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Gym protects the heart

New research conducted by the São Paulo Research Foundation in South America shows that exercise helps rid heart cells of dysfunctional mitochondria.

Cleansing mechanism

“Basically, we discovered that aerobic training facilitates the removal of dysfunctional mitochondria from heart cells,” said Professor Julio Ferreira, a researcher who formed part of a project which was funded by the São Paulo Research Foundation. Mitochondria are the organelles in charge of providing energy to cells. “The removal of dysfunctional mitochondria increases the supply of ATP [adenosine triphosphate, the molecule that stores energy for the cell] and reduces the production of toxic molecules, such as oxygen free radicals and reactive aldehydes, an excess of which damages the cell structure.”

Ferreira and colleagues proved exercise regulates a cellular cleansing mechanism known as autophagy, the discovery of which led Japanese scientist Yoshinori Ohsumi to win the 2016 Nobel Prize in Medicine.

Ferreira explained further: “Instead of degrading isolated proteins, this system creates a vesicle [autophagosome] around dysfunctional organelles and transports all this material at once to the lysosome, a sort of incinerator. The lysosome contains enzymes that destroy cell waste. However, we observed that autophagic flux is interrupted in the heart of a rat with heart failure and that there’s a buildup of dysfunctional mitochondria.”

Big difference

Small mitochondria accumulated but disappeared when scientists placed rats as part of their experiment on a treadmill. The rats would run at 60 percent of their capacity for 60 minutes once a day, five days a week for a duration of eight weeks.

“The exercise restored the process of dysfunctional cardiac mitochondria removal. The benefits of exercise were abolished when we blocked autophagy pharmaceutically or genetically.”

The scientists compared these results with rats with heart failure that had remained sedentary and a group of sedentary rats without induced heart failure.

“In the sick rats that remained sedentary, cardiac function fell by 30 percent in the eight-week period, whereas in the trained group, it increased by 40 percent compared with the pre-training condition,” Ferreira said. “All in all, therefore, the difference between these two groups in terms of cardiac function was 70 percent,” said Ferreira.

“Physical exercise does increase the size of the heart, but this increase is proportional to the improvement in cardiac function. The dilation caused by heart failure relates to loss of cardiac function. So our results show that exercise not only prevents but also reverses the damage caused by heart failure.”

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