Mário Pedro Bernardes is a big strong man. At 5 feet tall, he was always used to performing tasks that required physical strength. He was a cameraman on a TV network for years, and in the reports he carried a 7-kilogram camera on his shoulders. But in 2012, at age 47, he had to retire. Mario did a test to participate as a healthy volunteer in a study and found that his heart was not good. A virus infection, probably ancient, had caused injuries to the heart muscle and the organ no longer pumped the blood as it should. He had developed heart failure, a complex problem that reduces the heart’s ability to distribute blood through the body and is one of the leading causes of death in Brazil.
An infarction that occurred months later left Mario hospitalized for a week in an ICU and worsened the condition. When he was discharged, he was retired due to disability and his cardiologist at the time recommended that he not do any physical activity. You should take the medicines to help your heart function and could at most carry out “light walking”. But even this he could not. “I walked a block and had to stop to rest; if I spoke, I would tire before that, “said Mario on a morning of November this year, shortly after a training session in which he pedaled for 40 minutes an exercise bicycle in one of the laboratories of the Heart Institute (InCor) of the University of São Paulo (USP).
Mario is one of nearly 150 volunteers who in recent years have gone through an InCor training program to evaluate the effect of physical exercise on the health of people with heart failure. Directed by the physiologist Carlos Eduardo Negrão, the program has been helping to demonstrate that along with the use of medications, regular practice of physical exercise is fundamental to restore the health of those who have a sick heart. “Of the people who participated in the training, the vast majority improved,” says researcher Lígia Antunes-Corrêa, a member of the group.
Only those who are in stable clinical condition, obtained with the aid of medication, participate in the program. Researchers evaluate the cardiopulmonary capacity of each individual and prepare a progressive training plan until the desired level of physical exercise is achieved. The goal is to perform 40 minutes of aerobic exercise and another 20 exercises of muscular endurance and flexibility three times a week. The training lasts four months, long enough to start redeeming quality of life and the ability to perform many of daily activities such as bathing alone or walking to the supermarket, lost with heart failure.
“After I did the training for the first time, I felt more disposed,” said Mario, who is now at age 50 and participates in a second study conducted by Negrão’s group. Much of that provision, however, disappeared when Mario stopped exercising. “The effect of exercise is lost when training is discontinued,” explained Ligia.
“Regular practice of physical exercise is mandatory for people with heart failure with adequate clinical control,” says Negrão, director of InCor’s Cardiovascular Rehabilitation and Exercise Physiology Unit. Since the late 1990s he and his team have been demonstrating that exercise helps stabilize – and often reverse – the changes that heart failure causes in the body, working in a complementary way to medications.
In nearly 20 years, her group’s work, in parallel to that of teams in Europe and the United States, has identified some of the changes in exercise-induced biochemical, cellular and tissue levels. These alterations rebalance the functioning of the muscular, vascular and endocrine systems and help explain how regular physical exercise improves the well-being of those with heart failure.
The evidence accumulated during this period led to physical exercise being incorporated into the strategies for the treatment of heart failure recommended by the Brazilian Society of Cardiology (SBC), the American College of Cardiology and the American College of Sports Medicine. “Until the 1990s, there were doubts about the benefits of exercise and resting was recommended,” says Dirceu Rodrigues de Almeida, president of the Heart Failure Department at SBC and responsible for the Division of Heart Failure and Cardiac Transplantation at the Federal University of São Paulo (Unifesp). Since then, a lot of that has changed. “Even in the 1990s, evidence began to emerge that physical exercise increased the patients’ well-being and in the following decade it was understood how he minimized and, eventually,
In the United States, where about 3% of the population has heart failure, most cases result from the infarction. In Brazil, where about 200 thousand new cases emerge every year, the pattern is somewhat different, as shown by a study conducted by SBC with 1,263 patients seen in 51 centers in the country. Here, 30% of cases are a consequence of the infarction, 20% of untreated hypertension and another 11% of Chagas’ disease, the main cause in the Central West region of the country ( see data ) .
All these situations end up injuring the heart muscle – especially the left ventricle, which drives the blood throughout the body – and compromise the pumping capacity of the heart. When the blood does not have the necessary force to penetrate the organs and muscles, compensation mechanisms are immediately triggered. The kidneys release into the blood the protein renin, which triggers a sequence of chemical reactions that end up generating the fragment of protein (peptide) angiotensin II. This peptide causes fluid retention in the body and reduces the size of blood vessels. At the same time, it stimulates the sympathetic nervous system to send commands that increase the contraction force and frequency of heart beats, and further reduce the caliber of vessels in less vital organs. It is an adaptive mechanism,
For some time this effect is good and even desirable because it partially compensates for the lack of heart strength. It ensures the supply of blood and nutrients to the muscles of those who climb a flight of stairs or perform other daily activities. “But keeping the system activated is costly for the body as well as deleterious,” explains Igor Lucas Gomes-Santos of the InCor team.
This effort causes anatomical and functional changes in the diseased heart. It becomes more spherical and pumps blood even less efficiently. Another problem is the marked loss of muscle mass (cachexia). Almost half of people with heart failure lose weight a lot because their muscles start to wither, the reason for their weakness and tiredness.
Excess angiotensin II in the circulation and the activated sympathetic nervous system, sending continuous stimulation to the blood vessels to keep the caliber reduced (vasoconstriction), end up modifying the supply of oxygen and nutrients (glucose) to the muscle cells. They bypass the problem by triggering an alternative source of energy production. They begin to consume their own proteins in a series of chemical reactions that do not rely on oxygen and lead to the accumulation of lactic acid, the same compound responsible for muscle pain after intense physical training. “These people live as if they are in constant physical exhaustion,” says cardiologist Maria Janieire Alves of Negrão’s team. “Some of them feel tired and short of breath just combing their hair,” adds Lígia.
It’s not just. In addition to using proteins to generate energy, the muscles present another imbalance, said in 2012 the team of researcher Patricia Chakur Brum, collaborator of Negrao. In her laboratory at the School of Physical Education and Sports of USP, she and researchers Aline Villa Nova Bacurau and Telma Cunha analyzed the functioning of skeletal muscle cells of rodents and humans with heart failure and verified that, in both cases, these cells degrading rather than synthesizing proteins, leading to muscle atrophy. Investigating further, Patricia observed an increase in inflammation and the production of reactive oxygen species, molecules that damage muscle proteins. A quality control system identifies defective proteins and routes them to a disassembly line,
Also in 2012, Júlio Cesar Ferreira, a former doctoral student from Patrícia and now a professor at the Institute of Biomedical Sciences at USP, also found that there were problems with the quality control of heart muscle proteins. By analyzing rodent and human heart cells operated on to replace heart valves, he found that the proteins produced by them were of poorer quality and compromised the organ’s contraction capacity.
Patricia and two researchers guided by her doctorate – Alessandra Medeiros, Unifesp in Baixada Santista, and Natale Rolim, from the Norwegian University of Science and Technology – demonstrated that aerobic physical exercise reversed the changes in the functioning of the heart muscle. For two months, they put insufficient rodents to run on a treadmill for an hour a day, five times a week. After the training, there was improvement in the quality control in the proteins of the heart cells, which started to contract better. In the skeletal muscles, protein degradation decreased. “Exercise improves physical fitness by improving the functioning of the skeletal and cardiac muscles,” says Patricia.
The regular practice of physical exercise also undoes the imbalance caused by angiotensin II in muscles. Trained rodents produce in their muscle cells compounds that transform angiotensin II into a smaller molecule: angiotensin 1-7. This version of angiotensin causes blood vessels to dilate and reduces cardiac remodeling. “The effects of exercise are complementary to those of drugs, which can not, for example, completely inhibit or permanently inhibit the action of angiotensin II,” says Gomes-Santos.
Exercise also restores blood flow in the muscles by reducing the activity of the sympathetic nervous system. In a study of 26 people with heart failure, Lígia compared the sympathetic nervous system functioning of 13 who trained one hour a day three times a week for four months with 13 others who had only been given a recommendation to maintain their lifestyle. She found that the exercise restored the functioning of cells that detect movement (mechanical receptors) and chemical compounds (chemical receptors) located in the musculature and near the blood vessels. These receptors control the activation of the sympathetic nervous system during muscle contractions and are dysregulated in heart failure. As a result of the training, people’s hearts beat faster and their breathing was less breathy during physical exertion. “Exercise seems to normalize everything that is changed,” says Gomes-Santos.
Despite good evidence, regular physical exercise is still far from being part of the lives of those with heart failure, according to SBC’s Dirceu de Almeida. Three reasons contribute to this: many doctors are still unaware of the benefits of exercise and have the patient rest; lack of cardiovascular rehabilitation centers in Brazilian hospitals; and patients are not aware of the severity of the disease.
“Before beta-blockers were used to treat heart failure, which reduced sympathetic nervous system activity, the mean life expectancy was one year after diagnosis; today, these people live up to 10 years, “says Maria Janieire. “The challenge is with training to improve their quality of life and reduce cardiac decompensation.” She followed a group of people with advanced heart failure who had been active for a year and then were given guidance to stay active. Only 40% continued to exercise. “In the group that trained, 10% died,” he says. In what did not exercise, the mortality was 50%.