RESUMEN
Objective: Our study aimed to explore whether physical condition might affect the association between genetic predisposition for Alzheimer's Disease (AD) and AD incidence. Methods: The sample of participants consisted of 561 community-dwelling adults over 64 years old, without baseline dementia (508 cognitively normal and 53 with mild cognitive impairment), deriving from the HELIAD, an ongoing longitudinal study with follow-up evaluations every 3 years. Physical condition was assessed at baseline through walking time (WT), while a Polygenic Risk Score for late onset AD (PRS-AD) was used to estimate genetic predisposition. The association between WT and PRS-AD with AD incidence was evaluated with Cox proportional hazard models adjusted for age, sex, education years, global cognition score and APOE ε-4 genotype. Then, the association between WT and AD incidence was investigated after stratifying participants by low and high PRS-AD. Finally, we examined the association between PRS-AD and AD incidence after stratifying participants by WT. Results: Both WT and PRS-AD were connected with increased AD incidence (p < 0.05), after adjustments. In stratified analyses, in the slow WT group participants with a greater genetic risk had a 2.5-fold higher risk of developing AD compared to participants with lower genetic risk (p = 0.047). No association was observed in the fast WT group or when participants were stratified based on PRS-AD. Conclusions: Genetic predisposition for AD is more closely related to AD incidence in the group of older adults with slow WT. Hence, physical condition might be a modifier in the relationship of genetic predisposition with AD incidence.
RESUMEN
This study examined the phenomenon of transient hypoglycemia and metabolic responses to pre-exercise carbohydrate (CHO) maltodextrin ingestion in cycling and running on the same individuals. Eleven active males cycled or ran for 30 min at 80% maximal heart rate (HRmax) after ingestion of either 1g/kg body mass maltodextrin (CHO-Cycle and CHO-Run respectively) or placebo (PL-Cycle and PL-Run) solutions. Fluids were ingested 30min before exercise in a double-blind and random manner. Blood glucose and serum insulin were higher before exercise in CHO (mean CHO-Cycle+CHO-Run) (Glucose: 7.4 ± 0.3 mmol·l-1; Insulin: 59 ± 10 mU·l-1) compared to placebo (mean PL-Cycle+PL-Run) (Glucose: 4.7 ± 0.1 mmol·l-1; Insulin: 8 ± 1 mU·l-1) (p<0.01), but no differences were observed during exercise among the 4 conditions. Mean blood glucose did not drop below 4.1 mmol·l-1 in any trial. However, six volunteers in CHO-Cycle and seven in CHO-Run experienced blood glucose concentration ≤ 3.5 mmol·l-1 at 20min of exercise and similar degree of transient hypoglycemia in both exercise modes. No association was found between insulin response to maltodextrin ingestion and drop in blood glucose during exercise. Blood lactate increased with exercise more in cycling compared to running, and plasma free fatty acids (FFA) concentrations were higher in placebo compared to CHO irrespective of exercise mode (p<0.01). The ingestion of maltodextrin 30min before exercise at about 80% HRmax produced similar glucose and insulin responses in cycling and running in active males. Lactate was higher in cycling, whereas maltodextrin reduced FFA concentrations independently of exercise mode.
