Academic literature on the topic 'Peripheral muscles'
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Journal articles on the topic "Peripheral muscles"
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Bergmeister, Konstantin D., Martin Aman, Silvia Muceli, et al. "Peripheral nerve transfers change target muscle structure and function." Science Advances 5, no. 1 (2019): eaau2956. http://dx.doi.org/10.1126/sciadv.aau2956.
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Selective nerve transfers surgically rewire motor neurons and are used in extremity reconstruction to restore muscle function or to facilitate intuitive prosthetic control. We investigated the neurophysiological effects of rewiring motor axons originating from spinal motor neuron pools into target muscles with lower innervation ratio in a rat model. Following reinnervation, the target muscle’s force regenerated almost completely, with the motor unit population increasing to 116% in functional and 172% in histological assessments with subsequently smaller muscle units. Muscle fiber type populations transformed into the donor nerve’s original muscles. We thus demonstrate that axons of alternative spinal origin can hyper-reinnervate target muscles without loss of muscle force regeneration, but with a donor-specific shift in muscle fiber type. These results explain the excellent clinical outcomes following nerve transfers in neuromuscular reconstruction. They indicate that reinnervated muscles can provide an accurate bioscreen to display neural information of lost body parts for high-fidelity prosthetic control.
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MacIntosh, Brian R., and M. Reza S. Shahi. "A peripheral governor regulates muscle contraction." Applied Physiology, Nutrition, and Metabolism 36, no. 1 (2011): 1–11. http://dx.doi.org/10.1139/h10-073.
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Active skeletal muscles are capable of keeping the global [adenosine triphosphate (ATP)] reasonably constant during exercise, whether it is mild exercise, activating a few motor units, or all-out exercise using a substantial mass of muscle. This could only be accomplished if there were regulatory processes in place not only to replenish ATP as quickly as possible, but also to modulate the rate of ATP use when that rate threatens to exceed the rate of ATP replenishment, a situation that could lead to metabolic catastrophe. This paper proposes that there is a regulatory process or “peripheral governor” that can modulate activation of muscle to avoid metabolic catastrophe. A peripheral governor, working at the cellular level, should be able to reduce the cellular rate of ATP hydrolysis associated with muscle contraction by attenuating activation. This would necessarily cause something we call peripheral fatigue (i.e., reduced contractile response to a given stimulation). There is no doubt that peripheral fatigue occurs. It has been demonstrated in isolated muscles, in muscles in situ with no central nervous system input, and in intact human subjects performing voluntary exercise with small muscle groups or doing whole-body exercise. The regulation of muscle activation is achieved in at least 3 ways (decreasing membrane excitability, inhibiting Ca2+release through ryanodine receptors, and decreasing the availability of Ca2+in the sarcoplasmic reticulum), making this a highly redundant control system. The peripheral governor attenuates cellular activation to reduce the metabolic demand, thereby preserving ATP and the integrity of the cell.
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Little, James W., Kim Burchiel, and Paul Nutter. "Tremor and peripheral nerve entrapment." Journal of Neurosurgery 64, no. 1 (1986): 145–47. http://dx.doi.org/10.3171/jns.1986.64.1.0145.
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✓ A patient is described in whom pain, paresthesias, weakness, and resting tremor gradually developed 8 years after an ulnar nerve transposition. Electromyography revealed that the tremor occurred at 4 to 5 Hz, was abolished by voluntary muscle contraction, and was localized to ulnar-innervated muscles. Ulnar nerve conduction was focally slowed at the elbow; therefore, ulnar neurolysis was performed and a fusiform neuroma-in-continuity was found. Mechanically tapping the neuroma elicited repetitive discharges at 4 to 5 Hz in the intrinsic muscles of the hand; these discharges were abolished by anesthetic block proximal to the neuroma. Although the pain, paresthesias, and weakness were abolished by the neurolysis, the tremor persisted. Possible neurophysiological mechanisms underlying the appearance of tremor with peripheral nerve entrapment are discussed.
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Bond Jr., Vernon, Arthur T. Johnson, Paul Vaccaro, et al. "Lower Leg High-Intensity Resistance Training and Peripheral Hemodynamic Adaptations." Canadian Journal of Applied Physiology 21, no. 3 (1996): 209–17. http://dx.doi.org/10.1139/h96-017.
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High-intensity resistance (HIR) training has been associated with muscle hypertrophy and decreased microvascular density that might produce a blood flow limitation. The effect of HIR training on lower leg maximal blood flow and minimum vascular resistance (Rmin) during reactive hyperemia were investigated in 7 healthy males. The gastrocnemius-soleus muscles of one leg were trained using maximal isokinetic concentric contractions for 4 weeks; the nontrained leg was the control. Lower leg blood flow was measured by venous occlusion plethysmography. Lower leg muscle volume was determined using magnetic resonance imaging. Peak isokinetic torque increased in both the trained (T) and nontrained (NT) legs (p <.05). Lower leg muscle volume increased by 2% in the T leg only (p <.05). In the T leg, maximal blood flow decreased and Rmin increased (p <.05); no hemodynamic change was detected in the NT leg. It is concluded that HIR training of the calf muscles is associated with a decrease in hyperemia-induced blood flow; thereby, indicating a blood flow limitation to the calf muscles. Key words: Isokinetic strength training, reactive hyperemia
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Bell, D. G., P. Tikuisis, and I. Jacobs. "Relative intensity of muscular contraction during shivering." Journal of Applied Physiology 72, no. 6 (1992): 2336–42. http://dx.doi.org/10.1152/jappl.1992.72.6.2336.
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The intensity of cold-induced shivering, quantified by surface electromyography (EMG) and then expressed as a function of the maximal myoelectrical activity (integrated EMG) obtained during a maximum voluntary contraction (MVC), was examined in this study in individuals classified by body fat. In addition, the relationship between shivering and metabolic rate (MR) and the relative contribution of various muscle groups to total heat production were studied. Ten seminude male volunteers, 5 LEAN (less than 11% body fat) and 5 NORM (greater than 15% body fat) were exposed to 10 degrees C air for 2 h. EMG of six muscle groups (pectoralis major, rectus abdominis, rectus femoris, gastrocnemius, biceps brachii, and brachioradialis) was measured and compared with the EMG of each muscle's MVC. A whole body index of shivering, determined from the mass-weighted intensity of shivering of each muscle group, was correlated with MR. After the initial few minutes of exposure, only the pectoralis major, rectus femoris, and biceps brachii continued to increase their intensity of shivering. Shivering intensity was higher in the central muscles, ranging from 5 to 16% of MVC compared with that in the peripheral muscles, which ranged from 1 to 4% of MVC. Shivering intensities were similar in the peripheral muscles for the LEAN and NORM groups, whereas differences occurred in the trunk muscles for the pectoralis major and rectus abdominis. The whole body index of shivering correlated significantly with each individual's increase in MR (r = 0.63–0.97).(ABSTRACT TRUNCATED AT 250 WORDS)
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CARTER, A.-J., F. KRISTMUNDSDOTTIR, J. GILMOUR, and M. A. GLASBY. "Changes in Muscle Cytoarchitecture after Peripheral Nerve Injury and Repair." Journal of Hand Surgery 23, no. 3 (1998): 365–69. http://dx.doi.org/10.1016/s0266-7681(98)80059-4.
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The aim of this study was to assess the changes which occurred in the rat in target muscles after the injury and repair of a specific peripheral nerve, using several clinically-appropriate surgical techniques. There were alterations in the size, shape, morphology and cytochemical architecture of the fibres of the target muscles. These changes were marked when transection and repair of the nerve was compared with the less-severe crush injury. The method of repair did not correlate significantly with the occurrence of changes in muscle cytoarchitecture. The results suggest that the extent of cell loss and the changes in muscle fibre architecture were influenced by the type of injury, rather than by the method of repair.
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Gea, Joaquim, Alvar Agustí, and Josep Roca. "Pathophysiology of muscle dysfunction in COPD." Journal of Applied Physiology 114, no. 9 (2013): 1222–34. http://dx.doi.org/10.1152/japplphysiol.00981.2012.
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Muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD) and may involve both respiratory and locomotor (peripheral) muscles. The loss of strength and/or endurance in the former can lead to ventilatory insufficiency, whereas in the latter it limits exercise capacity and activities of daily life. Muscle dysfunction is the consequence of complex interactions between local and systemic factors, frequently coexisting in COPD patients. Pulmonary hyperinflation along with the increase in work of breathing that occur in COPD appear as the main contributing factors to respiratory muscle dysfunction. By contrast, deconditioning seems to play a key role in peripheral muscle dysfunction. However, additional systemic factors, including tobacco smoking, systemic inflammation, exercise, exacerbations, nutritional and gas exchange abnormalities, anabolic insufficiency, comorbidities and drugs, can also influence the function of both respiratory and peripheral muscles, by inducing modifications in their local microenvironment. Under all these circumstances, protein metabolism imbalance, oxidative stress, inflammatory events, as well as muscle injury may occur, determining the final structure and modulating the function of different muscle groups. Respiratory muscles show signs of injury as well as an increase in several elements involved in aerobic metabolism (proportion of type I fibers, capillary density, and aerobic enzyme activity) whereas limb muscles exhibit a loss of the same elements, injury, and a reduction in fiber size. In the present review we examine the current state of the art of the pathophysiology of muscle dysfunction in COPD.
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Grumbles, Robert M., Patrick Wood, Michelle Rudinsky, Anna M. Gomez, and Christine K. Thomas. "Muscle Reinnervation with Delayed or Immediate Transplant of Embryonic Ventral Spinal Cord Cells into Adult Rat Peripheral Nerve." Cell Transplantation 11, no. 3 (2002): 241–50. http://dx.doi.org/10.3727/096020198390003.
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Muscle denervation is common in various neuromuscular diseases and after trauma. It induces skeletal muscle atrophy. Only muscle reinnervation leads to functional recovery. In previous studies, denervated adult rat muscles were rescued by transplantation of embryonic day 14–15 (E14–15) ventral spinal cord cells into a nearby peripheral nerve. In the present study, changes were made in the environment into which the cells were placed to test whether reinnervation was improved by: 1) prior nerve degeneration, induced by sciatic nerve transection 1 week before cell transplantation; 2) transplantation of 1 million versus 5 million cells; 3) addition of nerve growth factor (NGF) to the transplant. Ten weeks after cell transplantation, axons had grown from all of the transplants. The numbers of myelinated axons that regenerated into the tibial, medial (MG), and lateral gastrocnemius-soleus (LGS) nerves were similar across treatments. The mean diameters of large LGS axons (>6 μm) were significantly larger with nerve degeneration before transplantation. The mean diameters of MG and LGS axons were significantly larger with transplantation of 1 million versus 5 million cells. Silver-stained experimental and control lateral gastronemius (LG) muscles showed axons that terminated at motor end plates. Nodal and terminal sprouts were more common in reinnervated muscles (45–63% of all end plates) than in control muscles (10%). Electrical stimulation of the transplants induced weak contractions in 39 of 47 MG muscles (83%) and 33 of 46 LG muscles (72%) but at higher voltages than needed to excite control muscles. The threshold for MG contraction was lower with transplantation of 1 million cells, while LG thresholds were lower without NGF. The cross-sectional area of whole LG muscles was significantly larger with cell transplantation (immediate or delayed) than with media alone, but all of these muscle areas were reduced significantly compared with control muscle areas. These data suggest that delayed transplantation of fewer cells without NGF assists regeneration of larger diameter axons and prevents some muscle atrophy.
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Choe, Myoung-Ae, Kyung Hwa Kim, Gyeong Ju An, Kyung-Sook Lee, and Margaret Heitkemper. "Hindlimb Muscle Atrophy Occurs From Peripheral Nerve Damage in a Rat Neuropathic Pain Model." Biological Research For Nursing 13, no. 1 (2011): 44–54. http://dx.doi.org/10.1177/1099800410382291.
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Objective: The purpose of this study was to examine the effect of neuropathic pain produced by peripheral nerve damage on mass, myofibrillar protein content, and cross-sectional areas of Type I and II fibers of rat hindlimb muscles. Method: Adult male Sprague-Dawley rats were assigned to one of three groups: a pain group (n = 10) that underwent ligation and cut of the left L5 spinal nerve, a sham group (n = 10) that underwent a sham cut procedure, or a control group (n = 10) that underwent no procedures. The withdrawal threshold test was done to assess pain threshold on each of Days 1—7 and 14. Activity, body weight, and food intake were measured daily for 2 weeks. At 15 days, rats were anesthetized and the bilateral soleus, plantaris, and gastrocnemius muscles dissected. Results: At 15 days postligation, the pain group had significant decreases in total dietary intake, body weight, activity, and muscle weight as compared to sham and control animals. Muscle weight and cross-sectional area of Type II fiber of the ipsilateral soleus, plantaris, and gastrocnemius muscles decreased as did myofibrillar protein content of the ipsilateral plantaris and gastrocnemius muscles. Muscle weight of the contralateral gastrocnemius muscle decreased, as did myofibrillar protein content and cross-sectional area of Type II fiber of the contralateral plantaris muscle. Conclusion: Hindlimb muscle atrophy occurs in both ipsilateral and contralateral sides following induction of neuropathic pain by unilateral peripheral nerve damage. Muscle changes of the ipsilateral side are more pronounced than those of the contralateral side.
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Kogo, Mikihiko, Munehiro Hamaguchi, and Tokuzo Matsuya. "Observation of Velopharyngeal Closure Patterns following Isolated Stimulation of Levator Veli Palatini and Pharyngeal Constrictor Muscles." Cleft Palate-Craniofacial Journal 33, no. 4 (1996): 273–76. http://dx.doi.org/10.1597/1545-1569_1996_033_0273_oovcpf_2.3.co_2.
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This study, using mongrel dogs, showed the individual movements caused by the levator veli palatini muscle (LVP) and pharyngeal constrictor (PC) contraction, induced by electrical stimulation to each peripheral motor nerve. Each bilateral peripheral motor nerve of the LVP and PC muscles was isolated and stimulated electrically to induce the individual contraction of bilateral LVP and PC muscles. The movements were visualized by use of a fiberscope. Vertical movement of the middle soft palate was observed mainly at LVP contraction. Circular closure in the posterior region of the velopharynx was induced by contraction of the PC muscle. The posterior and lateral wall movements clearly occurred following PC contraction.
Dissertations / Theses on the topic "Peripheral muscles"
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HOWARD, JAMES DAVID. "CENTRAL AND PERIPHERAL FACTORS UNDERLYING BILATERAL INHIBITION DURING MAXIMAL EFFORTS." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184067.
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It has been shown that maximal, bilateral efforts result in both a force and EMG deficit when compared to maximal, unilateral activation of the same musculature. It is unclear whether this deficit is the result of interactions of central or peripheral origin. The first aim study investigated the bilateral performance index (BPI (%) = [100 x bilateral force/(right unilateral + left unilateral forces)] - 100) for maximal, isometric, extensor torques about the knee joint in three groups of subjects: untrained (never lifted weights), cyclists (leg musculature trained reciprocally), and weightlifters (legs trained bilaterally). The BPI for the weightlifters (+7.0 ± 5.0%) was significantly (p < 0.05) greater than the BPI of the cyclists (-4.0 ± 6.3%) or the untrained subjects (-9.7 ± 5.2%). These results indicate that the inhibitory mechanisms previously proposed to act during bilateral efforts are inadequate, and that excitatory factors must be present to achieve a BPI > 0. The second aim study showed that the BPI can be altered as a result of three weeks of bilateral isometric strength training. The BPI's for the control and unilateral training groups were not significantly different pre- to posttraining. However, the BPI of the bilateral training group increased significantly (p < 0.05) from -3.7 ± 6.9% prior to training, to +4.2 ± 4.4% after training. These findings indicate that bilateral strength training can alter the relationship between unilateral and bilateral force output. The third aim study demonstrated that subjects with a positive BPI (+6.8 ± 4.3%) responded differently to an afferent perturbation (electrical stimulation) than subjects with a negative BPI (-10.0 ± 5.2%). The negative BPI group showed a 5.7 ± 3.4% facilitation in force during contralateral electrical stimulation. This was significantly (p < 0.05) less than the 16.5 ± 7.5% facilitation shown by the positive BPI group. These results indicate that afferent feedback can alter the force output in the contralateral limb, and may thereby play a role in unilateral-bilateral force differences.
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Swisher, Anne K. "The effect of emphysema on adaptation of peripheral skeletal muscle to different loading conditions in the Syrian golden hamster." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3008.
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Thesis (Ph. D.)--West Virginia University, 2003.<br>Title from document title page. Document formatted into pages; contains vii, 141 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Wang, Wendy. "Changes in the Electromyographic Activity and Joint Moments due to the Self-reinnervation of the Lateral Gastrocnemius and Soleus Muscles." Thesis, Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/52115.
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Peripheral nerve injuries can cause serious health problems and result in lifelong disabilities. Although researchers have been studying peripheral nerve injuries, patients may not regain complete function of their muscles even after surgeries to repair their nerves are performed. However, animal studies have shown that after peripheral nerve cut and repair (muscle self-reinnervation), stretch-reflex in the affected muscles does not recover, which may affect the muscle electromyographic (EMG) activity of all muscle synergists, as well as joint kinematics. The aim of this study is to determine the effects of the self-reinnervation of the lateral gastrocnemius (LG) and soleus (SO) muscles in the hind limb of felines on the mean EMG activity of the intact synergist medial gastrocnemius (MG), as well as the moments at the knee and ankle joints during different walking conditions: level (0%), downslope (-50%), and upslope (+50%). The EMG activity and joint kinematics were recorded on the three different walking conditions before and 12 weeks after the self-reinnervation of LG and SO when these muscles recovered their activity. The self-reinnervation of the two muscles caused the MG EMG activity to increase for all walking conditions. However, the changes in the knee and ankle moments differed depending on the three different walking conditions. It was concluded that the changes in EMG and joint moments after self-reinnervation could be caused by the absence of stretch-reflex in the affected muscles and/or changes in physiological properties of muscles.
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Ausín, Herrero Pilar 1974. "Estructura, biología y función muscular esquelética en mujeres con EPOC." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/403649.
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La disfunción muscular es una importante afectación sistémica en la EPOC, con un origen multifactorial e impacto en la actividad física, capacidad de ejercicio, calidad de vida y mortalidad de los pacientes. Hasta el momento se sabe que existen diferencias clínicas, funcionales y biológicas de la enfermedad en relación al sexo. Sin embargo no se ha analizado en profundidad si existen también diferencias respecto de la disfunción y estructura muscular. Objetivo: Analizar las diferencias en la presentación clínica y específicamente en la función, estructura y biología musculares, en función del sexo. Métodos: Se incluyeron 21 mujeres y 19 hombres con EPOC estable así como 8 mujeres y 7 hombres sanos. Se analizaron variables clínicas, de función pulmonar y muscular, actividad física y capacidad de esfuerzo así como marcadores de inflamación sistémica y pulmonar (condensado exhalado). Además se realizó biopsia abierta del vastus lateralis del cuádriceps a todos los sujetos, estudiándose la estructura (tipo y tamaño de fibras, así como signos histológicos de daño-regeneración) e inflamación musculares. Resultados: Las pacientes con EPOC presentan más signos histológicos de daño en el músculo cuádriceps que los hombres con la enfermedad a pesar de que los niveles de afectación funcional, estado nutricional, inflamación sistémica y actividad física fueron similares. Este fenómeno era evidente aún en estadios moderados de la enfermedad. Sin embargo, los signos precoces de regeneración muscular fueron inferiores en las mujeres con EPOC respecto de los varones. Así mismo, el shift hacia un aumento en la proporción de fibras de tipo II fue también inferior en las mujeres con EPOC. Asimismo, las mujeres con EPOC presentan mayor disminución de fuerza muscular, de la capacidad de esfuerzo y de los niveles de vitamina D, así como una tendencia a una superior percepción de la disnea. También se confirma la ausencia de relaciones en los niveles de inflamación entre los compartimentos sistémico, pulmonar y muscular. Conclusiones: Las mujeres con EPOC presentan una afectación muscular diferenciada de los varones con mayores signos de daño, menores de reparación y menor shift hacia fibras de tipo II. Existen diferentes factores que se asocian a la afectación muscular en estas mujeres, como los niveles de vitamina D, la hipoxia o el nivel de actividad física, aunque no pueden descartarse otros como la acción estrogénica que también podrían contribuir a estas diferencias.<br>Skeletal muscle dysfunction is an important systemic manifestation of the COPD. This dysfunction has a multifactorial origin that provokes significant impact on physical activity, exercise tolerance, quality of life and mortality of the patients. Several studies have showed differences related to gender in disease expression including symptoms, functional aspects and biology, however the effect of gender in muscle dysfunction in COPD is so far an unexplored area. Aim: to determine whether gender modifies clinical presentation and functional status of the disease, with special focus on muscle structure, biology and function. Methods: 21 female and 19 male COPD patients as well as 8 healthy women and 7 healthy men were consecutively recruited. Anthropometry, body composition, lung function, symptoms, health-related quality of life, physical activity, limb muscle function, exercise capacity, markers of systemic and pulmonary (breath condensate) inflammation were assessed in all the subjects. Open biopsies of the vastus lateralis muscle were obtained in all the subjects and analysis of muscle structure (fiber typing, fiber size and muscle damage-regeneration signs) and muscular inflammation were performed. Results: COPD women showed more evident histological signs of muscle injury in quadriceps muscle than COPD men in spite of similar functional and nutritional impairment, systemic inflammation and physical activity between both groups. This phenomenon was evident even in moderate stage of the disease. However the early regeneration signs were lower in COPD women compare to COPD men. Moreover, muscular shift from type I to type II fibers was also lower in women COPD in comparison with COPD men. Furthermore, women COPD showed lower quadriceps force, exercise capacity and vitamin D and higher perception of dyspnoea in COPD women. It also confirms the lack of relationship between systemic, pulmonary and muscular inflammation. Conclusions: COPD women show differences in muscular structure compared to COPD men with more signs of injury, less signs of regeneration and lower shift from type I to type II fibers. There are some factors related to muscular dysfunction in COPD women as vitamin D levels, hypoxia or level of physical activity, however other factors as oestrogens activity could also contribute to these differences.
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Salazar, Degracia Anna 1991. "Mechanisms of muscle wasting in cachexia models : therapeutic implications." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/666924.
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La caquexia afecta negativamente a los pacientes con enfermedades crónicas y sobre todo en el cáncer. Las estrategias terapéuticas son aún limitadas. Los beta2-agonistas (formoterol) y el soporte nutricional (L-carnitina) pueden atenuar los efectos deletéreos en el músculo. En la presente tesis, el tratamiento con formoterol y L-carnitina indujo efectos beneficiosos (peso corporal y muscular, estructura, apoptosis, proteólisis y vías de señalización) en el diafragma y músculos de las extremidades en un modelo experimental de caquexia cancerosa (hepatoma ascitico Yoshida AH-130, en ratas). En ratones con caquexia cancerosa (células de adenocarcinoma del pulmón LP07), el tratamiento del tumor con anticuerpos monoclonales (anti-PD1, anti-CTLA4, anti-CD137, y anti-CD19) indujo efectos beneficiosos de la misma índole como consecuencia de la disminución del tamaño y la carga tumoral. En esta tesis se ha demostrado que diversas vías de señalización y mecanismos implicados en la degradación proteica y muscular se ven atenuadas, mejorando las características fenotípicas y funcionales de los músculos diafragma y periféricos en respuesta a diversas estrategias terapéuticas. (165 palabras)<br>Cachexia negatively affects patients with chronic diseases and especially in cancer. Therapeutic strategies are still limited. The beta2-agonists (formoterol) and the nutritional support (L-carnitine) can attenuate the deleterious effects in the muscle. In this thesis, treatment with formoterol and L-carnitine induced beneficial effects (total body and muscle weights, structure, apoptosis, proteolysis and signaling pathways) in the diaphragm and limb muscles in an experimental model of cancer cachexia (AH-130 Yoshida hepatoma ascites cells, in rats). In mice with cancer cachexia (LP07 lung adenocarcinoma cells), treatment of the tumor with monoclonal antibodies (anti-PD1, anti-CTLA4, anti-CD137, and anti-CD19) induced beneficial effects of the same kind as a consequence of the decrease in size and tumor burden. This thesis has shown that various signaling pathways and mechanisms involved in protein and muscle degradation are attenuated, improving the phenotypic and functional characteristics of the diaphragm and peripheral muscles in response to various therapeutic strategies. (149 words)
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Williams, Craig. "Peripheral muscle fatigue during intense exercise." Thesis, University of Chichester, 2005. http://eprints.chi.ac.uk/840/.
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The role of adenine nucleotide metabolism is central to the electro-mechanical processes in muscular contraction. Interventions which alter the cellular micro-environment can impact on the fatigue response during exercise possibly mediated by the balance between ATP and ADP. This thesis examined the response of biochemical and physiological markers of muscle fatigue in dietary interventions aimed to alter the cellular environment. Contractile measures included force and relaxation times from contractions of the knee extensors, whilst biochemical markers included anunonia and lactate after voluntary isometric and incremental cycle exercise. Evoked contractile measurements afforded experimental objectivity independent of voluntary intervention whilst the voluntary measures afforded greater transferability. In Chapter 3 the relaxation time response to a train of evoked fatiguing contractions varied depending on the choice of relaxation method (upper exponential, lower exponential, 60-40 exponential, 100-75,95-45,75-37.5,75-25%). Methods describing the earlier portions of the relaxation curve slowed less during fatigue than those comprising the latter portions. Intra-session variability ranged from 1.3 to 5.02% and inter-session variation ranged from 2.85 to 6.97% dependent upon the adopted relaxation method. Such variability was comparable with other laboratories demonstrating significant intervention-induced changes. This has implications for future studies in the choice of relaxation method and magnitude of change necessary for identification of intervention-induced changes. In chapter 4 the magnitudes of change in MVC and time to fatigue in a voluntary isometric contraction between creatine and placebo supplementation were -3% and 2% respectively. The fatigue-induced slowing of evoked relaxation times was greater by -4% and these changes were not significant. The differences in markers of adenine nucleotide degradation after creatine and placebo supplementation were also insignificant. In chapter 5 the creatine supplementation-induced change in the decline in evoked force during a fatiguing train was -1 % but was insignificant. For the voluntary and evoked relaxation times, in chapter 5, the magnitude of changes between placebo and creatine supplementation were <1 %, and insignificant. The ingestion of NaHCO, accelerated the loss of evoked force during a fatiguing train, with a trend towards shorter relaxation times that was only evident in the 100-75% method. Bicarbonate ingestion resulted in higher plasma lactate but had minimal effect on markers of adenine nucleotide degradation. The rate of evoked force loss was greater when muscle glycogen stores were reduced by exercise and low CHO diet and this trend was reversed by additionally supplementing with creatine, but this was not associated with similar trends in markers of nucleotide degradation during incremental cycling. A novel finding of this study was that reducing muscle glycogen resulted in a more severe slowing of relaxation times that was reversed when combined with creatine supplementation. In this thesis the changes in the biochemical markers of ADP homeostasis (NH,) by dietary interventions were insignificant. However, the force and relaxation time responses may highlight the functional importance of maintaining ADP homeostasis. The fatigue-induced slowing of evoked relaxation times was different depending on the chosen method. Despite a smaller relative slowing during fatigue the 100-75% method appeared to be most sensitive to dietary interventions.
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Fitton, Anthony Robert. "Muscle recovery following peripheral nerve injury and repair." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418071.
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Askew, Christopher D. "Exercise intolerance in peripheral arterial disease." Queensland University of Technology, 2002. http://eprints.qut.edu.au/15869/.
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Patients with Peripheral Arterial Disease have a reduced capacity for exercise, the exact causes of which are poorly understood. This thesis investigated alternative testing procedures that aim to provide a more complete and precise description of the exercise capacities of these patients. Furthermore, the potential roles of gastrocnemius muscle fibre morphometry, capillary supply and glycogen stores in the exercise tolerance of PAD patients were studied.
Study one aimed to determine the effect of test repetition on maximal exercise performance and test-to-test variability in PAD patients using an incremental treadmill walking test (T) (n=5), an incremental cycle test (C) (n=5), and incremental endurance (PF-endurance) and maximal strength (PF-strength) plantar flexion tests (n=5). Tests were conducted once per week for eight weeks. Performance was stable on the T (~530 s) and C (~500 s) tests across the eight weeks. Test-to-test variance on T decreased from 16%CV (CV: coefficient of variation) to 6%CV (p=.21,NS), and from ~8%CV to 2%CV on C (p<.05) over the eight week period. Variance of peak gas exchange variables tended to decrease with performance variance on both tests; however, other physiological variables, and the associated variance levels, were stable throughout the study. PF strength (635-712N) gradually increased over the initial 2-3 weeks (p<.05) which was accompanied by a reduction in variance from ~8%CV to ~3%CV (p<.05). Similarly, PF endurance increased over the first two weeks (~32,000 to 41500 N.s-1) while variance of this measure fell from ~21%CV to ~10%CV (p<.05) over the study duration. It is concluded that the implementation of familiarisation sessions leads to a reduction in whole body and local calf muscular performance variance in patients with PAD.
Using a randomised crossover design, study two aimed to compare performance and the physiological and symptomatic responses between a T test and a C test in 16 patients with PAD. Peak exercise time on C (690 s) was greater than that on T (495 s); however the two were significantly correlated (n=16, r=.69, p<.05). Peak HR (120 bpm), VO2 (~1.22 l.min-1) and rate pressure product (~20') did not differ between the two tests, nor did the post exercise ankle pressure (T: 56; C: 61 mmHg). In two subjects with lower back pain during C, the ankle pressure of their "worst" limbs failed to fall by >10mmHg. Performance on both the T and C tests was closely related to the onset of leg symptoms; however the site of pain during C was much more variable than during T. Incremental cycle testing would overcome some of the limitations of treadmill testing (e.g. measurement of mechanical work), and it appears to be an acceptable alternative for measuring the exercise capacity and physiological exercise responses in known claudicants. Use of cycle ergometry for the diagnosis of PAD requires testing in the general population.
Study three aimed to compare whole body (T test and C test) and local calf muscular (PF strength and endurance) exercise performance between 16 PAD patients (age: 63 ± 2; BMI: 25.9 ± 1.1) and 13 healthy, sedentary control (CON) subjects (age: 62 ± 1; BMI: 25.9 ± 0.4), and to describe relationships between the whole body and local calf muscular exercise capacities within the two groups. Furthermore, this study aimed to compare several histochemical characteristics of the medial gastrocnemius muscle fibres between PAD and CON, and to establish whether these factors were related to the exercise capacities of both groups. Maximal performance on T was 59% lower in the PAD group compared with the CON group, as was performance on C (50%), PF strength (25%), and PF endurance (58%). Compared with CON, PAD patients had a lower estimated calf muscle mass and a slight reduction (10%) in muscle fibre size (p=.14, NS). They also had a lower proportion of type I fibres (PAD: 49%; CON: 62%) that was offset by a greater proportion of type IIA fibres (PAD: 27%; CON: 16%), and a reduction in the capillary contacts per muscle fibre (PAD: 1.63; CON: 2.12) compared with CON. When expressed relative to fibre area there were no differences in capillarisation between PAD and CON; however this index was significantly related to resting and post exercise ABI in the PAD patients. There were no differences in the mixed muscle [glycogen], nor the optical density of glycogen in the individual fibres, between the two groups. PF endurance was poorly predictive of walking performance, and did not correlate with any of the morphological variables in both groups. Calf muscle mass correlated with PF strength (r=.59 - .62), and strength was correlated with T performance (r= .61 - .63) in both groups. In the PAD patients, T performance was correlated with the cross sectional area (n=12, r=.72, p<.05), capillary contacts (n=10, r=.81, p<.05) and glycogen density (n=9, r=.81, p<.05) of type I fibres. This study confirms that a reduction in calf strength, which appears to be mediated through muscle atrophy, plays some role in the reduced exercise capacity of claudicants. While both fibre area and capillary supply seem to be of relevance to the exercise capacity of PAD patients, these two factors are closely linked and further research is required to establish the determinants, and relative importance of both. An important, and possibly limiting role of carbohydrate oxidisation in PAD patients is supported by the strong relationship between type I glycogen stores and whole body exercise capacity.
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Ross, Jessica L. "Peripheral Mechanisms of Ischemic Myalgia." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504803397585968.
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Gibson, H. "Peripheral excitatory and contractile mechanisms underlying fatigue resistance of human skeletal muscle." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384344.
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Experiments have been designed to investigate the physiological factors influencing the interrelationship between excitation and force generation that may counteractt he processesle ading to a decline in force (fatigue) during stimulatedi sometric contractions of the human adductor pollicis in vivo. Indices of isometric force, relaxation and contraction rates and evoked compound muscle action potentials (CMAP) were measured during defined patterns of stimulated activity (via the motor nerve). A computerized stimulator controller for precise generation of trains of electrical impulses was developed for this purpose. Forces generated at different frequencies were reproducible on separate occasions. Using an ascending frequency stimulation protocol (1-100Hz) the relationship between force decline and excitation (measured as the amplitude of the surface evoked CMAP) appeared to be dependent on stimulation frequency during ischaemic and nonoccluded activity. At high frequencies (50-100Hz), a `safety factor' was apparent, allowing preservation of force despite a marked fall in excitation, whereas at low frequencies (1-10Hz) force initially potentiated and then declined in excess of excitation. Maximum relaxation rate was reduced at all stimulation frequencies and was independent of stimulation frequency. Contractile activity performed was shown to be linearly related to maximum relaxation rate over a frequency range of 20-100Hz for up to 30max. seconds. Contractile activity performed was therefore used as a measure of the metabolic cost of a contraction. Force failure appeared to depend upon the numbers of stimuli delivered, independent of frequency, rather than on contractile activity performed, suggesting that electrophysiological factors are of importance in contributing to fatigue. Further studieso n CMAP characteristicsd emonstrateda broadeningo f the action potential, reflecting a slowing of conduction velocity, which is thought to lead to `runin' of action potentials, and hencet he reduction of CMAP amplitude associatedw ith the high-frequency `safety factor'. The broadening of the action potential recovered immediately during ischaemic conditions at 100Hz following 2400 stimuli but did not recover following prolonged activity at 20Hz until circulation was restored, whereas CMAP amplitude recovered immediately at both frequencies, suggesting that slowing of conduction velocity may be dependent on metabolic factors at low stimulation frequencies which in turn may depend on the contractile history of the muscle. Patients with myophosphorylase deficiency (and thus unable to utilize glycogen), were studied to investigate the importance of energy supply. A failure of ischaemic recovery of the CMAP amplitude and no broadening of the CMAP after stimulated activity at 20Hz was observed, suggesting a failure of excitation of individual muscle cells occurs resulting in force failure in these individuals. Reversing the pattern of stimulation resulted in an initial enhancement of low frequency (10Hz) force and a prolonged maintenance of this force throughout the period of contraction studied. This was independent of slowing of relaxation or excitation. The initial force enhancement may result from the increased slowing of relaxation, and in addition, a form of post-tetanic twitch potentiation operates to counteract the decline in force despite a loss in excitation. In conclusion, during stimulated contractile activity of the adductor pollicis, mechanisms act to maintain or increase force generated per action potential distal to the sarcolemmal membrane, at both high and low frequencies of stimulation, thereby counteracting mechanisms that lead to fatigue. It is postulated that the alterations in intramuscular processes may allow voluntary isometrically contracting muscle to optimize force production at the onset of a contraction where high motor unit discharge rates are initially developed, delaying or eliminating the influence of excitation failure which would lead to contractile failure once maximal force is achieved, and subsequently to optimize contractile activation in the light of possible excitation failure as motor unit discharge rates decline. These findings may have important functional implications and may form the basis of physiological strategies for optimizing force production in the development of stimulation regimes for `functional electrical stimulation' or to any area of skeletal muscle research in which fatigue resistance is of importance.
Books on the topic "Peripheral muscles"
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Workshop Conference Hoechst-Werk Albert (1987 Frankfurt, Germany). Muscle ischaemia: Functional and metabolic aspects. Edited by Hudlicka O and Okyayuz-Baklouti I. C. Wolf, 1988.
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Justin, Mowchun, and Grudem Jon, eds. Peripheral nerve and muscle disease. Oxford University Press, 2009.
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M, Magro Albert, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Central and peripheral mechanisms of cardiovascular regulation. Plenum Press, 1986.
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Fisher, Wendy Jayne. Central and peripheral components of the human pressor response: Effects of skeletal muscle training status annd chronic heart failure. University of Birmingham, 1999.
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Ubolsakka, Chulee. Cardiovascular responses to external compression and peripheral oedema during rest and exercise in man: A role for a muscle mechanoreflex? University of Birmingham, 2001.
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Cai, Bonnie Bao Yan. Sex-related differences in the suppressive effects of peripheral morphine but not GABA on reflex jaw muscle activity evoked by glutamate application to the TMJ region in rats. National Library of Canada, 2001.
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Rafferty, Gerrard, and John Moxham. Assessment of Peripheral and Respiratory Muscle Strength in ICU. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0047.
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Skeletal muscle weakness affecting the respiratory and peripheral muscles is common in critically ill patients and can lead to difficulties in weaning, prolonged ICU admission, and significant morbidity in survivors. A number of techniques can be used to assess muscle strength. In the peripheral muscles, volitional techniques employing scoring systems or portable hand dynamometers are relatively simple and quick to use, requiring little or no specialist equipment. Such techniques can, however, only be applied to conscious and cooperative patients, preventing assessment of muscle weakness in many ICU patients. The volitional requirement also limits the ability to distinguish poor motivation and impaired cognition from true loss of muscle function. Non-volitional techniques involving motor nerve stimulation provide measures of muscle force production in non-cooperative patients but require specialist equipment. Normative data for comparative purposes are limited. Also, it is not clear which peripheral muscle best reflects generalized muscle weakness. Measurements of maximal inspiratory and expiratory pressures are widely used to assess respiratory muscle strength in ICU patients and are applicable to patients who can make some respiratory effort. As with all tests requiring patient cooperation, reliability is limited. Phrenic nerve stimulation allows direct, non-volitional assessment of diaphragm and phrenic nerve function, and normative values for comparative purposes are available. Magnetic phrenic nerve stimulation is well tolerated, can be performed in the presence of vascular catheters, and is used to document respiratory muscle weakness and track progression in critically ill patients.
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Shaibani, Aziz. Weakness of the Neck Muscles. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0010.
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The neck is furnished by dozens ofmuscles for flexion, extension, lateral bending, and rotation. It carries a 10-pound head at least two-thirds of every day. These muscles are under delicate central control, and they are subject to different central and peripheral malfunctions. Differential involvement of the neck flexors versus extensors helps in diagnosing different neuromuscular disorders. Weakness of the cervical extensors leads to head drop, a troubling condition that is caused by many neuromuscular disorders. Movement disorders such as cervical dystonia and Parkinson disease may also lead to head drop, causing confusion with neuromuscular causes such as myasthenia gravis and ALS. Head protrusion of the elderly (camptocormia) is a different entity.
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Shaibani, Aziz. Weakness of the Neck Muscles. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0010.
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The neck is furnished by tens of muscles for flexion, extension, lateral bending, and rotation. It carries a 10-pound head for at least two-thirds of every day. These muscles are under delicate central control, and they are subject to different central and peripheral malfunctions. Differential involvement of the neck flexors’ Vs extensors helps with the diagnosis of various neuromuscular disorders. Weakness of the cervical extensors leads to head drop, a troubling condition that is caused by many neuromuscular disorders. Movement disorders such as cervical dystonia and Parkinson disease lead to head drop, causing confusion with neuromuscular causes such as myasthenia gravis (MG) and amyotrophic lateral sclerosis (ALS). Head protrusion of the elderly (camptocormia) is a different entity.
Book chapters on the topic "Peripheral muscles"
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Puente-Maestu, Luis, François Maltais, André Nyberg, and Didier Saey. "Peripheral muscles." In Pulmonary Rehabilitation. CRC Press, 2020. http://dx.doi.org/10.1201/9781351015592-10.
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Stager, Joel M. "Peripheral Adaptations: The Skeletal Muscles." In Handbook of Sports Medicine and Science: Swimming. Blackwell Science Ltd, 2008. http://dx.doi.org/10.1002/9780470698761.ch3.
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Schaakxs, D. "Research on Peripheral Nerves and Muscles." In Movement Disorders of the Upper Extremities in Children. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-53622-0_25.
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Tizian, C., and L. Döbler. "Isolated Traumatic Nerve Lesions of the Extensor Pollicis Longus and Brevis Muscles." In Peripheral Nerve Lesions. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75611-5_41.
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Jacobson, Marcus. "Development of Nerve Connections with Muscles and Peripheral Sense Organs." In Developmental Neurobiology. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-4954-0_9.
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Anderson, Janice R. "Peripheral Neuropathy." In Atlas of Skeletal Muscle Pathology. Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4866-2_6.
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Wåhlin-Larsson, B., and J. Ulfberg. "Peripheral Muscle Changes." In Restless Legs Syndrome/Willis Ekbom Disease. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6777-3_9.
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Penkert, Götz, and Hisham Fansa. "Muscle and Tendon Transfer." In Peripheral Nerve Lesions. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-09232-3_10.
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Vital, Anne. "Combined muscle and nerve biopsy." In Peripheral nerve disorders. John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118618424.ch2.
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Penkert, Götz, and Hisham Fansa. "Principles of Free Neurovascular Muscle Transplantation." In Peripheral Nerve Lesions. Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-09232-3_12.
Full textConference papers on the topic "Peripheral muscles"
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Ueda, Jun, Lauren Lacey, Melih Turkseven, et al. "Robotic Neuromuscular Facilitation for Regaining Neural Activation in Hemiparetic Limbs." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-48085.
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This paper introduces an effective engineered rehabilitation system for understanding and inducing functional recovery of hemiparetic limbs based on the concept of timing-dependent induction of neural plasticity. Limb motor function is commonly impaired after neurologic injury such as stroke, with hemiparesis being one of the major impairments. In an emerging unique intervention for hemiparesis, named repetitive facilitation exercise, or RFE, a therapist manually applies brief mechanical stimuli to the peripheral target muscles (e.g., tapping, stretching of tendon/muscle) immediately before a patient intends to produce a movement with the muscle. The practice of this rehabilitation procedure by a skilled therapist often leads to dramatic rehabilitation outcomes. However, unskilled therapists, most likely due to the inaccuracy of the timing of peripheral stimulation in reference to the intention of movement (i.e. motor command), are unable to recreate the same rehabilitation results. Robotic rehabilitation, on the other hand, can improve the reliability and efficacy of the operation by satisfying the timing precision required by the therapy. This study demonstrates the use of a pneumatically-driven MRI-compatible robot for RFE assessment. The pressure dynamics of the system is studied for an accurate estimation on the time of response of the robot. The required temporal precision of the therapy is obtained and the use of the device is validated through experiments on a human subject.
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Christ, Daniel, Tad Driver, and Xiangrong Shen. "Reducing Energy Consumption of Pneumatic Artificial Muscles With Component Integration." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-5920.
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Pneumatic artificial muscle (PAM) is a class of flexible muscle-like actuator with low structure weight and high power density. In this paper, an integrated PAM design is presented, which incorporates peripheral elements, especially the control valves, in the interior space of the actuator to reduce the size and complexity of the entire system. More importantly, the incorporated components are expected to largely eliminate the dead volume in the PAM actuator, and improve its energy efficiency. An energy consumption analysis is presented, which estimates the maximum percentage of achievable energy savings. A practical design, incorporating standard poppet valves is also presented. To demonstrate the energy saving effect of the proposed design, experiments were conducted with a commercial PAM actuator modified to incorporate a solid bar. Experimental results indicate an energy savings of up to 13%, which is expected to increase significantly with the custom-made integrated PAM actuators in the future.
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Pascual, Sergi, Carme Casadevall, Juana Martínez-Llorens, et al. "Functional Blockade Of TNF-Alpha And Myogenic Differentiation In Cells From Peripheral Muscles Of COPD Patients." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4264.
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Resqueti, Vanessa, Jéssica Cavalcanti, Kardec Alecxandro Aguiar, et al. "Electrical activity behavior of respiratory and peripheral muscles during incremental shuttle walking test in asthmatic subjects." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4825.
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Turkseven, Melih, Ilya Kovalenko, Euisun Kim, and Jun Ueda. "Analysis of a Tele-Operated MRI-Compatible Vane Actuator for Neuromuscular Facilitation in Hemiparetic Limbs." In ASME 2015 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/dscc2015-9992.
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This paper analyzes the suitability of pneumatically driven, MRI-compatible vane actuators for stroke rehabilitation, particularly functional recovery of hemiparetic limbs. Hemiparesis patients suffer a sudden loss of motor skills in the upper-limb due to brain injury, such as stroke. As an emerging physio-therapy technique for hemiparesis, named repetitive facilitation exercise, or RFE, a therapist manually applies brief mechanical stimuli to the peripheral target muscles (e.g., tapping, stretching of tendon/muscle) followed by wrist pronation/supination immediately before a patient intends to produce a movement with the muscle. In an earlier study, a robotic system that replicates the mechanical tendon stimulation part of RFE procedure in MRI with the required timing precision has been developed and tested by the authors to investigate the underlying principles of functional recovery via RFE. This work presents the design of a vane actuator that fits into the tight space in MR-scanners, and analyzes its dynamic performance via a detailed pneumatic system model. The analysis indicates that a pneumatically driven, tele-operated vane actuator can satisfy the dynamic requirements of the targeted rehabilitation procedure.
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Ghriallais, Ríona Ní, and Mark Bruzzi. "Effects of Knee Flexion on Stented Peripheral Arteries: A Computational and In Vitro Study." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53224.
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The femoropopliteal (FP) artery is a branch of the femoral artery, the main artery in the upper leg, providing blood to all muscles and superficial tissues in the thigh. It is the largest of the femoral artery branches, composed of the superficial femoral artery (SFA) in the proximal region and popliteal artery (PA) in the distal region which runs below the knee. It is characterised by its tortuous geometry, associating a high atherosclerotic plaque burden with it. However, due to the dynamic forces of the SFA and PA, peripheral stents are reported to have the highest failure rates, predominantly due to bending [1]. Worst case bending can be seen in regions of the SFA/PA behind and just above the knee [2] and this is detrimental to stent patency.
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Gülekon, Nadir. "Diabetes asociated neuropathy in peripheral nerves which innervate leg muscles: An immunohistochemical study performed using histomorphometry and S100." In 15th International Congress of Histochemistry and Cytochemistry. LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-66.
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Kunafina, Tatyana, Aleksander Grigorievich Chuchalin, Andrey Staniislavovich Belevskiy, and Natalia Nicolaevna Meshcheriakova. "Effectiveness of peripheral muscles neuromuscular electrical stimulation (NMES) as the rehabilitation of severe chronic obstructive pulmonary disease (COPD) patients." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa837.
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Tang, Yan, and Alexander Leonessa. "Functional Electrical Stimulation of a Quadriceps Muscle Using a Neural-Network Adaptive Control Approach." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41817.
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Functional electrical stimulation (FES) has been used to facilitate persons with paralysis in restoring their motor functions. In particular, FES-based devices apply electrical current pulses to stimulate the intact peripheral nerves to produce artificial contraction of paralyzed muscles. The aim of this work is to develop a model reference adaptive controller of the shank movement via FES. A mathematical model, which describes the relationship between the stimulation pulsewidth and the active joint torque produced by the stimulated muscles in non-isometric conditions, is adopted. The direct adaptive control strategy is used to address those nonlinearities which are linearly parameterized (LP). Since the torque due to the joint stiffness component is non-LP, a neural network (NN) is applied to approximate it. A backstepping approach is developed to guarantee the stability of the closed loop system. In order to address the saturation of the control input, a model reference adaptive control approach is used to provide good tracking performance without jeopardizing the closed-loop stability. Simulation results are provided to validate the proposed work.
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Whitcomb, Julie E., Vincent A. Barnett, Timothy W. Olsen, and Victor H. Barocas. "Iris Stiffening Following Drug Stimulation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176013.
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Glaucoma is a general term for the deterioration of the optic nerve head usually associated with an increase of intraocular pressure (IOP). Certain types of glaucoma are associated directly with the displacement of the iris from its normal morphology [1]. For example, angle closure glaucoma and pigment dispersion syndrome involve abnormal anterior or posterior displacement of the iris, respectively [2]. In angle closure, the abnormal position of the peripheral iris blocks aqueous humor access to the outflow pathway (trabecular meshwork), increasing the IOP. Although there has been a considerable amount of ultrastructural characterization of the iris [3], to our knowledge, there as been little done on the mechanical characterization of the iris other than a previous study by Heys and Barocas on passive bovine irides [4]. To have a complete understanding of these it requires that we understand the mechanical properties of the iris in both its passive and stimulated states. Mechanical analysis of the iris requires the consideration of its two constituent muscles, the inner sphincter iridis and the outer dilator pupillae, see Fig. 1. The sphincter iridis is innervated parasympathetically whereas the dilator is innervated sympathetically.