Regular exercise reduces the development of painful diabetic neuropathy in animals—apparently related to increased expression of a protective substance called “heat shock protein” 72 (Hsp72), reports an experimental study 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.