BACKGROUND: The acute impact of different types of physical activity on glycemic control in type 1 diabetes has not been well quantified. OBJECTIVES: Our objective was to estimate the rate of change (RoC) in glucose concentration induced acutely during the performance of structured exercise and at recovery in subjects with type 1 diabetes. METHODS: We searched for original articles in the PubMed, MEDLINE, Scopus, and Cochrane databases. Search terms included type 1 diabetes, blood glucose, physical activity, and exercise. Eligible studies (randomized controlled trials and non-randomized experiments) encompassed controlled physical activity sessions (continuous moderate [CONT], intermittent high intensity [IHE], resistance [RESIST], and/or a resting reference [REST]) and reported excursions in glucose concentration during exercise and after its cessation. Data were extracted by graph digitization to compute two RoC measures from population profiles: RoCE during exercise and RoCR in recovery. RESULTS: Ten eligible studies were found from 540 publications. Meta-analyses of exercise modalities versus rest yielded the following: RoCE -4.43 mmol/L h(-1) (p < 0.00001, 95% confidence interval [CI] -6.06 to -2.79) and RoCR +0.70 mmol/L h(-1) (p = 0.46, 95% CI -1.14 to +2.54) for CONT vs. REST; RoCE -5.25 mmol/L·h(-1) (p < 0.00001, 95 % CI -7.02 to -3.48) and RoCR +0.72 mmol/L h(-1) (p = 0.71, 95% CI -3.10 to +4.54) for IHE vs. REST; RoCE -2.61 mmol/L h(-1) (p = 0.30, 95% CI -7.55 to +2.34) and RoCR -0.02 mmol/L h(-1) (p = 1.00, 95% CI -7.58 to +7.53) for RESIST vs. REST. CONCLUSIONS: Novel RoC magnitudes RoCE, RoCR reflected rapid decays of glycemia during CONT exercise and gradual recoveries immediately afterwards. RESIST showed more constrained decays, whereas discrepancies were found for IHE.
BACKGROUND: The acute impact of different types of physical activity on glycemic control in type 1 diabetes has not been well quantified. OBJECTIVES: Our objective was to estimate the rate of change (RoC) in glucose concentration induced acutely during the performance of structured exercise and at recovery in subjects with type 1 diabetes. METHODS: We searched for original articles in the PubMed, MEDLINE, Scopus, and Cochrane databases. Search terms included type 1 diabetes, blood glucose, physical activity, and exercise. Eligible studies (randomized controlled trials and non-randomized experiments) encompassed controlled physical activity sessions (continuous moderate [CONT], intermittent high intensity [IHE], resistance [RESIST], and/or a resting reference [REST]) and reported excursions in glucose concentration during exercise and after its cessation. Data were extracted by graph digitization to compute two RoC measures from population profiles: RoCE during exercise and RoCR in recovery. RESULTS: Ten eligible studies were found from 540 publications. Meta-analyses of exercise modalities versus rest yielded the following: RoCE -4.43 mmol/L h(-1) (p < 0.00001, 95% confidence interval [CI] -6.06 to -2.79) and RoCR +0.70 mmol/L h(-1) (p = 0.46, 95% CI -1.14 to +2.54) for CONT vs. REST; RoCE -5.25 mmol/L·h(-1) (p < 0.00001, 95 % CI -7.02 to -3.48) and RoCR +0.72 mmol/L h(-1) (p = 0.71, 95% CI -3.10 to +4.54) for IHE vs. REST; RoCE -2.61 mmol/L h(-1) (p = 0.30, 95% CI -7.55 to +2.34) and RoCR -0.02 mmol/L h(-1) (p = 1.00, 95% CI -7.58 to +7.53) for RESIST vs. REST. CONCLUSIONS: Novel RoC magnitudes RoCE, RoCR reflected rapid decays of glycemia during CONT exercise and gradual recoveries immediately afterwards. RESIST showed more constrained decays, whereas discrepancies were found for IHE.
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