Question of the Day #1
A 32-year-old man is evaluated for significant blood glucose elevations associated with exercise. The patient has a 22-year history of type 1 diabetes mellitus. He reports that after a recent 6 AM five-mile run, his blood glucose level was 386 mg/dL (21.4 mmol/L); the level was 297 mg/dL (16.5 mmol/L) just before the run and 215 mg/dL (11.9 mmol/L) at bedtime the night before. He took no insulin and ate no food in the morning before his run. During the run, he felt slow and fatigued but was significantly better after drinking water and giving himself insulin. The patient had one episode of diabetic ketoacidosis 15 years ago. Medications are insulin detemir, 16 units/d in the morning, and insulin lispro, 4 to 6 units before each meal, depending on his preprandial blood glucose level and expected carbohydrate intake. Physical examination findings, including vital signs, are normal.
Which of the following is the most likely cause of his postexercise hyperglycemia?
A Excess nocturnal carbohydrate intake
C Inadequate insulin replacement
D Nocturnal hypoglycemia
Source: MKSAP 16
- Hypoinsulinemia causes increased hepatic glucose output and decreased peripheral glucose uptake, which results in a higher blood glucose level and, ultimately, a higher hemoglobin A1c value; prolonged exercise, which further stimulates hepatic glucose release, exacerbates this condition.
Diagnose postexercise hyperglycemia.
This patient’s significantly increased blood glucose level after running most likely results from baseline hypoinsulinemia exacerbated by the physiologic changes associated with prolonged exercise, such as stimulation of hepatic glucose release. A patient who has had type 1 diabetes mellitus for more than 20 years, including one episode of diabetic ketoacidosis, will be completely insulin deficient. Although long-acting, the treatment effect of insulin detemir does not always last a full 24 hours. The fact that his blood glucose level was 215 mg/dL (11.9 mmol/L) at bedtime the night before his run and was even higher the next morning before exercise suggests that he had low levels of insulin present in his system during the night and before starting his run. This hypoinsulinemia most likely triggered increased hepatic gluconeogenesis. In the absence of sufficient plasma insulin, the glucose could not be absorbed by the muscles and other tissues, and his blood glucose level continued to increase. Appropriate treatment is to adjust his insulin regimen to ensure adequate insulin replacement before running to minimize the expected physiologic changes associated with exercise.
Excess carbohydrate intake in the evening would likely contribute to his noted elevated bedtime and pre-exercise blood glucose levels but would not independently account for the significant rise in his blood glucose level after exercise.
Although this patient may have some degree of gastroparesis given the duration of his diabetes, this disorder is an unlikely explanation for an increased blood glucose level 12 hours or more since he last ate.
Early morning blood glucose elevations may occur in response to the nocturnal hypoglycemia associated with diabetes therapy. Although this patient had an elevated morning blood glucose level before running, his bedtime measurement also was elevated, and he took no additional insulin beyond his single dose of long-acting insulin the morning before. Therefore, nocturnal hypoglycemia is unlikely to be the cause of this patient’s exercise-associated hypoglycemia.
- Temple MY, Bar-Or O, Riddell MC. The reliability and repeatability of the blood glucose response to prolonged exercise in adolescent boys with IDDM. Diabetes Care. 1995;18(3):326-332. PMID: 7555475