Stretch Therapies May Help Heal Injured Tissue
By Jennifer Nachbur Article published April 23, 2008
For ten years, Dr. Helene Langevin's translational research has focused on acupuncture and the mechanisms at work in connective tissue. Her latest publication in the Journal of Cellular Physiology reports an important finding; in a mouse model, stretching decreased the fibrotic response to injury and helped maintain functionality.
The implications of these findings, says Langevin, a research associate professor of neurology, are enormous, and have already informed the next steps of her ongoing clinical research study on low back pain, which is examining how abnormal versus normal connective tissue might relate to back pain.
According to Langevin, if you compare the connective tissue to a sandwich, the loose connective tissue in the middle is the meat and mayonnaise and the thicker connective tissue on the outside is the bread. "When there's an injury like a muscle tear or sprain, there is no movement of the outer connective tissue and the two slices of bread get stuck," explains Langevin.
Her team's hypothesis maintained that if there is an injury and inflammation, one does not move as much. Since connective tissue needs to move to be healthy, this lack of movement could lead to abnormal connective tissue and may be the underlying problem in people with low back pain.
In the Journal of Cellular Physiology study, Langevin's team aimed to find out whether treatment with acupuncture or stretching, such as yoga, massage, or physical therapy, could make abnormal connective tissue normal. To determine an answer to this question, the researchers induced a micro injury into connective tissue on only one side and then let it heal. This healing process involves the production of collagen. Their goal was to elicit only enough response to ensure functionality. There were two groups — one involving gentle stretching following the injury and another involving no stretching following the injury.
"In the stretching group, there was no statistical difference between the injured and non-injured models," said Langevin. She and her team found that in the no stretching group, there was more collagen deposition. Through imaging, the group could see where fibroblasts were making new collagen. They examined TGF-beta1, a cytokine/signaling molecule that causes fibrosis, and took tissue samples to measure how much TGF-beta1 the body was making. In the stretching group, the body made less, implying that TGF-beta1 could be an important mechanism for how all types of stretching therapies work.
"This is a well known concept in PT," says Langevin. "If you stretch connective tissue, it will remodel. An example of this response is a broken arm; when it is in the cast for a long time, one loses functionality of the limb."
The next step for Langevin, who is in the middle of conducting a low back pain study through the General Clinical Research Center, is to apply what she and her team learned in their mouse model study, and find out how the connective tissue in patients with low back pain got thicker. "Thicker connective tissue is not bad alone," explains Langevin. "It is when it is also disorganized that is a problem. Then it's not functional."
For more information about Langevin's clinical research, please contact Debbie Stevens-Tuttle at 802-656-5552.