Strenuous exercise does not suppress immune system

Agencies
April 23, 2018

Researchers have debunked a nearly four-decade-old myth that strenuous exercisesuppresses the immune system. A study, conducted by the Department for Health at the University of Bath, reinterprets scientific findings from the last few decades and emphasises that exercise – instead of dampening immunity – may instead be beneficial for immune health.

In a detailed analysis of research articles that have been published since the 1980s, this new review of the literature has reinterpreted findings, based on fundamental principles of immunology and exercise physiology, to clarify misconceptions and misinterpretations that have formed over the years.

In their study, the authors explain that, for competitors taking part in endurance sports, exercise causes immune cells to change in two ways. Initially, during exercise, the number of some immune cells in the bloodstream can increase dramatically by up to 10 times, especially ‘natural killer cells’ which deal with infections.

After exercise, some cells in the bloodstream decrease substantially – sometimes falling to levels lower than before exercise started, and this can last for several hours.

Many scientists previously interpreted this fall in immune cells after exercise to be immune-suppression. However strong evidence suggests that this does not mean that cells have been ‘lost’ or ‘destroyed’, but rather that they move to other sites in the body that are more likely to become infected, such as the lungs.

Scientists know that these cells are not ‘destroyed’ for three main reasons. First, most evidence shows that cells return to normal levels within several hours, which is far too quick for them be ‘replaced’ with new cells. Second, studies in humans have shown that these cells have the ability to leave the bloodstream and travel to other body sites.

Third, studies with laboratory animals have shown by labelling immune cells, that following exercise, these labelled cells accumulate in the lungs, and other places, because they go there to look for infections.

The authors, therefore, suggest that low numbers of immune cells in the bloodstream in the hours after exercise, far from being a sign of immune-suppression, are in fact a signal that these cells, primed by exercise, are working in other parts of the body.

Dr John Campbell from the University’s Department for Health explained: “It is increasingly clear that changes happening to your immune system after a strenuous bout of exercise do not leave your body immune-suppressed. In fact, evidence now suggests that your immune system is boosted after exercise – for example we know that exercise can improve your immune response to a flu jab.”

Co-author, Dr James Turner added: “Given the important role exercise has for reducing the risk of cardiovascular disease, cancer and type II diabetes, the findings from our analysis emphasise that people should not be put off exercise for fear that it will dampen their immune system. Clearly, the benefits of exercise, including endurance sports, outweigh any negative effects which people may perceive.”

The authors suggest that although a strenuous exercise bout itself will not increase the likelihood of catching an infection, other factors might.

First, attending any event where there is a large gathering of people, increases your chance of infection. Second, public transport, particularly airline travel over long distances, where sleep is disrupted, may also increase your infection risk. Other factors, like eating an inadequate diet, getting cold and wet, and psychological stress, have all been linked to a greater chance of developing infections.

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Agencies
July 24,2020

Colorado, Jul 24: A new study has found that physical stress in one's job may be associated with faster brain ageing and poorer memory.

Aga Burzynska, an assistant professor in the Department of Human Development and Family Studies, and her research team connected occupational survey responses with brain-imaging data from 99 cognitively normal older adults, age 60 to 79. They found that those who reported high levels of physical stress in their most recent job had smaller volumes in the hippocampus and performed poorer on memory tasks. The hippocampus is the part of the brain that is critical for memory and is affected in both normal ageing and in dementia.

Their findings were published this summer in Frontiers in Human Neuroscience under the research topic 'Work and Brain Health Across the Lifespan.'

"We know that stress can accelerate physical ageing and is the risk factor for many chronic illnesses," Burzynska said. "But this is the first evidence that occupational stress can accelerate brain and cognitive ageing."

She added that it is important to understand how occupational exposures affect the ageing of our brains.

"An average American worker spends more than eight hours at work per weekday, and most people remain in the workforce for over 40 years," Burzynska said. "By pure volume, occupational exposures outweigh the time we spend on leisure social, cognitive and physical activities, which protect our ageing minds and brains."

Physical demands at work

Burzynska explained that the association between "physical stress" and brain/memory were driven by physical demands at work. These included excessive reaching, or lifting boxes onto shelves, not necessarily aerobic activity. This is important because earlier work by Burzynska and her colleagues showed that leisure aerobic exercise is beneficial for brain health and cognition, from children to very old adults. Therefore, the researchers controlled for the effects of leisure physical activity and exercise.

As expected, leisure physical activity was associated with greater hippocampal volume, but the negative association with physical demands at work persisted.

"This finding suggests that physical demands at work may have parallel yet opposing associations with brain health," Burzynska explained. "Most interventions for postponing cognitive decline focus on leisure, not on your job. It's kind of unknown territory, but maybe future research can help us make some tweaks to our work environment for long-term cognitive health."

She added that the results could have important implications for society.

"Caring for people with cognitive impairment is so costly, on economic, emotional and societal levels," Burzynska said. "If we can support brain health earlier, in middle-aged workers, it could have an enormous impact."

The researchers considered and corrected for several other factors that could be related to work environment, memory and hippocampus, such as age, gender, brain size, educational level, job title, years in the occupation and general psychological stress.

One piece of the puzzle

"The research on this topic is so fragmented," Burzynska said. "One previous study linked mid-life managerial experience with greater hippocampus volume in older age. Another showed that taxi drivers had larger hippocampi than a city's bus drivers, presumably due to the need to navigate. In our study, job complexity and psychological stress at work were not related to hippocampal volume and cognition. Clearly, our study is just one piece of the puzzle, and further research is needed."

The magnetic resonance imaging (MRI) data used for the study was collected at the University of Illinois Urbana-Champaign between 2011 and 2014.

CSU researchers now can collect MRI data with the new 3T scanner at the University's Translational Medicine Institute.

With this new capability, Burzynska, along with Michael Thomas and Lorann Stallones of CSU's Department of Psychology, is launching a new project, "Impact of Occupational Exposures and Hazards on Brain and Cognitive Health Among Aging Agricultural Workers," which will involve collecting MRI brain scans and identifying risk and protective factors that could help the agricultural community age successfully. The project recently obtained funding as an Emerging Issues Short-Term Project from the High Plains Intermountain Center for Agricultural Health and Safety.

The Department of Human Development and Family Studies is part of CSU's College of Health and Human Sciences.

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News Network
February 21,2020

Washington, Feb 21: The fat around arteries may play an important role in keeping the blood vessels healthy, according to a study in rats that may affect how researchers test for treatments related to plaque buildup, as seen in conditions leading to heart attack.

The study, published in the journal Scientific Reports, noted that the fat, known as perivascular adipose tissue, or PVAT, helps arteries let go of muscular tension while under constant strain.

According to the researchers, including Stephanie W. Watts from the Michigan State University in the US, this feature is similar to how the bladder expands to accommodate more liquid, while at the same time keeping it from spilling out.

"In our study, PVAT reduced the tension that blood vessels experience when stretched," Watts said.

"And that's a good thing, because the vessel then expends less energy. It's not under as much stress," she added.

According to Watts and her team, PVAT has largely been ignored by researchers believing its main job was to store lipids and do little more.

Until now, she said, scientists only divided blood vessels into three parts, the innermost layer called the tunica intima, the middle layer called the tunica media, and the outermost layer called the tunica adventitia.

Watts believes PVAT is the fourth layer, which others have called tunica adiposa.

Tunica, she said, meant a membranous sheath enveloping or lining an organ, and adiposa is a synonym for fat.

"For years, we ignored this layer -- in the lab it was thrown out. In the clinic it wasn't imaged. But now we're discovering it may be integral to our blood vessels," Watts said.

"Our finding redefines what the functional blood vessels are, and is part of what can be dysfunctional in diseases that afflict us, including hypertension. We need to pay attention to this layer of a blood vessel because it does far more than we originally thought," she added.

Earlier studies, Watts said, had shown that PVAT plays a role in the functioning of blood vessels, finding that it secretes substances that can cause blood vessels to relax as well as substances that can cause it to contract.

In the current study, the researchers decided to test whether PVAT provides a structural benefit to arteries by assisting the function of stress relaxation.

They tested the thoracic aorta in rats, and found those with intact PVAT had more stress relaxation than those without.

The study revealed that the pieces of artery with surrounding fat had measurably relaxed more than those without.

Watts and her colleagues then tested other arteries, and were able to duplicate the same response.

"It's not something you see only in this particular vessel or this particular species or this particular strain. But that maybe it's a general phenomenon," she said.

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Agencies
January 12,2020

Washington D.C., Jan 12: Disruption in one night's sleep can lead to getting Alzheimer's disease, a recent study has stated.

The interruption in the sound sleep for a single night aggravates the level of tau protein in any young male's body, thus gives rise to the chances of developing the disease.

According to CNN, the report was published on Wednesday in neurology, the medical journal of the American Academy of Neurology.

"Our study focuses on the fact that even in young, healthy individuals, missing one night of sleep increases the level of tau in blood suggesting that over time, such sleep deprivation could possibly have detrimental effects," says study author Dr Jonathan Cedernaes, a neurologist at Uppsala University in Sweden.

As defined by the Alzheimer's Association, tau is the name of a protein that helps in stabilizing the internal structure of the brain's nerve cells. An abnormal build-up of tau protein in the body can end up in causing interior cells to fall apart and eventually developing Alzheimer's.

"When you get more of that deep sleep and you get the REM sleep in the normal amounts, that improves clearance of abnormal proteins which we think is good," said Mayo Clinic neurologist Dr Donn Dexter, not the study author but a fellow of the American Academy of Neurology.

Earlier studies have also shown that getting deprived of sleep can allow higher tau development and accumulation. Thus that poor sleep can hasten the development of cognitive issues.

Researchers caution that the study is small and inconclusive, and acknowledged they were not able to determine what the increased levels might mean.

"This study raises more questions than answers," agreed Dexter on a concluding note, sharing, "What this is telling us is that we have to dig more deeply. Despite something we do for a third of our lives, we know so little about sleep and we're learning every day, particularly when it comes to sleep and dementia."

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