(DCP026) AEROBIC COOLDOWN AFTER FASTED RESISTANCE EXERCISE MODERATES INCREASES IN POST-EXERCISE CGM AND CAPILLARY GLUCOSE FOR ADULTS WITH TYPE 1 DIABETES
Friday, October 27, 2023
15:15 – 15:30 EST
Location: ePoster Screen 10
Disclosure(s):
Reid McClure, MSc: No financial relationships to disclose
Jane E. Yardley, PhD - Associate Professor: No relevant disclosure to display
Background: Fasted resistance exercise (RE) causes hyperglycemia in individuals with type 1 diabetes (T1D). Guidelines for managing T1D and RE recommend aerobic cooldowns to correct post-exercise hyperglycemia. This strategy has never been tested. This study tested if an aerobic cooldown could stabilise blood glucose concentration following 45 minutes of fasted, morning RE.
METHODS AND RESULTS: Sixteen T1D adults [median(IQR); age= 23.0(7.5) years; BMI= 25.4(4.8) kg·m-2; diabetes duration= 9.5(8.8) years, HbA1c= 7.1(1.2); 7F/9M] completed two 45-minute, fasted RE sessions in random order. One session involved an immediate post-exercise 10-minute cycle ergometer cooldown (CD) at 30% of aerobic capacity followed by a 20-minute seated recovery. The other involved a 30-minute seated recovery only (NC). We measured capillary blood glucose (CBG) pre/post RE, 10 and 30 minutes post RE (recovery). We monitored BG by CGM, capturing RE, recovery and post-recovery periods (6 hours and overnight). We calculated the percentage change in CBG (pre to post exercise). We examined the CGM glucose trajectory using linear mixed-effects models while controlling for individual-level differences. We examined CGM metrics for post-recovery periods according to current international recommendations.
CBG increased during RE in both conditions [median(IQR); NC: 19%(-6,33), CD: 10%(-5,25); p=0.2]. Compared to NC, CD stabilised CBG by diminishing the increase at 10 [median(IQR); NC: 22%(5,48), CD: 8%(-10,23); p=0.0076] and 30 minutes [NC: 20%(9,55), CD: 9%(-5,29); p=0.039] post RE (Figure1a). CGM glucose had similar trajectory during both recovery conditions [slope per 30 minutes (95%CI); NC: 0.21(0.078, 0.34), CD: 0.054(-0.08, 0.19) mmol/l/30minutes, p=0.1] (Figure1b). There was no difference in the time spent in hyperglycemia (>10mmol/l) 6 hours post RE [NC: 36%(10,61), CD: 35%(10,50); p=0.5] or overnight [NC: 0%(0,42), CD: 27%(2,69); p=0.2] however, CGM traces suggested that glucose continued to rise for up to 2 hours post recovery after NC (Figure 2). In both instances, hypoglycemia (3.0-3.9 mmol/l) was minimal 6 hours post RE [NC: 0%(0,0), CD: 0%(0,2.8); p=0.8] and overnight [NC: 0%(0,2), CD: 0%(0,0); p=0.6] respectively.
Conclusion: Fasted RE causes BG to increase and remain elevated during the post-exercise period, with low risk of hypoglycemia during exercise and following 6-hour and overnight periods. An aerobic cooldown has the potential to stabilise glucose and prevent acute post-exercise hyperglycemia, but may be more effective if combined with treatment (e.g., correction dose).