Research Paper I Open Access I Released under (CC BY-NC) license
Exercise Physiology
Sara Shahsavari Babokani; Hamid Mohebbi
Abstract
Aim: This study was conducted to determine the influence of nutrition and aerobic exercise on the signaling pathway of ER stress in the liver. Methods: A total of 18 male wistar rats, aged 5 weeks and weighing approximately 167 grams, were randomly divided into three groups: normal diet (ND), high-fat ...
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Aim: This study was conducted to determine the influence of nutrition and aerobic exercise on the signaling pathway of ER stress in the liver. Methods: A total of 18 male wistar rats, aged 5 weeks and weighing approximately 167 grams, were randomly divided into three groups: normal diet (ND), high-fat diet (HFD), and high-fat diet with aerobic exercise (HFD+EX). The rats in the HFD+EX group underwent exercise training three times per week for 12 weeks with an intensity of 68-80% of their maximum aerobic velocity. After completing the training, liver tissue samples were collected from all rats to measure the expression changes of Chop, Atf6, Perk, and Bax genes, as well as liver fat accumulation. Data analysis was conducted using the one-way ANOVA test. Finding: Higher liver fat content and higher expression of Chop, Atf6, Perk, and Bax, was observed in the HFD rats. In the HFD+EX group, liver fat content, Chop and Perk gene expression were lower than in the HFD group. In the HFD+EX group reduction of Atf6 and Bax genes, was not statistically significant (p>0.05). Conclusion: High fat diet can activate the unfolded protein response (UPR) pathway by elevating ER stress. This can lead to high expression of the Bax gene in liver cells. However, regular exercise can be an effective way to prevent the accumulation of liver fat by reducing UPR activation. This is due to its potential to lower the expression of Chop, Atf6, and Perk gene.
Research Paper I Open Access I Released under (CC BY-NC) license
Exercise Physiology
Armin Farahnak; Javad Mehrabani; Hamid Arazi
Abstract
Introduction and purpose: The effect of exercise training on supplying the energy needs of muscle tissues is one of the important questions in training adaptation. Along with exercise, taking some nutrition supplements can improve cellular function. Combining supplements together with concurrent training ...
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Introduction and purpose: The effect of exercise training on supplying the energy needs of muscle tissues is one of the important questions in training adaptation. Along with exercise, taking some nutrition supplements can improve cellular function. Combining supplements together with concurrent training is a new considerable approach. Therefore, the aim of the present study was to determine the effect of aerobic-resistance trainings and mixed supplementation (L-arginine/caffeine/L-carnitine) on angiogenic factors and hypoxia-inducible factor 1 (VEGF and HIF-1a) in inactive obese men.Methods: 28 inactive obese men (age 37.02±3.89, height 1.74±0.66 and BMI 34.04±1.24) were randomly were divided into three groups of aerobic-resistance training/combined supplementation (n: 10), aerobic-resistance training/placebo (n: 9) and combined supplement/detraining (n: 9). Aerobic (30 min 55-75% HRmax), resistance trainings (40-45 min/50-70% 1-RM) and a mixed supplement were including 1000 mg of L-arginine, 200 mg of caffeine and 1000 mg of L-carnitine that were performed during 10 weeks (3 session a week).Findings: The results of the MANCOVA test showed that the aerobic-resistance exercises training with moderate intensity in intraction with the mixed supplement (L-arginine/caffeine/L-carnitine) significantly increased the blood levels of angiogenesis indicators including VEGF (p=0.001) and significantly decreased the levels of HIF1-a (p=0.0001) in inactive obese men.Conclusion: In summary, the results of the present study showed that the aerobic-resistance training with moderate intensity in intraction with the mixed supplement (L-arginine/caffeine/L-carnitine) were increased angiogenic and hypoxi istimulation factors in inactive obese men.
