Dragon boat exercise reshapes the temporal-spatial dynamics of the brain.

Although exercise training has been shown to enhance neurological function, there is a shortage of research on how exercise training affects the temporal-spatial synchronization properties of functional networks, which are crucial to the neurological system. This study recruited 23 professional and 24 amateur dragon boat racers to perform simulated paddling on ergometers while recording EEG. The spatiotemporal dynamics of the brain were analyzed using microstates and omega complexity.

Characteristics of changes in the functional status of the brain before and after 1,000 m all-out paddling for different levels of dragon boat athletes.

Purposes: Dragon boat is a traditional sport in China, but the brain function characteristics of dragon boat athletes are still unclear. Our purpose is to explore the changing characteristics of brain function of dragon boat athletes at different levels before and after exercise by monitoring the changes of EEG power spectrum and microstate of athletes before and after rowing.

Methods: Twenty-four expert dragon boat athletes and 25 novice dragon boat athletes were selected as test subjects to perform the 1,000 m all-out paddling exercise on a dragon boat dynamometer.

Comparison of Electroencephalogram Power Spectrum Characteristics of Left and Right Dragon Boat Athletes after 1 km of Rowing.

Purpose: This study aimed to detect differences in post-exercise brain activity between the left and right paddlers due to exercise by analyzing the resting-state electroencephalogram (EEG) power spectrum before and after exercise. Methods: Twenty-one right paddlers and twenty-two left paddlers completed a 1 km all-out test on a dragon boat ergometer, and their heart rate and exercise time were recorded. EEG signals were collected from superficial brain layers before and after exercise; then, the EEG power spectrum was extracted and compared in different frequency bands.

Therapeutic Effect and Metabolic Mechanism of A Selenium-Polysaccharide from Green Tea on Chronic Fatigue Syndrome.

green tea was considered a medicine food homology plant to improve chronic fatigue Ssyndrome (CFS) in China. The aim of this research was to study the therapeutic effect of selenium-polysaccharides (Se-TP) from green tea on CFS and explore its metabolic mechanism. A CFS-rats model was established in the present research and Se-TP was administrated to evaluate the therapeutic effect on CFS.

Detection of Urine Metabolites in a Rat Model of Chronic Fatigue Syndrome before and after Exercise.

The aim of the present study was to elucidate the metabolic mechanisms associated with chronic fatigue syndrome (CFS) via an analysis of urine metabolites prior to and following exercise in a rat model. A rat model of CFS was established using restraint-stress, forced exercise, and crowded and noisy environments over a period of 4 weeks. Behavioral experiments were conducted in order to evaluate the model.

Exercise training reduces insulin resistance in postmyocardial infarction rats.

Myocardial infarction (MI) induces cardiac dysfunction and insulin resistance (IR). This study examines the effects of MI-related IR on vasorelaxation and its underlying mechanisms, with a specific focus on the role of exercise in reversing the impaired vasorelaxation. Adult male Sprague-Dawley rats were divided into three groups: Sham, MI, and MI+Exercise.

Acetylcholine inhibits tumor necrosis factor α activated endoplasmic reticulum apoptotic pathway via EGFR-PI3K signaling in cardiomyocytes.

Previous findings have shown that acetylcholine (ACh) decreased hypoxia-induced tumor necrosis factor alpha (TNF α) production, thus protected against cardiomyocyte injury. However, whether and how ACh affects TNF α-induced endoplasmic reticulum (ER) stress and cell apoptosis remain poorly defined. This study was aimed at determining the effect of ACh in H9c2 cells after TNF α stimulation.

Aerobic interval training attenuates mitochondrial dysfunction in rats post-myocardial infarction: roles of mitochondrial network dynamics.

Aerobic interval training (AIT) can favorably affect cardiovascular diseases. However, the effects of AIT on post-myocardial infarction (MI)-associated mitochondrial dysfunctions remain unclear. In this study, we investigated the protective effects of AIT on myocardial mitochondria in post-MI rats by focusing on mitochondrial dynamics (fusion and fission).

Aerobic interval training protects against myocardial infarction-induced oxidative injury by enhancing antioxidase system and mitochondrial biosynthesis.

1. Aerobic interval training (AIT) exerts beneficial effects on cardiovascular disease. However, its cardioprotective mechanisms are not fully understood.

Amlodipine ameliorates endothelial dysfunction in mesenteric arteries from spontaneously hypertensive rats.

1. Endothelial dysfunction plays a critical role in the development and progression or pathogenesis of hypertension. Amlodipine, a calcium channel blocker, is an effective antihypertensive agent.

Exercise improves the dilatation function of mesenteric arteries in postmyocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism.

Myocardial infarction (MI) has been shown to induce endothelial dysfunction in peripheral resistance arteries and thus increase peripheral resistance. This study was designed to investigate the underlying mechanisms of post-MI-related dysfunctional dilatation of peripheral resistance arteries and, furthermore, to examine whether exercise may restore dysfunctional dilatation of peripheral resistance arteries. Adult male Sprague-Dawley rats were divided into three groups: sham-operated, MI, and MI + exercise.

[Alterations in aortic vasomotor function in rats with chronic heart failure and its mechanism].

The aim of the present study was to investigate the alterations in thoracic aortic vasomotor function in rats with chronic heart failure (CHF) post myocardial infarction (MI), and then explored the possible mechanism of pathological changes. Male Sprague-Dawley rats were divided into sham and CHF groups randomly. The CHF model group of rats was generated by ligating the left anterior descending artery.