Facial Reanimation Utilizing Combined Orthodromic Temporalis Muscle Flap and End-to-Side Cross-Face Nerve Grafts

Individuals with facial paralysis of 6 months or more without evidence of clinical or electromyographic improvement have been successfully reanimated utilizing an orthodromic temporalis transfer in conjunction with end-to-side cross-face nerve grafts. The temporalis muscle insertion is released from the coronoid process of the mandible and sutured to a fascia lata graft that is secured distally to the commissure and paralyzed hemilip. The orthodromic transfer of the temporalis muscle overcomes the concave temporal deformity and zygomatic fullness produced by the turning down of the central third of the muscle (Gillies procedure) while yielding stronger muscle contraction and a more symmetric smile. The muscle flap is combined with cross-face sural nerve grafts utilizing end-to-side neurorrhaphies to import myelinated motor fibers to the paralyzed muscles of facial expression in the midface and perioral region. Cross-face nerve grafting provides the potential for true spontaneous facial motion. We feel that the synergy created by the combination of techniques can perhaps produce a more symmetrical and synchronized smile than either procedure in isolation.Nineteen patients underwent an orthodromic temporalis muscle flap in conjunction with cross-face (buccal-buccal with end-to-side neurorrhaphy) nerve grafts. To evaluate the symmetry of the smile, we measured the length of the two hemilips (normal and affected) using the CorelDRAW X3 software. Measurements were obtained in the pre- and postoperative period and compared for symmetry.There was significant improvement in smile symmetry in 89.5 % of patients.Orthodromic temporalis muscle transfer in conjunction with cross face nerve grafts creates a synergistic effect frequently producing an aesthetic, symmetric smile.This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors at www.spinger.com/00266.

Proteomic Analysis of Gastrocnemius Muscle in Rats with Streptozotocin-Induced Diabetes and Chronically Exposed to Fluoride

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Metabolic and functional effects of beta-hydroxy-beta-methylbutyrate (HMB) supplementation in skeletal muscle

Beta-hydroxy-beta-methylbutyrate (HMB) is a metabolite derived from leucine. The anti-catabolic effect of HMB is well documented but its effect upon skeletal muscle strength and fatigue is still uncertain. In the present study, male Wistar rats were supplemented with HMB (320 mg/kg per day) for 4 weeks. Placebo group received saline solution only. Muscle strength (twitch and tetanic force) and resistance to acute muscle fatigue of the gastrocnemius muscle were evaluated by direct electrical stimulation of the sciatic nerve. The content of ATP and glycogen in red and white portions of gastrocnemius muscle were also evaluated. The effect of HMB on citrate synthase (CS) activity was also investigated. Muscle tetanic force was increased by HMB supplementation. No change was observed in time to peak of contraction and relaxation time. Resistance to acute muscle fatigue during intense contractile activity was also improved after HMB supplementation. Glycogen content was increased in both white (by fivefold) and red (by fourfold) portions of gastrocnemius muscle. HMB supplementation also increased the ATP content in red (by twofold) and white (1.2-fold) portions of gastrocnemius muscle. CS activity was increased by twofold in red portion of gastrocnemius muscle. These results support the proposition that HMB supplementation have marked change in oxidative metabolism improving muscle strength generation and performance during intense contractions.

Effects of moderate electrical stimulation on reactive species production by primary rat skeletal muscle cells: Cross talk between superoxide and nitric oxide production

The effects of a moderate electrical stimulation on superoxide and nitric oxide production by primary cultured skeletal muscle cells were evaluated. The involvement of the main sites of these reactive species production and the relationship between superoxide and nitric oxide production were also examined. Production of superoxide was evaluated by cytochrome c reduction and dihydroethidium oxidation assays. Electrical stimulation increased superoxide production after 1?h incubation. A xanthine oxidase inhibitor caused a partial decrease of superoxide generation and a significant amount of mitochondria-derived superoxide was also observed. Nitric oxide production was assessed by nitrite measurement and by using 4,5-diaminofluorescein diacetate (DAF-2-DA) assay. Using both methods an increased production of nitric oxide was obtained after electrical stimulation, which was also able to induce an increase of iNOS content and NF-?B activation. The participation of superoxide in nitric oxide production was investigated by incubating cells with DAF-2-DA in the presence or absence of electrical stimulation, a superoxide generator system (xanthinexanthine oxidase), a mixture of NOS inhibitors and SOD-PEG. Our data show that the induction of muscle contraction by a moderate electrical stimulation protocol led to an increased nitric oxide production that can be controlled by superoxide generation. The cross talk between these reactive species likely plays a role in exercise-induced maintenance and adaptation by regulating muscular glucose metabolism, force of contraction, fatigue, and antioxidant systems activities. J. Cell. Physiol. 227: 25112518, 2012. (c) 2011 Wiley Periodicals, Inc.

Effect of N-acetylcysteine on markers of skeletal muscle injury after fatiguing contractile activity

The effects of N-Acetylcysteine (NAC), an unspecific antioxidant, on fatiguing contractile activity-induced injury were investigated. Twenty-four male Wistar rats were randomly assigned to two groups. The placebo group (N=12) received one injection of phosphate buffer (PBS) 1 h prior to contractile activity induced by electrical stimulation. The NAC group (NAC; N=12) received electrical stimulation for the same time period and NAC (500 mg/kg, i.p.) dissolved in PBS 1 h prior to electrical stimulation. The contralateral hindlimb was used as a control, except in the analysis of plasma enzyme activities, when a control group (rats placebo group not electrically stimulated and not treated) was included. The following parameters were measured: tetanic force, muscle fatigue, plasma activities of creatine kinase (CK) and lactate dehydrogenase (LDH), changes in muscle vascular permeability using Evans blue dye (EBD), muscle content of reactive oxygen species (ROS) and thiobarbituric acid-reactive substances (TBARS) and myeloperoxidase (MPO) activity. Muscle fatigue was delayed and tetanic force was preserved in NAC-treated rats. NAC treatment decreased plasma CK and LDH activities. The content of muscle-derived ROS, TBARS, EBD and MPO activity in both gastrocnemius and soleus muscles were also decreased by NAC pre-treatment. Thus, NAC has a protective effect against injury induced by fatiguing contractile activity in skeletal muscle.

Peroxisome proliferator-activated receptor {gamma} coactivator 1{alpha} (PGC-1{alpha}) promotes skeletal muscle lipid refueling in vivo by activating de novo lipogenesis and the pentose phosphate pathway

Exercise induces a pleiotropic adaptive response in skeletal muscle, largely through peroxisome proliferator-activated receptor coactivator 1 (PGC-1 ). PGC-1 enhances lipid oxidation and thereby provides energy for sustained muscle contraction. Its potential implication in promoting muscle refueling remains unresolved, however. Here, we investigated a possible role of elevated PGC-1 levels in skeletal muscle lipogenesis in vivo and the molecular mechanisms that underlie PGC-1 -mediated de novo lipogenesis. To this end, we studied transgenic mice with physiological overexpression of PGC-1 and human muscle biopsies pre- and post-exercise. We demonstrate that PGC-1 enhances lipogenesis in skeletal muscle through liver X receptor -dependent activation of the fatty acid synthase (FAS) promoter and by increasing FAS activity. Using chromatin immunoprecipitation, we establish a direct interaction between PGC-1 and the liver X receptor-responsive element in the FAS promoter. Moreover, we show for the first time that increased glucose uptake and activation of the pentose phosphate pathway provide substrates for RNA synthesis and cofactors for de novo lipogenesis. Similarly, we observed increased lipogenesis and lipid levels in human muscle biopsies that were obtained post-exercise. Our findings suggest that PGC-1 coordinates lipogenesis, intramyocellular lipid accumulation, and substrate oxidation in exercised skeletal muscle in vivo.

Muscle metabolites: functional MR spectroscopy during exercise imposed by tetanic electrical nerve stimulation

Permission from the ethics committee and informed consent were obtained. The purpose of this study was to prospectively evaluate a method developed for the noninvasive assessment of muscle metabolites during exercise. Hydrogen 1 magnetic resonance (MR) spectroscopy peaks were measured during tetanic isometric muscle contraction imposed by supramaximal repetitive nerve stimulation. The kinetics of creatine-phosphocreatine and acetylcarnitine signal changes (P < .001) could be assessed continuously before, during, and after exercise. The control peak (trimethylammonium compounds), which served as an internal reference, did not change. This technique-that is, functional MR spectroscopy-opens the possibility for noninvasive diagnostic muscle metabolite testing in a clinical setting.

Impaired metabolic modulation of α-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle

The neuronal isoform of nitric oxide synthase (nNOS) is highly expressed in mammalian skeletal muscle, but its functional role has not been defined. NO has been implicated in the local metabolic regulation of blood flow in contracting skeletal muscle in part by antagonizing sympathetic vasoconstriction. We therefore hypothesized that nNOS in skeletal muscle is the source of the NO mediating the inhibition of sympathetic vasoconstriction in contracting muscle. In the mdx mouse, a model of Duchenne muscular dystrophy in which dystrophin deficiency results in greatly reduced expression of nNOS in skeletal muscle, we found that the normal ability of skeletal muscle contraction to attenuate α-adrenergic vasoconstriction is defective. Similar results were obtained in mutant mice that lack the gene encoding nNOS. Together these data suggest a specific role for nNOS in the local metabolic inhibition of α-adrenergic vasoconstriction in active skeletal muscle.

Identification of the endogenous smooth muscle myosin phosphatase-associated kinase

Ca2+ sensitization of smooth muscle contraction involves inhibition of myosin light chain phosphatase (SMPP-1M) and enhanced myosin light chain phosphorylation. Inhibition of SMPP-1M is modulated through phosphorylation of the myosin targeting subunit (MYPT1) by either Rho-associated kinase (ROK) or an unknown SMPP-1M-associated kinase. Activated ROK is predominantly membrane-associated and its putative substrate, SMPP-1M, is mainly myofibrillar-associated. This raises a conundrum about the mechanism of interaction between these enzymes. We present ZIP-like kinase, identified by “mixed-peptide” Edman sequencing after affinity purification, as the previously unidentified SMPP-1M-associated kinase. ZIP-like kinase was shown to associate with MYPT1 and phosphorylate the inhibitory site in intact smooth muscle. Phosphorylation of ZIP-like kinase was associated with an increase in kinase activity during carbachol stimulation, suggesting that the enzyme may be a terminal member of a Ca2+ sensitizing kinase cascade.

Cocaine: mechanism of inhibition of a muscle acetylcholine receptor studied by a laser-pulse photolysis technique.

Effects of cocaine on the muscle nicotinic acetylcholine receptor were investigated by using a chemical kinetic technique with a microsecond time resolution. This membrane-bound receptor regulates signal transmission between nerve and muscle cells, initiates muscle contraction, and is inhibited by cocaine, an abused drug. The inhibition mechanism is not well understood because of the lack of chemical kinetic techniques with the appropriate (microsecond) time resolution. Such a technique, utilizing laser-pulse photolysis, was recently developed; by using it the following results were obtained. (i) The apparent cocaine dissociation constant of the closed-channel receptor form is approximately 50 microM. High carbamoylcholine concentration and, therefore, increased concentrations of the open-channel receptor form, decrease receptor affinity for cocaine approximately 6-fold. (ii) The rate of the receptor reaction with cocaine is at least approximately 30-fold slower than the channel-opening rate, resulting in a cocaine-induced decrease in the concentration of open receptor channels without a concomitant decrease in the channel-opening or -closing rates. (iii) The channel-closing rate increases approximately 1.5-fold as the cocaine concentration is increased from 20 to 60 microM but then remains constant as the concentration is increased further. The results are consistent with a mechanism in which cocaine first binds rapidly to a regulatory site of the receptor, which can still form transmembrane channels. Subsequently, a slow step (t1/2 approximately 70 ms) leads to a receptor form that cannot form transmembrane channels, and acetylcholine receptor-mediated signal transmission is, therefore, blocked. Implications for the search for therapeutic agents that alleviate cocaine poisoning are mentioned.

Muscular contraction and the reflex control of movement,

"A chronological list of important contributions to the physiology of muscle": p. 53-55.

Unravelling the complexity of muscle impairment in chronic neck pain

Exercise interventions are deemed essential for the effective management of patients with neck pain. However, there has been a lack of consensus on optimal exercise prescription, which has resulted from a paucity of studies to quantify the precise nature of muscle impairment, in people with neck pain. This masterclass will present recent research from our laboratory, which has utilized surface electromyography to investigate cervical flexor muscle impairment in patients with chronic neck pain. This research has identified deficits in the motor control of the deep and superficial cervical flexor muscles in people with chronic neck pain, characterized by a delay in onset of neck muscle contraction associated with movement of the upper limb. In addition, people with neck pain demonstrate an altered pattern of muscle activation, which is characterized by reduced deep cervical flexor muscle activity during a low load cognitive task and increased activity of the superficial cervical flexor muscles during both cognitive tasks and functional activities. The results have demonstrated the complex, multifaceted nature of cervical muscle impairment, which exists in people with a history of neck pain. In turn, this has considerable implications for the rehabilitation of muscle function in people with neck pain disorders. (C) 2004 Elsevier Ltd. All rights reserved.

Maternal creatine supplementation during pregnancy prevents long-term changes in diaphragm muscle structure and function after birth asphyxia

Using a model of birth asphyxia, we previously reported significant structural and functional deficits in the diaphragm muscle in spiny mice, deficits that are prevented by supplementing the maternal diet with 5% creatine from mid-pregnancy. The long-term effects of this exposure are unknown. Pregnant spiny mice were fed control or 5% creatine-supplemented diet for the second half of pregnancy, and fetuses were delivered by caesarean section with or without 7.5 min of in-utero asphyxia. Surviving pups were raised by a cross-foster dam until 33±2 days of age when they were euthanized to obtain the diaphragm muscle for ex-vivo study of twitch tension and muscle fatigue, and for structural and enzymatic analyses. Functional analysis of the diaphragm revealed no differences in single twitch contractile parameters between any groups. However, muscle fatigue, induced by stimulation of diaphragm strips with a train of pulses (330 ms train/sec, 40 Hz) for 300 sec, was significantly greater for asphyxia pups compared with controls (p<0.05), and this did not occur in diaphragms of creatine + asphyxia pups. Birth asphyxia resulted in a significant increase in the proportion of glycolytic, fast-twitch fibres and a reduction in oxidative capacity of Type I and IIb fibres in male offspring, as well as reduced cross-sectional area of all muscle fibre types (Type I, IIa, IIb/d) in both males and females at 33 days of age. None of these changes were observed in creatine + asphyxia animals. Thus, the changes in diaphragm fatigue and structure induced by birth asphyxia persist long-term but are prevented by maternal creatine supplementation.

Systemic inflammatory responses to maximal versus submaximal lengthening contractions of the elbow flexors

We compared changes in markers of muscle damage and systemic inflammation after submaximal and maximal lengthening muscle contractions of the elbow flexors. Using a cross-over design, 10 healthy young men not involved in resistance training completed a submaximal trial (10 sets of 60 lengthening contractions at 10% maximum isometric strength, 1 min rest between sets), followed by a maximal trial (10 sets of three lengthening contractions at 100% maximum isometric strength, 3 min rest between sets). Lengthening contractions were performed on an isokinetic dynamometer. Opposite arms were used for the submaximal and maximal trials, and the trials were separated by a minimum of two weeks. Blood was sampled before, immediately after, 1 h, 3 h, and 1-4 d after each trial. Total leukocyte and neutrophil numbers, and the serum concentration of soluble tumor necrosis factor-alpha receptor 1 were elevated after both trials (P < 0.01), but there were no differences between the trials. Serum IL-6 concentration was elevated 3 h after the submaximal contractions (P < 0.01). The concentrations of serum tumor necrosis factor-alpha, IL-1 receptor antagonist, IL-10, granulocyte-colony stimulating factor and plasma C-reactive protein remained unchanged following both trials. Maximum isometric strength and range of motion decreased significantly (P < 0.001) after both trials, and were lower from 1-4 days after the maximal contractions compared to the submaximal contractions. Plasma myoglobin concentration and creatine kinase activity, muscle soreness and upper arm circumference all increased after both trials (P < 0.01), but were not significantly different between the trials. Therefore, there were no differences in markers of systemic inflammation, despite evidence of greater muscle damage following maximal versus submaximal lengthening contractions of the elbow flexors.

Relationship of moderate and low isometric lumbar extension through architectural and muscular activity variables: a cross sectional study

Background No study relating the changes obtained in the architecture of erector spinae (ES) muscle were registered with ultrasound and different intensities of muscle contraction recorded by surface EMG (electromyography) on the ES muscle was found. The aim of this study was analyse the relationship in the response of the ES muscle during isometric moderate and light lumbar isometric extension considering architecture and functional muscle variables. Methods Cross-sectional study. 46 subjects (52% men) with a group mean age of 30.4 (±7.78). The participants developed isometric lumbar extension while performing moderate and low isometric trunk and hip extension in a sitting position with hips flexed 90 degrees and the lumbar spine in neutral position. During these measurements, electromyography recordings and ultrasound images were taken bilaterally. Bilaterally pennation angle, muscle thickness, torque and muscle activation were measured. This study was developed at the human movement analysis laboratory of the Health Science Faculty of the University of Malaga (Spain). Results Strong and moderate correlations were found at moderate and low intensities contraction between the variable of the same intensity, with correlation values ranging from 0.726 (Torque Moderate – EMG Left Moderate) to 0.923 (Angle Left Light – Angle Right Light) (p < 0.001). This correlation is observed between the variables that describe the same intensity of contraction, showing a poor correlation between variables of different intensities. Conclusion There is a strong relationship between architecture and function variables of ES muscle when describe an isometric lumbar extension at light or moderate intensity. Keywords: Ultrasonography; Surface electromyography; Thickness; Pennation angle; Erector spinae