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. 2021 Apr 9:12:664211.
doi: 10.3389/fphys.2021.664211. eCollection 2021.

Maximal Fat Oxidation During Exercise Is Already Impaired in Pre-pubescent Children With Type 1 Diabetes Mellitus

Affiliations

Maximal Fat Oxidation During Exercise Is Already Impaired in Pre-pubescent Children With Type 1 Diabetes Mellitus

Solenne Fel et al. Front Physiol. .

Abstract

Objective: We evaluated substrate utilization during submaximal exercise, together with glycemic responses and hormonal counter-regulation to exercise, in children with type 1 diabetes mellitus (T1DM). Methods: Twelve pre-pubescent children with T1DM and 12 healthy children were matched by sex and age. Participants completed a submaximal incremental exercise test to determine their fat and carbohydrate oxidation rates by indirect calorimetry. Levels of glycemia, glucagon, cortisol, growth hormone, noradrenaline, adrenaline, and insulin were monitored until 120 min post-exercise. Results: Absolute peak oxygen uptake (VO2 peak) was significantly lower in the children with T1DM than in the healthy controls (1131.4 ± 102.5 vs. 1383.0 ± 316.6 ml.min-1, p = 0.03). Overall carbohydrate and lipid oxidation rates were the same in the two groups, but for exercise intensities, higher than 50% of VO2 peak, fat oxidation rate was significantly lower in the children with T1DM. The absolute maximal lipid oxidation rate was significantly lower in the T1DM children (158.1 ± 31.6 vs. 205.4 ± 42.1 mg.min-1, p = 0.005), and they reached a significantly lower exercise power than the healthy controls (26.4 ± 1.2 vs. 35.4 ± 3.3 W, p = 0.03). Blood glucose responses to exercise were negatively correlated with pre-exercise blood glucose concentrations (r = -0.67; p = 0.03). Conclusion: Metabolic and hormonal responses during sub-maximal exercise are impaired in young children with T1DM.

Keywords: glucose metabolism; glycemia; metabolic; pediatric; physical activity.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Study design.
Figure 2
Figure 2
The oxidation rates of carbohydrates (A) and fat (B), in conjunction with power output (C) according to the percentage of VO2 peak. Individual regression for heart rate (HR) vs. the corresponding relative VO2 peak for children with type 1 diabetes mellitus (T1DM) and healthy controls (D). Data are means ± SD.
Figure 3
Figure 3
Comparison of absolute (A) and relative (B) maximal fat oxidation rate (MFO). Power (C), percentage of VO2 peak (D), respiratory exchange ratio (E), and heart rate (F) at the MFO. Boxes represent interquartile ranges. Whiskers give minimum and maximum values. Data are mean (x) and median (−).
Figure 4
Figure 4
Blood concentrations of insulin (A), adrenaline (B), noradrenaline (C), growth hormone (D), cortisol (E), glucagon (F), and glycemia (G) in healthy controls (solid line) and children with T1DM (dotted line). Incremental exercise starts at T0 and finishes at T20. Data are means ± SD. Significantly different between healthy controls and T1DM children at p < 0.05. ∗∗Significantly different at p < 0.001. ǂSignificantly different from T0 at p < 0.05. ǂ ǂSignificantly different from T0 at p < 0.001.
Figure 5
Figure 5
Individual pre-exercise glycemia values according to the drop in glycemia during post-exercise in children with T1DM. The change in glucose concentrations during exercise was calculated from the delta of the end of exercise (T20) and pre-exercise value (T0). Two of the blood glucose data at T20 are missing due to an analytical problem.

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