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
April 17,2020

Washington DC, Apr 17: In recent research, scientists have linked the emotional, social and psychiatric problems in children and adolescents with higher levels of genetic vulnerability for adult depression. The study implies that the genetics passed from parents may be linked with psychiatric problems in children and adolescents and may also leading to depression in adults.

University of Queensland scientists made the finding while analysing the genetic data of more than 42,000 children and adolescents from seven cohorts across Finland, the Netherlands, Norway, Sweden and the UK.

Professor Christel Middeldorp said that researchers have also found a link with a higher genetic vulnerability for insomnia, neuroticism and body mass index.

"By contrast, study participants with higher genetic scores for educational attainment and emotional well-being were found to have reduced childhood problems," Professor Middeldorp said.

"We calculated a person's level of genetic vulnerability by adding up the number of risk genes they had for a specific disorder or trait and then made adjustments based on the level of importance of each gene We found the relationship was mostly similar across ages," Middeldorp added.

The results indicate there are shared genetic factors that affect a range of psychiatric and related traits across a person's lifespan.

Middeldorp said that around 50 per cent of children and adolescents with psychiatric problems, such as attention deficit hyperactivity disorder (ADHD), continue to experience mental disorders as adults, and are at risk of disengaging with their school community among other social and emotional problems.

"Our findings are important as they suggest this continuity between childhood and adult traits is partly explained by genetic risk," the Professor said.

"Individuals at risk of being affected should be the focus of attention and targeted treatment," Middeldorp continued.

"Although the genetic vulnerability is not accurate enough at this stage to make individual predictions about how a person's symptoms will develop over time, it may become so in the future, in combination with other risk factors. And, this may support precision medicine by providing targeted treatments to children at the highest risk of persistent emotional and social problems," Middeldorp added.

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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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