Abstract:The primary purpose of the study was to evaluate whether a pericardiectomy (PERI) alters training- or myocardial infarction (MI)-induced left ventricular hypertrophy (LVH), chamber geometry, gene expression and/or running performance. Mice were randomized into 6 groups: naïve control (CONT)-sedentary (Sed), CONT-trained (Tr), PERI-Sed, PERI-Tr, MI-Sed and MI-Tr. MI mice also received a pericardiectomy as part of the MI surgical procedure. 10 weeks of treadmill running resulted in enhanced running performance-t… Show more
“…To the best of our knowledge, no previous study has examined the apoptosis signaling pathway in response to METH and HIIT. However, the results of the present study agree with those of Delfan et al [ 33 ], Lu et al [ 24 ], and Wolff et al [ 26 ]. Delfan et al [ 33 ] and Lu et al [ 24 ] suggested that HIIT reduces caspase-3 gene expression in rat models of diabetes and myocardial infarction.…”
Section: Discussionsupporting
confidence: 93%
“…Delfan et al [ 33 ] and Lu et al [ 24 ] suggested that HIIT reduces caspase-3 gene expression in rat models of diabetes and myocardial infarction. Additionally, Wolff et al [ 26 ] showed that treadmill training (15° inclination and 22 m/min) increases the melusin mRNA concentration in myocardial infarction and pericardiectomy mice.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, Banaei et al [ 25 ] showed that rats with myocardial ischemia–reperfusion injury showed no reduction in caspase-3 protein in response to HIIT. Moreover, Wolff et al [ 26 ] observed that 10 weeks of training on a treadmill increased the melusin mRNA concentration in rats with myocardial infarction and pericardiectomy.…”
Chronic methamphetamine use increases apoptosis, leading to heart failure and sudden cardiac death. Previous studies have shown the importance of high-intensity interval training (HIIT) in reducing indices of cardiac tissue apoptosis in different patients, but in the field of sports science, the molecular mechanisms of apoptosis in methamphetamine-dependent rats are still unclear. The present article aimed to investigate the changes in cardiac apoptosis markers in methamphetamine-dependent rats in response to HIIT. Left ventricular tissue was used to evaluate caspase-3, melusin, FAK, and IQGAP1 gene expression. Rats were divided into four groups: sham, methamphetamine (METH), METH-control, and METH-HIIT. METH was injected for 21 days and then the METH-HIIT group performed HIIT for 8 weeks at 5 sessions per week. The METH groups showed increased caspase-3 gene expression and decreased melusin, FAK, and IQGAP1 when compared to the sham group. METH-HIIT showed decreased caspase-3 and increased melusin and FAK gene expression compared with the METH and METH-control groups. The IQGAP1 gene was higher in METH-HIIT when compared with METH, while no difference was observed between METH-HIIT and METH-control. Twenty-one days of METH exposure increased apoptosis markers in rat cardiac tissue; however, HIIT might have a protective effect, as shown by the apoptosis markers.
“…To the best of our knowledge, no previous study has examined the apoptosis signaling pathway in response to METH and HIIT. However, the results of the present study agree with those of Delfan et al [ 33 ], Lu et al [ 24 ], and Wolff et al [ 26 ]. Delfan et al [ 33 ] and Lu et al [ 24 ] suggested that HIIT reduces caspase-3 gene expression in rat models of diabetes and myocardial infarction.…”
Section: Discussionsupporting
confidence: 93%
“…Delfan et al [ 33 ] and Lu et al [ 24 ] suggested that HIIT reduces caspase-3 gene expression in rat models of diabetes and myocardial infarction. Additionally, Wolff et al [ 26 ] showed that treadmill training (15° inclination and 22 m/min) increases the melusin mRNA concentration in myocardial infarction and pericardiectomy mice.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, Banaei et al [ 25 ] showed that rats with myocardial ischemia–reperfusion injury showed no reduction in caspase-3 protein in response to HIIT. Moreover, Wolff et al [ 26 ] observed that 10 weeks of training on a treadmill increased the melusin mRNA concentration in rats with myocardial infarction and pericardiectomy.…”
Chronic methamphetamine use increases apoptosis, leading to heart failure and sudden cardiac death. Previous studies have shown the importance of high-intensity interval training (HIIT) in reducing indices of cardiac tissue apoptosis in different patients, but in the field of sports science, the molecular mechanisms of apoptosis in methamphetamine-dependent rats are still unclear. The present article aimed to investigate the changes in cardiac apoptosis markers in methamphetamine-dependent rats in response to HIIT. Left ventricular tissue was used to evaluate caspase-3, melusin, FAK, and IQGAP1 gene expression. Rats were divided into four groups: sham, methamphetamine (METH), METH-control, and METH-HIIT. METH was injected for 21 days and then the METH-HIIT group performed HIIT for 8 weeks at 5 sessions per week. The METH groups showed increased caspase-3 gene expression and decreased melusin, FAK, and IQGAP1 when compared to the sham group. METH-HIIT showed decreased caspase-3 and increased melusin and FAK gene expression compared with the METH and METH-control groups. The IQGAP1 gene was higher in METH-HIIT when compared with METH, while no difference was observed between METH-HIIT and METH-control. Twenty-one days of METH exposure increased apoptosis markers in rat cardiac tissue; however, HIIT might have a protective effect, as shown by the apoptosis markers.
“…Indicators of endurance training adaption suggest that our trained mice underwent sufficient training, because we report higher maximal running velocities as well as higher heart weight/ body weight for both sexes. Further, previous work from our group reports elevated citrate synthase activity in the quadriceps femoris of mice who underwent a similar training protocol [12]. Thus perhaps differences (physiological, psychological) exist between forced and voluntary exercise that explain the differences between males and females in our data.…”
Section: Discussionsupporting
confidence: 55%
“…An exhaustive exercise test was performed using a modified graded protocol as previously published [12,13]. Briefly, the test began at 15 m/min for the SED group and 20 m/min for TR group.…”
Ischemic heart disease presents with significant differences between sexes.
Endurance exercise protects the heart against ischemic disease and also
distinctly impacts male and female patients through unidentified mechanisms,
though some evidence implicates 5′-AMP-activated protein kinase (AMPK).
The purpose of this investigation was to assess the impact of training and sex
on cardiac AMPK activation following exhaustive exercise. AMPK activation was
measured in trained and sedentary mice of both sexes. Trained mice ran on a
treadmill at progressively increasing speeds and duration for 12 weeks. Trained
and sedentary mice of both sexes were euthanized immediately following
exhaustive exercise and compared to sedentary controls. Endurance training
elicited adaptations indicative of aerobic adaptation including higher max
running velocities and cardiac hypertrophy with no differences between males and
females. AMPK activity was higher in male compared to females, and trained
exhibited higher AMPK activity compared to sedentary mice. In response to
training, male mice activated AMPK more robustly than female mice. Chronic
exercise training increases the ability to activate cardiac AMPK in response to
exhaustive exercise in a sex-specific manner. Understanding the interaction
between exercise and sex is vital for use of exercise as medicine for heart
disease in both men and women.
Regulated necrosis (necroptosis) plays a pivotal role in the extent of cardiomyocyte loss and the development of post-ischemic adverse remodelling and cardiac dysfunction following myocardial I/R injury. Although HIIT has been reported to give rise to cardioprotection against MI, but the detailed knowledge of its molecular targets for treatment of MI is still not available. The LAD of Male Wistar rats was occluded to induce MI for 30 min and reperfusion for eight weeks. We investigated the effect of long-term HIIT for eight weeks on lipid peroxidation, SOD activity and GSH content using ELISA assay. Cardiac function, fibrosis, and infarct size were assessed by echocardiography, Masson's trichrome and Evans Blue/TTC dual staining respectively. The expressions of gene markers of myocardial hypertrophy, fibrosis and key mediators of necroptosis were measured using RT-PCR and western blotting assay respectively. The results indicated that HIIT reduced lipid peroxidation, infarct size and improved endogenous antioxidant system and heart function. Significant decreases in mRNA levels of procollagen α1(I), α1(III), and fibronectin1were observed following HIIT. Moreover, that HIIT significantly decreased the expression of key mediators of necroptosis induced by MI (P < 0.05). There were no significant differences in β-MHC mRNA level in different groups. The findings of study suggest that HIIT might exert cardioprotective effects against post-ischemic adverse remodeling through targeting necroptosis process. Likewise, cardioprotective effects of HIIT in coping with myocardial I/R injury may be associated with RIP1-RIP3-MLKL axis. These findings establish a critical foundation for higher efficiency of exercise-based cardiac rehabilitation post-MI and future research.
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