During brief high-intensity exercise, your muscles rely on their glycogen stores and to a lesser extent blood glucose, but relatively little fat. Shorter, intense activities such as sprinting or power lifting are mostly anaerobic activities that cause your muscles to rapidly use high-energy phosphate compounds (ATP and more), and, if they last longer than ten seconds, glycogen stores in muscles. High-intensity exercise causes a strong response of your nervous system (the one that controls “flight or fight” responses, the sympathetic nervous system), which can be further worsened by the mental stress of competition, resulting in the release of adrenaline and other hormones that raise your blood glucose levels. Such activities generally cause a transient rise in your blood sugars that may require additional insulin to correct. Uncorrected, blood glucose levels may remain elevated for two to three hours afterwards, even if normal prior to exercise. Athletes, however, must guard against hypoglycemia resulting from ongoing muscle glycogen replacement in their muscles post-exercise, which is largely insulin independent until glycogen levels increase, particularly during the “window of opportunity” from 30 minutes up to two hours after physical activity.
Athletes with diabetes who train regularly, on the whole, exhibit a heightened sensitivity to insulin, which allows blood glucose to enter their muscle cells more efficiently both acutely and chronically with exercise. Acute changes likely result from heightened muscle glycogen repletion following workouts. However, one study reported that following a competitive marathon, athletes with type 1 diabetes who kept their blood sugars normal had unchanged insulin sensitivity on the morning after the event despite significant glycogen depletion. Under such conditions, it is likely that enhanced fat use following exhaustive exercise, which occurs normally even in non-diabetic individuals, combined with some degree of muscular damage to create a transient state of insulin resistance that usually resolves in a day or two.
Chronic changes in insulin sensitivity, on the other hand, are attributed to adaptive changes in your muscle tissue resulting in enhanced insulin-mediated glucose transport by insulin-sensitive glucose transporter (GLUT4) proteins and lower glucose production by the liver. Aerobic training also results in an increase in the proportion of fats used during low- or moderate-intensity activity. Using fats more effectively spares some muscle glycogen and blood glucose and allows for better control of your blood sugars during activities. These changes in fuel utilization in response to training, though, will result in a need for smaller adjustments to your carbohydrate or insulin intake to maintain control over your blood sugars compared to the period of time prior to training. Therefore, training adaptations lower your overall insulin needs, regardless of the insulin regimen that you use. Your exercise must be consistent, though, as this heightened state of insulin action begins to decline after only one to two days of inactivity.
Similar to aerobic activities, resistance training also enhances insulin sensitivity and blood glucose utilization. Skeletal muscle is a metabolically active tissue that takes up more glucose (through glycogen synthesis) than many other body tissues; therefore, athletes with diabetes who gain muscle mass from doing resistance work also have lower overall insulin requirements and must lower their insulin doses both acutely and chronically.
In the next blog, I’ll talk more about the importance of nutrition and carbohydrate intake in controlling your blood sugars during exercise.