and those in between. Red muscle, which gets its color in part from mitochondria, prevails in people who engage in endurance training, such as marathon runners. White muscle dominates in the bodies of weightlifters and sprinters — people who require short, intense bursts of energy. “Most people are in the middle and have a mix of red and white,” Lin said. When you exercise, nerves signal your muscles to contract, and the muscle needs energy. In response to a signal to lift a heavy weight, white muscles use glycogen to generate adenosine triphosphate (ATP) — energy the cells can use to complete the task. While this process, called glycolysis, can produce a lot of power for a short time, the glycogen fuel soon depletes. However, if the brain tells the muscle to run a slow and steady long-distance race, the mitochondria in red muscles primarily use fat oxidation instead of glycogen breakdown to generate ATP. The supply of energy lasts much longer but doesn’t provide the burst of strengththat comes from glycolysis. People with diabetes see whitening of the mix of muscle. “For a long time, the red-to-white shift was thought to make muscle less responsive to insulin, a hormone that lowers blood sugar,” Lin said. “But this idea is far from proven. You lose red muscle when you age or develop diabetes, but is that really the culprit?” Further studies led the team to focus on a protein called BAF60c, a sort of “zip code” mechanism that tells the cells when and how to express certain genes. The Lin team made a transgenic mouse model to increase BAF60c only in the skeletal muscle. One of the first things they noticed was that mice with more BAF60c had muscles that looked paler. Using mouse treadmills, they compared the endurance of BAF60c mice to a control group of normal mice, and found that the BAF60c transgenic mice could only run about 60 percent of the time that the control group could before tiring. “White muscle uses glycogen, and the transgenic mice depleted theirmuscles’ supplies of glycogen very quickly,” Lin said. After some follow-up experiments to figure out exactly which molecules were controlled by BAF60c, Lin and his team were confident that they had identified major players responsible for promoting white muscle formation. Now that they knew how to make more white muscle in animals, they wanted to determine whether white muscle was a deleterious or an adaptive characteristic of diabetes. The team induced obesity in mice by feeding them the “Super Size Me” diet, Lin said. On a high-fat diet, a mouse will double its body weight in two to three months. They found that obese mice with BAF60c transgene were much better at controlling blood glucose. “The results are a bit of a surprise to many people,” Lin said. “It really points to the complexity in thinking about muscle metabolism and diabetes.” In humans, resistance training promotes the growth of white muscle and helps in lowering blood glucose. If future studies in humans determine thatthe BAF60c pathway is indeed the way in which cells form white muscle and in turn optimize metabolic function, the finding could lead to researching the pathway as a drug target. “We know that this molecular pathway also works in human cells. The real challenge is to find a way to target these factors,” Lin said. Health-e-Solutions comment: So resistance training builds white muscles, which use glycogen for quick energy. Endurance training builds red muscles, which use ketones for long-lasting energy. An exercise regimen that employs both types of exercise would probably be a great way to help with blood sugar control. As one of the five pillars supporting thriving health, an integral part of the Health-e-Solutions lifestyle always includes a consistent . We want to help you realize the importance of exercise, but also the complexities involved in #BloodSugarControl with diabetes while incorporating exercise into your daily routine. Our downloadable, printable report on equips you tomake exercise with diabetes, particularly insulin-dependent diabetes, more manageable, fun, and practical. Journal Reference: Zhuo-Xian Meng, Siming Li, Lin Wang, Hwi Jin Ko, Yongjin Lee, Dae Young Jung, Mitsuharu Okutsu, Zhen Yan, Jason K Kim, Jiandie D Lin. Baf60c drives glycolytic metabolism in the muscle and improves systemic glucose homeostasis through Deptor-mediated Akt activation. Nature Medicine, 2013; DOI:
