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NEWS
INDEX
Archives
2007
July
Research
suggests fitness may reduce inflammation
Melissa
Mitchell, News Editor
217-333-5491; melissa@uiuc.edu
Released
7/5/07
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Click
photo to enlarge |
Photo
by L. Brian Stauffer |
| Jeffrey A. Woods, professor of kinesiology and community health, and Victoria J. Vieira, a predoctoral fellow in kinesiology and community health and in nutritional sciences, are co-authors of a new study. Their research may help explain some of the underlying biological mechanisms that take place as a result of regular exercise. |
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CHAMPAIGN, Ill. —
Although a number of studies have suggested that regular exercise reduces
inflammation – a condition that is predictive of cardiovascular
and other diseases, such as diabetes – it’s still not clear
whether there is a definitive link. And if such a link exists, the nature
of the relationship is by no means fully understood.
A recent study by kinesiology and community health researchers at the
University of Illinois provides new evidence that may help explain some
of the underlying biological mechanisms that take place as the result
of regular exercise. According to the researchers, that knowledge could
potentially lead to a better understanding of the relationship between
exercise and inflammation.
The objective of their research was to examine the independent effect
of parasympathetic tone – in this case, determined by assessing
heart-rate recovery after exercise – on circulating levels of
C-reactive protein (CRP). Parasympathetic tone and its inverse function
– sympathetic tone – are components of the autonomic nervous
system. CRP, which is secreted by the liver, circulates in the bloodstream
and is a biomarker for inflammation in the body.
“The sympathetic nervous system speeds things up, and the parasympathetic
slows things down,” said Victoria J. Vieira, a predoctoral fellow
in kinesiology and community health
and in nutritional sciences,
and the primary author and designer of the study, published in a recent
issue of the Journal of the American Geriatrics Society. “So when
you’re exercising, your sympathetic nervous system will be on,
increasing your heart rate, your respiration, etc. Once you stop, your
body always tries to get back to homeostasis. So the parasympathetic
nervous system kicks in to get everything back down to baseline levels.”
Co-author and kinesiology and community health professor Jeffrey A.
Woods said cardiologists are already routinely gauging CRP levels in
much the same way they look at lipids panels to assess cholesterol levels.
“Certainly, that’s being done in the cardiovascular disease
realm, but I think (it may be effectively used as a monitor) for other
diseases, such as Alzheimer’s, diabetes and metabolic syndrome,”
he said.
Woods said the main question motivating the current research was, “What
factors are related to CRP in the elderly?”
“We’ve known that as people age, their CRP levels go up,”
Vieira said. “That’s one of the reasons why older individuals
are more prone to develop inflammation-related diseases such as diabetes
and heart disease. So we just wanted to look at what’s predicting
those levels of CRP in an average older population that is relatively
healthy.”
Perhaps the most notable result of the study, according to the researchers,
relates to heart-rate recovery following exercise.
“The quicker the individuals were able to get back to their resting
heart rate after a strenuous exercise test was inversely related to
their CRP,” Vieira said. “In other words, individuals who
had better parasympathetic tone had lower levels of inflammation.
“And the reason we’re excited about this is that exercise
is a great way to improve parasympathetic tone. When you exercise –
that is the sympathetic/parasympathetic communication – your sympathetic
goes up, and when you stop exercising, your parasympathetic kicks in
to bring you back to normal. An untrained person will take a while to
get their heart rate back down to resting. A trained person’s
heart rate will come back down very quickly.”
The cross-sectional study focused on baseline test results from 132
sedentary, independently living individuals aged 60 to 83 (47 males;
85 females) who had been recruited to participate in the Immune Function
Intervention Trial (ImFIT), a randomized longitudinal trial designed
by Woods and funded by the National Institute on Aging to examine the
relationship between exercise and immune function.
Participants included only individuals who did not take medications
that included corticosteroids, which could interfere with immune measurements.
Smokers and/or those with severe arthritis, a history of cancer or inflammatory
disease, chronic obstructive pulmonary disorder, uncontrolled diabetes
mellitus, congestive heart failure, recent illness or vaccination, or
a positive stress test were excluded.
The physical fitness of subjects was assessed through a battery of tests
that measured such variables as fatigue, blood pressure, oxygen intake
and carbon dioxide elimination and heart-rate recovery in conjunction
with exercise on a walking treadmill. Tests also were administered to
determine the subjects’ levels of physical activity, physical
fitness, emotional stress and body composition (bone density and body
fat). Blood samples also were drawn to measure CRP levels.
“The major criterion we were looking at was their fitness level,”
Vieira said. “A strength of our study is that we have very good
data on their fitness levels.”
And while other studies have explored the relationship between exercise
and inflammation, another unique aspect of the U. of I. research, Vieira
said, is that “no other studies have adjusted for fitness and
body fat percentages simultaneously to really get at that question,
‘Is exercise independently reducing CRP levels, or is it modulated
through a decrease in adiposity (body fat)?’ ”
Because the
study was cross-sectional – meaning the researchers essentially
took a snapshot of the participants’ reactions and measurements
at a single, fixed point only – Vieira said it was important to
note that “we can’t say anything about cause and effect
relationships.”
However, Woods said, “it gives you some idea of what factors are
related, and then you test those in a more rigorous manner.”
Vieira said the research “certainly suggests that fitness may
be associated with a decrease in inflammation even independent of body
fat and several things, and the mechanism may involve a parasympathetic
anti-inflammatory reflex.”
“We know inflammation is bad. We know it increases as we age,
with stress and other things,” she said. “So if we can decrease
that to protect ourselves somehow by just adopting a physically active
lifestyle, that’s definitely an advantage.”
And while the study confirms the conclusions of previous research by
others indicating that high body fat is related to high inflammation
and high fitness to low inflammation, “the unique part of this
paper is that controlling for those, we also show that high parasympathetic
tone is related to low inflammation,” Woods said.
“And it’s even independent of their fitness level,”
Vieira interjected.
“Fitness, fatness and parasympathetic tone appear to be important,”
Woods said, summing up the findings. “And at least according to
our results, parasympathetic tone might even be more important than
those other factors.”
Co-authors with Vieira and Woods of the study are U. of I. kinesiology
and community health professors Ellen Evans and Edward McAuley, and
graduate student Rudy J. Valentine.
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