UNLABELLED: Acute physical exercise usually enhances insulin sensitivity. We examined the effect of a competitive 42 km marathon run on glucose uptake and lipid oxidation in 7 runners with insulin-dependent diabetes mellitus (IDDM), aged 36 +/- 3 yr, BMI 23.9 +/- 0.5 kg m-2, VO2max 46 +/- 1 ml kg-1 min-1, HbA1c 7.7 +/- 0.3%, duration of diabetes 16 +/- 5 yr, runtime 3 h 47 +/- 8 min. On the marathon day, they reduced pre-race insulin doses by 26 +/- 8%, and ingested 130 +/- 33 g carbohydrate before, 91 +/- 26 g during, and 115 +/- 20 g after the race. During the run, blood glucose concentration fell from 14.4 +/- 2.0 to 7.4 +/- 3.0 mmol l-1 (p < 0.05) and serum insulin from 51 +/- 8 to 33 +/- 8 pmol l-1 (p < 0.05). Serum NEFA increased by 4-fold (p < 0.05), but fell to the normal level by next morning. Muscle glycogen content was 56% lower (p < 0.05) and glycogen synthase fractional activity 40% greater (p < 0.05) in the morning after the marathon as compared to the resting control day. In spite of glycogen depletion, whole body glucose disposal (euglycaemic insulin clamp) was unchanged, while glucose oxidation (indirect calorimetry) was decreased by 49% (p < 0.05) and lipid oxidation increased by 41% (p < 0.01). There was an inverse correlation between the rates of lipid oxidation and glucose uptake after the marathon (r = -0.75; p < 0.05). IN CONCLUSION: after successfully managed marathon running in patients with IDDM, insulin sensitivity was not increased in spite of low glycogen content and enhanced glycogen synthase activity after marathon, probably because of increased lipid oxidation.
UNLABELLED: Acute physical exercise usually enhances insulin sensitivity. We examined the effect of a competitive 42 km marathon run on glucose uptake and lipid oxidation in 7 runners with insulin-dependent diabetes mellitus (IDDM), aged 36 +/- 3 yr, BMI 23.9 +/- 0.5 kg m-2, VO2max 46 +/- 1 ml kg-1 min-1, HbA1c 7.7 +/- 0.3%, duration of diabetes 16 +/- 5 yr, runtime 3 h 47 +/- 8 min. On the marathon day, they reduced pre-race insulin doses by 26 +/- 8%, and ingested 130 +/- 33 g carbohydrate before, 91 +/- 26 g during, and 115 +/- 20 g after the race. During the run, blood glucose concentration fell from 14.4 +/- 2.0 to 7.4 +/- 3.0 mmol l-1 (p < 0.05) and serum insulin from 51 +/- 8 to 33 +/- 8 pmol l-1 (p < 0.05). Serum NEFA increased by 4-fold (p < 0.05), but fell to the normal level by next morning. Muscle glycogen content was 56% lower (p < 0.05) and glycogen synthase fractional activity 40% greater (p < 0.05) in the morning after the marathon as compared to the resting control day. In spite of glycogen depletion, whole body glucose disposal (euglycaemic insulin clamp) was unchanged, while glucose oxidation (indirect calorimetry) was decreased by 49% (p < 0.05) and lipid oxidation increased by 41% (p < 0.01). There was an inverse correlation between the rates of lipid oxidation and glucose uptake after the marathon (r = -0.75; p < 0.05). IN CONCLUSION: after successfully managed marathon running in patients with IDDM, insulin sensitivity was not increased in spite of low glycogen content and enhanced glycogen synthase activity after marathon, probably because of increased lipid oxidation.
Authors: G Perseghin; G Lattuada; F De Cobelli; A Esposito; F Costantino; T Canu; P Scifo; F De Taddeo; P Maffi; A Secchi; A Del Maschio; L Luzi Journal: Diabetologia Date: 2005-11-01 Impact factor: 10.122