We used Drosophila melanogaster as an animal model system to study the impact of exercise training initiated early in life on cardiac function using a well-established model of inherent myogenic properties of the heart and discussed the changes on myosin, a myocardial contractile protein. We also explored the effect of early physical exercise on organismal aging by analyzing the wake-sleep pattern using a Drosophila activity monitor system. We found that a variety of arrhythmias are part of the heart spectrum in old flies after a lifetime of physical exercise as evidenced by reducing the incidence of fibrillations and increasing the occurrence of bradycardias. Maintenance of myocardial myosin levels may be an underlying contributor to these exercise-induced improvements in cardiac function at an advanced age. Moreover, we found that exercise training resulted in improved sleep quality by ameliorating age-related sleep inefficiency, fragmentation and sleep consolidation.
Mild normobaric hypoxia (NH) and modest exercise have multiple beneficial effects on health, but the changes in physiological function induced by NH and/or exercise remain unclear. The purpose of this investigation was to examine the specific effects of NH and/or exercise on cardiac function and myocardial structure and behavior including sleep-activity and negative geotaxis in aged Drosophila. We also assessed the survival rate of flies after hypoxia and/or exercise. One-thousand wild-type w 1118 virgin female flies were randomly divided into four groups and treated with NH and/or exercise from ages 3-6 weeks. We found that exercise remarkably delayed the decline of actin and myosin and the age-related changes in cardiac structure, improved abnormal cardiac contraction, and enhanced the cardiac pumping force by inducing cardiac hypertrophy and delaying deterioration of cardiac contractility and diastolic compliance, and improved abnormal heart contraction. NH also increased the content of actin and myosin, but induced a decrease in heart diameter and heart rate, as well as an increase in the number of mitochondria and deeper sleep, which may be the manifestation of energy saving under long-term hypoxia. Both NH and exercise improved sleep quality and climbing ability of aged flies, as well as extended the maximum life span, which shows the benefits of hypoxia and exercise. Finally, the superposition of NH and exercise did not impart any obvious physiological and behavior improvement. Therefore, it is necessary to further explore the appropriate combination of hypoxia and exercise.
The aim of this study was to evaluate the potential neurotrophic factors and expression of neurotrophin receptors in peripheral blood mononuclear cells linked with the antidepressant action of exercise intervention during protracted methamphetamine (METH) abstinence. Materials and Methods: A total of 72 male METH addicts, including 47 individuals with depression and 25 individuals without depression, were recruited in this study. Individuals with depression were divided into the depression control group and the depression exercised group. Consequently, 12 weeks of supervised exercise intervention was applied. Depression and anxiety were analyzed; plasma brain-derived neurotrophic factor (BDNF), neuronal growth factor (NGF), neurotrophin-3 (NT-3), NT-4, and proBDNF levels were tested using enzyme-linked immunosorbent assay; the mRNA expressions of TrkA, TrkB-FL, TrkB-T1, TrkCB, and P75NTR in peripheral blood mononuclear cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Results: NT-4 plasma levels were correlated with depression (r = −0.330, p = 0.005), which remained significant after Bonferroni correction. In addition, the BDNF and NT-3 levels in the plasma were significantly correlated with depression (r = −0.268, p = 0.023; r = −0.259, p = 0.028), but did not reach significance after Bonferroni correction. The BDNF, NT-3, and NT-4 plasma levels were significantly different between the depressive control group and the depressive exercise group using pre-exercise values as the covariate. The fold changes in TrkB-FL and TrkB-T1 mRNA in peripheral blood mononuclear cells between the post-exercise and pre-exercise demonstrated a remarkable decrease (fold change = −11.056 and −39.055).
Apolipoprotein B plays an essential role in systemic lipid metabolism, and it is closely related to cardiovascular diseases. Exercise-training can regulate systemic lipid metabolism, improve heart function, and improve exercise capacity, but the molecular mechanisms involved are poorly understood. We used a Drosophila model to demonstrate that exercise-training regulates the expression of apoLpp (a homolog of apolipoprotein B) in cardiomyocytes, thereby resisting heart insufficiency and low exercise capacity caused by obesity. The apoLpp is an essential lipid carrier produced in the heart and fat body of Drosophila. In a Drosophila genetic screen, low expression of apoLpp reduced obesity and cardiac dysfunction induced by a high-fat diet (HFD). Cardiac-specific inhibition indicated that reducing apoLpp in the heart during HFD reduced the triglyceride content of the whole-body and reduced heart function damage caused by HFD. In exercise-trained flies, the result was similar to the knockdown effect of apoLpp. Therefore, the inhibition of apoLpp plays an important role in HFD-induced cardiac function impairment and low exercise capacity. Although the apoLpp knockdown of cardiomyocytes alleviated damage to heart function, it did not reduce the arrhythmia and low exercise capacity caused by HFD. Exercise-training can improve this condition more effectively, and the possible reason for this difference is that exercise-training regulates climbing ability in ways to promote metabolism. Exercise-training during HFD feeding can down-regulate the expression of apoLpp, reduce the whole-body TG levels, improve cardiac recovery, and improve exercise capacity. Exercise-training can downregulate the expression of apoLpp in cardiomyocytes to resist cardiac function damage and low exercise capacity caused by HFD. The results revealed the relationship between exercise-training and apoLpp and their essential roles in regulating heart function and climbing ability.
Cardiovascular disease (CVD) places a heavy burden on older patients and the global healthcare system. A large body of evidence suggests that exercise training is essential in preventing and treating cardiovascular disease, but the underlying mechanisms are not well understood. Here, we used the Drosophila melanogaster animal model to study the effects of early-life exercise training (Exercise) on the aging heart and lifespan. We found in flies that age-induced arrhythmias are conserved across different genetic backgrounds. The fat body is the primary source of circulating lipoproteins in flies. Inhibition of fat body apoLpp (Drosophila apoB homolog) demonstrated that low expression of apoLpp reduced the development of arrhythmias in aged flies but did not affect average lifespan. At the same time, exercise can also reduce the expression of apoLpp mRNA in aged flies and have a protective effect on the heart, which is similar to the inhibition of apoLpp mRNA. Although treatment of UAS-apoLpp RNAi and exercise alone had no significant effect on lifespan, the combination of UAS-apoLpp RNAi and exercise extended the average lifespan of flies. Therefore, we conclude that UAS-apoLpp RNAi and exercise are sufficient to resist age-induced arrhythmias, which may be related to the decreased expression of apoLpp mRNA, and that UAS-apoLpp RNAi and exercise have a combined effect on prolonging the average lifespan.www.aging-us.com AGINGremodeling, obesity, and even sudden cardiac death, which threatens health [10][11][12]. However, there is considerable difficulty and complexity in studying cardiac aging due to long life spans and genetic redundancy in mammals. Therefore, we utilized the Drosophila model to design this experiment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.