Abstract: Long-term aerobic exercise can improve heart function, but the underlying mechanism of exercise's protective effect on the heart remains unclear.

Recently, in Circulation Research, researchers from the Air Force Military Medical University of China stated that the improvement of the heart function by long-term exercise is related to a new cardioprotective exercise factor, exosome miR-342-5p.

Epidemiology and animal experiments have shown that exercise can not only reduce the risks of cardiovascular disease, but also can directly protect myocardium and reduce myocardial ischemia-reperfusion injury. An in-depth study of the cardioprotective mechanism of exercise will facilitate the promotion of exercise and the development of new cardioprotective drugs.

Exosomes are nano-sized vesicles secreted by cells. They can mediate the transmission of information between distant organs and tissues through the miRNAs and proteins carried by them, and participate in the systemic regulation of the body. Studies have shown that exercise can induce the release of circulating exosomes and change their protein composition, and a variety of motility factors exist in exosomes, so exosomes can act as a carrier of these factors to protect the heart muscle.
In this research, the researchers conducted animal experiments and human experiments separately.

In the experimental study of rats, it was found that the area of myocardial infarction after myocardial ischemia and reperfusion in rats in the long-term swimming training group was smaller, and the content of lactate dehydrogenase (LDH) in serum was also lower. Subsequently, the researchers isolated the exosomes in the rat blood and incubated the extracted exosomes with damaged cardiomyocytes. It was found that the exosomes extracted from the rats in the swimming group could significantly reduce the apoptosis of the injured cardiomyocytes.

Next, the researchers verified whether the exosomes extracted from the exercise group could reduce cardiomyocyte apoptosis and reduce cardiomyocyte injury after ischemia-reperfusion in vivo. The researchers injected exosomes into the heart of normal mice and modeled them 48 hours later. The results showed that the exosomes extracted from the exercise group can significantly reduce the area of myocardial infarction, improve heart function, increase the maximum rate of increase/decrease of left ventricular pressure, and reduce left ventricular end-diastolic pressure.
Correspondingly, the test results of human experiments are consistent with those of rats. The researchers collected blood samples from rowers and untrained students, extracted the exosomes from them, and incubated them with damaged cardiomyocytes. The results showed that the exosomes extracted from the rowers’ blood could inhibit apoptosis, reduce LDH, and increase the survival rate of cells.

The results of human and animal experiments suggest that exosomes produced after long-term exercise can indeed protect damaged cardiomyocytes. So, which component of exosomes is at work?

The researchers found through exosome sequencing that the miRNAs in the exosomes of the training group and the control group were very different, and 11 kinds of miRNAs were significantly up-regulated in the exercise group, including miR-3571, miR-1-3p, miR-342-5p, miR-122-5p, etc.

The research results proved that long-term exercise can affect cardiomyocytes through exosomes and exert cardioprotective functions, revealing a new mechanism of long-term exercise to protect the heart. The research has important application value for the prevention and treatment of clinical ischemic heart disease, such as the development of new therapies based on miRNA to treat heart disease. But for healthy people, more exercise, more benefits!

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