Exploring the relationship between physical literacy levels, engagement and emotionality in physical education classes / Explorando a relação entre os níveis de alfabetização física, engajamento e emotividade nas aulas de educação física

ABSTRACT For the researchers, physical literacy (AFi) is the objective to be achieved in Physical Education, for seeking competent subjects, capable of adhering to physical activity throughout their lives, with continuous personal, social, affective, and physical development. Quantitative, descriptive-correlational research was carried out, with a non-experimental design and a non-probabilistic sample of 322 subjects, students from 12 to 18 years old from private, public, and subsidized schools in Talca, Chile. The aim was to relate the level of AFi, engagement and perceived emotionality. Data were collected by the Perceived Physical Literacy Instrument (PPLI), Behavioral Engagement Questionnaire (BEQ) and Scale for Mood Assessment (EVEA). A positive relationship was identified with a higher level of physical literacy, higher levels of happiness (r=0.37) and emotional engagement (r=0.54), decreasing the indexes of hostility (r=-0.25) and the private establishments reach the highest levels of anxiety (X̅=3.2). It is concluded that the higher the level of AFi, the greater the commitment and the greater the regulation of emotional factors.

RESUMO A alfabetização física (AFi) é o objetivo para os pesquisadores na Educação Física, buscando sujeitos competentes e capazes de aderir à atividade física ao longo de suas vidas, com desenvolvimento contínuo pessoal, social, afetivo e físico. Esta pesquisa é de natureza quantitativa, descritiva-correlacional, com um desenho não experimental e uma amostra não probabilística de 322 sujeitos, estudantes de 12 a 18 anos de escolas particulares, municipais e subsidiadas na cidade de Talca, Chile. O objetivo foi relacionar o nível de AFi, comprometimento e emocionalidade percebida. Os dados foram coletados por meio do Perceived Physical Literacy Instrument (PPLI), Behavioral Engagement Questionnaire (BEQ) e Escala de Avaliação do Estado de Ânimo (EVEA). Identificou-se uma relação positiva com um maior nível de alfabetização física, maior nível de alegria (r=0,37) e comprometimento emocional (r=0,54), diminuindo os índices de hostilidade (r=-0,25). As escolas particulares atingem os níveis mais altos de ansiedade (X̅=3,2). Conclui-se que um maior nível de AFi está associado a um maior comprometimento e maior regulação dos fatores emocionais.

Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system, by increasing the expression of atrogin-1 and MuRF-1. In addition, myostatin activates the NF-κB signaling pathway. Renin-angiotensin system (RAS) also regulates muscle mass. Angiotensin (1-7) (Ang-(1-7)) has anti-atrophic properties in skeletal muscle. In this paper, we evaluated the effect of Ang-(1-7) on muscle atrophy and signaling induced by myostatin. The results show that Ang-(1-7) prevented the decrease of the myotube diameter and myofibrillar protein levels induced by myostatin. Ang-(1-7) also abolished the increase of myostatin-induced reactive oxygen species production, atrogin-1, MuRF-1, and TNF-α gene expressions and NF-κB signaling activation. Ang-(1-7) inhibited the activity mediated by myostatin through Mas receptor, as is demonstrated by the loss of all Ang-(1-7)-induced effects when the Mas receptor antagonist A779 was used. Our results show that the effects of Ang-(1-7) on the myostatin-dependent muscle atrophy and signaling are blocked by MK-2206, an inhibitor of Akt/PKB. Together, these data indicate that Ang-(1-7) inhibited muscle atrophy and signaling induced by myostatin through a mechanism dependent on Mas receptor and Akt/PKB.

The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice.

Angiotensin (1-7) (Ang-(1-7)) is a bioactive heptapeptide with a short half-life and has beneficial effects in several tissues - among them, skeletal muscle - by preventing muscle atrophy. Dendrimers are promising vehicles for the protection and transport of numerous bioactive molecules. This work explored the use of a neutral, non-cytotoxic hydroxyl-terminated poly(amidoamine) (PAMAM-OH) dendrimer as an Ang-(1-7) carrier. Bioinformatics analysis showed that the Ang-(1-7)-binding capacity of the dendrimer presented a 2:1 molar ratio. Molecular dynamics simulation analysis revealed the capacity of neutral PAMAM-OH to protect Ang-(1-7) and form stable complexes. The peptide coverage ability of the dendrimer was between ~50% and 65%. Furthermore, an electrophoretic mobility shift assay demonstrated that neutral PAMAM-OH effectively bonded peptides. Experimental results showed that the Ang-(1-7)/PAMAM-OH complex, but not Ang-(1-7) alone, had an anti-atrophic effect when administered intraperitoneally, as evaluated by muscle strength, fiber diameter, myofibrillar protein levels, and atrogin-1 and MuRF-1 expressions. The results of the Ang-(1-7)/PAMAM-OH complex being intraperitoneally injected were similar to the results obtained when Ang-(1-7) was systemically administered through mini-osmotic pumps. Together, the results suggest that Ang-(1-7) can be protected for PAMAM-OH when this complex is intraperitoneally injected. Therefore, the Ang-(1-7)/PAMAM-OH complex is an efficient delivery method for Ang-(1-7), since it improves the anti-atrophic activity of this peptide in skeletal muscle.

High Fat Diet-Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis.

Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.