Como eu faço no Coração de Atleta: avaliação dos diferentes tipos de adaptação ao exercício / My approach to "Athlete'S Heart": evaluation of the different types of adaptation to exercise

A prática regular de esportes pode induzir adaptações no coração, sendo essa condição comumente chamada de "coração de atleta". As alterações observadas incluem dilatação das câmaras cardíacas, aumento da espessura miocárdica, melhora do enchimento ventricular, aumento da trabeculação do ventrículo esquerdo (VE), dilatação da veia cava inferior, entre outras. Essas alterações também podem ser observadas em algumas doenças cardíacas, como cardiomiopatia (CMP) dilatada, hipertrófica e outras. Dessa forma, os exames de imagem cardíaca são fundamentais na identificação dessas alterações e na diferenciação entre o "coração de atleta" e uma possível cardiopatia.(AU)

Exercise-induced adaptation may occur in amateur and professional athletes. This condition is commonly named "athlete's heart". The alterations observed include dilation of the heart chambers, increased myocardial thickness, improved ventricular filling, increased left ventricular trabeculation, dilation of the inferior vena cava, among others. These changes can also be observed in some heart diseases, such as dilated, hypertrophic and other cardiomyopathies (CMP). Thus, cardiac imaging tests are fundamental in identifying these alterations and in differentiating between "athlete's heart" and possible heart disease. (AU)

Athlete's heart in a Brazilian paralympic judo team. Case series study

ABSTRACT BACKGROUND: Athlete's heart is a term describing the cardiovascular effects of long-term conditioning among highly trained athletes. It is a variation of normal standards. DESIGN AND SETTING: Case series study at the cardiology division of a public university hospital. METHODS: We studied 14 visually handicapped paralympic athletes (8 men) in the national judo team. They were 26.3 ± 6.4 years old, with body mass index 25 ± 14, and had been practicing judo for 9.2 ± 7.9 years. Clinical evaluations, electrocardiograms, exercise testing and echocardiograms were performed by independent observers. RESULTS: Signs of athlete's heart were found in all athletes, comprising left ventricular hypertrophy (5 cases), sinus bradycardia (5), T-wave juvenile pattern (3), T wave juvenile pattern (3), left atrial hypertrophy (2) and increased left ventricular volume (9 cases; 62.22 ± 6.46 ml/m2). There were very strong correlations between left ventricular mass/body surface and endurance time (r: 0.91) and estimated peak oxygen uptake (r: 0.8). The correlations between left ventricular internal diastolic dimension and endurance time (r: 0.91) and estimated peak oxygen uptake (r: 0.8) were strong. Despite increased left ventricular dimensions (4 cases), atrial dimensions (1) and relative wall thickness (4), all athletes had normal left ventricular mass/body surface (89.98 ± 21.93 g/m²). The exercise testing was normal: exercise duration 706 ± 45 seconds and estimated peak oxygen uptake 62.70 ± 9.99 mlO2/min. CONCLUSIONS: Signs of athlete's heart were seen frequently in the paralympic judo team. These demonstrated the presence of mild cardiac adaptations to training.

Resposta Hipertrofica da Associacao de Hormonio Tireoidiano e de Exercicio Fisico no Coracao de Ratos / Hypertrophic response of the Association of Thyroid Hormone and Exercise in the Heart of Rats

Fundamento: A hipertrofia cardíaca constitui um dos componentes do remodelamento cardíaco e ocorre em resposta a aumento da atividade ou da sobrecarga funcional do coração. Objetivo: Avaliar a resposta hipertrófica da associação do hormônio tireoidiano e do exercício físico no coração de ratos. Método: Foram utilizados 37 ratos da linhagem Wistar, machos, adultos, distribuídos aleatoriamente em quatro grupos: controle, hormônio (HT), exercício (E), hormônio tireoidiano e exercício (H + E). O grupo hormônio recebeu diariamente levotiroxina sódica por gavagem, na dose de 20 μg de hormônio tireoidiano/100 g de peso corporal; o grupo exercício realizou natação cinco vezes por semana, com peso adicional correspondente a 20% do peso corporal, durante seis semanas; no grupo H + E foram aplicados simultaneamente os tratamentos dos grupos HT e E. A estatísica utilizada foi a análise de variância complementada, quando necessário, pelo teste de Tukey e o teste de correlação de Pearson. Resultados: O T4 foi mais elevado nos grupos HT e H + E. O peso total do coração foi maior nos grupos que receberam hormônio tireoidiano, e o peso ventricular esquerdo foi maior no grupo HT. O diâmetro transversal dos cardiomiócitos aumentou nos grupos HT, E e H + E. A porcentagem de colágeno foi maior nos grupos E e H + E. A análise da correlação entre as variáveis apresentou distintas respostas. Conclusão: A associação do hormônio tireoidiano com exercício físico de elevada intensidade produziu hipertrofia cardíaca e gerou um padrão hipertrófico não correlacionado diretamente ao grau de fibrose. .

Background: Cardiac hypertrophy is a component of cardiac remodeling occurring in response to an increase of the activity or functional overload of the heart. Objective: Assess hypertrophic response of the association of thyroid hormone and exercise in the rat heart. Methods: We used 37 Wistar rats, male, adults were randomly divided into four groups: control, hormone (TH), exercise (E), thyroid hormone and exercise (H + E); the group received daily hormone levothyroxine sodium by gavage at a dose of 20 μg thyroid hormone/100g body weight, the exercise group took swimming five times a week, with additional weight corresponding to 20% of body weight for six weeks; in group H + E were applied simultaneously TH treatment groups and E. The statistics used was analysis of variance, where appropriate, by Tukey test and Pearson correlation test. Results: The T4 was greater in groups TH and H + E. The total weight of the heart was greater in patients who received thyroid hormone and left ventricular weight was greater in the TH group. The transverse diameter of cardiomyocytes increased in groups TH, E and H + E. The percentage of collagen was greater in groups E and H + E Correlation analysis between variables showed distinct responses. Conclusion: The association of thyroid hormone with high-intensity exercise produced cardiac hypertrophy, and generated a standard hypertrophy not directly correlated to the degree of fibrosis. .

Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants

Among the molecular, biochemical and cellular processes that orchestrate the development of the different phenotypes of cardiac hypertrophy in response to physiological stimuli or pathological insults, the specific contribution of exercise training has recently become appreciated. Physiological cardiac hypertrophy involves complex cardiac remodeling that occurs as an adaptive response to static or dynamic chronic exercise, but the stimuli and molecular mechanisms underlying transduction of the hemodynamic overload into myocardial growth are poorly understood. This review summarizes the physiological stimuli that induce concentric and eccentric physiological hypertrophy, and discusses the molecular mechanisms, sarcomeric organization, and signaling pathway involved, also showing that the cardiac markers of pathological hypertrophy (atrial natriuretic factor, β-myosin heavy chain and α-skeletal actin) are not increased. There is no fibrosis and no cardiac dysfunction in eccentric or concentric hypertrophy induced by exercise training. Therefore, the renin-angiotensin system has been implicated as one of the regulatory mechanisms for the control of cardiac function and structure. Here, we show that the angiotensin II type 1 (AT1) receptor is locally activated in pathological and physiological cardiac hypertrophy, although with exercise training it can be stimulated independently of the involvement of angiotensin II. Recently, microRNAs (miRs) have been investigated as a possible therapeutic approach since they regulate the translation of the target mRNAs involved in cardiac hypertrophy; however, miRs in relation to physiological hypertrophy have not been extensively investigated. We summarize here profiling studies that have examined miRs in pathological and physiological cardiac hypertrophy. An understanding of physiological cardiac remodeling may provide a strategy to improve ventricular function in cardiac dysfunction.