also stimulate metaboreceptors. Once activated, group III and IV sensory impulses are transmitted to cardiovascular control centers within the brain stem where they are integrated and processed. Activation of the reflex results in an increase in efferent sympathetic nerve activity and a withdrawal of parasympathetic nerve activity. These actions result in the precise alterations in cardiovascular hemodynamics requisite to meet the metabolic demands of working skeletal muscle. Coordinated activity by this reflex is altered after the development of cardiovascular disease, generating exaggerated increases in sympathetic nerve activity, blood pressure, heart rate, and vascular resistance. The basic components and operational characteristics of the reflex, the techniques used in human and animals to study the reflex, and the emerging evidence describing the dysfunction of the reflex with the advent of cardiovascular disease are highlighted in this review.
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Miller, A. D., and S. Nonaka. "Mechanisms of abdominal muscle activation during vomiting." Journal of Applied Physiology 69, no. 1 (July 1, 1990): 21–25. http://dx.doi.org/10.1152/jappl.1990.69.1.21.
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The possible contribution of spinal reflexes to abdominal muscle activation during vomiting was assessed in decerebrate cats. The activity of these muscles is partly controlled by bulbospinal expiratory neurons in the caudal ventral respiratory group (VRG). In a previous study it was found that the abdominal muscles are still active during vomiting after midsagittal lesion of the axons of these neurons between C1 and the obex (A.D. Miller, L.K. Tan, and I. Suzuki. J. Neurophysiol. 57: 1854-1866, 1987). The present experiments indicate that this postlesion activity was due to spinal stretch reflexes because 1) such midsagittal lesions eliminate abdominal muscle nerve activity during fictive vomiting in paralyzed cats in which there are no abdominal stretch reflexes, 2) the abdominal muscles are activated during vomiting by spinal reflexes after upper thoracic cord transections, and 3) the normal 100-ms delay between diaphragmatic and abdominal activation during vomiting is reduced to approximately 20-25 ms after both types of lesions, which is consistent with postlesion abdominal reflex activation. Our results also suggest that, during normal vomiting, abdominal stretch and tension reflexes have only a minor role if any and abdominal muscle activation is probably mediated primarily or exclusively by expiratory neurons in the caudal ventral respiratory group. However, our finding that phrenic activity is reduced both during vomiting after thoracic transections and during fictive vomiting after paralysis is consistent with a contribution of reflex activity from abdominal and/or intercostal muscles to phrenic discharge during normal vomiting.
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Leevers, A. M., and J. D. Road. "Abdominal muscle activity during hypercapnia in awake dogs." Journal of Applied Physiology 77, no. 3 (September 1, 1994): 1393–98. http://dx.doi.org/10.1152/jappl.1994.77.3.1393.
Full textAbstract:
We previously found the internal abdominal muscle layer to be preferentially recruited during expiratory threshold loading in anesthetized and awake dogs. Expiratory threshold loading increases end-expiratory lung volume and hence can activate reflex pathways such as tonic vagal reflexes, which could influence abdominal muscle recruitment. Our objectives in the present study were to determine the effects of hypercapnia on abdominal muscle activation and the pattern of recruitment in awake dogs. Five tracheotomized dogs were chronically implanted with sonomicrometer transducers and fine-wire electromyogram (EMG) electrodes in each of the four abdominal muscles: transversus abdominis, internal oblique, external oblique, and rectus abdominis. Muscle length changes and EMG activity were studied in the awake dog at rest and during CO2 rebreathing. CO2 rebreathing produced a tripling of tidal volume and activation of the abdominal muscles. Despite the increase in tidal volume, there was no significant change in abdominal muscle end-inspiratory length. Both tonic and phasic expiratory shortening were greater in the internal muscle layer (transversus abdominis and internal oblique) than in the external muscle layer (external oblique and rectus abdominis). We conclude that the internal abdominal muscles are preferentially recruited by hypercapnia and vagal reflexes probably do not contribute to this differential recruitment but that segmental reflexes may be involved. The mechanical consequences of this recruitment are discussed.
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Matsukawa, K., P. T. Wall, L. B. Wilson, and J. H. Mitchell. "Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (August 1, 1994): H821—H827. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h821.
Full textAbstract:
Reflex response of cardiac sympathetic nerve activity (CSNA) during static contraction of the triceps surae muscle was studied using anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. CSNA increased 48 +/- 13% immediately after the onset of contraction, which was abolished by cutting the L4-S1 dorsal roots. This rapid increase in CSNA preceded rises in heart rate (13 +/- 1 beats/min) and arterial blood pressure (33 +/- 6 mmHg). When tension development was altered by changing the frequency of ventral root stimulation or the initial muscle length, the CSNA increase depended on the tension developed. Passive stretch of the muscle, which primarily activates mechanoreceptors, increased CSNA by 41 +/- 22%. When the contraction was sustained for 5 min, CSNA remained elevated throughout the contraction despite a fall in tension, suggesting that the later increase in CSNA is caused by factors other than a mechanical event of contraction (e.g., metabolic products). Thus it is suggested that cardiac sympathetic outflow is stimulated due to a reflex arising from the contracting muscle. The increase in CSNA at the initiation of contraction is likely to be caused by a reflex from muscle mechanoreceptors, which is followed by a subsequent increase due to a reflex from muscle metaboreceptors.
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Victor, R. G., and D. R. Seals. "Reflex stimulation of sympathetic outflow during rhythmic exercise in humans." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 6 (December 1, 1989): H2017—H2024. http://dx.doi.org/10.1152/ajpheart.1989.257.6.h2017.
Full textAbstract:
The aim of this study was to determine whether a chemically generated reflex arising in nonischemic skeletal muscle normally increases sympathetic outflow during rhythmic exercise. To accomplish this aim, we recorded muscle sympathetic nerve activity (MSNA, peroneal nerve) in conscious humans during exercise interventions designed to alter the relationship between muscle blood flow and metabolic demand. Under normal conditions, MSNA increased during moderate but not during mild levels of rhythmic handgrip (0.67 Hz) and one-arm cycling (0.83 Hz). MSNA remained elevated when the moderate level of rhythmic handgrip was followed by forearm vascular occlusion, a maneuver that sustains muscle chemoreflex stimulation. Complete arm vascular occlusion was needed to increase MSNA during mild arm cycling, whereas even partial vascular occlusion greatly amplified the stimulation of MSNA normally produced by the moderate level of arm cycling. We conclude that a chemically generated reflex arising in nonischemic working muscle plays an important role in the normal activation of sympathetic discharge to nonexercising leg muscles during moderate but not during mild levels of rhythmic arm exercise.
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Rowell, L. B., and D. S. O'Leary. "Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes." Journal of Applied Physiology 69, no. 2 (August 1, 1990): 407–18. http://dx.doi.org/10.1152/jappl.1990.69.2.407.
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The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.
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Ebert, T. J. "Reflex activation of sympathetic nervous system by ANF in humans." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (September 1, 1988): H685—H689. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h685.
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Recent studies in experimental animal preparations suggest that ANF might alter sympathetic nervous system function. In the present investigation, direct recordings of postganglionic muscle sympathetic nerve activity were obtained from the peroneal nerve of conscious human volunteers. These data and hemodynamic parameters were recorded before and during infusions of atrial natriuretic factor (ANF, 99–126) or placebo (isotonic saline) in 10 subjects. Base-line ANF (36.5 +/- 3.8) increased to 329 +/- 22 pg/ml during 20-min infusions of ANF (15 ng.kg-1.min-1). This did not alter heart rate or blood pressure but reduced central venous pressure (CVP) by 47 +/- 10% (P less than 0.01). Base-line-integrated sympathetic activity (14.4 +/- 2.4 bursts/min) increased 30 +/- 12% during ANF infusion (P less than 0.05). However, when CVP was fixed at control levels with head-down tilt or lower body positive pressure, sympathetic activity was unchanged from pre-ANF base-line levels. These data indicate that exogenous infusions of ANF reduced CVP and unloaded cardiopulmonary baroreceptors. This elicits reflex increases of muscle sympathetic efferent activity. When CVP is maintained at control levels, ANF does not alter sympathetic neural outflow to muscles.
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Tantucci, Claudio, Selma Mehiri, Alexandre Duguet, Thomas Similowski, Isabelle Arnulf, Marc Zelter, Jean-Philippe Derenne, and Joseph Milic-Emili. "Application of negative expiratory pressure during expiration and activity of genioglossus in humans." Journal of Applied Physiology 84, no. 3 (March 1, 1998): 1076–82. http://dx.doi.org/10.1152/jappl.1998.84.3.1076.
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The application of negative expiratory pressure (NEP) at end expiration has been shown to cause reflex-mediated activation of the genioglossus muscle in awake humans. To test whether a reflex contraction of pharyngeal dilator muscles also occurs in response to NEP applied in early expiration, the effect on genioglossus muscle reflex activity of NEP pulses of 500 ms, given 0.2 s after the onset of expiration and during the end-expiratory pause, was assessed in 10 normal awake subjects at rest. The raw and integrated surface electromyogram of the genioglossus (EMGgg) was recorded with airflow and mouth pressure under control conditions and with NEP ranging from −3 to −10 cmH2O. Intraoral EMGgg was also recorded under the same experimental conditions in two subjects. The application of NEP at the end-expiratory pause elicited a consistent reflex response of EMGgg in seven subjects with a mean latency of 68 ± 5 ms. In contrast, when NEP was applied at the onset of expiration, EMGgg reflex activity was invariably observed in only one subject. No relationship was found between steady increase or abrupt fall in expiratory flow and the presence or the absence of a reflex activity of genioglossus during sudden application of NEP at the beginning of expiration. Our results show that a reflex activity of genioglossus is elicited much more commonly during application of NEP at the end rather than at the onset of expiration. These findings also suggest that when NEP is applied in early expiration to detect intrathoracic flow limitation the absence of upper airways narrowing does not imply the occurrence of a reflex-mediated activation of genioglossus and vice versa.
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Kim, Jong Kyung, Shawn G. Hayes, Angela E. Kindig, and Marc P. Kaufman. "Thin-fiber mechanoreceptors reflexly increase renal sympathetic nerve activity during static contraction." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 2 (February 2007): H866—H873. http://dx.doi.org/10.1152/ajpheart.00771.2006.
Full textAbstract:
The renal vasoconstriction induced by the sympathetic outflow during exercise serves to direct blood flow from the kidney toward the exercising muscles. The renal circulation seems to be particularly important in this regard, because it receives a substantial part of the cardiac output, which in resting humans has been estimated to be 20%. The role of group III mechanoreceptors in causing the reflex renal sympathetic response to static contraction remains an open question. To shed some light on this question, we recorded the renal sympathetic nerve responses to static contraction before and after injection of gadolinium into the arterial supply of the statically contracting triceps surae muscles of decerebrate unanesthetized and chloralose-anesthetized cats. Gadolinium has been shown to be a selective blocker of mechanogated channels in thin-fiber muscle afferents, which comprise the afferent arm of the exercise pressor reflex arc. In decerebrate ( n = 15) and chloralose-anesthetized ( n = 12) cats, we found that gadolinium (10 mM; 1 ml) significantly attenuated the renal sympathetic nerve and pressor responses to static contraction (60 s) after a latent period of 60 min; both responses recovered after a latent period of 120 min. We conclude that thin-fiber mechanoreceptors supplying contracting muscle are involved in some of the renal vasoconstriction evoked by the exercise pressor reflex.
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Augé, Wayne K., and David S. Morrison. "Assessment of the Infraspinatus Spinal Stretch Reflex in the Normal, Athletic, and Multidirectionally Unstable Shoulder." American Journal of Sports Medicine 28, no. 2 (March 2000): 206–13. http://dx.doi.org/10.1177/03635465000280021101.
Full textAbstract:
To examine neural aspects of motor control in the glenohumeral joint, this study evaluates utilization of an innate spinal segmental pathway, the spinal stretch reflex, as an investigational tool that reflects neural circuitry. The purpose of this study was to determine if this reflex could be evoked from the infraspinatus muscle, if the testing apparatus and protocol for elicitation were reliable, and if the reflex response varies between groups of subjects and therefore could be useful clinically. These reflex characteristics were evaluated in the infraspinatus muscle, since rotator cuff muscle activity in subjects with glenohumeral instability exhibits differences in electromyographic activity and coordination patterns, implicating its role in dynamic stability. Normal shoulders were compared with athletic shoulders and shoulders with multidirectional instability. The spinal stretch reflex was elicited in a controlled and reliable manner. Shoulders with multidirectional instability exhibited a more-prominent spinal stretch reflex response than normal shoulders, whereas athletic shoulders exhibited a more-quiescent spinal stretch reflex response. As the spinal stretch reflex probably plays a role in motor control, variation in this reflex profile may reflect some differences in development that contribute to the variable expression of dynamic glenohumeral stability. This study suggests that the spinal stretch reflex profile may be a useful clinical tool to assist in discriminating between the normal and pathologic state. This information may also be useful in the evaluation of new treatment approaches exploiting spinal cord plasticity and spinal stretch reflex mutability through neuromuscular training.
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Tolu, E., and M. Pugliatti. "The Vestibular System Modulates Masseter Muscle Activity." Journal of Vestibular Research 3, no. 2 (February 1, 1993): 163–71. http://dx.doi.org/10.3233/ves-1993-3205.
Full textAbstract:
The aim of this study was to investigate whether, and in what way, the vestibular input may influence the activity of the masseter muscles. The variations in the spontaneous electrical activity and the evoked responses in the masseter motor units to natural or electrical activation of the vestibular afferents were recorded in anesthetized guinea pigs. The effects of a unilateral lesion of the labyrinth on the firing rate of the masseter motor units were also studied. Results show that: 1) vestibular input elicited an excitatory tonic control on masseter muscle activity; 2) a faster labyrinthine control is driven to the contralateral than the homolateral masseter muscles; 3) vestibular macular input does exert an asymmetrical control on masseteric muscles of both sides, in relation to the head displacement in space. The latencies of responses recorded from the masseter motor units suggest that polysynaptic pathways are involved in connecting the vestibular system to the trigeminal complex. The possible anatomical substrates for this vestibulomasseteric reflex are discussed.
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Hill, J. M., C. M. Adreani, and M. P. Kaufman. "Muscle reflex stimulates sympathetic postganglionic efferents innervating triceps surae muscles of cats." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 1 (July 1, 1996): H38—H43. http://dx.doi.org/10.1152/ajpheart.1996.271.1.h38.
Full textAbstract:
Two neural mechanisms contribute to the cardiovascular responses to exercise. The first, central command, proposes a parallel activation of central locomotor and brain stem circuits controlling cardiovascular function. The second, the muscle reflex, proposes that contraction-activated group III and IV afferents increase cardiovascular function. In humans, whole nerve recordings of sympathetic discharge suggest that central command increases sympathetic outflow to skin but not to skeletal muscle and that the muscle reflex increases sympathetic outflow to skeletal muscle but not to skin. We therefore tested the hypothesis that the muscle reflex, but not central command, increases the discharge of single sympathetic postganglionic efferents innervating the triceps surae muscles of decerebrate unanesthetized cats. Central command was evoked by electrical stimulation of the mesencephalic locomotor region. The reflex was evoked by electrical stimulation of the tibial nerve, which in turn contracted the triceps surae muscles. Hexamethonium abolished spontaneous and evoked activity, verifying that the recordings were from sympathetic postganglionic fibers. The discharge of 13 efferents was increased by static contraction (from 0.6 +/- 0.2 to 1.0 +/- 0.3 imp/s; P < 0.05) but was not increased by central command (from 0.6 +/- 0.2 to 0.8 +/- 0.2 imp/s; P > 0.05). Nevertheless, the discharge of nine efferents, not increased by central command before alpha-adrenergic blockade (from 0.5 +/- 0.2 to 0.9 +/- 0.4 imp/s; P > 0.05), was increased after blockade (from 1.3 +/- 0.2 to 3.2 +/- 0.8 imp/s; P < 0.05). We conclude that the muscle reflex stimulates sympathetic postganglionic efferents innervating the vasculature of skeletal muscle. Furthermore, baroreceptors appear to buffer the central command-induced increases in the discharge of these efferents.
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Guieu, Régis, Olivier Blin, Jean Pouget, and Georges Serratrice. "Nociceptive Threshold and Physical Activity." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 1 (February 1992): 69–71. http://dx.doi.org/10.1017/s0317167100042566.
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ABSTRACT:Previous studies using subjective tools to measure pain have shown that muscle exercise can have analgesic effects in man. The nociceptive leg flexion reflex (or RIII reflex) is a useful objective tool for assessing human pain. In this study, the pain threshold was assessed using the nociceptive flexion reflex in six high-level athletes 1) at rest in comparison with 8 control subjects and 2) after exercise requiring the production of a 200-Watt force over a period of 20 minutes. The nociceptive flexion reflex threshold at rest was found to be spontaneously higher in the athletes than in the controls. Physical activity resulted in a significant increase (+53%) in the threshold of the nociceptive reflex in the athletes. The role of stress-induced analgesia, the reduction in perceived intensity of stimuli during movement, and the release of opioids are discussed.
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Ryan, Stephen, Walter T. McNicholas, Ronan G. O'Regan, and Philip Nolan. "Upper airway muscle paralysis reduces reflex upper airway motor response to negative transmural pressure in rat." Journal of Applied Physiology 94, no. 4 (April 1, 2003): 1307–16. http://dx.doi.org/10.1152/japplphysiol.00052.2002.
Full textAbstract:
The reflex upper airway (UA) motor response to UA negative pressure (UANP) is attenuated by neuromuscular blockade. We hypothesized that this is due to a reduction in the sensitivity of laryngeal mechanoreceptors to changes in UA pressure. We examined the effect of neuromuscular blockade on hypoglossal motor responses to UANP and to asphyxia in 15 anesthetized, thoracotomized, artificially ventilated rats. The activity of laryngeal mechanoreceptors is influenced by contractions of laryngeal and tongue muscles, so we studied the effect of selective denervation of these muscle groups on the UA motor response to UANP and to asphyxia, recording from the pharyngeal branch of the glossopharyngeal nerve ( n = 11). We also examined the effect of tongue and laryngeal muscle denervation on superior laryngeal nerve (SLN) afferent activity at different airway transmural pressures ( n = 6). Neuromuscular blockade and denervation of laryngeal and tongue muscles significantly reduced baseline UA motor nerve activity ( P < 0.05), caused a small but significant attenuation of the motor response to asphyxia, and markedly attenuated the response to UANP. Motor denervation of tongue and laryngeal muscles significantly decreased SLN afferent activity and altered the response to UANP. We conclude that skeletal muscle relaxation reduces the reflex UA motor response to UANP, and this may be due to a reduction in the excitability of UA motor systems as well as a decrease of the response of SLN afferents to UANP.
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Ashby, P., A. Mailis, and J. Hunter. "The Evaluation of “Spasticity”." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 497–500. http://dx.doi.org/10.1017/s0317167100037987.
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ABSTRACT:Lesions of the upper motor neuron cause: 1. Alterations in segmental reflex activity. For example increased tendon jerks and velocity dependent stretch reflexes ("spasticity"), clonus, the clasp knife response, release of flexion reflexes and extensor plantar reflexes. 2. Impaired ability to activate motoneurons rapidly and selectively. Voluntary movements may also be restrained by co-contraction of antagonists muscles, by segmental reflexes (enhanced during voluntary effort) or by contractures. A combination of these factors may impair overall functional ability. Segmental reflexes, voluntary power and overall functional abilities can be assessed using clinical scoring systems. Recordings of muscle length, tension andEMG offer more objective measures of reflex and voluntary activity and of overall functions such as locomotion, and can separate weakness from co-contraction, spasticity from contracture. Methods are now available for exploring individual (transmitter specific) segmental reflex pathways and descending pathways in man. Lesions of the upper motor neuron are complicated by secondary changes in segmental neurons. Segmental reflex activity and muscle mechanics depend on the immediate past history of events. These factors must be taken into account.
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Bonasera, S. J., and T. R. Nichols. "Mechanical actions of heterogenic reflexes linking long toe flexors with ankle and knee extensors of the cat hindlimb." Journal of Neurophysiology 71, no. 3 (March 1, 1994): 1096–110. http://dx.doi.org/10.1152/jn.1994.71.3.1096.
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1. To study the means whereby ankle biomechanics are represented in the interneuronal circuitry of the spinal cord we examined stretch-evoked reflex interactions between the physiological extensors flexor hallucis longus (FHL) and flexor digitorum longus (FDL) as well as their interactions with gastrocnemius (G), soleus (S), and the quadriceps group (Q) in 34 unanesthetized decerebrate cats. To evoke stretch, DC motors provided ramp-hold-release length changes to tendons detached from their bony insertions. Semiconductor myographs measured resultant muscle force response. Reflexes were examined under both quiescent (no active force generation) and activated conditions; muscle activation was achieved through either crossed-extension or flexion reflexes. 2. FHL and FDL share mutual excitatory stretch-evoked interactions under most conditions examined. These interactions depended on muscle length, were asymmetric (with FHL contributing a larger magnitude of reflex excitation onto FDL), and occurred at a latency of 16 ms. Mutual Ia synergism previously described for these two muscles provides a basis for all of the above findings. Our data demonstrate that for this muscle pair, reflex connectivities revealed at the intracellular level can be extrapolated to cover the entire motoneuron pool; further, our data directly demonstrate the net mechanical result of ensemble synaptic events. 3. FHL was found to share strong, mutually inhibitory stretch-evoked interactions with G, S, and Q. Stepwise regression statistical analyses determined that these interactions depended on recipient muscle force and donor muscle force. These reflex interactions all occurred at a latency of 28 +/- 4 (SE) ms. Further, the heterogenic inhibition between FHL/G and FHL/S was attenuated by strychnine infusion (intravenous) but unaffected by either mecamylamine, picrotoxin, or baclofen infusion (intravenous, intrathecal). Disynaptic Ib inhibition previously described among hindlimb extensors provides a basis for the above findings; our data demonstrate that under certain conditions the ensemble activity of this system can cause a dramatic decline in whole muscle force output. 4. By contrast, FDL was found to share mutually inhibitory, stretch-evoked reflex interactions with G, S, and Q that were much weaker than those observed between FHL and these same muscles. The small magnitude of inhibition observed in these interactions made it difficult to assess reflex latency or to determine the factor(s) that best predicted the heterogenic inhibition. 5. This study provides further evidence of intrinsic differences in interneuronal organization between muscles whose activity occurs in a periodic manner during locomotion ("stereotypical") and a muscle whose locomotor activity is characterized by both periodic and nonperiodic components ("facultative").(ABSTRACT TRUNCATED AT 400 WORDS)
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Matsukawa, K., P. T. Wall, L. B. Wilson, and J. H. Mitchell. "Reflex responses of renal nerve activity during isometric muscle contraction in cats." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 5 (November 1, 1990): H1380—H1388. http://dx.doi.org/10.1152/ajpheart.1990.259.5.h1380.
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Renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), and heart rate (HR) were measured during isometric muscle contraction of a hindlimb in chloralose-anesthetized cats. In 14 cats RSNA, AP, and HR increased during a 1-min contraction by 45%, 39 mmHg, and 11 beats/min, respectively; however, in three cats there was a brief initial decrease in RSNA followed by an increase. In 11 cats isometric contraction was maintained for 5 min by alternate stimulation of the L7 and S1 ventral roots. In the first 1 min of sustained contraction, there was a positive correlation (gamma = 0.58, P less than 0.005) between RSNA and tension development. Thereafter RSNA remained elevated despite a tension decrease, and there was no significant correlation between these changes. The RSNA response to contraction of both hindlimbs was greater than that to contraction of either hindlimb alone. Passive stretch of the hindlimb muscle significantly increased RSNA. Thus the initial increase in RSNA during sustained contraction is likely due to activation of muscle mechanoreceptors, whereas the later increase is probably caused by activation of the muscle metaboreceptors.
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Fitzpatrick, R., D. Burke, and S. C. Gandevia. "Loop gain of reflexes controlling human standing measured with the use of postural and vestibular disturbances." Journal of Neurophysiology 76, no. 6 (December 1, 1996): 3994–4008. http://dx.doi.org/10.1152/jn.1996.76.6.3994.
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1. In this study we measured the loop gain of postural reflexes in standing human subjects. Reflex activity is conventionally described in terms of the muscle activation arising from a perturbation, but in this study the ability of the evoked muscle activity to correct the perturbation was also measured, and the behavior of the entire feedback loop is described. 2. A weak continuous random perturbation was applied at waist level to standing subjects. The effects of the perturbation on body sway and soleus electromyogram (EMG) were identified by cross-correlation, and spectral analysis was used to estimate the open-loop reflex transmission characteristics (i.e., sway to EMG). Under the same conditions, activity in the leg muscles was evoked by galvanic vestibular stimulation with the use of a continuous randomly varying current. The effects on soleus EMG and the subsequent body sway were identified by cross-correlation. This allowed calculation of the open-loop muscle and load behavior (i.e., EMG to sway). From these open-loop reflex and muscle and load transfer functions, the loop gain and phase were calculated. 3. In addition to the gain of the feedback loop, the study describes the transmission characteristics of reflex responses in the leg muscles associated with body sway and the effects of excluding visual and proprioceptive contributions to the response; the transfer function of human soleus with a stimulus that preserves the normal recruitment of motoneurons, including the effects of different load conditions on the muscle; and the transmission characteristics of vestibular pathways that evoke responses in the leg muscles during standing in situations that might modify the reflexes. 4. When standing, the loop gain of reflex feedback is approximately unity and is unchanged by eye closure and stability of support. Reflex transmission introduced a marked phase advance, and this served to offset most of the phase lag introduced by muscle and load. The residual phase lag could explain the frequency of tremor observed during standing (6–8 Hz). 5. The gain of the feedback loop (approximately 1) is higher than suggested by both previous estimates and theoretical considerations, but is still insufficient to explain the stability of normal human standing. This implies that, although sensory information is used to control posture, it does not do so exclusively through a negative feedback control process. The experimental findings are consistent with a reflex response based on a feed-forward process, and this would result in prediction of the response necessary to counteract a postural disturbance.
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Yang, Yuan, Teodoro Solis-Escalante, Jun Yao, Frans C. T. van der Helm, Julius P. A. Dewald, and Alfred C. Schouten. "Nonlinear Connectivity in the Human Stretch Reflex Assessed by Cross-Frequency Phase Coupling." International Journal of Neural Systems 26, no. 08 (October 4, 2016): 1650043. http://dx.doi.org/10.1142/s012906571650043x.
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Communication between neuronal populations is facilitated by synchronization of their oscillatory activity. Although nonlinearity has been observed in the sensorimotor system, its nonlinear connectivity has not been widely investigated yet. This study investigates nonlinear connectivity during the human stretch reflex based on neuronal synchronization. Healthy participants generated isotonic wrist flexion while receiving a periodic mechanical perturbation to the wrist. Using a novel cross-frequency phase coupling metric, we estimate directional nonlinear connectivity, including time delay, from the perturbation to brain and to muscle, as well as from brain to muscle. Nonlinear phase coupling is significantly stronger from the perturbation to the muscle than to the brain, with a shorter time delay. The time delay from the perturbation to the muscle is 33 ms, similar to the reported latency of the spinal stretch reflex at the wrist. Source localization of nonlinear phase coupling from the brain to the muscle suggests activity originating from the motor cortex, although its effect on the stretch reflex is weak. As such nonlinear phase coupling between the perturbation and muscle activity is dominated by the spinal reflex loop. This study provides new evidence of nonlinear neuronal synchronization in the stretch reflex at the wrist joint with respect to spinal and transcortical loops.
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Johnson, Michael D., Alain Frigon, Marie-France Hurteau, Charlette Cain, and C. J. Heckman. "Reflex wind-up in early chronic spinal injury: plasticity of motor outputs." Journal of Neurophysiology 117, no. 5 (May 1, 2017): 2065–74. http://dx.doi.org/10.1152/jn.00981.2016.
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In this study we evaluate temporal summation (wind-up) of reflexes in select distal and proximal hindlimb muscles in response to repeated stimuli of the distal tibial or superficial peroneal nerves in cats 1 mo after complete spinal transection. This report is a continuation of our previous paper on reflex wind-up in the intact and acutely spinalized cat. To evaluate reflex wind-up in both studies, we recorded electromyographic signals from the following left hindlimb muscles: lateral gastrocnemius (LG), tibialis anterior (TA), semitendinosus (ST), and sartorius (Srt), in response to 10 electrical pulses to the tibial or superficial peroneal nerves. Two distinct components of the reflex responses were considered, a short-latency compound action potential (CAP) and a longer duration bout of sustained activity (SA). These two response types were shown to be differentially modified by acute spinal injury in our previous work (Frigon A, Johnson MD, Heckman CJ. J Physiol 590: 973-989, 2012). We show that these responses exhibit continued plasticity during the 1-mo recovery period following acute spinalization. During this early chronic phase, wind-up of SA responses returned to preinjury levels in one muscle, the ST, but remained depressed in all other muscles tested. In contrast, CAP response amplitudes, which were initially potentiated following acute transection, returned to preinjury levels in all muscles except for Srt, which continued to show marked increase. These findings illustrate that spinal elements exhibit considerable plasticity during the recovery process following spinal injury and highlight the importance of considering SA and CAP responses as distinct phenomena with unique underlying neural mechanisms. NEW & NOTEWORTHY This research is the first to assess temporal summation, also called wind-up, of muscle reflexes during the 1-mo recovery period following spinal injury. Our results show that two types of muscle reflex activity are differentially modulated 1 mo after spinal cord injury (SCI) and that spinal reflexes are altered in a muscle-specific manner during this critical period. This postinjury plasticity likely plays an important role in spasticity experienced by individuals with SCI.
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Schotland, J. L., and W. Z. Rymer. "Wipe and flexion reflexes of the frog. II. Response to perturbations." Journal of Neurophysiology 69, no. 5 (May 1, 1993): 1736–48. http://dx.doi.org/10.1152/jn.1993.69.5.1736.
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1. To evaluate the hypothesis that the neural control of sensorimotor transformations may be simplified by using a single control variable, we compared the movement kinematics and muscle activity patterns [electromyograms (EMGs)] of the frog during flexion withdrawal and the hind limb-hind limb wipe reflex before and after adding an external load. In addition, the flexibility of spinal cord circuitry underlying the hind limb-hind limb wipe reflex was evaluated by comparing wipes before and after removal of one of the contributing muscles by cutting a muscle nerve. 2. The kinematics of the movements were recorded using a WATSMART infrared emitter-detector system and quantified using principal-components analysis to provide a measure of the shape (eigenvalues) and orientation (eigenvector coefficients) of the movement trajectories. The neural pattern coordinating the movements was characterized by the latencies and magnitudes of EMGs of seven muscles acting at the hip, knee, and ankle. These variables were compared 1) during flexion withdrawal and the initial movement segment of the limb during the hind limb-hind limb wipe reflex in both unrestrained movements and in movements executed when a load equal to approximately 10% of the animal's body weight was attached to a distal limb segment and 2) during the initial movement segment of the wipe reflex before and after cutting the nerve to the knee flexor-hip extensor, iliofibularis. 3. Addition of the load had no discernible effect on the end-point position of the foot during either reflex. However, during the loaded flexion reflex, the ankle joint did not move until after the hip and knee joints had moved to their normal positions. This delayed flexion of the ankle was accompanied by large increases in the magnitude of EMG activity in two ankle muscles that exceeded the levels found during unrestrained movements. Significant changes in the temporal organization of the EMG pattern accompanied the change in joint angle relations during flexion withdrawal. 4. Despite the addition of an external load, all animals successfully and reliably removed the stimulus during the wipe reflex, and the relative timing of both the EMG pattern and joint angle motion was preserved. 5. Immediately after section of the nerve to a single muscle (iliofibularis), all animals successfully and reliably removed the stimulus during the wipe reflex. The relative timing of muscle activation was preserved, accompanied by a reduction in the activity level of gluteus magnus, a muscle with action reciprocal to iliofibularis.(ABSTRACT TRUNCATED AT 400 WORDS)
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Thexton, A. J., A. W. Crompton, and R. Z. German. "Electromyographic activity during the reflex pharyngeal swallow in the pig: Doty and Bosma (1956) revisited." Journal of Applied Physiology 102, no. 2 (February 2007): 587–600. http://dx.doi.org/10.1152/japplphysiol.00456.2006.
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The currently accepted description of the pattern of electromyographic (EMG) activity in the pharyngeal swallow is that reported by Doty and Bosma in 1956; however, those authors describe high levels of intramuscle and of interindividual EMG variation. We reinvestigated this pattern, testing two hypotheses concerning EMG variation: 1) that it could be reduced with modern methodology and 2) that it could be explained by selective detection of different types of motor units. In eight decerebrate infant pigs, we elicited radiographically verified pharyngeal swallows and recorded EMG activity from a total of 16 muscles. Synchronization signals from the video-radiographic system allowed the EMG activity associated with each swallow to be aligned directly with epiglottal movement. The movements were highly stereotyped, but the recorded EMG signals were variable at both the intramuscle and interanimal level. During swallowing, some muscles subserved multiple functions and contained different task units; there were also intramuscle differences in EMG latencies. In this situation, statistical methods were essential to characterize the overall patterns of EMG activity. The statistically derived multimuscle pattern approximated to the classical description by Doty and Bosma (Doty RW, Bosma JF. J Neurophysiol 19: 44–60, 1956) with a leading complex of muscle activities. However, the mylohyoid was not active earlier than other muscles, and the geniohyoid muscle was not part of the leading complex. Some muscles, classically considered inactive, were active during the pharyngeal swallow.