Angiotensin converting enzyme (ACE) and interleukin 1 activities were assayed simultaneously in the serum free medium from the unstimulated peripheral blood monocytes from 32 patients with rheumatoid arthritis

BackgroundThe control of immunological alterations becomes important during in-season training, as a result of increased incidence of infectious diseases, and may assist in avoiding interruptions to training due to illness.ObjectiveThe aim of the present study was to evaluate 28 weeks of chronic immune modulations in female volleyball athletes.MethodsThe sample was composed of twelve athletes aged 19.47 ± 2.49 years, height 1.78 ± 0.08 cm, and body mass 66.77 ± 7.8 kg. Leukocytes, individual immune cell count, interleukin (IL)-2, IL-6, and tumor necrosis factor (TNF)-α plasma cytokines were measured during the competitive period.ResultsResults revealed that immune variables were correlated with symptoms of upper respiratory tract infections and training-load indicators, indicating a possible marker of immune status. There was a statistically significant increase in total leukocytes, neutrophils, and monocyte count, a decrease in lymphocytes, and an increase in upper respiratory tract infection symptoms, with no change in IL-2, IL-6, and TNF-α. Correlations between subjective levels of tiredness, total leukocyte count, and neutrophils with upper respiratory tract infection symptoms were observed.ConclusionIn conclusion, these correlations can represent important tools to access the immune status of an athlete during long training periods, preventing a possible immunosuppressive status.

In the last decade, molecular biology has contributed to define some of the cellular events that trigger skeletal muscle hypertrophy. Recent evidence shows that insulin like growth factor 1/phosphatidyl inositol 3-kinase/protein kinase B (IGF-1/PI3K/Akt) signaling is not the main pathway towards load-induced skeletal muscle hypertrophy. During load-induced skeletal muscle hypertrophy process, activation of mTORC1 does not require classical growth factor signaling. One potential mechanism that would activate mTORC1 is increased synthesis of phosphatidic acid (PA). Despite the huge progress in this field, it is still early to affirm which molecular event induces hypertrophy in response to mechanical overload. Until now, it seems that mTORC1 is the key regulator of load-induced skeletal muscle hypertrophy. On the other hand, how mTORC1 is activated by PA is unclear, and therefore these mechanisms have to be determined in the following years. The understanding of these molecular events may result in promising therapies for the treatment of muscle-wasting diseases. For now, the best approach is a good regime of resistance exercise training. The objective of this point-of-view paper is to highlight mechanotransduction events, with focus on the mechanisms of mTORC1 and PA activation, and the role of IGF-1 on hypertrophy process.

Since its discovery, myostatin (MSTN) has been at the forefront of muscle therapy research because intrinsic mutations or inhibition of this protein, by either pharmacological or genetic means, result in muscle hypertrophy and hyperplasia. In addition to muscle growth, MSTN inhibition potentially disturbs connective tissue, leads to strength modulation, facilitates myoblast transplantation, promotes tissue regeneration, induces adipose tissue thermogenesis and increases muscle oxidative phenotype. It is also known that current advances in gene therapy have an impact on sports because of the illicit use of such methods. However, the adverse effects of these methods, their impact on athletic performance in humans and the means of detecting gene doping are as yet unknown. The aim of the present review is to discuss biosynthesis, genetic variants, pharmacological/genetic manipulation, doping and athletic performance in relation to the MSTN pathway. As will be concluded from the manuscript, MSTN emerges as a promising molecule for combating muscle wasting diseases and for triggering wide-ranging discussion in view of its possible use in gene doping. Uniterms:Myostatin. Myostatin/genetic variants. Myostatin/pharmacological inhibitors. Gene doping. Gene therapy. Physical performance. Skeletal muscle.Desde sua descoberta, a miostatina (MSTN) entrou na linha de frente em pesquisas relacionadas às terapias musculares porque mutações intrínsecas ou inibição desta proteína tanto por abordagens farmacológicas como genéticas resultam em hipertrofia muscular e hiperplasia. Além do aumento da massa muscular, a inibição de MSTN potencialmente prejudica o tecido conectivo, modula a força muscular, facilita o transplante de mioblastos, promove regeneração tecidual, induz termogênese no tecido adiposo e aumenta a oxidação na musculatura esquelética. É também sabido que os atuais avanços em terapia gênica têm uma relação com o esporte devido ao uso ilícito de tal método. Os efeitos adversos de tal abordagem, seus efeitos no desempenho de atletas e métodos para detectar doping genético são, contudo, desconhecidos. O objetivo da presente revisão de literatura foi discutir biossíntese, variantes genéticas, manipulação genética e farmacológica, e doping relacionado à via da MSTN. Como será concluído do manuscrito, a MSTN emerge como uma molécula promissora para combater doenças atróficas musculares e para gerar muitas discussões devido à sua possível utilização em doping genético. Unitermos:Miostatina. Miostatina/variantes genéticas. Miostatina/inibidores farmacológicos. Doping genético. Desempenho atlético. Músculo esquelético.

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