Although a diagnosis of type 1 diabetes (T1D) should not limit a person’s ability to compete at the highest level of sport, considerations must be made to manage glycemia both during exercise and in the postexercise recovery period, according to a consensus statement published in Lancet Diabetes Endocrinology.
Significant progress has been made in the understanding of how to manage glycemia following exercise in people with T1D, with a general consensus that T1D should not limit a person’s desire to have an active lifestyle. However, research evaluating postexercise recovery is limited. According to Christoph Stettler, MD, of the Department of Diabetes, Endocrinology, Nutritional Medicine, and Metabolism at the University of Bern in Switzerland and colleagues, the primary focus of such research has been on insulin or nutrition-focused strategies to manage glycemia before and/or during exercise.
To rectify this, Dr Stettler and colleagues sought to create an up-to-date consensus statement addressing postexercise recovery and glucose management for endurance athletes with T1D.
Understanding Physiologic Processes
The postexercise period is defined as the time following an exercise regimen until a new exercise regimen is initiated. Data have shown that exercise can influence glycemia both during and after exercise and may persist for 48 hours or longer due to changes in insulin sensitivity and muscle glucose uptake.
Compared with the average person, professional or endurance athletes train more frequently than every 48 hours, often training more than once per day. For these individuals, late-onset hypoglycemia following exercise is common. Implementing an improved postexercise recovery routine, though, can reduce the risk. Conversely, high-intensity exercise that exceeds the lactate threshold can result in immediate postexercise hyperglycemia, which data have found is more commonly associated with fasting morning exercise and moderately intense aerobic exercise.
To understand the requirements of individuals with T1D in this population of endurance or high-performing athletes, it is crucial to understand the physiologic mechanisms that occur following exercise.
For people with and without T1D, carbohydrates are the primary fuel source when exercising at an intensity higher than 70% of the maximum rate of oxygen consumption (VO2max). However, in people with T1D, these changes are associated with greater carbohydrate oxidation at higher exercise intensities.
Several studies evaluating exercise-associated fuel metabolism in T1D populations and the effect of plasma glucose and insulin concentrations have been published. One such study found that despite the presence of “substantially higher” systemic insulin and glucose concentrations, no major differences exist between people with and without T1D in terms of substrate oxygen or hepatic glycogen breakdown. Another study identified a higher rate of carbohydrate oxidation in hyperglycemia compared with euglycemia and inverse findings for lipid oxidation.
Lipid oxidation is the primary fuel source in the period after exercise and leads to decreases in respiratory exchange ratio, “even in conditions of high carbohydrate feeding.” Lipid oxidation from both intra- and extramuscular sources is elevated to meet necessary fuel requirements, an important biological process that allows for the replenishment of liver and skeletal muscle glycogen stores following an exercise session.
Muscle glycogen resynthesis begins as soon as exercise is concluded, with the most rapid activity occurring during the first 5 to 6 hours of the recovery period. It occurs in a biphasic pattern: an initial rapid phase (minutes to hours) that requires no insulin to be present, followed by a long-lasting, insulin-dependent phase (up to 72 hours). Muscle glycogen typically returns to pre-exercise concentrations within 24 to 36 hours, as long as sufficient levels of carbohydrates are ingested.
Recovery Phase Guidance
For people without diabetes who are seeking rapid recovery and a quick return to peak performance, suggested carbohydrate intake is 1.0 g/kg/h to 1.3 g/kg/h for the first 4 hours of recovery, with frequent 30-minute eating intervals thereafter. For those with T1D, a deep understanding of glycogen resynthesis physiology might help reduce the risk of hyper- and hypoglycemia.
Following exercise, the muscle cell membrane permeability to glucose increases, resulting in an initial “rapid phase” of glycogen resynthesis — independent of insulin signaling that typically lasts between 30 and 60 minutes. The rate of resynthesis during this crucial period can “rapidly decline in the absence of exogenous carbohydrate,” according to studies, but there is limited research on this process in people with T1D.
The insulin-dependent phase follows as the second phase of glycogen resynthesis. In this phase, additional considerations may be required for athletes with T1D due to the exogenous administration of insulin. Consuming carbohydrates directly after exercise plays an important role in the rate of glycogen synthesis during this phase.
In the mid to late postexercise period (3 to 12 hours after exercise), insulin sensitivity can be high, resulting in a risk of postexercise hypoglycemia. Athletes with T1D should consider this and adjust bolus and/or basal insulin doses accordingly. No existing studies quantify the adaptations in insulin needed in the postexercise period. As such, Dr Stettler and colleagues recommend a reduction in bolus insulin of 20% to 50% at the first recovery meal, as well as a similar reduction in basal insulin.
Hepatic glycogen is less well studied than skeletal muscle glycogen, likely due to the difficulty of accessing tissue samples. However, new noninvasive technology in the form of C-magnetic resonance spectroscopy has allowed researchers to begin studying this process.