<p> </p> <p><strong>Objective:</strong> Maintenance of glycemic control during and following exercise remains a major challenge for individuals with type 1 diabetes. Glycemic responses to exercise may differ by exercise type (aerobic, interval, resistance), and the effect of activity type on glycemic control following exercise remains unclear.</p> <p><strong>Research Design-Methods: </strong>The Type 1 Diabetes Exercise Initiative (T1Dexi) was a real-world study of at-home exercise. Adult participants were randomly assigned to complete six structured aerobic, interval, or resistance exercise sessions over 4-weeks. Participants self-reported study and non-study exercise, food intake, and insulin dosing (multiple-daily injection [MDI] users) using a custom smart phone application, and provided pump data (pump users), heart rate, and continuous glucose monitoring (CGM) data.</p> <p><strong>Results: </strong>497 adults with type 1 diabetes, mean±SD age 37±14 years, HbA1c 6.6±0.8% (49±8.7 mmol/mol) assigned to structured aerobic (N=162), interval (N=165), or resistance (N=170) exercise were analyzed. Mean change in glucose during assigned exercise was -18±39, -14±32, and -9±36 mg/dL for aerobic, interval, and resistance, respectively (P<0.001), with similar results for closed loop, standard pump, and MDI users. Time-in-range 70-180 mg/dL [3.9-10.0 mmol/L] was higher during the 24-hours following study exercise when compared to days without exercise (76±20% vs. 70±23%; P<0.001).</p> <p><strong>Conclusion: </strong>Adults with type 1 diabetes experienced the largest drop in glucose level with aerobic followed by interval and resistance exercise, regardless of insulin delivery modality. Even in well controlled adults with type 1 diabetes, days with structured exercise sessions contributed to clinically meaningful improvement in glucose time-in-range but may have slightly increased time below range.</p>
Prolonged exercise causes blood glucose (BG) to decrease in well insulinized individuals with insulin-dependent diabetes mellitus (IDDM). In an attempt to determine the influence of pre-exercise BG (BGpre), and carbohydrate (CHO) ingestion on the rate of drop in BG, 8 adolescent males with IDDM participated in 2 experimental protocols (A & B) spaced 1-4 weeks apart. In protocol A, subjects drank water during 60 min. of moderate intensity cycle ergometry exercise, 75min after insulin injection and a standardized breakfast. Total CHO utilization was determined based on respiratory exchange ratio and O2 uptake. In protocol B, subjects ingested a CHO beverage (13C enriched, 8% glucose solution, 18mmol-1 NaCl) equal to the amount of CHO utilized in protocol A, during an identical exercise challenge. Percent exogenous CHO (CHOexo) oxidation was calculated in protocol B using the expired13 CO2/12CO2 ratio. Total CHO utilization was 85±25g (mean±SD) in protocol A and CHOexo oxidation was 13±4% in protocol B. The rate of drop in BG was higher in protocol A than in B (9.1±3.8 vs 3.6±3.3 mmol-1·65min-1, respectively) The rate of drop was correlated to BGpre in protocol A (r=.86, p<0.01) and marginally so in protocol B (r=.64, p=0.08). Percent CHOexo oxidation was not correlated with BGpre (r=.08). These data suggest that pre-exercise blood glucose influences the rate of drop in blood glucose but does not influence CHOexo oxidation.
There are currently no guidelines regarding the carbohydrate (CHO) dosage required to prevent exercise-induced hypoglycemia in children with insulin-dependent diabetes mellitus (IDDM). To prevent hypoglycemia by matching glucose ingestion with total-CHO utilization, 20 adolescents with IDDM attended 2 trials: control (CT; drinking water) and glucose (GT; drinking 6-8% glucose). Participants performed 60 min of moderate-intensity cycling 100 min after insulin injection and breakfast. CT's total-CHO utilization during exercise was determined using indirect calorimetry. In GT, participants ingested glucose in the amount equal to total CHO utilization in the CT. A total of 9 participants had BG <4.0 mmol/L in CT compared to 3 in GT ( p < .05). In conclusion, glucose ingestion equal to total-CHO utilization attenuates the drop in blood glucose and reduces the likelihood of hypoglycemia during exercise in adolescents with IDDM.
Introduction: Somatostatin may be elevated in diabetes, which can reduce glucagon secretion at mealtimes and during hypoglycemia. In this pilot study, we investigated the effect of a sustained low-dose delivery of a novel SSTR2a (ZT-01), using a mini-osmotic pump, on oral glucose tolerance (OGT) and response to an insulin-induced hypoglycemia challenge in a T2D rat model. Methods: Male Sprague Dawley rats (n=4/5 per group) were placed on a high-fat diet (3 weeks) then injected with low-dose streptozotocin (35 mg/kg), inducing T2D. Basal bolus insulin was administered for 7 days (2-3 units/day) to maintain fed-state glycemia targeting 12-25 mmol/L, after which the rats were treated with ZT-01 (0.18 mg/day) or vehicle using implanted mini-osmotic pumps (Alzet). An OGT test on day 3 was followed by a hypoglycemic challenge (12U regular insulin) on day 5. Results: Drug and vehicle groups displayed similar glycemic levels in the fasted state and post oral glucose ingestion. Glycemia was also similar prior to insulin challenge and there was no difference in basal glucagon between groups, but SSTR2a treatment attenuated the drop in blood glucose after bolus insulin. Conclusion: Sustained exposure to low-dose SSTR2a does not appear to affect basal glucose or glucagon levels, nor affect the response to OGT but may improve the glucose response to insulin-induced hypoglycemia in this T2D model. Disclosure N. Aleali: None. N. C. D'souza: None. D. Shakeri: None. E. Simonson: None. R. Liggins: Employee; Zucara Therapeutics, Stock/Shareholder; Zucara Therapeutics. O. Chan: None. M. C. Riddell: Advisory Panel; Zealand Pharma A/S, Zucara Therapeutics, Indigo Diabetes, Consultant; Lilly Diabetes, Eli Lilly and Company, Jaeb Center for Health Research, Speaker's Bureau; Dexcom, Inc., Novo Nordisk, Sanofi, Stock/Shareholder; Supersapiens, Zucara Therapeutics. Funding GlycoNet (CD-85); Zucara Therapeutics Inc.
