Efeitos dos treinamentos físicos aeróbicos e resistido sobre a atrofia muscular esquelética na insuficiência cardíaca / Effects of aerobic and resistance exercise training on skeletal muscle atrophy induced by heart failure

A insuficiência cardíaca é uma síndrome que envolve múltiplos sistemas e mecanismos compensatórios neuro-hormonais, acompanhada de altos índices de morbidade e mortalidade, caracterizadas por sintomas clínicos como fadiga, dispnéia e intolerância aos esforços físicos. Além do comprometimento cardíaco, observam-se importantes alterações periféricas, como a atrofia muscular esquelética, a qual contribui para o mau prognóstico e para o aumento da mortalidade dos pacientes. Estudos têm demonstrado que essa atrofia muscular pode ser causada por um desbalanço entre vias de síntese e degradação protéica, pricipalmente pelo aumento da ativação do sistema proteolítico ubiquitina-proteassoma e pela diminuição da ativação da via IGF-1/Akt. O treinamento físico, estratégia não farmacológica no tratamento da insuficiência cardíaca, tem se mostrado capaz de atenuar ou reverter o quadro de miopatia esquelética encontrado nessa síndrome. Portanto, foi objetivo da presente revisão discutir em maiores detalhes a atrofia muscular esquelética observada na insuficiência cardíaca e os efeitos dos treinamentos físicos aeróbicos e resistido sobre esta condição. Embora o treinamento físico aeróbico, de moderada ou alta intensidade, não seja conhecido por promover aumento da massa muscular esquelética, alguns estudos demonstram que este tipo de treinamento promove adaptações importantes na regulação da massa muscular na insuficiência cardíaca, prevenindo a atrofia e, consequentemente, contribuindo para a melhora da tolerância ao esforço físico. Por outro lado, o treinamento físico resistido parece ser mais eficaz em atenuar ou reverter a atrofia muscular esquelética presente na insuficiência cardíaca.

Heart failure is a complex syndrome involving multiple systems and neurohumoral compensatory mechanisms accompanied by high morbidity and mortality, and it is characterized by clinical signs such as fatigue, dyspneia, and exercise intolerance. Although heart failure is a syndrome of cardiac origin, it promotes changes in other tissues, such as skeletal muscle, where modifications of muscle phenotype and the loss of skeletal muscle mass observed in heart failure contribute to poor prognosis and increased mortality of patients. Studies have show that skeletal muscle atrophy is caused by an imbalance between the process of protein synthesis and degradation, mainly due to increased activation of ubiquitin-proteasome proteolytic system and decreased activation of IGF-1/Akt pathway. Exercise training, a non-pharmacological strategy to treat heart failure, has been shown to attenuate or reverse the skeletal myopathy in this syndrome. this review aimed to discuss in details the muscular atrophy observed in heart failure and the effects of aerobic and resistance exercise training on skeletal muscle atrophy induced by this conditions. Although aerobic exercise training, at moderate or high intensity, is not known for promoting skeletal muscle hypertrophy, some studies show that this type of exercise training promotes major changes in skeletal muscle mass in heart failure, preventing atrophy and consequently contributing to improved exercise tolerance. On the other hand, resistance exercise training appears to be more effective in attenuating or reversing the skeletal muscle atrophy in heart failure. However, the benefits promoted by aerobic exercise training in many aspects of heart failure are more established in the literature and should be considered in the treatment of this syndrome in association with resistance exercise training, in order to obtain better results.

Clinical Implications caused by the agenesis of the RectusAbdominal Muscle’s (MRA) inferior venter

The rectus abdominal muscle is part of the anterior abdominal wall, having three to six bellies. In only oneof the 106 dissections already made in the “Faculdade de Ciências Médicas de Minas Gerais” AnatomyLaboratory was found a male cadaver who did not have inferior venter of this muscle bilaterally. Instead, at theleft side, was found a tendon that measured 5.5 cm laterally and 12 cm medially, and at the right side, therewas the same variation with a 15.5 cm length tendon, rising in the upper branch of the pubis and crest pubis.Despite being a rare variation, individuals who have showed it have increased potential for physiological andsurgical complications, in case they need interventions using inferior rectus abdominis muscle venter’s snips.

Congenital contractural arachnodactyly with neurogenic muscular atrophy: case report

We report the case of a 3-1/2-year-old girl with hypotonia, multiple joint contractures, hip luxation, arachnodactyly, adducted thumbs, dolichostenomelia, and abnormal external ears suggesting the diagnosis of congenital contractural arachnodactyly (CCA). The serum muscle enzimes were normal and the needle electromyography showed active and chronic denervation. The muscle biopsy demonstrated active and chronic denervation compatible with spinal muscular atrophy. Analysis of exons 7 and 8 of survival motor neuron gene through polymerase chain reaction did not show deletions. Neurogenic muscular atrophy is a new abnormality associated with CCA, suggesting that CCA is clinically heterogeneous

Linear scleroderma. A unique presentation.

A rare case of linear scleroderma with plaques of morphea in hemicorporeal distribution and subclinical systemic involvement is presented. Its possibility of progression into systemic sclerosis, which has not been reported earlier, is discussed.

Aspecto histopatológico de massas sarcoplásmicas em forma de "meia-lua" no hipertireoidismo: relato de caso / Histopathological aspects of sarcoplasmics deposits in semilunar form in hyperthyroidism: a case report

Apresenta-se um caso de amiotrofia no curso de hipertireoidismo. Ao exame microscópico do tecido muscular, observaram-se massas sarcoplásmicas hialinas dispostas na periferia das fibras, que, em cortes transversais, apareciam com a forma de "meia-lua" ("crescentes"), corando-se de róseo-pálida pelo método da hematoxilina-eosina e em azul-claro pelo tricrômico de Gomori