Thesis (MScPhysio)--Stellenbosch University, 2015 / ENGLISH ABSTRACT: Background: The use of computers at school, university, work and for social media is growing and whilst neck pain is common in the general population, computer users have an even higher prevalence. Incorrect workstation ergonomics have been identified as a risk factor for the development of neck pain in computer workers. Aims: To assess the effect of adjusting chair and monitor height of a female office worker’s computer workstation on work related neck and upper back pain intensity, comfort of her sitting posture and disability. Methods: An N=1 study was conducted using the A-B-C design consisting of a computer workstation adjustment involving chair and monitor height of a female office worker. The effect of the intervention was evaluated using the Visual Analogue Scale (VAS) to measure neck and upper back pain intensity and comfort of sitting position, and the Neck Disability Index to measure disability. The effect of the intervention was assessed over the three phases, consisting of four weeks each. During these phases, the participant could continue with her usual computer work. The results were compiled and tabulated. Results: A reduction in neck and upper back pain intensity as well as an increase in sitting comfort position were found. However these improvements were not statistically or clinically significant. The effect size for pain intensity was 0.76 and for sitting comfort 0.21. The participant reported no disability as measured by the Neck Disability Index, at the start and at the end at the end of the study. Conclusion: The vertical adjustment of this female office worker’s chair and monitor height according to her anthropometrics improved neck and upper back pain intensity and comfort of sitting position. This ergonomic workstation intervention could form part of a practical management option for computer users with neck and upper back pain. Further research is recommended to establish whether these findings are generalizable to the wider community of computer users. / AFRIKAANSE OPSOMMING: Probleemstelling: Die gebruik van rekenaars by skole, universiteite, werksplekke en vir sosiale doeleindes neem toe. Nek pyn kom dikwels in die algemene bevolking voor, maar dit is meer prevalent in rekenaargebruikers. ‘n Werkstasie wat nie ergonomies korrek opgestel is nie, is geidentifiseer as ‘n risikofaktor vir die ontwikkeling van nekpyn in rekenaar werkers. Doelwitte: Om te bepaal of aanpassings in die stoel- en beeldskerm hoogte van ‘n vroulike kantoor werker se rekenaar werkstasie, ‘n effek het op werksverwante nek en boonste rug pyn, sitgemak en funksionele vermoë. Methode: Die N=1 studie met ‘n A-B-C ontwerp is onderneem en het bestaan uit n rekenaar werkstasie aanpassing waarby die hoogte van die stoel en beeldskerm van ‘n vroulike relenaargebruiker aangepas is. Die effek van die intervensie is ge-evalueer deur middle van die visueel analoogskaal (VAS) om pyn en sitgemak te bepaal; en die Nek Ongeskiktheids Indeks (NOI) om gestremtheid te bepaal. Die effek van die intervensie is oor drie fases, wat elk bestaan het uit vier weke, evalueer. Gedurende die fases, kon die deelnemer met haar gewone rekenaarwerk voortgaan. Die resultate is saamgestel en getabuleer. Resultate: Daar was ‘n vemindering in die intensiteit van nekpyn, boonste rug pyn en die sitgemak van die individu het ook verbeter. Hierdie verbeteringe was egter nie statisties of klinies betekenisvol nie. Die effek grootte vir pyn intensiteit was 0.76 en vir sitgemak was 0.21. Die deelnemer het geen gestremdheid gerapporteer, soos gemeet met die NOI met aanvangs van die studie of teen die einde van die studie nie. Gevolgtrekking: Die vertikale hoogte-aanpassing van die stoel en beeldskerm van hierdie vroulike rekenaar werker volgens haar antropometrie het bygedra tot ‘n verbetering in nek en boonste rug pyn, asook sitgemak. Hierdie ergonomiese werkstasie intervensie kan deel vorm van die praktiese hantering van nek en boonste rug pyn in rekenaargebruikers. Verdere navorsing wod aanbeveel om te bepaal of hierdie bevindinge veralgemeenbaar is na die wyer gemeenskap van rekenaarverbruikers.

Thesis (MSc)--University of Stellenbosch, 2007. / ENGLISH ABSTRACT: Tumour necrosis factor alpha (TNFα) is a pleiotropic cytokine and has a wide variety of dose dependent cellular effects ranging from cell growth and differentiation, to inducing apoptosis. It has long been implicated in muscle and non-muscle inflammatory disorders, such as muscle wasting in chronic disease states, and rheumatoid arthritis. However, a physiological role for TNFα in muscle regeneration has been proposed as elevated levels of the cytokine are present when muscle regeneration processes are initiated: TNFα is secreted by infiltrating inflammatory cells, and by injured muscle fibres. Adult skeletal muscle contains a population of resident stem cell-like cells called satellite cells, which become activated, proliferate and differentiate following muscle injury to bring about repair of damaged muscle. Much research on the effects of TNFα on satellite cell differentiation has been conducted in recent years. It is however difficult to get a complete characterisation of the cytokine’s action as all models used slightly differ. We aimed therefore at providing comprehensive assessment of the effects of increasing doses of chronically supplemented TNFα on differentiating C2C12 cells. Cells were allowed to differentiate with or without TNFα supplementation for 7 days. Differentiation was induced at day 0. The effect on differentiation was assessed at days 1, 3, 5, and 7 by western blot analysis, and supplementary immunohistochemical analysis at days 1, 4, and 7 of markers of differentiation - muscle regulatory factors: MyoD and myogenin, markers of the cell cycle p21, PCNA, and the integral signalling molecule, p38MAPK. TNFα supplementation at day 1 tended to positively regulate early markers of differentiation. With continued supplementation however, markers of differentiation decreased dose dependently in treated cultures as the initial effect appeared to be reversed: A trend towards a dose dependent decrease in MyoD, myogenin and p21 protein existed in treated cultures at days 3, 5, and 7. These findings were significant at day 5 (p21, p<0.05), and day 7 (myogenin, p<0.05). A significant dose dependent decrease in p38 phosphorylation was evident at day 3 (p<0.05), while phospho-p38 was dose dependently increased at day 7 (p<0.05). Taken together, these data show that TNFα supplementation for 24 hours following the induction of differentiation in vitro, tends to increase levels of early markers of differentiation, and with continued TNFα supplementation decrease markers of differentiation in a dose dependent fashion. This study provides a comprehensive characterisation of the dose and time dependent effects of TNFα on satellite cell differentiaton in vitro. The model system used in the current study, allows us to make conclusions on more chronic disease states. / AFRIKAANSE OPSOMMING: Tumor nekrose faktor alfa (TNFα) is ‘n pleiotropiese sitokien wat ‘n wye verskeidenheid, dosis afhanklike, sellulêre effekte te weeg bring. Hierdie sellulêre effekte sluit sel groei en differensiasie tot sel dood in. TNFα is by beide spier en niespier inflammatoriese stoornisse soos spier tering in kroniese siektetoestande, en rumatiese artritis betrek. ‘n Fisiologiese rol vir TNFα is egter voorgestel aangesien verhoogde vlakke van die sitokien tydens inisiasie van spier herstel meganismes teenwoordig is: TNFα word deur infiltrerende inflammatoriese selle, asook deur beseerde spier vesels afgeskei. Volwasse skeletspier bevat ‘n populasie stamselagtige selle, sogenoemde satelliet selle. Laasgenoemde word geaktiveer, prolifereer en differensieër volgende spierbesering, om sodoende herstel van beskadigde spier te weeg te bring. Baie navorsing op die effekte van TNFα op satelliet sel differensiasie is onlangs uitgevoer. Dit is egter aansienlik moeilik om volgens hierdie navorsing‘n algehele beeld van TNFα se aksies te vorm aangesien alle modelle wat gebruik word verskil. Ons doel was daarom om ‘n omvangryke assessering van toenemende konsentrasies kronies gesupplementeerde TNFα op differensieërende C2C12 selle op ‘n enkele model uit te voer. Selle was vir 7 dae met of sonder TNFα supplementasie gedifferentieër. Differensiasie was by Dag 0 geïnduseer. TNFα se effek op differensiasie is op dae 1, 3, 5, en 7 deur middel van western blot analise geassesseer. Aanvullende immunohistochemiese bepalings op dae 1, 4, en 7 is verder deurgevoer. Merkers vir differensiasie het die spier regulatoriese faktore MyoD en miogenien, sel siklus merkers p21 en PCNA, asook die integrale sein transduksie molekule p38MAPK ingesluit. TNFα supplementasie by dag 1 het geneig om vroeë merkers van differensiasie positief te reguleer. Met voortdurende supplementasie is die vroeë positiewe effekte (op ‘n dosis afhanklike manier) egter omgekeer: ‘n neiging teenoor (‘n dosis afhanklike) vermindering in MyoD, miogenien en p21 proteïen het in behandelde kulture op dae 3, 5, en 7 bestaan. Hierdie bevindinge was beduidend by dag 5 (p21, p<0.05), en dag 7 (miogenien, p<0.05). A beduidende dosis afhanklike afname in p38 fosforilasie was duidelik by dag 3 (p<0.05), terwyl fosfo-p38 by dag 7 verhoog het met verhoogde konsentrasie TNFα (p<0.05). Bogenoemde saamgevat, dui aan dat TNFα supplementasie 24h volgende die induksie van differensiasie in vitro, verhoogde vlakke van vroeë differnsiasie merkers te weeg bring. Met voortdurende TNFα supplementasie, word differensiasie merkers egter met toenemende dosis verminder. Hierdie studie voorsien ‘n omvattende karakterisering van die dosis- en tyd afhanklike effekte van TNFα op satelliet sel differesiasie in vitro. Die model sisteem in hierdie studie gebruik, maak afleidings oor meer kroniese siektetoestande moontlik.

Aim:  The overall aim of this thesis was to explore the development of a video-supported interactive learning model for movement awareness among nursing students. Methods:  Study I was a cross-sectional survey regarding prevalence and impact of musculoskeletal symptoms (MSS) among nursing students. In the remaining three studies a learning model was developed and explored; II - the inter-personal interaction (qualitative content analysis), III - the students’ experiences of using the learning model (phenomenological hermeneutics), IV - the students’ learning processes (hermeneutic approach). Results: 143 of the 224 respondents in study I reported MSS during the previous 12 months and of those 91 reported impact on physical daily life activities. The odds ratio for reporting MSS study year 3 was 4.7 (95% CI: 2.1 – 10.7). Study II shows that the students’ movement awareness and self-analysis developed when encountering their own movement through video feedback. Studies III and IV show that the facilitator’s reflective and responsive approach appears to be essential in creating interaction and a permitting learning atmosphere. The students became emotionally and cognitively challenged and personally engaged, were motivated to change by discovering details in their movements and gained a greater understanding of the relationship between their own movements and current or risk for future MSS. They also experienced emotional, cognitive and bodily confusion, which was interpreted as a necessary step in the changing process. Conclusion: MSS among nursing students appears to be a problem and education regarding ergonomic movements and principles is suggested to be emphasized in the nursing curriculum. The video-supported learning model enabled encountering and discovering one’s own body and movement in different ways, which facilitated reflection and motivation for change, which was supported by the facilitator’s reflective approach. The learning model, which could contribute to multifactorial ergonomic interventions, could also support movement awareness and learning in practical learning situations within education and rehabilitation. Further research needs to study the model in different contexts and in relation to MSS prevention.

Several surgically corrective procedures are considered to treat Adult Acquired Flatfoot Deformity (AAFD) patients, relieve pain, and restore function. Procedure selection is based on best practices and surgeon preference. Recent research created patient specific models of Adult Acquired Flatfoot Deformity (AAFD) to explore their predictive capabilities and examine effectiveness of the surgical procedure used to treat the deformity. The models’ behavior was governed solely by patient bodyweight, soft tissue constraints, and joint contact without the assumption of idealized joints. The current work expanded those models to determine if an alternate procedure would be more effective for the individual. These procedures included one hindfoot procedure, the Medializing Calcaneal Osteotomy (MCO), and one of three lateral column procedures: Evans osteotomy, Calcaneocuboid Distraction Arthrodesis (CCDA), Z osteotomy and the combination procedures MCO & Evans osteotomy, MCO & CCDA, and MCO & Z osteotomy all used in combination with a tendon transfer. The combination MCO & Evans and MCO & Z procedures were shown to provide the greatest amount of correction for both forefoot abduction and hindfoot valgus. However, these two procedures significantly increased the joint contact force, specifically at the calcaneocuboid joint, and ground reaction force along the lateral column. With exception to the lateral bands of the plantar fascia and middle spring ligament, the strain present in the plantar fascia, spring, and deltoid ligaments decreased after all procedures. The use of patient specific computational models provided the ability to investigate effects of alternate surgical corrections on restoring biomechanical function in flatfoot patients.

Submitted in partial compliance with the requirements for the Master's Degree in Technology : Chiropractic, Durban University of Technology, Durban, South Africa, 2015. / Introduction: Symptoms associated with large breasts result from bra strap chafing, poor body posture, headaches, neck, shoulder, thoracic and lower back pain. There is a paucity of literature quantifying objective data regarding the effect of breast size on posture. Therefore correct bra sizing may improve posture, however this is undetermined. This study aimed to investigate the effect of bra correction on selected postural parameters in order to determine its relevance in a clinical setting. Methodology: Sixty five females who met the inclusion criteria had the following parameters recorded: age, height, weight, body mass index, occupation, and underbust and overbust bra size. An anterior-posterior, right and left lateral digital photographs were taken before and after bra correction. These were then processed using the Posture Pro software. The data was analysed using the latest version of SPSS. The results were presented by means of standard deviations and ranges and differences between pre and post measures were performed with an ANOVA. Results: It was found that there was no correlation between changes in any of the four parameters from pre to post correction, which changed significantly with postural correction (4/43 post correction significant readings) and the demographic variables. Most participants changed to a larger cup sizes after correction which is in line with Greenbaum, (2003) who found that participants tend to buy a smaller bra size. In this study 3% of the study population changed to a bigger cup size and 97% wore bras that were too tight. Similar to the findings of Wood eta/., (2008) who found that 70% of the study population wore bras that are too small and 10% wore bras that were too big. Conclusion: In the study on effect of incorrect bra size on selected postural parameters it was found the there were four parameters that changed significantly with p<O, 05 [ANOVA]. Further investigation needs to be done on a larger sample size, age group range, BMI and different demographic. / PDF copy unavailable. please refer to hard copy for full text information / M

L'imagerie médicale joue un rôle majeur dans l'identification, la caractérisation et le bilan d'extension des lésions tumorales du système ostéo-articulaire. La grande majorité de ces néoplasies est bénigne et il est important de savoir les reconnaître et les distinguer des lésions malignes. Ces dernières ont un pronostic beaucoup plus sombre et sont l'objet d'une prise en charge nettement plus agressive. L'IRM est actuellement la technique de choix pour l'évaluation des tumeurs ostéo-articulaires. Malgré une très haute sensibilité pour la détection des tumeurs osseuses et des parties molles, un grand nombre de lésions identifiées ne sont pas caractérisables. Récemment des nouvelles techniques d'imagerie fonctionnelle sont apparues permettant une évaluation tumorale au niveau biochimique et cellulaire. Ces techniques, initialement conçues pour l'évaluation des tumeurs cérébrales comme la perfusion, la diffusion et la spectroscopie ont commencé à être utilisées pour l'évaluation des néoplasies ostéo-articulaires avec des résultats préliminaires prometteurs. Parallèlement, avec le développement en scanner de systèmes de détection à large surface et l'échographie de contraste, l'étude de la perfusion tumorale basée sur ces méthodes est plus accessible en pratique courante. L'imagerie fonctionnelle reste, néanmoins peu accessible en dehors de la recherche. Des difficultés techniques inhérentes à l'application clinique de ces nouvelles méthodes et l'hétérogénéité histologique des tumeurs ostéo-articulaires constituent encore un obstacle important. Dans ce travail la performance diagnostique de plusieurs méthodes d'imagerie fonctionnelle en pratique courante a été évaluée. En autre, des améliorations permettant une augmentation de la qualité d'image et une réduction des artéfacts des méthodes fonctionnelles ont été testées. Secondairement, les performances diagnostiques de différentes méthodes de perfusion tumorale (échographie, tomodensitométrie et imagerie par résonance magnétique) ont été comparées / Medical imaging plays a major role in the identification, characterization and staging of tumor lesions of the musculoskeletal system. The vast majority of these neoplasms are benign and it is important to recognize and distinguish them from malignant lesions. Malignant lesions carry a worse prognosis and are usually treated aggressively. MRI is currently the method of choice for evaluating musculoskeletal tumors. Despite a high sensitivity for the detection of bone and soft tissue tumors, a large number of identified lesions remain indeterminate in origin after imaging work-up. In recent years, new functional imaging techniques, which allow tumor evaluation in a biochemical and cellular level, have emerged. These techniques such as perfusion, diffusion weighted imaging and MR spectroscopy, originally designed for the evaluation of brain tumors, began to be used for the evaluation of musculoskeletal neoplasms with promising preliminary results. Meanwhile, with the development of wide area-detector CT systems and contrast enhanced ultrasound (CEUS) new ways of assessing tumor perfusion became available in clinical practice. Functional imaging nevertheless remains largely inaccessible outside research oriented imaging centers. The clinical application of these new methods is hindered by various factors, which include the great histological heterogeneity of musculoskeletal tumors and patient related technical difficulties. In this project, the diagnostic performance of several functional imaging methods in clinical practice was assessed. Additionally tools for image quality improvement and artifact reduction were tested. Finally, the diagnostic performance of different perfusion methods (ultrasound, computed tomography and magnetic resonance imaging) was compared

Yeung Sai Mo, Simon. / "June 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 255-278). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Soccer players change direction repeatedly throughout a game, making agility an important component of their performance. The purpose of this project was to identify how anatomical and physical characteristics influence agility performance among soccer players. The influences of anthropometry, strength, and power on agility performance in soccer players were investigated. The participants were NCAA Division I soccer players (N = 65). Anthropometric measures included height, body mass, percent body fat, lean body mass. Strength was evaluated using an isometric mid-thigh pull, and power was measured by vertical jumps. In correlation analysis, agility performance showed a statistically significant correlation (p<0.05) with peak power (PP) from 0kg and 20kg counter-movement jumps (r=-.379 & r=-.364 respectively) for the male players. Also for the males, percent body fat showed significant correlations (p<0.05) with Average 2 (r=-.438), 3 (r=-.411), and All (r=-.436). I conclude that the anthropometric measures evaluated have little influence on agility performance.

PURPOSE The purpose of this study was to determine if performing static active knee extension hamstring stretching using the Pneumex Pro-Vibe vibrating platform increased acute hamstring range of motion (ROM) greater than traditional static active knee extension hamstring stretching. METHODS: A within subject design was utilized with subjects undergoing static stretching with vibration and without vibration (conditions counterbalanced). Pre- and post-test active and passive ROM was measured for the right leg, with subjects first undergoing a 5-minute warm-up on a stationary bicycle. Supine active knee extension was performed on the Pro-Vibe platform with and without vibration. The stretch was held 3 times each for 30 seconds, with a 20-second rest period between each stretch. Vibration was set at 30 Hz at the “high” amplitude setting. Active hamstring ROM was measured via active knee extension using a goniometer with the leg in 90° of hip flexion. Passive ROM was measured via clinician-assisted knee extension with the leg in 90° of hip flexion. RESULTS: A 2-way repeated measures ANOVA was performed for passive ROM, and revealed a significant main effect for condition, F (1, 23) = 0.5875, p < 0.05, and time, F (1, 23) = 5.029, p < 0.05. Another repeated measures ANOVA was performed for active ROM with the same factors, and revealed a significant time by condition interaction, F (1, 23) = 4.730, p < 0.05, and a significant main effect for time, F (1, 23) = 18.612, p < 0.001. Post-hoc paired samples t-tests determined the difference between the pre-test and post-test measurements for each condition. Active ROM showed a significant difference pre-test to post-test for the vibration condition, t (23) = -5.41, p < 0.001. The vibration condition also resulted in significantly different pre-test vs. post-test measurements on passive ROM, t (23) = -2.55, p < 0.05. In both cases the average ROM was higher for the post-test. DISCUSSION: Three 30-second active knee extension hamstring stretches using a vibrating platform are sufficient to cause significant acute increases in hamstring ROM. These findings suggest this device may be useful when desiring increased hamstring ROM.

Els mitocondris són orgànuls citoplasmàtics que tenen un paper fonamental en múltiples processos biològics com l’oxidació de substrats i la producció d’ATP, la senyalització cel•lular, l’apoptosi, el control del cicle cel•lular i l’homeòstasi del calci. Els mitocondris són orgànuls dinàmics, que pateixen canvis de morfologia regulats per processos de fusió i de fissió. Existeix un equilibri entre ambdós processos que és indispensable per a la correcta funció mitocondrial. Les proteïnes que participen directament en la fusió mitocondrial en mamífers són les mitofusines (Mfn1 i Mfn2), localitzades a la membrana mitocondrial externa i OPA1, situada a la membrana mitocondrial interna. Diferents estudis han demostrat que la proteïna Mfn2, a més de promoure la fusió dels mitocondris, també està implicada en la interacció entre els mitocondris i el reticle endoplasmàtic i que participa en la regulació del cicle cel•lular i del metabolisme mitocondrial. Per altra banda, l’expressió de Mfn2 es troba disminuïda en múscul esquelètic en situacions de resistència a la insulina, com l’obesitat o la diabetis de tipus 2, que a la vegada es caracteritzen per una alterada activitat mitocondrial. En base a aquestes observacions, l’objectiu principal de la present tesi doctoral ha estat estudiar els efectes de la modulació de l’expressió de Mfn2 sobre el metabolisme i la bioenergètica mitocondrial en múscul esquelètic. Amb aquest propòsit hem expressat una forma truncada de Mfn2 (hMfn2Δ614-757) o bé hem reprimit l’expressió de Mfn2 endògena en el model cel•lular C2C12 i en múscul esquelètic de ratolí. Per dur a terme aquest objectiu hem generat 3 models de ratolí diferents: el model d’expressió transitòria de la forma hMfn2Δ614-757; el model de repressió transitòria de Mfn2 i el ratolí knockdown de Mfn2. Els dos primers models han estat generats mitjançant la tècnica de l’electrotransferència d’ADN en múscul esquelètic. La sobreexpressió de la forma hMfn2Δ614-757 en cèl•lules C2C12 diferenciades incrementa el consum d’oxigen mitocondrial en situació basal i també en desacoblar la cadena de transport d’electrons de la síntesi d’ATP, suggerint una major capacitat respiratòria dels miotubs que expressen la hMfn2Δ614-757. En múscul esquelètic de ratolí, l’expressió d’aquesta forma de Mfn2 causa una estimulació de la taxa d’oxidació de glucosa així com un increment de la Respiratory Control Ratio (RCR). La inducció del metabolisme mitocondrial observada en sobreexpressar la forma hMfn2Δ614-757 no és deguda a un augment de la massa mitocondrial, sinó a un increment en l’expressió i l’activitat d’alguns dels complexes de la cadena respiratòria mitocondrial. La repressió de Mfn2 en miotubs C2C12 produeix un increment en la respiració no associada a la producció d’ATP o proton leak i una disminució en el potencial de membrana mitocondrial. Aquests resultats indiquen que la repressió de Mfn2 provoca el desacoblament de la cadena de transport d’electrons i la síntesi d’ATP, suggerint una disminució de l’eficiència de la fosforilació oxidativa. Els músculs dels ratolins knockdown de Mfn2 presenten una reducció de la taxa d’oxidació de glucosa i de la Respiratory Control Ratio. A més, la repressió de Mfn2 disminueix l’activitat del complex IV de la cadena respiratòria. En conjunt aquests resultats suggereixen que la disminució de l’expressió de Mfn2 origina una disfunció del sistema de transport electrònic mitocondrial. També cal remarcar que els ratolins knockdown de Mfn2 presenten una major susceptibilitat a desenvolupar resistència a la insulina en resposta a l’envelliment o a una dieta rica en greixos. La disfunció mitocondrial i l’augment en la producció d’espècies reactives d’oxigen (ROS) observats en el múscul esquelètic d’aquests ratolins podrien explicar aquesta major susceptibilitat. / Mitochondria are cellular organelles that play a fundamental role in many cellular functions, such as substrates oxidation, ATP production, apoptosis and calcium economy. Mitochondria are dynamic organelles that can fuse and divide; the balance between both processes is crucial for a correct mitochondrial function. The most relevant proteins described to date involved in the regulation of mitochondrial fusion are mitofusins 1 and 2 (Mfn1 and Mfn2, respectively) and OPA1. Substantial data indicates that Mfn2 is also a key regulator of cell cycle and mitochondrial metabolism. On the other hand, Mfn2 expression is reduced in skeletal muscle of obese subjects and type 2 diabetic patients, situations characterized by altered mitochondrial activity. Based on these observations, the main objective of this thesis was the study of the metabolic role of Mfn2 in skeletal muscle. We have studied the metabolic effects caused by the manipulation of Mfn2 expression in mice skeletal muscle in vivo. By means of DNA electrotransfer technologies, we have expressed a truncated Mfn2 mutant in skeletal muscle and we have also repressed endogenous Mfn2 expression with microRNAs. We have also generated a skeletal muscle Mfn2 knockout mouse model (Mfn2 KO). The expression of truncated Mfn2 mutant in tibialis stimulated glucose oxidation and increased the Respiratory Control Ratio (RCR). It also increased the expression of subunits Cox4 of OXPHOS complex IV and Atp5a1 of complex V. We observed these metabolic effects in absence of changes in mitochondrial content. The repression of Mfn2 in mice skeletal muscle caused a marked reduction in the expression of subunit Cox4 of OXPHOS complex IV, accompanied with a 20% of decrease in COX activity. In this case we neither observed differences in mitochondrial content. Skeletal muscle from Mfn2 KO mice showed a decrease in glucose oxidation and in the RCR. In addition, Mfn2 KO mice showed a higher susceptibility to develop insulin resistance in response to aging or a high fat diet. Mitochondrial dysfunction and the increased ROS production observed in skeletal muscle of these mice could explain this higher susceptibility.