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Why is strenuous exercise good for heart failure?

MADRID, 12 Dic. (EUROPA PRESS) –

High intensity interval training strengthens the heart even more than moderate exercise. Now researchers from the Norwegian University of Science and Technology have found several answers to what makes hard workouts so effective.

“Our research in rats with heart failure shows that exercise reduces disease severity, improves heart function, and increases work capacity. And training intensity is really important in achieving this effect,” explains Thomas Stolen, one of the leaders of the study, which has been published in the ‘Journal of Molecular and Cellular Cardiology’.

The researchers went to great lengths to investigate what happens inside the tiny cells of the heart muscle after regular exercise. “We found that exercise improves important properties both in the way the heart muscle cells handle calcium and in the conduction of electrical signals in the heart. These improvements allow the heart to beat more vigorously and may counteract heart rhythm disorders. life-threatening, “says Stolen.

For a heart to be able to beat strongly, regularly and in sync, many functions have to work together. Every time the heart beats, the sinus node (the heart’s own pacemaker) sends electrical impulses to the rest of the heart. These electrical impulses are called action potentials.

All cells of the heart muscle are enclosed by a membrane. At rest, the electrical voltage inside the cell membrane is negative compared to the voltage outside. The difference between the voltage on the outside and inside of the cell membrane is called the resting membrane potential.

When action potentials reach cardiac muscle cells, they need to overcome the resting membrane potential of each cell to depolarize the cell wall. When this happens, calcium can flow into the cell through channels in the cell membrane.

Calcium initiates the actual contraction of the heart muscle cells. When this process is complete, calcium is transported out of the cell or back to its storage location within each cell of the heart muscle. From there, the calcium is ready to contribute to a new contraction the next time an action potential passes quickly.

If the electrical conduction of the heart or the calcium delivery system fails, the risk is that fewer cells of the heart muscle contract, the contraction of each cell is weak, and the electrical signals become chaotic, so that the chambers of the heart begin to stir.

“All of these processes are dysfunctional when someone has heart failure. Action potentials last too long, the resting potential of cells is too high, and the transport function of calcium channels in the cell wall is disturbed. Calcium is then constantly escaping from its storage sites within each cell of the heart muscle, “says the researcher.

Normally, the sinus node causes the human heart to beat 50 to 80 times per minute at rest. This is enough to supply all organ and cell systems in the body with the amount of oxygen-rich blood they need to function properly.

When we get up for a walk, our heart automatically begins to beat a little faster and pump a little harder so that the blood supply adapts to the increased activity level. The higher the intensity of the activity, the harder the heart has to work.

Exercise strengthens the heart so it can pump more blood to the rest of the body with each beat. This way, the sinus node can take it a bit easier, and well-trained people have a lower resting heart rate than people who haven’t done regular resistance training.

At the other end of the continuum are people with heart failure. Here the pumping capacity of the heart is so weak that the organs no longer receive enough blood to maintain proper function. People with heart failure have a low tolerance for exercise and often become out of breath with minimal effort. In other words, increasing the pumping capacity of the heart is absolutely crucial for the quality of life and health of people with heart failure.

In healthy rats, the heart pumped 75 percent of the blood with each contraction. In rats with heart failure, this measure of pumping ability, called the ejection fraction, dropped to 20 percent. The ejection fraction increased to 35 percent after six to eight weeks with almost daily interval training sessions on a treadmill. The rats did four-minute intervals at about 90 percent of their maximum capacity.

“Interval training also significantly improved the conditioning of the rats. After the training period, their fitness level was actually better than untrained rats that had not had a heart attack,” Stolen argues.

The effect was clear when the researchers tried to induce ventricular fibrillation in the hearts of the diseased rats – they only succeeded in this in one of the nine animals that had completed interval training. By comparison, they had no problem inducing fibrillation in all the heart failure rats that had not exercised.

Until now, the research group had shown that exercise improves calcium management in diseased heart muscle cells in several ways. Training also makes the heart’s electrical wiring system more functional. In addition, they showed that exercise counteracted the processes that cause the heart to become large and stiff. Together, these improvements make each heart beat more powerful and reduce the severity of heart failure. The risk of dangerous ventricular fibrillation was also reduced.

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