O exercício resistido dinâmico é recomendado, em complemento ao aeróbico, para indivíduos hipertensos. O aumento da pressão arterial durante sua execução se faz, primordialmente, pelo aumento da resistência vascular periférica, porém o aumento do débito cardíaco também parece estar envolvido. A elevação da pressão arterial parece ser exacerbada em hipertensos não medicados. Entretanto, grande parte dos hipertensos está sob terapêutica medicamentosa e vários fazem uso de -bloqueadores, que reduzem o débito cardíaco pela diminuição da resposta taquicárdica e inotrópica à estimulação simpática. Assim, é possível supor que o uso de -bloqueadores reduza o aumento da pressão arterial nos exercícios resistidos. Porém, pelo nosso conhecimento, este efeito ainda não foi estudado. Assim, esta investigação teve por objetivo investigar o efeito do atenolol sobre a resposta da pressão arterial durante o exercício resistido de diferentes intensidades. Foram estudados 10 hipertensos essenciais com pressão arterial sistólica/diastólica sob placebo entre 140 e 160/90 e 105 mmHg. Os pacientes foram estudados após 6 semanas de uso de placebo e de atenolol, sendo que os indivíduos estavam cegos para a medicação. Em cada fase, os voluntários fizeram o exercício de extensão de joelhos na cadeira extensora até a exaustão, seguindo 3 protocolos realizados em ordem aleatória: a) uma série em 100% de 1RM (repetição máxima), b) três séries em 40% de 1RM e; c) três séries em 80% de 1RM. Antes, durante e após os exercícios, a pressão arterial foi medida diretamente na artéria radial. Os dados foram comparados pelo teste t student ou pela ANOVA de dois fatores para amostras repetidas. Quando necessário, foi utilizado o post-hoc de Newman-Keuls e aceito como significante o índice de P≤0,05. Verificou-se que o atenolol reduziu os valores absolutos atingidos pela pressão arterial sistólica durante a execução do exercício nas três intensidades (valores máximos: 100% = 186±4 vs. 215±7, 80% = 224±7 vs. 247±9 e 40% = 223±7 vs. 252±16, mmHg, P≤0,05). Além disso, ele reduziu o aumento desta pressão arterial na 1ª série do exercício nas 3 intensidades (100% = +38±5 vs. +54±9; 80% = +68±11 vs. +84±13 e 40% = +69±7 vs. +84±14, mmHg, P≤0,05). Em relação à pressão arterial diastólica, o atenolol diminuiu os valores máximos absolutos e o aumento desta pressão arterial (126±6 vs. 145±6 e +41±6 vs. +52±6, mmHg, P≤0,05) no exercício em 100% de 1RM, mas não a alterou nas demais intensidades. Dessa forma, é possível concluir que o atenolol foi eficaz em atenuar tanto o valor absoluto quanto a resposta da pressão arterial sistólica durante o exercício resistido de diferentes intensidades em hipertensos, conferindo-lhes uma certa proteção cardiovascular. Este achado reforça o conceito de que o aumento do débito cardíaco é um mecanismo importante para o aumento da pressão arterial sistólica durante este tipo de exercício / Dynamic resistance exercise is recommended in association to aerobic exercise for hypertensive patients. Blood pressure increase during this kind of exercise is mainly due to an increase in peripheral vascular resistance, however, an increase in cardiac output might also be involved. This blood pressure increase seems to be exacerbated in non-medicated hypertensives. Nevertheless, most of the hypertensives are taking medications, and some of them are receiving -blockers, which decreases cardiac output by the inhibition of sympathetic-induced increase on heart rate and cardiac contractility. Thus, -blockers might decrease blood pressure rise during resistance exercise which, to our knowledge, has not been studied yet. Hence, the aim of this study was to verify the effects of the selective -blocker atenolol on blood pressure increase during dynamic resistance exercise of different intensities. Ten essential hypertensives with systolic/diastolic blood pressures under placebo condition maintained among 140 and 160/90 and 105 mmHg were recruited. These volunteers were studied after 6 weeks of placebo and atenolol treatment, and they were blinded for the medication used. In each phase, the volunteers executed, in a random order, 3 protocols of knee extension exercise until fatigue: a) 1 set at 100% of 1 repetition maximum (1RM); b) 3 sets at 40% of 1RM; c) 3 sets at 80% of 1RM. Before, during and after the exercises, intra-arterial radial blood pressure was measured. Data were compared by paired student t-test and by two-way ANOVA for repeated measures. Newman-Keuls post-hoc test was applied when necessary. P≤0.05 was considered as significant. Atenolol decreased the absolute value achieved by systolic blood pressure during the exercise performed at the 3 intensities (maximum values: 100% = 186±4 vs. 215±7, 80%= 224±7 vs. 247±9 e 40% = 223±7 vs. 252±16, mmHg, P≤0.05). Moreover, atenolol also reduced systolic blood pressure increase in the first set of exercise at the 3 intensities (100% = +38±5 vs. +54±9; 80% = +68±11 vs. +84±13 e 40% = +69±7 vs. +84±14, mmHg, P≤0.05). In regard to diastolic blood pressure, atenolol decreased its absolute values and its increase during exercise performed at 100% of 1RM (126±6 vs. 145±6 e +41±6 vs. +52±6, mmHg, P≤0.05), but it did not change diastolic blood pressure at the other exercise intensities. In Conclusion, atenolol therapy was effective in reducing both, systolic blood pressure absolute values and increase during resistance exercise of different intensities in hypertensive subjects; given them some cardiovascular protection. This result enhances the belief that cardiac output increase is important for blood pressure enhancement during this kind of exercise

Bakgrund: Fysisk aktivitet har flera positiva effekter på hälsan. Fysisk aktivitet på recept är en behandlingsmetod mot olika ohälsotillstånd, samt i preventivt syfte. Fysisk aktivitet på recept kan förskrivas av legitimerad vårdpersonal, exempelvis sjuksköterskor.  Syfte: Att beskriva patienters upplevelser av följsamhet till fysisk aktivitet på recept. Metod: Kvalitativ litteraturöversikt med induktiv ansats där tio vetenskapliga artiklar sammanställdes efter analys av materialet enligt Fribergs femstegsanalys.  Resultat: Tre kategorier formades: individuella påverkansfaktorer, sociala påverkansfaktorer och yttre påverkansfaktorer. Individuella påverkansfaktorer berörde exempelvis symtom och tidigare erfarenheter. Sociala faktorer var till exempel stöd från familj och närstående samt vårdpersonal. Yttre påverkansfaktorer handlade bland annat om tid och ekonomi. Slutsats: Både yttre och inre faktorer påverkade följsamheten till receptet. Orsakerna till följsamhet/icke följsamhet var ofta multifaktoriella och komplexa. Vårdpersonalen som förskriver receptet behöver vara lyhörda för patientens behov och förutsättningar. Som förskrivande vårdpersonal är det även viktigt att erbjuda stöd och uppföljningar. / Background: Physical activity (PA) has several beneficial effects on health. Physical activity on prescription (PAP) is a non-medical treatment method and is also used to prevent future illness. Health care practioners with a legitimation – e.g. nurses - can prescribe PAP. Aim: To describe patients experiences of compliance to physical activity on prescription.  Method: A qualitative literature review with inductive approach. Ten articles with qualitative design were analyzed and compiled through Friberg’s analyze in five steps.  Results: The result was organized in three main categories: individual factors, social influential factors and external factors. Individual factors was for example symptoms and previous experience. Social factors was for example support from family, friends and healthcare staff. External factors was for example time and economy. Conclusion: Both external and internal factors had impact on the participants adherence to PAP. The reasons explained by the participants were multifactorial and complex. Health care professionals who prescribe physical activity need to be responsive to the patients` needs and prerequisites. It is also important to offer support and follow-ups.

Epidermolysis bullosa simplex (EBS) and epidermolytic ichthyosis (EI) are rare skin fragility diseases characterized by intra-epidermal blistering due to autosomal dominant-negative mutations in basal (KRT5 or KRT14) and suprabasal (KRT1 or KRT10) keratin genes,  respectively. Despite vast knowledge in the disease pathogenesis, the pathomechanisms are not fully understood, and no effective remedies exist. The purpose of this work was to search for keratin gene mutations in EBS patients, to develop in vitro models for studying EBS and EI, and to investigate novel pharmacological approaches for both diseases. We identified both novel and recurrent KRT5 mutations in all studied EBS patients but one which did not show any pathogenic keratin mutations. Using cultured primary keratinocytes from EBS patients, we reproduced a correlation between clinical severity and cytoskeletal instability in vitro. Immortalized keratinocyte cell lines were established from three EBS and three EI patients with different phenotypes using HPV16-E6E7. Only cell lines derived from severely affected patients exhibited spontaneous keratin aggregates under normal culture conditions. However, heat stress significantly induced keratin aggregates in all patient cell lines. This effect was more dramatic in cells from patients with a severe phenotype. In organotypic cultures, the immortalized cells were able to differentiate and form a multilayered epidermis reminiscent of those observed in vivo. Addition of two molecular chaperones, trimethylamine N-oxide dihydrate (TMAO) and sodium 4-phenylbutyrate (4-PBA), reduced the keratin aggregates in both stressed and unstressed EBS and EI keratinocytes, respectively. The mechanism of action of TMAO and 4-PBA was shown to involve the endogenous chaperone system (Heat shock proteins e.g. Hsp70). Besides, MAPK signaling pathways also seemed to be incriminated in the pathogenesis of EBS. Furthermore, depending on which type of keratin is mutated, 4-PBA up-regulated Hsp70 and KRT4 (possibly compensating for mutated KRT1/5), and down-regulated KRT1 and KRT10, which could further assist in protecting EBS and EI cells against stress. In conclusion, novel and recurrent pathogenic keratin mutations have been identified in EBS. Immortalized EBS and EI cell lines that functionally reflect the disease phenotype were established. Two pharmacologic agents, TMAO and 4-PBA, were shown to be promising candidates as novel treatment of heritable keratinopathies in this in vitro model.