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Neurotrophins and cognitive functions in T1D compared with healthy controls

Journal Contribution - Journal Article

Subtitle:effects of a high-intensity exercise

Exercise is known to have beneficial effects on cognitive function. This effect is greatly favored by an exercise-induced increase in neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1), especially with high-intensity exercises (HIE). As a complication of type 1 diabetes (T1D), a cognitive decline may occur, mostly ascribed to hypoglycaemia and chronic hyperglycaemia. Therefore, the purpose of this study was to examine the effects of acute HIE on cognitive function and neurotrophins in T1D and matched controls. Ten trained T1D (8 males, 2 females) participants and their matched (by age, sex, fitness level) controls were evaluated on 2 occasions after familiarization: a maximal test to exhaustion and an HIE bout (10 intervals of 60 s at 90% of their maximal wattage followed by 60 s at 50 W). Cognitive tests and analyses of serum BDNF, IGF-1, and free insulin were performed before and after HIE and following 30 min of recovery. At baseline, cognitive performance was better in the controls compared with the T1D participants (p < 0.05). After exercise, no significant differences in cognitive performance were detected. BDNF levels were significantly higher and IGF-1 levels were significantly lower in T1D compared with the control group (p < 0.05) at all time points. Exercise increased BDNF and IGF-1 levels in a comparable percentage in both groups (p < 0.05). In conclusion, although resting levels of serum BDNF and IGF-1 were altered by T1D, comparable increasing effects on BDNF and IGF-1 in T1D and healthy participants were found. Therefore, regularly repeating acute HIE could be a promising strategy for brain health in T1D.

Journal: Applied Physiology, Nutrition & Metabolism
ISSN: 1715-5312
Issue: 1
Volume: 40
Pages: 20-27
Publication year:2015
  • VABB Id: c:vabb:395138
  • Scopus Id: 84920686025
  • WoS Id: 000347300400003
  • ORCID: /0000-0002-2808-044X/work/53627943
  • ORCID: /0000-0002-7163-8752/work/70057741
  • ORCID: /0000-0001-7553-9957/work/83183148
  • ORCID: /0000-0002-2690-5479/work/84574542
CSS-citation score:2