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Researchers determine how much oxygen the brain needs

The brain has a high energy demand and reacts very sensitively to oxygen deficiency. LMU neurobiologists have now succeeded for the first time in directly correlating oxygen consumption with the activity of certain nerve cells.

The brain requires a disproportionate amount of energy compared to its body mass. This energy is mainly generated by aerobic metabolic processes that consume considerable amounts of oxygen. Therefore, the oxygen concentrations in the brain are an important parameter that influences the function of nerve cells and glial cells. However, how much oxygen is consumed in the brain and how this is related to neuronal activity was so far largely unknown. LMU neurobiologists Hans Straka, Suzan Özugur, and Lars Kunz have now succeeded for the first time in directly measuring this in the intact brain and correlating it with nerve cell activity. The scientists report on their results in the journal BMC Biology.

In an already established animal model—tadpoles of the clawed frog Xenopus laevis—the scientists used electrochemical sensors to determine the concentration of oxygen in the brain and in one of the brain ventricles. They were able to specifically control the amount of oxygen available to the brain as well as inhibit nerve cell activity with the help of pharmacological substances. Using the example of nerve cells that control eye movements, the scientists succeeded in directly recording the relationship between oxygen consumption and nerve cell activity.

“We have found that the brain is anoxic in a normal air-saturated environment, which means that no oxygen can be measured,” says Straka. The complete oxygen was therefore immediately used by the cells to synthesize energy-rich substances. If more than twice the atmospheric oxygen concentration was available, the energy metabolism was saturated and oxygen was abundantly present in the brain.

“We were also able to show that during normal operation only about 50 percent of the oxygen is used for nerve cell activity,” says Straka. “So the other 50 percent are required for glial cells and for maintaining the basic metabolic rate of nerve cells. However, nerve cells with increased activity consume more oxygen.”

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Fat check: Researchers find explanation for stress’ damage in brown fat

In their search for what triggers the damaging side-effects caused by acute psychological stress, Yale researchers found an answer by doing a fat check.

In the face of psychological stress, an immune system response that can significantly worsen inflammatory responses originates in brown fat cells, the Yale team reports June 30 in the journal Cell.

Since the hormones associated with stress, cortisol and adrenaline, generally decrease inflammation, it has long puzzled researchers how stress can worsen health problems such as diabetes and autoimmune disease as well as depression and anxiety.

“In the clinic, we have all seen super-stressful events that make inflammatory disease worse, and that never made sense to us,” said Dr. Andrew Wang, assistant professor of internal medicine and immunobiology, and corresponding author of the study.

Cortisol and adrenaline, hormones released in the classic “flight or fight” stress response, generally suppress the immune system, not activate it. These hormones also initiate a massive metabolic mobilization that provides fuel to the body as it addresses threats.

The scientists found that it was an immune system cell—the cytokine interleukin-6 (IL-6)—that triggers inflammation in times of stress. IL-6 has also been shown to play a role in autoimmune diseases, cancer, obesity, diabetes, depression and anxiety.

Wang and colleagues began to study the role of IL-6 in stress after a simple observation: When the researchers drew blood from mice, a very stressful procedure, the blood showed elevated levels of the cytokine.

In a series of experiments in mice, designed by Hua Qing and Reina Desrouleaux in Wang’s lab, the researchers found that IL-6, which is usually secreted in response to infections, was induced by stress alone and worsened inflammatory responses in the stressed animals.

And to their surprise, they found that in times of stress IL-6 was secreted in brown fat cells, which are most known for their roles in regulating metabolism and body temperature. When signals from the brain to brown fat cells are blocked, stressful events no longer worsened inflammatory responses.

“This was a completely unexpected finding,” said Qing, a postdoctoral associate at Yale School of Medicine.

The researchers reasoned that IL-6 must play another role in the “fight or flight” response besides triggering inflammation. They learned it also helps prepare the body to increase production of glucose in anticipation of threats. The brown fat cell response causes IL-6 levels to peak well after the metabolic production of glucose and the release of cortisol and adrenaline. This may explain why stress can trigger inflammation even while immune-suppressing hormones are being released, the researchers said.

Blocking IL-6 production not only protected stressed mice from inflammation, it also made them less agitated when placed in a stressful environment.

Wang and his team also suspect IL-6 may play a role in mental health disorders such as depression and anxiety. Wang observes that many of symptoms of depression, such as loss of appetite and sex drive, mimic those caused by infectious diseases such as the flu—so-called “sickness behaviors”—that can be triggered by IL-6.

Existing drugs designed to treat autoimmune diseases such as rheumatoid arthritis block the activity of IL-6. Preliminary findings suggest these drugs may help alleviate symptoms of depression, the authors note. There is also preliminary evidence that IL-6 may also play a role in diabetes and obesity as well.

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Researchers identify multiple molecules that shut down SARS-Cov-2 polymerase reaction

SARS-CoV-2, the coronavirus causing the global COVID-19 pandemic, uses a protein called polymerase to replicate its genome inside infected human cells. Terminating the polymerase reaction will stop the growth of the coronavirus, leading to its eradication by the human host’s immune system.

Researchers at Columbia Engineering and the University of Wisconsin-Madison have identified a library of molecules that shut down the SARS-CoV-2 polymerase reaction, a key step that establishes the potential of these molecules as lead compounds to be further modified for the development of COVID-19 therapeutics. Five of these molecules are already FDA-approved for use in the treatment of other viral infections including HIV/AIDS, cytomegalovirus, and hepatitis B. The new study was published on June 18, 2020, in Antiviral Research.

The Columbia team initially reasoned that the active triphosphate of the hepatitis C drug sofosbuvir and its derivative could act as a potential inhibitor of the SARS-CoV-2 polymerase based on the analysis of their molecular properties and the replication requirements of both the hepatitis C virus and coronaviruses. Led by Jingyue Ju, Samuel Ruben-Peter G. Viele Professor of Engineering, professor of chemical engineering and pharmacology, and director of the Center for Genome Technology & Biomolecular Engineering at Columbia University, they then collaborated with Robert N. Kirchdoerfer, assistant professor of biochemistry and an expert in the study of coronavirus polymerases at University of Wisconsin-Madison’s Institute for Molecular Virology and the department of biochemistry.

In an earlier set of experiments testing the properties of the polymerase of the coronavirus that causes SARS, the researchers found that the triphosphate of sofosbuvir was able to terminate the virus polymerase reaction. They then demonstrated that sofosbuvir and four other nucleotide analogs (the active triphosphate forms of the HIV inhibitors Alovudine, Zidovudine, Tenofovir alafenamide, and Emtricitabine) also inhibited the SARS-CoV-2 polymerase with different levels of efficiency.

Using the molecular insight gained in these investigations, the team devised a strategy to select 11 nucleotide analog molecules with a variety of structural and chemical features as potential inhibitors of the polymerases of SARS-CoV and SARS-CoV-2. While all 11 molecules tested displayed incorporation, six exhibited immediate termination of the polymerase reaction, two showed delayed termination, and three did not terminate the polymerase reaction.

Prodrug medications of five of these nucleotide analogs (Cidofovir, Abacavir, Valganciclovir/Ganciclovir, Stavudine, and Entecavir) that terminate the SARS-CoV-2 polymerase reaction are FDA-approved for the treatment of other viral infections and their safety profiles are well established. Once the potency of the drugs to inhibit viral replication in cell culture is demonstrated in future investigations, then the candidate molecules and their modified forms may be evaluated for the development of potential COVID-19 therapies.

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Researchers find on-off switch for inflammation related to overeating

Researchers at Yale have identified a molecule that plays a key role in the body’s inflammatory response to overeating, which can lead to obesity, diabetes, and other metabolic diseases. The finding suggests that the molecule could be a promising therapeutic target to control this inflammation and keep metabolic diseases in check.

The study appears on June 29 in the Proceedings of the National Academy of Sciences.

When a person overeats, the body stores excess calories in the form of fat in the adipose tissue, or body fat, said lead author Xiaoyong Yang of Yale School of Medicine. As the amount of calories consumed continues to increase, this leads to inflammation in adipose tissue and the release of fatty acids into other tissues, including the liver and muscles.

“This is dangerous,” Yang said, “and leads to metabolic disorders like diabetes.”

Researchers were aware that overeating led to inflammation and metabolic diseases, but until now, they did not know the precise way that the body’s immune cells, such as macrophages—which react to excess calorie consumption—contributed to this process. The new research by Yang and team zeroed in on a pathway called O-GIcNAc signaling, which activates when a person overeats, instructing the cells to limit inflammation.

Inflammation happens when the body’s immune system reacts to injury or threat, and involves increased blood flow, capillary dilation, and an influx of white blood cells.

“The body is smart,” said Yang, associate professor of comparative medicine and of cellular & molecular physiology. “It tries to protect against inflammation when fat builds up in the body. We discovered a key pathway that quenches inflammation caused by overnutrition.”

In particular, the researchers found that OGT (O-GIcNAc transferase), an enzyme that activates GIcNAc signaling, was responsible for activating the body’s pro-inflammatory response by turning on or off a specific signaling pathway in macrophages.

“The macrophage can be a good guy or a bad guy,” Yang said. “It becomes a bad guy in overnutrition, secreting a lot of inflammatory factors. In other contexts, it’s a good guy and has an anti-inflammatory effect. We found out that OGT tries to stop the macrophage from becoming a bad guy—to stop the pro-inflammatory response.”

Their finding suggests that OGT could be a target for new therapies to suppress inflammation and improve health.

The study also sheds light on the workings of glutamine and glucosamine, nutritional supplements recommended by doctors for arthritis and inflammation of the joints, Yang said. While researchers have known that these supplements promote O-GlcNAc signaling and reduce inflammation, they did not know how this process worked.

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Researchers uncover effects of negative stereotype exposure on the brain

The recent killings of unarmed individuals such as George Floyd, Breonna Taylor, Ahmaud Arbery and Tony McDade have sparked a national conversation about the treatment of Black people—and other minorities—in the United States.

“What we’re seeing today is a close examination of the hardships and indignities that people have faced for a very long time because of their race and ethnicity,” said Kyle Ratner, an assistant professor of psychological and brain sciences at UC Santa Barbara. As a social psychologist, he is interested in how social and biological processes give rise to intergroup bias and feelings of stigmatization.

According to Ratner, “It is clear that people who belong to historically marginalized groups in the United States contend with burdensome stressors on top of the everyday stressors that members of non-disadvantaged groups experience. For instance, there is the trauma of overt racism, stigmatizing portrayals in the media and popular culture, and systemic discrimination that leads to disadvantages in many domains of life, from employment and education to healthcare and housing to the legal system.”

Concerned by negative rhetoric directed at Latinx individuals, Ratner and his lab have investigated how negative stereotype exposure experienced by Mexican-American students can influence the way their brains process information.

In a recent paper published in the journal Social Cognitive and Affective Neuroscience, the research team focuses on how negative stereotype exposure affects responses to monetary incentives. Their finding: The brains of Mexican-American students exposed to negative stereotypes anticipate rewards and punishments differently versus those who were not so exposed. The discovery, he said, is the first step in a series of studies that could help researchers understand neural pathways through which stigma can have detrimental effects on psychological and physical health.

‘I’m so tired of this’

Much existing research has focused on how experiencing stigma and discrimination triggers anger, racing thoughts and a state of high arousal. Although Ratner believes this is a reaction that people experience in some contexts, his recent work focuses on the psychological fatigue of hearing your group disparaged. “It’s this feeling of ‘oh, not again,’ or ‘I’m so tired of this,'” he said, describing a couple of reactions to the stress of managing self-definition in the face of negative stereotypes.

While noticing several years ago that experiencing stigma can produce this sense of withdrawal and resignation, Ratner was reminded of work he conducted earlier in his career relating stress to depressive symptoms.

“In work I was involved in over a decade ago, we showed that life stress can be associated with anhedonia, which is a blunted sensitivity to positive and rewarding information, such as winning money,” he said. “If you’re not sensitive to the rewarding things in life, you’re basically left being sensitive to all the frustrating things in life, without that positive buffer. And that’s one route to depression.”

Given that experiencing stigma can be conceptualized as a social stressor, Ratner wanted to investigate whether negative stereotype exposure might also relate to sensitivity to reward.

Reward Processing in the Brain

Ratner and his colleagues focused on the nucleus accumbens, a sub-cortical brain region that plays a central role in anticipating pleasure—the “wanting” stage of reward processing that motivates behaviors.

Using functional MRI to measure brain activity, the researchers asked Mexican-American UCSB students to view sets of video clips in rapid succession and then gave these students the opportunity to win money or avoiding losing money.

In the control group, the viewers were shown news and documentary clips of social problems in the United States that were relevant to the country in general—childhood obesity, teen pregnancy, gang violence and low high school graduation numbers.

In the stigmatized group, subjects were shown news and documentary clips covering the same four domains, but that singled out the Latinx community as the group specifically at risk for these problems.

“These videos were not overtly racist,” Ratner said of the stigmatizing clips. Rather, he explained, the videos tended to spend a disproportionate amount of attention on the association between specific social issues and their effects in the Latinx community, rather than presenting them as problems of American society as a whole. The clips were mostly from mainstream news agencies—the newscasters and narrators, he said, appeared to be “presenting facts as they understood them,” but the content of these clips reinforced negative stereotypes.

After repeated exposure to negative stereotypes, the research participants were asked to perform a Monetary Incentive Delay (MID) task, which required them to push a button whenever they saw a star on the screen. Pressing the button fast enough resulted in either winning money or avoiding losing money.

In those individuals shown the stigmatizing clips, the nucleus accumbens responded differently to waiting for the star to appear, as compared to those who viewed the control clips, a pattern that suggests that negative stereotype exposure was “spilling-over” to affect how participants were anticipating winning and losing money.

“We saw that something about watching these stigmatizing videos was later influencing the pattern of response within this brain region,” Ratner said. This suggests that the nucleus accumbens is representing the potential of winning and losing money differently in the brains of those who previously saw the stigmatizing videos than those who didn’t, he explained. The researchers also found that the group that saw the stigmatizing videos reported lower levels of arousal right before starting the MID task, consistent with stigmatizing experiences having a demotivating effect.

“The nucleus accumbens is very important for motivated behavior, and sparks of motivation are important for many aspects for everyday life,” Ratner said. A loss of motivation, he continued, is often experienced by those who perceive their situation as out of their control.

One reason negative stereotypes in the media and popular culture are so problematic is they make people feel stigmatized even when they are not personally targeted in their daily life by bigoted people, he explained. “It becomes something you can’t escape—similar to other stressors that are out of people’s control and have been shown to cause anhedonia.”

Ratner is careful to point out that this study merely scratches the surface of brain processes involved in intergroup reactions such as stigma—how the brain processes social motivations is far more complex and necessitates further study.

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Researchers seeking to understand the connection between SARS-CoV-2 and a deadly immune system malfunction

The name ‘cytokine storm’ is apt: It describes a furious gale-force swarm of molecules unleashed by the body’s immune system that causes extreme inflammation, tissue damage, even death. Cytokines—from the Greek cyto for cells and kinos for movement—are important in the fight against viral infections. But they worsen those same infections in the extreme, a phenomenon that is proving lethal for older COVID-19 patients.

“The immune system is a double-edged sword,” says Andrea Cox, a professor of medicine in the Johns Hopkins School of Medicine. “There’s a critical role for it in an antiviral response. But it also can be pro-inflammatory in a pathological way. It’s like trying to kill a bug with a hammer. You can put a hole in the wall while you’re trying to smush the bug.”

Cox is among several Hopkins scientists studying cytokine storms and their relationship to COVID-19. Her lab, which includes infectious disease postdoctoral fellow Andrew Karaba, is analyzing blood and lung tissue samples from infected patients to identify specific cytokines involved. They want to know why they turn dangerous, especially among the elderly.

Other researchers are testing drugs they hope will prevent the onset of cytokine storms, or stop them after they begin. The goal, ultimately, is to save those at greatest risk from this potentially deadly complication of SARS-CoV-2 infection.

Cox and her team are studying a range of illness, “looking for things found in very severe illness, and in those who are not very severely ill, to understand why some are getting sick and others not,” she says. “We want to narrow it down to the smallest number of things consistent among the groups. Cytokines are produced as part of an innate sensing pathway. If we can identify that overly active pathway, we can find ways to block it.”

There are several dozen cytokines—protein messengers—that affect the immune system. In some cases, they activate certain responses, while in others, they slow them down. Sometimes the system goes awry, triggering too many cytokines, too rapidly. This also occurs in auto-immune diseases, other infections, and as a side effect of certain immunotherapies.

In COVID-19, cytokine storms disproportionately strike the elderly, “for reasons that are not clear,” Cox says. “Immune system balance is regulated differently at different ages. It’s not that the immune system is weaker or stronger in older versus younger–but different. It’s possible that older people make a more damaging immune response than the young.”

Most commonly, patients seem to be holding their own against the initial SARS-CoV-2 infection before suddenly turning gravely ill. Often, the outcome is grim.

“Cytokines tell other cells to do things that in this case may enhance tissue damage and disease severity,” Cox says. “With blood vessels, for example, it can cause the vascular system to leak fluids and blood, and make it harder for oxygen to go where it’s supposed to go because there is fluid where oxygen should be, like in the lungs.”

Understanding a cytokine storm’s role in COVID-19 is a multidisciplinary effort at Hopkins, including researchers taking a new look at old drugs.

“It has been terrific to see people from all different fields [at JHU] respond,” says Russell Wesson, assistant professor of surgery in the School of Medicine, and a transplant surgeon. “People are looking at using different drugs to see their effect on COVID, and almost all of these efforts involve repurposing other drugs.”

Wesson is working with principal investigator Nada Alachkar, associate professor of medicine and medical director of the Incompatible Kidney Transplant Program, and scientists from the nephrology and infectious diseases groups in a multicenter study testing Clazakizumab, a medication that prevents organ rejection in kidney transplant recipients. It works by suppressing interleukin-6 (IL-6), an immune system cytokine found elevated in the sickest COVID-19 patients.

The clinical trial is double-blinded and placebo controlled, meaning neither the researchers nor the patients know who gets the drug or a harmless substitute. The subjects include patients who are seriously ill, including those on ventilators. “We know this drug very directly affects IL-6 and believe that neutralizing it will help stop cytokine storm, or prevent it from progressing,” Wesson says. “The study is blinded, but we have seen encouraging results, among them patients who have recovered rapidly.”

Researchers from the Kimmel Cancer Center, the divisions of rheumatology and infectious diseases, and the departments of neurology and neurosurgery, are testing another drug, Prazosin, an alpha blocker used to treat hypertension, enlarged prostate, and post-traumatic stress disorder. They think it could prevent cytokine storms by blocking a surge of molecules known as catecholamines, substances made in the brain and adrenal glands that—based on an earlier mouse study—typically precedes the onset of a cytokine storm.

The researchers first examined a national database of patients with Acute Respiratory Distress Syndrome, or ARDS, a condition characterized by fluid accumulation in the lungs, not unlike what happens with COVID-19. They found fewer deaths and less need for ventilators among those who had been taking drugs like Prazosin, leading them to speculate that the drug could similarly benefit patients with COVID-19.

“Between the preclinical data from animal models and the retrospective data from humans, we felt there was good rationale to test this concept with COVID-19,” says Chetan Bettegowda, a brain tumor specialist and professor of neurosurgery in the School of Medicine. The team, which also includes Bert Vogelstein, director of the Ludwig Center, professor of oncology and pathology, and a Howard Hughes Medical Institute investigator, and rheumatologist Maximilian Konig, a postdoctoral fellow, recently began a controlled trial to see if Prazosin, given early after infection, can stave off a cytokine storm. “This is a preventive approach,” Bettegowda says. “If patients are already manifesting signs of cytokine storm, it’s unlikely to work.”

For her part, Cox has long studied infectious diseases, so she is aware of the challenges posed by a newly identified virus.

“The problem with these pandemic viruses is that no one in the world has seen anything like them,” Cox says. “There is no immunity. What’s worse, the rules for who does well and who does badly are different for this virus than for other viruses, and, right now, we don’t understand the rules at all.”

For the others, the research represents a departure, albeit a welcome one, as they are glad to be involved in the fight.

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Researchers discover algorithms and neural circuit mechanisms of escape responses

Ordered and variable animal behaviors emerge to explore and adapt to the environment. They are generally considered as the combination of a series of stereotyped motor primitives. However, how the nervous system shapes the dynamics of motor sequences remains to be solved.

In a study published in eLife, Prof. Wen Quan from School of Life Sciences, University of Science and Technology of China (USTC) of the Chinese Academy of Sciences (CAS) has proposed algorithms and circuit mechanisms for the robust and flexible motor states of nematodes during escape responses.

Prof. Wen’s group investigated nematode Caenorhabditis elegans (C. elegans) to learn about neural circuit mechanisms that generate robust and flexible the motor sequences.

C. elegans are ideal subjects for their simple yet fully functional neural system with only 302 neurons, approximately 6400 chemical synapses and 890 electrical synapses. Early in the 1980s, the coupling image of neural networks were reconstituted at the synapse scale by the electron microscope, laying a solid foundation for the research on the neural circuit. Additionally, optical manipulation and detection are easily conducted considering C. elegans’ overall transparent bodies.

Potential threats like mechanical or thermal stimuli robustly trigger escape responses comprising stereotyped motor modules including forward movement, backward movement and turning movement. However, the sequence and timing of actions of every module vary from each other.

With the help of optogenetic technology, calcium image and computational models, the researchers discovered that the excitatory feedforward coupling accounts for certain motor sequences robustly triggered by stimuli, while a winner-take-all operation via mutual inhibition between motor modules realizes the flexible alteration of different motor patterns. Also, the plasticity of short-term synapses and the intrinsic noise of the nervous system play an important role in the sequence and timing of motor patterns.

Applying the coupling image of neural networks of C. elegans and molecular biological methods, the researchers further proved that electrical synapses contribute to feedforward coupling, whereas glutamatergic synapses contribute to inhibition between modules through glutamate-gated chloride expressed by downstream neurons.

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‘Stay at home but don’t stay still,’ researchers recommend

The adverse side effects of the social isolation measures implemented to combat COVID-19 include an increase in sedentary behavior and physical inactivity, which can contribute to a deterioration in cardiovascular health even in the short term. Older people and people with chronic diseases tend to be most affected.

The warning comes from a review article published in the American Journal of Physiology by researchers at the University of São Paulo’s Medical School (FM-USP) in Brazil. According to the authors, the slogan “Stay at home” broadcast by governments and chief medical officers is unquestionably valid under the present circumstances but should be coupled with another: “Don’t stay still.”

“You need at least 150 minutes of moderate to vigorous physical activity per week to be considered active by the World Health Organization [WHO] and medical associations. Gyms, fitness centers and sports facilities will be open to a limited extent in the months ahead, even after confinement and quarantine measures are lifted. Physical activity in the home is a worthwhile alternative,” said Tiago Peçanha, first author of the article. Peçanha has a postdoctoral research scholarship from FAPESP.

The article reviews the scientific literature to compile evidence for the effects of short periods of physical inactivity on the cardiovascular system. Some of the studies cited show that between one and four weeks of bed rest can lead to cardiac atrophy and significant narrowing of peripheral blood vessels. Peçanha stressed that this is an aggressive model and does not reflect what happens during social confinement or quarantine. “However, other experiments reviewed in the article are a good match,” he said.

In one of these experiments, volunteers were asked to reduce their physical activity so that they took less than 5,000 steps in a week instead of more than 10,000 steps as usual. At the end of the period, the researchers observed a reduction in the diameter of the brachial artery (the main blood vessel in the arm), loss of blood vessel elasticity, and damage to the endothelium (the inner cell lining of all veins and arteries).

In other experiments, volunteers stayed seated for periods varying between three and six hours. This amount of inactivity was sufficient to cause vascular alterations, an increase in inflammation markers, and a rise in postprandial blood sugar.

“This first group of alterations observed in the studies have to do with functionality. In healthy volunteers, the heart and blood vessels function differently in response to inactivity,” Peçanha said. “In an extended period of inactivity, the alterations tend to become structural and are harder to reverse.”

Prolonged inactivity is particularly harmful for people with cardiovascular diseases and other chronic health problems, such as diabetes, hypertension, obesity or cancer. In older people, it can also aggravate loss of muscle mass (sarcopenia) and increase the risk of falls, fractures and other injuries. The FM-USP group recently published an article on this topic in the Journal of the American Geriatrics Society.

“These groups that are more vulnerable to the effects of inactivity are also high-risk groups for COVID-19 and will be staying at home for months. Ideally, they should find ways of staying active, such as doing housework, going up and down stairs, taking short walks, playing with children, or dancing in the living room,” Peçanha said. “The scientific evidence shows that getting exercise in the home is safe and effectively helps control blood pressure, reduces blood lipids, and improves body composition, quality of life and sleep.”

For high-risk groups, especially people who are not habitually active, Peçanha recommends supervision by health professionals, which can be performed remotely using cameras, smartphone apps and other electronic devices. “Studies show that an online environment favoring social support and interaction tends to motivate people to keep fit,” he said.

Fresh evidence

Data published in recent months by companies that sell smartwatches and exercise tracking apps suggest that the number of daily steps taken by users since the start of confinement has fallen.

“For example, Fitbit’s blog presents data for 30 million users showing a 7%-38% decline in daily step counts during the week ending March 22,” Peçanha said. “In Brazil, an internet survey by Raphael Ritti-Dias involving over 2,000 volunteers showed more than 60% saying they reduced their physical activity after the start of confinement or lockdown. All this evidence is preliminary, but studies are in progress to measure the effects on health of physical inactivity during social restrictions.”

One of these studies is being conducted at FM-USP as part of the Thematic Project “Reducing sedentary time in clinical populations: the Take A Stand For Health Study”. The principal investigator is Bruno Gualano, a co-author of the American Journal of Physiology article.

“We’re working with clinical groups associated with the Thematic Project, such as women with rheumatoid arthritis, patients submitted to bariatric surgery, and elderly subjects with mild cognitive impairment. They’re encouraged to take more exercise in the form of daily activities such as walking the dog or getting off the bus two stops prior to their destination. The effects on their health are being studied,” Peçanha said.

Since the implementation of social restrictions to contain the pandemic, the researchers have monitored a group of female rheumatoid arthritis patients more closely to measure their level of physical activity and compare it with the pre-pandemic level. “The patients are wearing accelerometers [electronic devices that measure physical activity and distance covered in a set period] at home,” Peçanha said. “We call them frequently to ask about quality of life and diet. A few researchers visit them at home to measure body weight, body composition and blood pressure and to take blood samples.”

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