The Effects of Postprandial Exercise on Glucose Control in Individuals with Type 2 Diabetes: A Systematic Review.

BACKGROUND: Regulation of postprandial hyperglycemia is a major concern for individuals with type 2 diabetes. Exercise can reduce postprandial hyperglycemia by increasing contraction-mediated glucose uptake. However, there is no consensus with which to develop guidelines for optimal postprandial exercise timing and prescription. OBJECTIVE: The current systematic review was conducted to consolidate the literature surrounding the effects of postprandial exercise on glucose regulation in individuals with type 2 diabetes. METHODS: Electronic databases were searched on 17 February 2017. Inclusion criteria were: (1) trial was a randomized crossover trial; (2) subjects were diagnosed with type 2 diabetes; (3) a standardized meal was given; (4) exercise was initiated within three hours of the meal; (5) subjects were not treated with insulin. RESULTS: Twelve studies met the inclusion criteria, involving 135 participants (108 males, 20 females, seven unknown). The included studies varied greatly in their timing, duration, intensity, modality, and glucose measures. Postprandial aerobic exercise (11 studies) decreased short-term glucose area under the curve by 3.4-26.6% and 24-h prevalence of hyperglycemia by 11.9-65%. Resistance exercise (two studies) decreased the short-term glucose area under the curve by 30% and 24-h prevalence of hyperglycemia by 35%. CONCLUSION: Postprandial exercise may be an effective way to improve glucose control in individuals with type 2 diabetes. The most consistent benefits were seen in long-duration (≥ 45 min), moderate-intensity aerobic exercise. Resistance training also appears to be an effective modality. We recommend that individuals with type 2 diabetes focus on increasing energy expenditure after the largest meal of the day. More research is needed in this area to confirm the results of this systematic review and to provide clinicians with specific exercise recommendations.

Brain-derived neurotrophic factor mediates cognitive improvements following acute exercise.

The mechanisms causing improved cognition following acute exercise are poorly understood. This article proposes that brain-derived neurotrophic factor (BDNF) is the main factor contributing to improved cognition following exercise. Additionally, it argues that cerebral blood flow (CBF) and oxidative stress explain the release of BDNF from cerebral endothelial cells. One way to test these hypotheses is to block endothelial function and measure the effect on BDNF levels and cognitive performance. The CBF and oxidative stress can also be examined in relationship to BDNF using a multiple linear regression. If these hypotheses are true, there would be a linear relationship between CBF+oxidative stress and BDNF levels as well as between BDNF levels and cognitive performance. The novelty of these hypotheses comes from the emphasis on the cerebral endothelium and the interplay between BDNF, CBF, and oxidative stress. If found to be valid, these hypotheses would draw attention to the cerebral endothelium and provide direction for future research regarding methods to optimize BDNF release and enhance cognition. Elucidating these mechanisms would provide direction for expediting recovery in clinical populations, such as stroke, and maintaining quality of life in the elderly.