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1
Franz, Leonardo, Luciana Travan, Miriam Isola, Gino Marioni, and Renzo Pozzo. "Facial Muscle Activity Patterns in Clarinet Players: A Key to Understanding Facial Muscle Physiology and Dysfunction in Musicians." Annals of Otology, Rhinology & Laryngology 129, no. 11 (June 2, 2020): 1078–87. http://dx.doi.org/10.1177/0003489420931553.
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Objectives: Facial muscle activity is crucial to controlling musical performance in wind instrument playing. Facial muscle dysfunctions are common in wind instrument players, dramatically affecting their professional musical activity and potentially leading to disabling symptoms. The aim of this pilot study on a cohort of healthy clarinetists was to use surface electromyography to identify the facial muscle activity patterns involved in stabilizing the mouthpiece, controlling emission and articulation during musical tasks in physiological conditions, also comparing muscle activity between less and more experienced clarinetists (students vs postgraduates/professionals). Methods: Surface electromyographic measures of the sternocleidomastoid, masseter, mentalis, mylohyoid and buccinator muscles were obtained from eight healthy clarinet players (four students and four postgraduates/professionals) performing two standardized musical tasks. Results: Overall, mean IEMG activity was significantly lower for the sternocleidomastoid than for the other muscles ( P = .000), and for the mouthpiece-stabilizing muscles (masseter and mentalis) than for those directly involved in controlling emission and articulation (buccinator and mylohyoid muscles) ( P = .000). Regardless of the musical task, the mean IEMG values were significantly higher in the students for the masseter ( P = .0007), buccinator ( P = .0001) and mylohyoid (0.000), while they were significantly higher in the postgraduates/professionals for the mentalis ( P = .000). No significant differences emerged between the two groups for the sternocleidomastoid ( P = .207). Conclusions: These preliminary data reflect a significantly higher overall facial muscle activity in the less-experienced group, potentially resulting in an overload, whereas the more expert players had more optimized muscle activity patterns.
2
Hollowell, D. E., P. R. Bhandary, A. W. Funsten, and P. M. Suratt. "Respiratory-related recruitment of the masseter: response to hypercapnia and loading." Journal of Applied Physiology 70, no. 6 (June 1, 1991): 2508–13. http://dx.doi.org/10.1152/jappl.1991.70.6.2508.
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To test the hypothesis that a muscle that closes the jaw, the masseter, can be recruited by ventilatory stimuli, we studied the electromyographic activation of the masseter and genioglossus in seven normal awake males who were exposed in random order to progressive hyperoxic hypercapnia, inspiratory threshold loading (-40 cmH2O), and combined hypercapnia and loading. With hypercapnia, the masseter was generally recruited after the genioglossus had been activated. Once recruited, activation of both muscles increased linearly with increasing CO2. Combined hypercapnia and loading produced more activation than either stimulus alone. These data indicate that the masseter is activated by ventilatory stimuli that activate the genioglossus. Earlier recruitment of the genioglossus suggests that activation of the masseter serves to stabilize the mandible and allow the genioglossus to function as a more efficient dilator of the upper airway.
3
Cairns, Brian E., James W. Hu, Lars Arendt-Nielsen, Barry J. Sessle, and Peter Svensson. "Sex-Related Differences in Human Pain and Rat Afferent Discharge Evoked by Injection of Glutamate Into the Masseter Muscle." Journal of Neurophysiology 86, no. 2 (August 1, 2001): 782–91. http://dx.doi.org/10.1152/jn.2001.86.2.782.
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Animal studies have suggested that tissue injury–related increased levels of glutamate may be involved in peripheral nociceptive mechanisms in deep craniofacial tissues. Indeed, injection of glutamate (0.1–1 M, 10 μl) into the temporomandibular region evokes reflex jaw muscle responses through activation of peripheral excitatory amino acid receptors. It has recently been found that this glutamate-evoked reflex muscle activity is significantly greater in female than male rats. However, it is not known whether peripheral administration of glutamate, in the same concentrations that evoke jaw muscle activity in rats, causes pain in humans or activates deep craniofacial nociceptive afferents. Therefore we examined whether injection of glutamate into the masseter muscle induces pain in male and female volunteers and, since masseter afferent recordings were not feasible in humans, whether glutamate excites putative nociceptive afferents supplying the masseter muscle of male and female rats. Injection of glutamate (0.5 M or 1.0 M, 0.2 ml) into the masseter muscle of both men and women caused significantly higher levels of peak pain, duration of pain, and overall pain than injection of isotonic saline (0.2 ml). In addition, glutamate-evoked peak and overall muscle pain in women was significantly greater than in men. In rats of both sexes, glutamate (10 μl, 0.5 M) evoked activity in a subpopulation of masseter muscle afferents ( n = 36) that projected to the subnucleus caudalis, an important relay of noxious input from the craniofacial region. The largest responses to glutamate were recorded in muscle afferents with the slowest conduction velocities (2.5–5 m/s). Further, glutamate-evoked masseter muscle afferent activity was significantly greater in female than in male rats. These results indicate that glutamate injection into the masseter muscle evokes pain responses that are greater in women than men and that one possible mechanism for this difference may be a greater sensitivity to glutamate of masseter muscle afferents in females. These sex-related differences in acute experimental masseter muscle pain are particularly interesting given the higher prevalence of many chronic muscle pain conditions in women.
4
Türker, Kemal S., and Melissa Jenkins. "Reflex Responses Induced by Tooth Unloading." Journal of Neurophysiology 84, no. 2 (August 1, 2000): 1088–92. http://dx.doi.org/10.1152/jn.2000.84.2.1088.
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The reflex response of the masseter muscle to the rapid unloading of a single maxillary incisor tooth was studied. Unloading of a static force of 2 N in the horizontal direction resulted in a short-latency excitation, inhibition, and long-latency excitation of masseter muscle activity occurring at latencies of approximately 13, 20, and 40 ms, respectively, with a corresponding change in bite force occurring slightly later in each case. Following the blocking of periodontal input by the injection of local anesthetic around the stimulated tooth, inhibitory responses were abolished. Therefore, it is concluded that the observed masseteric inhibition was caused by the unloading of periodontal mechanoreceptors and thus that these receptors may contribute to the jaw unloading reflex.
5
Ayada, Kentaro, Makoto Watanabe, and Yasuo Endo. "Elevation of histidine decarboxylase activity in skeletal muscles and stomach in mice by stress and exercise." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2042—R2047. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2042.
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The effects of different types of stress (water bathing, cold, restraint, and prolonged walking) on histidine decarboxylase (HDC) activity in masseter, quadriceps femoris, and pectoralis superficial muscles, and in the stomach were examined in mice. All of these stresses elevated gastric HDC activity. Although water bathing, in which muscle activity was slight, was sufficiently stressful to produce gastric hemorrhage and to increase gastric HDC activity, it produced no detectable elevation of HDC activity in any of the muscles examined. The other stresses all elevated HDC activity in all three muscles. We devised two methods of restraint, one accompanied by mastication and the other not. The former elevated HDC activity in the masseter muscle, but the latter did not. These results suggest that 1) HDC activity in the stomach is an index of responses to stress, 2) the elevation of HDC activity in skeletal muscles during stress is induced partly or wholly by muscle activity and/or muscle tension, and 3) stress itself does not always induce an elevation of HDC activity in skeletal muscles.
6
Hollowell, D. E., and P. M. Suratt. "Mandible position and activation of submental and masseter muscles during sleep." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2267–73. http://dx.doi.org/10.1152/jappl.1991.71.6.2267.
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Movement of the mandible could influence pharyngeal airway caliber because the mandible is attached to the tongue and to muscles that insert on the hyoid bone. In normal subjects and patients with obstructive sleep apnea (OSA) we measured jaw position during sleep with strain gauges, as well as masseter and submental electromyograms, airflow, esophageal pressure, oximetry, electroencephalograms, and electrooculograms. Jaws of patients with OSA were open more than those of normal subjects at end expiration and opened further at end inspiration, particularly at the termination of apneas when the masseter and submental muscles contracted. Masseter activation occurred only in patients with OSA and in a pattern similar to that of submental muscles. Jaw opening at end expiration could narrow the upper airway, whereas opening at end inspiration could reflect efforts to expand the airway with tracheal tug and with submental muscle activation and efforts to open the mouth to allow mouth breathing. Masseter contraction does not close the jaw but may serve to stabilize it.
7
Evans, Marianna, Kevin Morine, Cyelee Kulkarni, and Elisabeth R. Barton. "Expression profiling reveals heightened apoptosis and supports fiber size economy in the murine muscles of mastication." Physiological Genomics 35, no. 1 (September 2008): 86–95. http://dx.doi.org/10.1152/physiolgenomics.00232.2007.
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Distinctions between craniofacial and axial muscles exist from the onset of development and throughout adulthood. The masticatory muscles are a specialized group of craniofacial muscles that retain embryonic fiber properties in the adult, suggesting that the developmental origin of these muscles may govern a pattern of expression that differs from limb muscles. To determine the extent of these differences, expression profiling of total RNA isolated from the masseter and tibialis anterior (TA) muscles of adult female mice was performed, which identified transcriptional changes in unanticipated functional classes of genes in addition to those attributable to fiber type. In particular, the masseters displayed a reduction of transcripts associated with contractile and cytoskeletal load-sensing and anabolic processes, and heightened expression of genes associated with stress. Associated with these observations was a significantly smaller fiber cross-sectional area in masseters, significantly elevated load-sensing signaling (phosphorylated focal adhesion kinase), and increased apoptotic index in masseters compared with TA muscles. Based on these results, we hypothesize that masticatory muscles may have a fundamentally different strategy for muscle design, compared with axial muscles. Specifically there are small diameter fibers that have an attenuated ability to hypertrophy, but an increased propensity to undergo apoptosis. These results may provide insight into the molecular basis for specific muscle-related pathologies associated with masticatory muscles.
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Hakim, Akhlaq W., Xudong Dong, and Brian E. Cairns. "TNFα Mechanically Sensitizes Masseter Muscle Nociceptors by Increasing Prostaglandin E2 Levels." Journal of Neurophysiology 105, no. 1 (January 2011): 154–61. http://dx.doi.org/10.1152/jn.00730.2010.
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TNFα induces mechanical sensitization of rat masseter muscle nociceptors, which takes 2–3 h to manifest and is mediated through activation of P55 and P75 receptors. This study was undertaken to determine whether TNFα induces nociceptor mechanical sensitization through the release of other algogenic substances such as glutamate, prostaglandin E2 (PGE2), and/or nerve growth factor (NGF), which have been shown to induce mechanical sensitization of muscle nociceptors. Masseter muscle homogenate levels of PGE2 and NGF were measured 3 h after injection of TNFα (1 μg) or vehicle control using commercially available kits. Interstitial glutamate concentration was measured after injection of TNFα or vehicle control using a glutamate-selective biosensor probe. Diclofenac, a cycloxygenase inhibitor that blocks the synthesis of PGE2, d-2-amino-5-phophonovaleric acid (APV), a competitive N-methyl-d-aspartate (NMDA) receptor antagonist, and a tyrosine kinase A (TrkA) receptor antibody, which blocks NGF-induced masseter muscle nociceptor sensitization, were used to assess the contribution of PGE2, glutamate, and NGF to TNFα-induced nociceptor sensitization. PGE2 and glutamate concentrations were significantly elevated 3 h after TNFα injection into the masseter muscle. Injection of diclofenac partially reversed the TNFα-induced decreases in the mechanical threshold (MT) of masseter muscle nociceptors, whereas vehicle control, APV, and TrkA antibody did not significantly alter nociceptor MT. These results suggest that TNFα-induced mechanical sensitization of masseter muscle nociceptors is mediated in part by increased PGE2 levels. The findings of this study support the hypothesis that TNFα induces a delayed mechanical sensitization of masseter muscle nociceptors indirectly by the release of PGE2.
9
Eason, Jane M., Gail A. Schwartz, Grace K. Pavlath, and Arthur W. English. "Sexually dimorphic expression of myosin heavy chains in the adult mouse masseter." Journal of Applied Physiology 89, no. 1 (July 1, 2000): 251–58. http://dx.doi.org/10.1152/jappl.2000.89.1.251.
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Little is known regarding the role of androgenic hormones in the maintenance of myosin heavy chain (MHC) composition of rodent masticatory muscles. Because the masseter is the principal jaw closer in rodents, we felt it was important to characterize the influence of androgenic hormones on the MHC composition of the masseter. To determine the extent of sexual dimorphism in the phenotype of masseter muscle fibers of adult (10-mo-old) C57 mice, we stained tissue sections with antibodies specific to type IIa and IIb MHC isoforms. Females contain twice as many fibers containing the IIa MHC as males, and males contain twice as many fibers containing the IIb MHC as females. There is a modest amount of regionalization of MHC phenotypes in the mouse masseter. The rostral portions of the masseter are composed mostly of type IIa fibers, whereas the midsuperficial and caudal regions contain mostly type IIb fibers. Using immunoblots, we showed that castration results in an increase in the expression of type IIa MHC fibers in males. Ovariectomy has no effect on the fiber type composition in females. We conclude that testosterone plays a role in the maintenance of MHC expression in the adult male mouse masseter.
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Schwarz, Peter B., and John H. Peever. "Dopamine triggers skeletal muscle tone by activating D1-like receptors on somatic motoneurons." Journal of Neurophysiology 106, no. 3 (September 2011): 1299–309. http://dx.doi.org/10.1152/jn.00230.2011.
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The dopamine system plays an integral role in motor physiology. Dopamine controls movement by modulation of higher-order motor centers (e.g., basal ganglia) but may also regulate movement by directly controlling motoneuron function. Even though dopamine cells synapse onto motoneurons, which themselves express dopamine receptors, it is unknown whether dopamine modulates skeletal muscle activity. Therefore, we aimed to determine whether changes in dopaminergic neurotransmission at a somatic motor pool affect motor outflow to skeletal muscles. We used microinjection, neuropharmacology, electrophysiology, and histology to determine whether manipulation of D1- and D2-like receptors on trigeminal motoneurons affects masseter and/or tensor palatini muscle tone in anesthetized rats. We found that apomorphine (a dopamine analog) activated trigeminal motoneurons and triggered a potent increase in both masseter and tensor palatini tone. This excitatory effect is mediated by D1-like receptors because specific D1-like receptor activation strengthened muscle tone and blockade of these receptors prevented dopamine-driven activation of motoneurons. Blockade of D1-like receptors alone had no detectable effect on basal masseter/tensor palatini tone, indicating the absence of a functional dopamine drive onto trigeminal motoneurons, at least during isoflurane anesthesia. Finally, we showed that D2-like receptors do not affect either trigeminal motoneuron function or masseter/tensor palatini muscle tone. Our results provide the first demonstration that dopamine can directly control movement by manipulating somatic motoneuron behavior and skeletal muscle tone.
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Ishii, Hisayoshi, Takeharu Niioka, Hidekazu Watanabe, and Hiroshi Izumi. "Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (August 2007): R729—R736. http://dx.doi.org/10.1152/ajpregu.00866.2006.
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The present study was designed to examine the effect of sympathetic tonic activity on parasympathetic vasodilation evoked by the trigeminal-mediated reflex in the masseter muscle in urethane-anesthetized rats. Sectioning of the superior cervical sympathetic trunk (CST) ipsilaterally increased the basal level of blood flow in the masseter muscle (MBF). Electrical stimulation of the peripheral cut end of the CST for 2 min using 2-ms pulses ipsilaterally decreased in a dependent manner the intensity (0.5–10 V) and frequency (0.1–5 Hz) of the MBF. The CST stimulation for 2 min at <0.5 Hz with 5 V using 2-ms pulses seems to be comparable with the spontaneous activity in the CST fibers innervating the masseter vasculature, because this stimulation restored the basal level of the MBF to the presectioned values. Parasympathetic vasodilation evoked by electrical stimulation of the central cut end of the lingual nerve in the masseter muscle was markedly reduced by CST stimulation for 2 min with 5 V using 2-ms pulses in a frequency-dependent manner (0.5–5 Hz). Intravenous administration of phentolamine significantly reduced the vasoconstriction induced by CST stimulation in a dose-dependent manner (0.1–1 mg/kg), but pretreatment with either phentolamine or propranolol failed to affect the sympathetic inhibition of the parasympathetic vasodilation. Our results suggest that 1) excess sympathetic activity inhibits parasympathetic vasodilation in the masseter muscle, and 2) α- and β-adrenoceptors do not contribute to sympathetic inhibition of parasympathetic vasodilation, and thus some other types of receptors must be involved in this response.
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Lambert, R. W., L. J. Goldberg, and S. H. Chandler. "Comparison of mandibular movement trajectories and associated patterns of oral muscle electromyographic activity during spontaneous and apomorphine-induced rhythmic jaw movements in the guinea pig." Journal of Neurophysiology 55, no. 2 (February 1, 1986): 301–19. http://dx.doi.org/10.1152/jn.1986.55.2.301.
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Vertical and horizontal movements of the lower jaw (mandible) of ketamine-anesthetized guinea pigs were recorded in association with electromyographic (EMG) activity in the anterior digastric, lateral pterygoid, medial pterygoid, and deep masseter muscles during spontaneously occurring rhythmic jaw movements (SRJMs) and during rhythmical jaw movements induced by the intravenous administration of apomorphine (ARJMs). Both ARJMs and SRJMs were near periodic and occurred at frequencies in the 2- to 5-Hz range. However, the profiles of the mandibular movements and associated patterns of jaw muscle EMG activity differed dramatically for SRJMs versus ARJMs. SRJMs were characterized by prominent lateral excursions of the mandible that occurred in association with both the jaw opening and closing movements. The lateral excursions were directed to the left side on some SRJM cycles and to the right side on others. The direction of the lateral component alternated irregularly, but no more than three consecutive cycles with horizontal movements to the same side were observed at any time. Each SRJM cycle was generated by the occurrence of one of two coordinated sequences of EMG activity. One sequence produced right-sided cycles, the other produced left-sided cycles. Each sequence was initiated by an EMG burst in the digastric muscle ipsilateral to the direction of the horizontal excursion of the mandible, followed by EMG bursts in the contralateral digastric, lateral pterygoid, and medial pterygoid muscles. The EMG bursts in the digastrics and contralateral lateral pterygoid muscles were associated with jaw opening and the initial stage of lateral movement. EMG activity in the contralateral medial pterygoid muscle was associated with the onset of closing and a second stage of lateral movement. Masseter muscle activity was also observed during SRJMs, but only in a subset of the animals tested (3 of 12). When present, the masseter activity began well after the onset of jaw closing. No significant horizontal mandibular movements were observed during ARJMs. The mandibular trajectories during opening and closing always remained close to the midline. The opening phase of ARJM cycles was associated with bilaterally synchronized activity in the digastric and lateral pterygoid muscles. The closing phase was associated with bilaterally symmetric activity in the masseter muscles. The medial pterygoid muscles displayed little or no EMG activity during ARJMs. The durations of the EMG bursts recorded in the masseter muscle were correlated with cycle time during SRJMs, as were the burst durations of the digastric and lateral pterygoid muscles during ARJMs.(ABSTRACT TRUNCATED AT 400 WORDS)
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Anapol, F., and S. W. Herring. "Length-tension relationships of masseter and digastric muscles of miniature swine during ontogeny." Journal of Experimental Biology 143, no. 1 (May 1, 1989): 1–16. http://dx.doi.org/10.1242/jeb.143.1.1.
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At incremental whole muscle lengths, active isometric and passive elastic forces were recorded from the masseter and digastric muscles of anaesthetized miniature pigs (Hanford) weighing 2.0-20.0 kg. Wet muscle mass and maximum tetanic tension values for masseter exceed those for digastric and increase more rapidly with body mass (age). At any body mass, masseter exceeds digastric in the ratio of optimum length (that length at which maximum tetanic tension is produced) to in situ muscle length (that length which corresponds to the jaw in a closed position) and the proportion of passive tension comprising total (passive plus active) tension. Passive elastic tension begins to rise in masseter at lengths as short as 87% of optimum (in younger pigs). In digastric, passive tension is absent until the muscle is stretched to a length slightly longer than optimum in younger pigs but occurs at shorter lengths in older pigs. Contractile properties explain functional differences between masseter and digastric more clearly than they explain ontogenetic changes in either muscle. The behavioural transition from infant suckling to adult mastication of solid food is best characterized by a disproportionate increase in mass (and force) of the masseter, relative to digastric, and increased reliance upon active (rather than passive) tension.
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Yang, J., and K. S. Türker. "Jaw Reflexes Evoked by Mechanical Stimulation of Teeth in Humans." Journal of Neurophysiology 81, no. 5 (May 1, 1999): 2156–63. http://dx.doi.org/10.1152/jn.1999.81.5.2156.
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Jaw reflexes evoked by mechanical stimulation of teeth in humans. The reflex response of jaw muscles to mechanical stimulation of an upper incisor tooth was investigated using the surface electromyogram (SEMG) of the masseter muscle and the bite force. With a slowly rising stimulus, the reflex response obtained on the masseter SEMG showed three different patterns of reflex responses; sole excitation, sole inhibition, and inhibition followed by excitation. Simultaneously recorded bite force, however, exhibited mainly one reflex response pattern, a decrease followed by an increase in the net closing force. A rapidly rising stimulus also induced several different patterns of reflex responses in the masseter SEMG. When the simultaneously recorded bite force was analyzed, however, there was only one reflex response pattern, a decrease in the net closing force. Therefore, the reflex change in the masseter muscle is not a good representative of the net reflex response of all jaw muscles to mechanical tooth stimulation. The net response is best expressed by the averaged bite force. The averaged bite force records showed that when the stimulus force was developing rapidly, the periodontal reflex could reduce the bite force and hence protect the teeth and supporting tissues from damaging forces. It also can increase the bite force; this might help keep food between the teeth if the change in force rate is slow, especially when the initial bite force is low.
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Scutter, Sheila D., and Kemal S. Türker. "Muscle Spindle Afferent Input to Motoneurons in Human Masseter." Journal of Neurophysiology 82, no. 1 (July 1, 1999): 505–7. http://dx.doi.org/10.1152/jn.1999.82.1.505.
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The H-reflex response in large and small single motor units in human deep anterior masseter was studied to investigate the distribution of muscle spindle afferents onto masseter motoneurons. We found that only the larger units displayed H-reflex responses. This indicates preferential distribution of muscle spindle input onto large motoneurons or a skewed distribution of tonic presynaptic inhibitory mechanisms.
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Williams, J. M., C. Johnson, R. Bales, G. Lloyd, L. Barron, and D. Quest. "Analysis of Temporalis and Masseter adaptation after routine dental treatment in the horse via surface electromyography." Comparative Exercise Physiology 10, no. 4 (January 1, 2014): 223–32. http://dx.doi.org/10.3920/cep143004.
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Limited knowledge of how routine dental treatment (rasping) alters the mastication cycle exists. To our knowledge, Masseter and Temporalis muscle activity after rasping has not been previously evaluated. A descriptive, experimental study compared muscle activity pre- and post-routine dental treatment using surface electromyography (sEMG) to investigate the hypothesis that Masseter activity would increase and Temporalis activity decrease, over a 6 week time period after routine dentistry. Motor unit action potential amplitude (MUAP) and peak amplitude contraction (PAC), for 5 chewing cycles, were measured using sEMG in the right and left Masseter and Temporalis muscles of 10 horses, selected opportunistically due to their dental pathology that required routine rasping (week 0). Routine dental treatment was undertaken and sEMG measurements repeated at 1, 3 and 6 weeks post treatment. Mean MUAP and PAC were calculated for each week and compared both across the cohort and for each horse. For the cohort: Temporalis MUAP fluctuated after rasping, but was only significant in the left muscle between weeks 0 and 6, and weeks 1 and 6 (P<0.02). PAC did not differ significantly, with the exception of a decrease occurring on the left from week 0 to 1 (P<0.01). Masseter activity varied throughout the investigation, but few significant differences were found. A non-significant but consistent reduction in magnitude of PAC was found. For the individuals: MUAP and PAC in the Masseter and Temporalis muscles varied (increased / decreased) on an individual basis throughout the six weeks post rasping, although only MUAP fluctuations between weeks were significant (P<0.01). Adaptation occurs in the Masseter and Temporalis of individual horses after routine rasping; this appears to be associated with kinematic changes within the chewing cycle and is still occurring 6 weeks post-treatment.
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English, Arthur W., and Gail Schwartz. "Development of sex differences in the rabbit masseter muscle is not restricted to a critical period." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1214–22. http://dx.doi.org/10.1152/japplphysiol.00953.2001.
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The proportions of muscle fibers of different phenotype in the adult rabbit masseter differ greatly in different sexes. These sex differences are not apparent in young adults, but arise under the influence of testosterone in the males. We examined whether this switch occurred during a critical period of postnatal development. Testosterone was administered to young adults 1, 2, or 4 mo after castration, and also to adult females. Samples of masseter muscle were taken at four monthly intervals after the onset of treatment and examined for the expression of different myosin heavy chain (MyHC) isoforms by using a panel of monoclonal antibodies. Despite the length of androgen deprivation, treatment with testosterone produced a marked MyHC isoform switch from α-slow/β to IIa. This male proportion of fibers of different phenotypes persisted well beyond the return of serum testosterone levels to pretreatment levels. Thus brief exposure to testosterone produces a permanent change in the proportions of masseter muscle fibers of different phenotypes, and the capacity for this change is not restricted to a critical period.
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Jung, Hak Hyun, Richard L. Lieber, and Allen F. Ryan. "Quantification of myosin heavy chain mRNA in somatic and branchial arch muscles using competitive PCR." American Journal of Physiology-Cell Physiology 275, no. 1 (July 1, 1998): C68—C74. http://dx.doi.org/10.1152/ajpcell.1998.275.1.c68.
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The purpose of this study was to quantify the type and amount of myosin heavy chain (MHC) mRNA within muscles of different developmental origins to determine whether the regulation of gene expression is comparable. Seven MHC isoforms were analyzed in rat adult limb (extensor digitorum longus, tibialis anterior, and soleus) and nonlimb (extraocular, thyroarytenoid, diaphragm, and masseter) muscles using a competitive PCR assay. An exogenous template that included oligonucleotide sequences specific for seven rat sarcomeric MHC isoforms (β-cardiac, 2A, 2X, 2B, extraocular, embryonic, and neonatal) as well as β-actin was constructed and used as the competitor. Only the extraocular muscle contained all seven isoforms. All seven muscles contained type 2A and type 2X MHC transcripts in varying percentages. As expected, the soleus muscle contained primarily β-cardiac MHC (87.8 ± 2.6%). Extraocular MHC was found only in the extraocular and thyroarytenoid muscles and in relatively small proportions (7.4 ± 1.5% and 4.0 ± 0.7%, respectively). Neonatal MHC was identified in extraocular (7.9 ± 0.3%), thyroarytenoid (4.4 ± 0.4%), and masseter (1.0 ± 0.2%) muscles, and embryonic MHC was identified both in extraocular (1.2 ± 0.5%) and, unexpectedly, in soleus (0.6 ± 0.1%) muscles. Absolute MHC mRNA mass was greatest in the masseter (106 pg/0.5 μg RNA) and least for the tibialis anterior (64 pg/0.5 μg RNA). These values suggest that MHC mRNA represents from 4 to 17% of the total mRNA pool in various skeletal muscles. Differences in MHC profile between somatic and branchial arch muscles suggest that the developmental origin of a muscle may, at least in part, be responsible for the MHC expression program that is implemented in the adult. An inverse relationship between the expression of β-cardiac and type 2B MHC transcripts across muscles was noted, suggesting that the expression of these two isoforms may be reciprocally regulated.
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Deriu, Franca, Eusebio Tolu, and John C. Rothwell. "A Sound-Evoked Vestibulomasseteric Reflex in Healthy Humans." Journal of Neurophysiology 93, no. 5 (May 2005): 2739–51. http://dx.doi.org/10.1152/jn.01005.2004.
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Averaged responses to loud clicks were recorded in the unrectified and rectified masseter electromyogram (EMG) of 18 healthy subjects. Unilateral clicks (0.1 ms, 3 Hz, 70–100 dB NHL), delivered during a steady masseter contraction, evoked bilateral responses that appeared to consist of 2 components on the basis of threshold, latency, and their appearance in rectified EMG. The lowest threshold response appeared as a p16 wave (onset 11–13 ms) in the unrectified EMG and corresponded with a 10- to 12-ms period of inhibition in the rectified EMG. Higher-intensity clicks recruited an earlier p11 response in the unrectified EMG (onset 7.0–9.2 ms) that sometimes appeared as an initial increase in the rectified EMG before suppression. The amplitude of the p11 wave scaled with background EMG level and was asymmetrically modulated by 30° tilt of the whole body. The threshold of the early p11/n15 wave in masseter was the same as the threshold for click-induced vestibulocollic reflexes. Single motor unit recordings demonstrated that responses in masseters corresponded to a silent period in unit firing that began earlier and lasted longer at 100 dB than at 80 dB. We propose that loud clicks induce 2 partially overlapping short-latency reflexes in masseter muscle EMG: a p11/n15 response, which we suggest is of vestibular origin, and a p16/n21 response, which we suggest is equivalent to the previously described jaw–acoustic reflex.
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Hakim, Akhlaq W., Xu-Dong Dong, Peter Svensson, Ujendra Kumar, and Brian E. Cairns. "TNFα Mechanically Sensitizes Masseter Muscle Afferent Fibers of Male Rats." Journal of Neurophysiology 102, no. 3 (September 2009): 1551–59. http://dx.doi.org/10.1152/jn.00326.2009.
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Behavioral evidence in rats indicates that injection of tumor necrosis factor alpha (TNFα) into skeletal muscle results in a prolonged mechanical sensitization without gross inflammation. To investigate whether a peripheral mechanism could underlie this effect, in the present study, TNFα (1 or 0.1 μg) was injected into the rat masseter muscle to assess its effect on the excitability and mechanical threshold (MT) of muscle nociceptors as well as on inflammation. Expression of TNFR1 (P55 receptors) and TNFR2 (P75 receptors) by the masseter muscle and trigeminal ganglion neurons that innervate that muscle was determined by Western blot and immunohistochemistry, respectively. The Evans blue dye technique was used at the end of the TNFα experiments to assess for plasma protein extravasation. In subsequent experiments to confirm the involvement of receptor activation in TNFα-induced effects, P55 or P75 receptor antibody was co-injected with TNFα. Intramuscular injection of 1 μg TNFα did not excite nociceptors but did significantly decrease MT compared with vehicle control. There was no evidence of gross inflammation 3 h after injection of TNFα. Co-injection of TNFα with P55 or P75 receptor antibodies attenuated TNFα-induced mechanical sensitization. P55 and P75 receptors were expressed by 29 and 62% of masseter nociceptors, respectively. These findings indicate that TNFα induces mechanical sensitization of masseter nociceptors that is mediated through activation of peripheral P55 and P75 receptors. These results support the hypothesis that a peripheral receptor mechanism could contribute to TNFα-induced noninflammatory mechanical sensitization of skeletal muscle previously reported in behaving rats.
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Tangel, D. J., W. S. Mezzanotte, E. J. Sandberg, and D. P. White. "Influences of NREM sleep on the activity of tonic vs. inspiratory phasic muscles in normal men." Journal of Applied Physiology 73, no. 3 (September 1, 1992): 1058–66. http://dx.doi.org/10.1152/jappl.1992.73.3.1058.
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Studies of sleep influences on human pharyngeal and other respiratory muscles suggest that the activity of these muscles may be affected by non-rapid-eye-movement (NREM) sleep in a nonuniform manner. This variable sleep response may relate to the pattern of activation of the muscle (inspiratory phasic vs. tonic) and peripheral events occurring in the airway. Furthermore, the ability of these muscles to respond to respiratory stimuli during NREM sleep may also differ. To systematically investigate the effect of NREM sleep on respiratory muscle activity, we studied two tonic muscles [tensor palatini (TP), masseter (M)] and two inspiratory phasic ones [genioglossus (GG), diaphragm (D)], also measuring the response of these muscles to inspiratory resistive loading (12 cmH2O.l-1.s) during wakefulness and NREM sleep. Seven normal male subjects were studied on a single night with intramuscular electrodes placed in the TP and GG and surface electrodes placed over the D and M. Sleep stage, inspiratory airflow, and moving time average electromyograph (EMG) of the above four muscles were continuously recorded. The EMG of both tonic muscles fell significantly (P less than 0.05) during NREM sleep [TP awake, 4.3 +/- 0.05 (SE) arbitrary units, stage 2, 1.1 +/- 0.2; stage 3/4, 1.0 +/- 0.2. Masseter awake, 4.8 +/- 0.6; stage 2, 3.3 +/- 0.5; stage 3/4, 3.1 +/- 0.5]. On the other hand, the peak phasic EMG of both inspiratory phasic muscles (GG and D) was well maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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Miyahara, T., N. Hagiya, T. Ohyama, and Y. Nakamura. "Modulation of human soleus H reflex in association with voluntary clenching of the teeth." Journal of Neurophysiology 76, no. 3 (September 1, 1996): 2033–41. http://dx.doi.org/10.1152/jn.1996.76.3.2033.
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1. To determine the effects of motor activity in the jaw on more general motor behavior, we examined the modulation of the soleus H reflex in association with voluntary clenching of the teeth in healthy adult volunteers. 2. The amplitude of the H reflex increased remarkably during teeth clenching. The increase during maximal teeth clenching was greater than that induced either by maximal voluntary isometric contraction of the wrist extensors or by maximal voluntary clenching of the fists. 3. The increase in amplitude of the soleus H reflex showed a positive correlation with the strength of teeth clenching, as monitored by recording electromyographic (EMG) activity from the masseter muscle. 4. The increase in amplitude of the H reflex associated with teeth clenching started before the onset of the EMG activity of the masseter muscle, reached a peak shortly after the onset, and then declined to a plateau that continued in parallel with the masseter EMG until the end of teeth clenching. 5. The increase in amplitude of the H reflex in association with teeth clenching was partially decreased during the inhibitory masseteric reflex evoked by innocuous electrical stimulation of the lip. 6. It is concluded that the soleus H reflex is facilitated in association with voluntary teeth clenching, and that descending influences from the cerebral cortex, as well as peripheral afferent impulses from the oral-facial region, are involved in this facilitation. It is proposed that oral motor activity can exert strong influences on the motor activity of the other parts of the body.
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Eriksson, Per-Olof, Gill S. Butler-Browne, and Lars-Eric Thornell. "Immunohistochemical characterization of human masseter muscle spindles." Muscle & Nerve 17, no. 1 (January 1994): 31–41. http://dx.doi.org/10.1002/mus.880170105.
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Escobar, Jeffery, Jason W. Frank, Agus Suryawan, Hanh V. Nguyen, Scot R. Kimball, Leonard S. Jefferson, and Teresa A. Davis. "Regulation of cardiac and skeletal muscle protein synthesis by individual branched-chain amino acids in neonatal pigs." American Journal of Physiology-Endocrinology and Metabolism 290, no. 4 (April 2006): E612—E621. http://dx.doi.org/10.1152/ajpendo.00402.2005.
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Skeletal muscle grows at a very rapid rate in the neonatal pig, due in part to an enhanced sensitivity of protein synthesis to the postprandial rise in amino acids. An increase in leucine alone stimulates protein synthesis in skeletal muscle of the neonatal pig; however, the effect of isoleucine and valine has not been investigated in this experimental model. The left ventricular wall of the heart grows faster than the right ventricular wall during the first 10 days of postnatal life in the pig. Therefore, the effects of individual BCAA on protein synthesis in individual skeletal muscles and in the left and right ventricular walls were examined. Fasted pigs were infused with 0 or 400 μmol·kg−1·h−1 leucine, isoleucine, or valine to raise individual BCAA to fed levels. Fractional rates of protein synthesis and indexes of translation initiation were measured after 60 min. Infusion of leucine increased ( P < 0.05) phosphorylation of eukaryotic initiation factor (eIF)4E-binding protein-1 and increased ( P < 0.05) the amount and phosphorylation of eIF4G associated with eIF4E in longissimus dorsi and masseter muscles and in both ventricular walls. Leucine increased ( P < 0.05) the phosphorylation of ribosomal protein (rp)S6 kinase and rpS6 in longissimus dorsi and masseter but not in either ventricular wall. Leucine stimulated ( P < 0.05) protein synthesis in longissimus dorsi, masseter, and the left ventricular wall. Isoleucine and valine did not increase translation initiation factor activation or protein synthesis rates in skeletal or cardiac muscles. The results suggest that the postprandial rise in leucine, but not isoleucine or valine, acts as a nutrient signal to stimulate protein synthesis in cardiac and skeletal muscles of neonates by increasing eIF4E availability for eIF4F complex assembly.
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Cairns, Brian E., Barry J. Sessle, and James W. Hu. "Activation of Peripheral GABAA Receptors Inhibits Temporomandibular Joint–Evoked Jaw Muscle Activity." Journal of Neurophysiology 81, no. 4 (April 1, 1999): 1966–69. http://dx.doi.org/10.1152/jn.1999.81.4.1966.
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Activation of peripheral GABAA receptors inhibits temporomandibular joint–evoked jaw muscle activity. We have previously shown that injection of mustard oil or glutamate into rat temporomandibular joint (TMJ) tissues, an experimental model of acute TMJ injury, can reflexly induce a prolonged increase in the activity of both digastric (jaw-opener) and masseter (jaw-closer) muscles. In this study, GABA was applied to the TMJ region by itself or in combination with glutamate, and the magnitude of evoked jaw muscle electromyographic (EMG) activity was measured. Application of GABA alone to the TMJ region did not evoke significant jaw muscle EMG activity when compared with normal saline controls. In contrast, co-application of GABA and glutamate into the TMJ region decreased the magnitude of glutamate-evoked EMG activity. This GABA-mediated inhibition of glutamate-evoked EMG activity followed an inverse dose-response relationship with an estimated median inhibitory dose (ID50) of 0.17 ± 0.05 (SE) μmol and 0.031 ± 0.006 μmol for the digastric and masseter muscles, respectively. Co-administration of the GABAA receptor antagonist bicuculline (0.05 μmol) but not the GABABreceptor antagonist phaclofen (0.05 or 0.15 μmol) reversed the suppressive actions of GABA, indicating that this action of GABA may be mediated by peripheral GABAA receptors located within the TMJ region. Our results suggest that activation of peripheral GABAA receptors located within the TMJ region could act to decrease the transmission of nociceptive information.
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Rousseff, Rossen T., Adnan J. Khuraibet, Asmahan F. Al-Shubaili, and Plamen Tzvetanov. "Stimulated jitter in the masseter muscle: Normative values." Muscle & Nerve 35, no. 2 (September 5, 2006): 243–45. http://dx.doi.org/10.1002/mus.20651.
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Ortu, Enzo, Franca Deriu, Antonio Suppa, Elena Giaconi, Eusebio Tolu, and John C. Rothwell. "Intracortical modulation of cortical-bulbar responses for the masseter muscle." Journal of Physiology 586, no. 14 (July 14, 2008): 3385–404. http://dx.doi.org/10.1113/jphysiol.2008.153288.
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Ishii, Hisayoshi, Takeharu Niioka, Emi Sudo, and Hiroshi Izumi. "Evidence for parasympathetic vasodilator fibres in the rat masseter muscle." Journal of Physiology 569, no. 2 (November 24, 2005): 617–29. http://dx.doi.org/10.1113/jphysiol.2005.087643.
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Kato, Takafumi, Yuji Masuda, Hayato Kanayama, Norimasa Nakamura, Atsushi Yoshida, and Toshifumi Morimoto. "Heterogeneous activity level of jaw-closing and -opening muscles and its association with arousal levels during sleep in the guinea pig." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R34—R42. http://dx.doi.org/10.1152/ajpregu.00205.2009.
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Exaggerated jaw motor activities during sleep are associated with muscle symptoms in the jaw-closing rather than the jaw-opening muscles. The intrinsic activity of antagonistic jaw muscles during sleep remains unknown. This study aims to assess the balance of muscle activity between masseter (MA) and digastric (DG) muscles during sleep in guinea pigs. Electroencephalogram (EEG), electroocculogram, and electromyograms (EMGs) of dorsal neck, MA, and DG muscles were recorded with video during sleep-wake cycles. These variables were quantified for each 10-s epoch. The magnitude of muscle activity during sleep in relation to mean EMG activity of total wakefulness was up to three times higher for MA muscle than for DG muscle for nonrapid eye movement (NREM) and rapid-eye-movement (REM) sleep. Although the activity level of the two jaw muscles fluctuated during sleep, the ratio of activity level for each epoch was not proportional. Epochs with a high activity level for each muscle were associated with a decrease in δEEG power and/or an increase in heart rate in NREM sleep. However, this association with heart rate and activity levels was not observed in REM sleep. These results suggest that in guinea pigs, the magnitude of muscle activity for antagonistic jaw muscles is heterogeneously modulated during sleep, characterized by a high activity level in the jaw-closing muscle. Fluctuations in the activity are influenced by transient arousal levels in NREM sleep but, in REM sleep, the distinct controls may contribute to the fluctuation. The above intrinsic characteristics could underlie the exaggeration of jaw motor activities during sleep (e.g., sleep bruxism).
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Peever, John H., Yuan-Yang Lai, and Jerome M. Siegel. "Excitatory Effects of Hypocretin-1 (Orexin-A) in the Trigeminal Motor Nucleus Are Reversed by NMDA Antagonism." Journal of Neurophysiology 89, no. 5 (May 1, 2003): 2591–600. http://dx.doi.org/10.1152/jn.00968.2002.
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Hypocretin-1 and -2 (Hcrt-1 and -2, also called orexin-A and -B) are newly identified neuropeptides synthesized by hypothalamic neurons. Defects in the Hcrt system underlie the sleep disorder narcolepsy, which is characterized by sleep fragmentation and the involuntary loss of muscle tone called cataplexy. Hcrt neurons project to multiple brain regions including cranial and spinal motor nuclei. In vitro studies suggest that Hcrt application can modulate presynaptic glutamate release. Together these observations suggest that Hcrt can affect motor output and that glutamatergic processes may be involved. We addressed these issues in decerebrate cats by applying Hcrt-1 and -2 into the trigeminal motor nucleus to determine whether these ligands alter masseter muscle activity and by pretreating the trigeminal motor nucleus with a N-methyl-d-aspartate (NMDA) antagonist to determine if glutamatergic pathways are involved in the transduction of the Hcrt signal. We found that Hcrt-1 and -2 microinjections into the trigeminal motor nucleus increased ipsilateral masseter muscle tone in a dose-dependent manner. We also found that Hcrt application into the hypoglossal motor nucleus increases genioglossus muscle activity. Pretreatment with a NMDA antagonist (d-(−)-2-amino-phosphonovaleric acid) abolished the excitatory response of the masseter muscle to Hcrt-1 application; however, pretreatment with methysergide, a serotonin antagonist had no effect. These studies are the first to demonstrate that Hcrt causes the excitation of motoneurons and that functional NMDA receptors are required for this response. We suggest that Hcrt regulates motor control processes and that this regulation is mediated by glutamate release in the trigeminal motor nucleus.
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Kayar, S. R., H. Hoppeler, B. Essen-Gustavsson, and K. Schwerzmann. "The similarity of mitochondrial distribution in equine skeletal muscles of differing oxidative capacity." Journal of Experimental Biology 137, no. 1 (July 1, 1988): 253–63. http://dx.doi.org/10.1242/jeb.137.1.253.
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A morphometric analysis was performed on horse muscle tissue to quantify mitochondrial distribution relative to capillaries. Samples of M. vastus medialis, M. semitendinosus, M. masseter and M. cutaneus thoracicus were preserved in a glutaraldehyde fixative for electron microscopy, or frozen for biochemical and histochemical analysis. These four muscles varied from highly oxidative in type, consisting nearly completely of type I fibres, in masseter, to highly glycolytic, primarily type IIb fibres, in cutaneus. In all four muscles, mitochondria were found in highest volume density near capillaries at the fibre border, with a sharp decline in volume density towards the fibre centre. This distribution was independent of myoglobin concentration, muscle fibre type and the activities of three key metabolic enzymes, citrate synthase, 3-OH-acyl-CoA dehydrogenase and lactate dehydrogenase.
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Kim, Jeong-su, Kenneth W. Hinchcliff, Mamoru Yamaguchi, Laurie A. Beard, Chad D. Markert, and Steven T. Devor. "Exercise training increases oxidative capacity and attenuates exercise-induced ultrastructural damage in skeletal muscle of aged horses." Journal of Applied Physiology 98, no. 1 (January 2005): 334–42. http://dx.doi.org/10.1152/japplphysiol.00172.2003.
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Exercise training improves functional capacity in aged individuals. Whether such training reduces the severity of exercise-induced muscle damage is unknown. The purpose of the present study was to determine the effect of 10 wk of treadmill exercise training on skeletal muscle oxidative capacity and exercise-induced ultrastructural damage in six aged female Quarter horses (>23 yr of age). The magnitude of ultrastructural muscle damage induced by an incremental exercise test before and after training was determined by electron microscopic examination of samples of triceps, semimembranosus, and masseter (control) muscles. Maximal aerobic capacity increased 22% after 10 wk of exercise training. The percentage of type IIa myosin heavy chain increased in semimembranosus muscle, whereas the percentage of type IIx myosin heavy chain decreased in triceps muscle. After training, triceps muscle showed significant increases in activities of both citrate synthase and 3-hydroxyacyl-CoA-dehydrogenase. Attenuation of exercise-induced ultrastructural muscle damage occurred in the semimembranosus muscle at both the same absolute and the same relative workloads after the 10-wk conditioning period. We conclude that aged horses adapt readily to intense aerobic exercise training with improvements in endurance, whole body aerobic capacity, and muscle oxidative capacity, and heightened resistance to exercise-induced ultrastructural muscle cell damage. However, adaptations may be muscle-group specific.
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INOKO, Yoshimi, Kimio SHIMIZU, Osami MORITA, and Masaki KOHNO. "Relationship between masseter muscle activity and sleep-disordered breathing." Sleep and Biological Rhythms 2, no. 1 (February 2004): 67–68. http://dx.doi.org/10.1111/j.1479-8425.2003.00068.x.
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Rasmussen, Tara, and Haley Tucker. "Loss of SMYD1 Results in Perinatal Lethality via Selective Defects within Myotonic Muscle Descendants." Diseases 7, no. 1 (December 20, 2018): 1. http://dx.doi.org/10.3390/diseases7010001.
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SET and MYND Domain 1 (SMYD1) is a cardiac and skeletal muscle-specific, histone methyl transferase that is critical for both embryonic and adult heart development and function in both mice and men. We report here that skeletal muscle-specific, myogenin (myoG)-Cre-mediated conditional knockout (CKO) of Smyd1 results in perinatal death. As early as embryonic day 12.5, Smyd1 CKOs exhibit multiple skeletal muscle defects in proliferation, morphology, and gene expression. However, all myotonic descendants are not afflicted equally. Trunk muscles are virtually ablated with excessive accumulation of brown adipose tissue (BAT), forelimb muscles are disorganized and improperly differentiated, but other muscles, such as the masseter, are normal. While expression of major myogenic regulators went unscathed, adaptive and innate immune transcription factors critical for BAT development/physiology were downregulated. Whereas classical mitochondrial BAT accumulation went unscathed following loss of SMYD1, key transcription factors, including PRDM16, UCP-1, and CIDE-a that control skeletal muscle vs. adipose fate, were downregulated. Finally, in rare adults that survive perinatal lethality, SMYD1 controls specification of some, but not all, skeletal muscle fiber-types.
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Khuraibet, Adnan J., Rossen T. Rousseff, Raed Behbehani, Asmahan F. K. Al-Shubaili, and Riyadh A. Khan. "Single-fiber electromyography of masseter muscle in myasthenia gravis." Muscle & Nerve 37, no. 4 (April 2008): 522–25. http://dx.doi.org/10.1002/mus.20921.
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Hamilton, Marc T., Jacqueline Etienne, Warren C. McClure, Brian S. Pavey, and Alisha K. Holloway. "Role of local contractile activity and muscle fiber type on LPL regulation during exercise." American Journal of Physiology-Endocrinology and Metabolism 275, no. 6 (December 1, 1998): E1016—E1022. http://dx.doi.org/10.1152/ajpendo.1998.275.6.e1016.
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The purpose of this study was to determine the influence of local contractile activity on lipoprotein lipase (LPL) regulation in skeletal muscle. Short-term voluntary run training increased LPL mRNA concentration and LPL immunoreactive mass about threefold in white skeletal muscles of the rat hindlimb (all P < 0.01). Training also increased total and heparin-releasable LPL enzyme activity in white hindlimb muscles and in postheparin plasma ( P< 0.05). Training did not enhance LPL regulation in a white muscle that was not recruited during running (masseter). LPL levels were already high in red skeletal muscles of control rats, and training did not result in a further rise. In resting rats, local electrical stimulation of a motor nerve to a predominantly white muscle caused a significant rise in LPL mRNA, immunoreactive mass, and enzyme activity relative to the contralateral control muscle of the same animals (all P < 0.01). Finally, LPL expression was several times greater in a red muscle (soleus) of rats with normal postural activity than rats with immobilized hindlimbs ( P < 0.01). In summary, these studies support the hypothesis that local contractile activity is required for increasing LPL expression during exercise training and for maintaining a high level of LPL expression in postural muscles.
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Yamane, Akira, Satonari Akutsu, Thomas G. H. Diekwisch, and Ryoichi Matsuda. "Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice." American Journal of Physiology-Cell Physiology 289, no. 1 (July 2005): C42—C48. http://dx.doi.org/10.1152/ajpcell.00577.2004.
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To determine whether muscle satellite cells and utrophin are correlated with the degree of damage in mdx skeletal muscles, we measured the area of the degenerative region as an indicator of myofiber degeneration in the masseter, gastrocnemius, soleus, and diaphragm muscles of mdx mice. Furthermore, we analyzed the expression levels of the paired box homeotic gene 7 ( pax7), m-cadherin (the makers of muscle satellite cells), and utrophin mRNA. We also investigated the immunolocalization of m-cadherin and utrophin proteins in the muscles of normal C57BL/10J (B10) and mdx mice. The expression level of pax7 mRNA and the percentage of m-cadherin-positive cells among the total number of cell nuclei in the muscle tissues in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there was no significant correlation between muscle damage and expression level for pax7 mRNA ( R = −0.140), nor was there a correlation between muscle damage and the percentage of satellite cells among the total number of cell nuclei ( R = −0.411) in the mdx mice. The expression level of utrophin mRNA and the intensity of immunostaining for utrophin in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there also was not a significant correlation between muscle damage and expression level of utrophin mRNA ( R = 0.231) in the mdx mice, although upregulated utrophin was incorporated into the sarcolemma. These results suggest that satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice.
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Orellana, Renan A., Pamela M. J. O'Connor, Jill A. Bush, Agus Suryawan, M. Carole Thivierge, Hanh V. Nguyen, Marta L. Fiorotto, and Teresa A. Davis. "Modulation of muscle protein synthesis by insulin is maintained during neonatal endotoxemia." American Journal of Physiology-Endocrinology and Metabolism 291, no. 1 (July 2006): E159—E166. http://dx.doi.org/10.1152/ajpendo.00595.2005.
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Sepsis promotes insulin resistance and reduces protein synthesis in skeletal muscle of adults. The effect of sepsis on insulin-stimulated muscle protein synthesis has not been determined in neonates, a highly anabolic population that is uniquely sensitive to insulin. Overnight fasted neonatal pigs were infused for 8 h with endotoxin [lipopolysaccharide (LPS), 0 and 10 μg·kg−1·h−1]. Glucose and amino acids were maintained at fasting levels, insulin was clamped at either fasting or fed (2 or 10 μU/ml) levels, and fractional protein synthesis rates were determined at the end of the infusion. LPS infusion induced a septic-like state, as indicated by a sustained elevation in body temperature, heart rate, and cortisol. At fasting insulin levels, LPS reduced fractional protein synthesis rates in gastrocnemius muscle (−26%) but had no effect on the masseter and heart. By contrast, LPS stimulated liver protein synthesis (+28%). Increasing insulin to fed levels accelerated protein synthesis rates in gastrocnemius (controls by +38%, LPS by +60%), masseter (controls by +50%, LPS by +43%), heart (controls by +34%, LPS by +40%), and diaphragm (controls by +54%, LPS by +29%), and the response to insulin was similar in LPS and controls. Insulin did not alter protein synthesis in liver, kidney, or jejunum in either group. These findings suggest that acute endotoxemia lowers basal fasting muscle protein synthesis in neonates but does not alter the response of protein synthesis to insulin.
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Hidaka, O., T. Morimoto, T. Kato, Y. Masuda, T. Inoue, and K. Takada. "Behavior of Jaw Muscle Spindle Afferents During Cortically Induced Rhythmic Jaw Movements in the Anesthetized Rabbit." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2633–40. http://dx.doi.org/10.1152/jn.1999.82.5.2633.
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The regulation by muscle spindles of jaw-closing muscle activity during mastication was evaluated in anesthetized rabbits. Simultaneous records were made of the discharges of muscle spindle units in the mesencephalic trigeminal nucleus, masseter and digastric muscle activity (electromyogram [EMG]), and jaw-movement parameters during cortically induced rhythmic jaw movements. One of three test strips of polyurethane foam, each of a different hardness, was inserted between the opposing molars during the jaw movements. The induced rhythmic jaw movements were crescent shaped and were divided into three phases: jaw-opening, jaw-closing, and power. The firing rate of muscle spindle units during each phase increased after strip application, with a tendency for the spindle discharge to be continuous throughout the entire chewing cycle. However, although the firing rate did not change during the jaw-opening and jaw-closing phases when the strip hardness was altered, the firing rate during the power phase increased in a hardness-dependent manner. In addition, the integrated EMG activity, the duration of the masseteric bursts, and the minimum gape increased with strip hardness. Spindle discharge during the power phase correlated with jaw-closing muscle activity, implying that the change in jaw-closing muscle activity associated with strip hardness was caused by increased spindle discharge produced through insertion of a test strip. The increased firing rate during the other two phases may be involved in a long-latency spindle feedback. This could contribute to matching the spatiotemporal pattern of the central pattern generator to that of the moving jaw.
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Butler-Browne, G. S., P. O. Eriksson, C. Laurent, and L. E. Thornell. "Adult human masseter muscle fibers express myosin isozymes characteristic of development." Muscle & Nerve 11, no. 6 (June 1988): 610–20. http://dx.doi.org/10.1002/mus.880110614.
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Yoneda, Hiroyuki, Fukie Niijima-Yaoita, Masahiro Tsuchiya, Hiroyuki Kumamoto, Makoto Watanbe, Hiroshi Ohtsu, Kazuhiko Yanai, et al. "Roles played by histamine in strenuous or prolonged masseter muscle activity in mice." Clinical and Experimental Pharmacology and Physiology 40, no. 12 (November 21, 2013): 848–55. http://dx.doi.org/10.1111/1440-1681.12167.
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Ramamani, A., M. M. Aruldhas, and P. Govindarajulu. "Differential response of rat skeletal muscle glycogen metabolism to testosterone and estradiol." Canadian Journal of Physiology and Pharmacology 77, no. 4 (April 1, 1999): 300–304. http://dx.doi.org/10.1139/y99-016.
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Although reports on sex steroids have implicated them as promoting protein synthesis and also providing extra strength to the skeletal muscle, it remains unclear whether sex steroids affect glycogen metabolism to provide energy for skeletal muscle functions, since glycogen metabolism is one of the pathways that provides energy for the skeletal muscle contraction and relaxation cycle. The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats.Key words: testosterone, estradiol, skeletal muscle, glycogen metabolism.
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Duhlmeier, Reinhard, Anja Hacker, Andrea Widdel, Wolfgang von Engelhardt, and Hans-Peter Sallmann. "Mechanisms of insulin-dependent glucose transport into porcine and bovine skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 1 (July 2005): R187—R197. http://dx.doi.org/10.1152/ajpregu.00502.2004.
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Euglycemic, hyperinsulinemic clamp tests have shown that adult ruminants are less insulin-sensitive than monogastric omnivores. The present study was carried out to elucidate possible cellular mechanisms contributing to this impaired insulin sensitivity of ruminants. Western blotting was used to measure glucose transporters 1 and 4 (GLUT1, GLUT4) in oxidative (musculus masseter and diaphragm) and glycolytic (musculus longissimus dorsi and semitendinosus) skeletal muscle in the crude membranes of pigs and cows. Muscles were characterized biochemically. To determine insulin-stimulated 3- O-d-[3H]-methylglucose (3- O-MG) uptake and GLUT4 translocation, porcine and bovine musculus semitendinosus strips were removed by open muscle biopsy and incubated without and with 0.1 or 20 mIU insulin/ml. GLUT4 translocation was analyzed using subcellular fractionation techniques to isolate partially purified plasma membranes and cytoplasmic vesicles and using Western blotting. GLUT4 protein contents were significantly higher in oxidative than in glycolytic muscles in pigs and cows. GLUT1 protein contents were significantly higher in glycolytic than in oxidative muscles in bovines but not in porcines. The 3- O-MG uptake into musculus semitendinosus was similar in both species. Maximum insulin-induced GLUT4 translocation into musculus semitendinosus plasma membrane was significantly lower in bovines than in porcines. These results indicate that GLUT1 is the predominant glucose transporter in bovine glycolytic muscles and that a reinforced insulin-independent glucose uptake via GLUT1 may compensate for the impaired insulin-stimulated GLUT4 translocation, resulting in a similar 3- O-MG uptake in bovine and porcine musculus semitendinosus. These findings may explain at least in part the impaired in vivo insulin sensitivity of adult ruminants compared with that of omnivorous monogastric animals.
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Tonndorf, M�nica L., and Alan G. Hannam. "Motor unit territory in relation to tendons in the human masseter muscle." Muscle & Nerve 17, no. 4 (April 1994): 436–43. http://dx.doi.org/10.1002/mus.880170412.
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Turturici, Marco, and Silvestro Roatta. "Compression-induced hyperaemia in the rabbit masseter muscle: a model to investigate vascular mechano-sensitivity of skeletal muscle." Physiological Measurement 34, no. 3 (February 12, 2013): 307–14. http://dx.doi.org/10.1088/0967-3334/34/3/307.
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Daimon, Shigeru, and Kazunori Yamaguchi. "Changes in respiratory activity induced by mastication during oral breathing in humans." Journal of Applied Physiology 116, no. 11 (June 1, 2014): 1365–70. http://dx.doi.org/10.1152/japplphysiol.01236.2013.
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We examined the effect of oral breathing on respiratory movements, including the number of respirations and the movement of the thoracic wall at rest and while chewing gum. Forty normal nose breathers were selected by detecting expiratory airflow from the mouth using a CO2 sensor. Chest measurements were recorded using a Piezo respiratory belt transducer, and electromyographic (EMG) activity of the masseter and trapezius muscles were recorded at rest and while chewing gum during nasal or oral breathing. Oral breathing was introduced by completely occluding the nostrils with a nose clip. During oral breathing, the respiration rate was significantly lower while chewing gum than while at rest ( P < 0.05). While chewing gum, the respiration rate was significantly lower during oral breathing than during nasal breathing ( P < 0.05). During oral breathing, thoracic movement was significantly higher while chewing gum than while at rest ( P < 0.05). Thoracic movement was significantly greater during oral breathing than during nasal breathing ( P < 0.05). The trapezius muscle exhibited significant EMG activity when chewing gum during oral breathing. The activity of the trapezius muscle coincided with increased movement of the thoracic wall. Chewing food while breathing through the mouth interferes with and decreases the respiratory cycle and promotes unusual respiratory movement of the thoracic wall, which is directed by the activity of accessory muscles of respiration.
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Cvetko, Erika, and Ida Eržen. "Effect of chronic uncontrollable stress on myosin heavy chain expression in rat masseter muscle." Pfl?gers Archiv European Journal of Physiology 442, no. 7 (September 1, 2001): r147—r149. http://dx.doi.org/10.1007/s004240100002.
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Davis, Teresa A., Marta L. Fiorotto, Philip R. Beckett, Douglas G. Burrin, Peter J. Reeds, Diane Wray-Cahen, and Hanh V. Nguyen. "Differential effects of insulin on peripheral and visceral tissue protein synthesis in neonatal pigs." American Journal of Physiology-Endocrinology and Metabolism 280, no. 5 (May 1, 2001): E770—E779. http://dx.doi.org/10.1152/ajpendo.2001.280.5.e770.
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We recently demonstrated in neonatal pigs that, with amino acids and glucose maintained at fasting levels, the stimulation of protein synthesis in longissimus dorsi muscle with feeding can be reproduced by a physiological rise in insulin alone. In the current report, we determine whether the response of protein synthesis to insulin in the neonatal pig is 1) present in muscles of different fiber types, 2) proportional in myofibrillar and sarcoplasmic proteins, 3) associated with increased translational efficiency and ribosome number, and 4) present in other peripheral tissues and in viscera. Hyperinsulinemic-euglycemic-amino acid clamps were performed in 7- and 26-day-old pigs infused with 0, 30, 100, or 1,000 ng · kg−0.66 · min−1 of insulin to reproduce insulin levels present in fasted, fed, refed, and supraphysiological conditions, respectively. Tissue protein synthesis was measured using a flooding dose ofl-[4-3H]phenylalanine. Insulin increased protein synthesis in gastrocnemius muscle and, to a lesser degree, masseter muscle. The degree of stimulation of protein synthesis by insulin was similar in myofibrillar and sarcoplasmic proteins. Insulin increased translational efficiency but had no effect on ribosome number in muscle. All of these insulin-induced changes in muscle protein synthesis decreased with age. Insulin also stimulated protein synthesis in cardiac muscle and skin but not in liver, intestine, spleen, pancreas, or kidney. The results support the hypothesis that insulin mediates the feeding-induced stimulation of myofibrillar and sarcoplasmic protein synthesis in muscles of different fiber types in the neonate by increasing the efficiency of translation. However, insulin does not appear to be involved in the feeding-induced stimulation of protein synthesis in visceral tissues. Thus different mechanisms regulate the growth of peripheral and visceral tissues in the neonate.
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Mohn, Christine, Olav Vassend, and Stein Knardahl. "Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women." Scandinavian Journal of Pain 3, no. 3 (July 1, 2012): 165–69. http://dx.doi.org/10.1016/j.sjpain.2011.12.001.
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AbstractBackground and purposeThe psychophysiological responses to and modulation of pressure pain stimulation are relatively new areas of investigation. The aims of the present study were to characterize subjective and cardiovascular (CV) responses to pressure pain stimulation, and to examine the relationship between CV responding and pain pressure pain sensitivity.MethodsThirty-nine pain-free, normotensive women were included in the study and tested during the follicular phase of their menstrual cycles. Pain threshold and tolerance were recorded at the right masseter muscle and the sternum, and visual analogue scales (VAS) were used to rate both pain intensity (the sensory dimension) and discomfort (the affective dimension). Mean arterial pressure (MAP), heart rate (HR), and facial and digital skin blood flux (SBF) were registered continuously.ResultsThe pain threshold and tolerance were significantly higher at the sternum compared with the masseter, but the level of affective distress was higher at the masseter tolerance point. No associations emerged between pressure pain threshold and tolerance stimulation levels, and the corresponding VAS ratings. Pressure pain stimulation of the masseter induced significant increases in MAP, HR, and a decrease in digital SBF. During sternum pressure stimulation a significant change in HR and digital SBF was observed. There were no significant correlations between CV responding and pressure pain sensitivity.ConclusionHealthy women seem to display higher pressure pain sensitivity at the masseter region relative to the sternum. Pressure pain stimulation was associated with significant changes in MAP, HR, and SBF, but was not modulated by CV responses. The validity of these findings is strengthened by our control for menstrual cycle events, weekend-related changes in physiology, and CV changes during pain stimulation.ImplicationsThis study extends previous reports of SBF sensitivity to electrocutaneous pain into the field of pressure stimulation. Moreover, this study suggests that the often demonstrated association between high BP and low pain sensitivity may not apply to pressure pain specifically. Alternatively, this finding adds to the literature of gender differences in the relationship between CV responding and acute pain sensitivity in general.
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Hoh, J. F. Y., and S. Hughes. "Immunocytochemical analysis of the perinatal development of cat masseter muscle using anti-myosin antibodies." Journal of Muscle Research and Cell Motility 10, no. 4 (August 1989): 312–25. http://dx.doi.org/10.1007/bf01758427.
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