Effect of Stanozolol and/or Cannabis Abuse on Hypertrophic Mechanism and Oxidative Stress of Male Albino Rat Cardiac Tissue in Relation to Exercise: A Sport Abuse Practice.

Adolescents commonly co-abuse many drugs including anabolic androgenic steroids either they are athletes or non-athletes. Stanozolol is the major anabolic used in recent years and was reported grouped with cannabis. The current study aimed at evaluating the biochemical and histopathological changes related to the hypertrophic effects of stanozolol and/or cannabis whether in condition of exercise practice or sedentary conditions. Adult male Wistar albino rats received either stanozolol (5 mg/kg, s.c), cannabis (10 mg/kg, i.p.), and a combination of both once daily for two months. Swimming exercise protocol was applied as a training model. Relative heart weight, oxidative stress biomarkers, cardiac tissue fibrotic markers were evaluated. Left ventricular morphometric analysis and collagen quantification was done. The combined treatment exhibited serious detrimental effects on the heart tissues. It increased heart tissue fibrotic markers (Masson's trichrome stain (p < 0.001), cardiac COL3 (p < 0.0001), and VEGF-A (p < 0.05)), lowered heart glutathione levels (p < 0.05) and dramatically elevated oxidative stress (increased malondialdehyde (p < 0.0001) and 8-OHDG (p < 0.0001)). Training was not ameliorating for the observed effects. Misuse of cannabis and stanozolol resulted in more hypertrophic consequences of the heart than either drug alone, which were at least largely assigned to oxidative stress, heart tissue fibrotic indicators, histological alterations, and morphometric changes.

Left Ventricular Hypertrophy in Hypertensive Athletes can be Reduced by Antihypertensive Medication Despite Continuing Intense Aerobic Exercise.

INTRODUCTION: Left ventricular hypertrophy (LVH) can be successfully reduced by antihypertensive medication. Both hypertension and aerobic exercise can cause increases in left ventricular mass (LV-mass). AIM: Therefore, hypertensive athletes with LVH were studied to investigate the effect of antihypertensive medication on LV-mass reduction despite continuing their regular intensive exercise programs. METHODS: 14 previously untreated hypertensive male athletes (A) with LVH and a prolonged history of endurance training where included in the study. 50 previously untreated inactive comparable hypertensives with LVH served as controls (C). For both groups inclusion criteria were blood pressure (BP) at rest: > 140/90 mmHg, BP during ergometry (at 100 W): > 200/100 mmHg and. LV-mass-index > 125 g/m2. Echocardiography was performed to calculate LV-mass and function before and after 3 years of antihypertensive medication. RESULTS: Despite regularly aerobic training throughout the treatment period, LV mass decreased from 164 ± 19 g/m2 before to 97 ± 16 g/m2 after 3 years of therapy (p < 0.001). Controls with identical pressures demonstrated a decrease from 149 ± 29 g/m2 to 87 ± 15 g m2. There were similar decreases in LV wall thicknesses in both groups, whereas diastolic dimensions did not change significantly. Moreover, there was an increase in fractional fiber shortening as a measure of LV pump function in both groups of 15% in A and 11% in C, respectively. CONCLUSIONS: In hypertensive athletes LVH due to hypertension can be reduced and LV-function can be improved by long-term antihypertensive medication despite regular aerobic exercise. Therefore, exercise does not interfere with the regression of LVH on account of antihypertensive therapy in hypertensive subjects.

Cardiac AT(1) receptor-dependent and IGF1 receptor-independent signaling is activated by a single bout of resistance exercise.

AT(1) receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that beta-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT/mTOR and ERK1/2 pathways may occur through the beta-arrestin-dependent pathway.

Hypertrophic response of the association of thyroid hormone and exercise in the heart of rats.

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.

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. .