Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans

Intermittent fasting and exercise provide neuroprotection from age-related cognitive decline. A link between these two seemingly distinct stressors is their capability to steer the brain away from exclusively glucose metabolism. This cerebral substrate switch has been implicated in upregulating brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie some of these neuroprotective effects. We examined the isolated and interactive effects of (1) 20-h fasting, (2) 90-min light exercise, and (3) high-intensity exercise on peripheral venous BDNF in 12 human volunteers. A follow-up study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 h decreased glucose and increased ketones (P < 0.0157) but had no effect on BDNF (P >= 0.4637). Light cycling at 25% of peak oxygen uptake (?VO2peak) increased serum BDNF by 6 +/- 8% (independent of being fed or fasted) and was mediated by a 7 +/- 6% increase in platelets (P < 0.0001). Plasma BDNF was increased from 336 pg l(-1) [46,626] to 390 pg l-1 [127,653] by 90-min of light cycling (P = 0.0128). Six 40-s intervals at 100% of ?V-O2peak increased plasma and serum BDNF, as well as the BDNF-per-platelet ratio 4-to 5-fold more than light exercise did (P < 0.0044). Plasma BDNF was correlated with circulating lactate during the high-intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407). Changes in cerebral shear stress - whether occurring naturally during exercise or induced experimentally with inspired CO2 - did not correspond with changes in BDNF (P >= 0.2730). BDNF responses to low-intensity exercise are mediated by increased circulating platelets, and increasing either exercise duration or particularly intensity is required to liberate free BDNF.

Automated summary

Intermittent fasting and exercise can protect the brain from age-related cognitive decline by promoting brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning, and memory. Low-intensity exercise increases BDNF through increased platelets, while high-intensity exercise is required to release free BDNF. Changes in cerebral shear stress do not correspond with changes in BDNF. Fasting decreases glucose and increases ketones, but has no effect on BDNF.