Anesthesia & Analgesia: Official Journal of the
International Anesthesia Research
Society
The underlying mechanism of exercise on the development of
diabetes-associated neuropathic pain is not well understood. Forced
exercise markedly delays the progression of tactile
hypersensitivity, but not thermal hyperalgesia. Study found
progressive exercise training markedly decreases
diabetes-associated neuropathic pain, including thermal
hyperalgesia and mechanical allodynia. Full results of this study
can be found in the February issue of Anesthesia
& Analgesia.,
official journal of the International Anesthesia Research Society
(IARS).
The
observations add to previous studies suggesting that "progressive
exercise training markedly decreased diabetes associated
neuropathic pain," write Yu-Wen Chen, PhD, of China Medical
University, Taichung, Taiwan, and colleagues. The link to Hsp72
offers a clue as to how exercise can prevent or slow the
development of neuropathy—a major complication of
diabetes.
Exercise
Reduces Diabetic Nerve Pain in Rats
Neuropathic
pain is a common and difficult-to-treat type of pain related to
nerve damage—most commonly caused by diabetes. Affecting about half
of patients with diabetes, diabetic neuropathy causes symptoms such
as numbness, tingling, or pain in the arms and legs.
Dr Chen
and colleagues examined the effects of exercise on neuropathy
caused by chemically-induced diabetes in rats. For a few weeks
after induction of diabetes, some animals were assigned to a
progressive treadmill exercise program.
Within
two weeks, the diabetic rats that did not exercise showed signs of
diabetic neuropathy, based on observable pain behaviors. These
included abnormal responses to temperature and pressure (thermal
and tactile hypersensitivity)—both characteristic of neuropathic
pain.
"In
contrast, diabetic rats undergoing exercise demonstrated delayed
progress of tactile and thermal hypersensitivity," Dr Chen and
colleagues write. The reduction in painful diabetic neuropathy was
associated with lesser increases in blood glucose levels after
induction of diabetes.
Previous
studies have suggested that neuropathic pain may be related to
expression of certain inflammation-promoting cytokines—such as
tumor necrosis factor-alpha and interleukin-6—which might be
reduced by exercise. In the new experiments, expression of
TNF-alpha and IL-6 in nerve tissue were significantly increased
after induction of diabetes, with no difference for exercising
versus non-exercising animals.
Findings
Suggest Role of Heat Shock Protein
However,
diabetic rats assigned to exercise showed increased expression of
Hsp72 in nerve tissues. Hsp 72 is one of a family of heat shock
proteins that play essential roles in protecting against cellular
damage caused by various types of stress (including heat stress).
Previous experiments have shown protective effects of Hsp72 in
other conditions, including neuropathy caused by mechanical nerve
injury.
Exercise
is commonly recommended for patients with various types of chronic
pain, and is routinely prescribed as part of treatment to control
diabetes. A growing body of evidence suggests that exercise may
also have beneficial effects in reducing painful diabetic
neuropathy.
The new
study provides support for the concept that exercise can slow the
progression of diabetic neuropathy. In the animal experiments,
exercise had short-term effects on abnormal responses to pain and
temperature, although long-term responses were unchanged.
The study
also adds new evidence that exercise may protect against diabetic
neuropathy by suppressing induced blood sugar levels while
increasing expression of Hsp72 in nerve tissues. The results may
present new opportunities for developing new, nondrug approaches
that can "delay or protect against the development of diabetic
peripheral nerve complications," Dr Chen and coauthors
conclude.
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