Glucose tolerance status associates with improvements in cognitive function following high-intensity exercise in adults with obesity.

PURPOSE: Obesity, insulin resistance (IR), and proinflammatory cytokines associate with cognitive decline. Numerous studies document cognitive benefits of acute exercise bouts in lean individuals. However, how co-morbidities such as obesity and IR influence cognitive changes induced by acute exercise is unclear. We examined the effects of acute high-intensity aerobic exercise on cognitive function in age-matched and BMI-matched obese adults with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) and in lean, NGT adults. METHODS: 49 adults (15 Lean, 18 Obese-NGT, 16 Obese-IGT) performed one session of high-intensity interval exercise (four cycles of 4-min at 75% Wmax with 3-min rest). Cognitive function testing and blood sampling were performed pre- and post-exercise. RESULTS: Following exercise, measurements of executive function and working memory were improved in Lean and Obese-NGT (p < 0.05), but not Obese-IGT. Changes in cognitive function following exercise negatively correlated with 2-hr glucose during an OGTT after controlling for body weight and body composition (rp = -0.40, p = 0.007). Serum levels of inflammatory cytokines IL-6 and CRP remained increased 60-minutes post-exercise in Obese-IGT, but not in Lean or Obese-NGT, which positively associated with 2-hr glucose during an OGTT (p < 0.01) and negatively with changes in cognitive function following exercise (p < 0.01). Greater insulin levels in Obese-IGT post-exercise also negatively correlated with changes in cognitive function following exercise (p < 0.01). CONCLUSION: Improvements in cognition following acute high-intensity exercise positively associate with glucose tolerance, independent of body weight and body composition. Further, poorer changes in cognitive performance following exercise associate with persistent peripheral inflammation.

A meal enriched in saturated fat acutely impairs cognitive performance in obese men.

BACKGROUND: Diets chronically high in saturated fat (SFA) associate with obesity and insulin resistance (IR), which in turn associate with cognitive decline and dementia. However, understanding how acute SFA consumption influences cognition is less clear despite short-term SFA-enriched diets inducing whole-body IR. We examined how consuming meals enriched with SFA or monounsaturated fat (MUFA) acutely influence cognitive function in lean and obese men. We hypothesized that greater diet-induced IR following a SFA-enriched meal would associate with decreased cognitive performance. METHODS: Twelve lean and 12 obese males ingested meals containing no fat (CTL), enriched with SFA, or enriched with MUFA in a single-blind, randomized fashion. Cognitive testing and blood sampling were performed pre- and 2 h post-meal. Oral glucose tolerance (OGTT) and body composition were also assessed. RESULTS: At baseline, fasting glucose, insulin, HOMA-IR, triglyceride, IL-6, and 2-hr glucose during an OGTT were higher in obese men (p < 0.001), while executive function (Stroop Test and Trail Making Test B-A) and working memory (Digit Span Test) were lower in obese men (p < 0.05). In response to the CTL and MUFA-enriched, no differences in cognitive measures were observed in lean or obese subjects. Following a SFA-enriched meal, obese subjects scored worse during cognitive testing (Stroop Test, Trail Making Test B-A, and Digit Span Test) compared to pre-meal scores (p < 0.05). These impairments in cognitive testing scores following the SFA-enriched meal associated with increased HOMA-IR (p < 0.01) and decreased plasma IL-6 (p < 0.05). No changes in cognitive function were observed in lean subjects following a SFA-enriched meal. CONCLUSIONS: These data demonstrate that cognitive performance of obese men acutely worsens following a high-SFA meal. Reductions in cognitive performance associated with increased IR, suggesting that diet-induced IR may acutely decrease cognitive function.