overview: Researchers report that six minutes of regular high-intensity exercise can slow brain aging and delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. High-intensity exercise increases the production of BDNF, a protein involved in memory, learning, and brain plasticity, and may protect the brain from age-related cognitive decline.
sauce: Physiological Society
Six minutes of high-intensity exercise may extend the lifespan of a healthy brain and delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
New research published in journal of physiology Short but intense cycling increases the production of specialized proteins essential for brain formation, learning and memory, showing that it may protect the brain from age-related cognitive decline.
This insight into exercise is part of the impetus to develop accessible, equitable and affordable non-pharmacological approaches that everyone can adopt to promote healthy aging.
A specialized protein called brain-derived neurotrophic factor (BDNF) promotes neuroplasticity (the brain’s ability to form new connections and pathways) and neuronal survival.
Animal studies have shown that increasing the availability of BDNF promotes memory formation and storage, enhances learning, and improves overall cognitive performance. Interest in BDNF for aging research has increased due to its neuroprotective properties.
Lead author Travis Gibbons of the University of Otago, New Zealand, said:
“We recognized the need to explore non-pharmacological approaches that could preserve the brain’s capacity for humans to naturally increase BDNF and use it to aid in healthy aging.”
To clarify the effects of fasting and exercise on BDNF production, researchers at the University of Otago, New Zealand compared the following factors to study their interacting effects alone:
- 20 hour fast
- Light exercise (90 minutes of low intensity cycling)
- Vigorous exercise (6 minutes of vigorous cycling)
- Combining fasting and exercise
They found that short but intense exercise, with or without long sessions of light exercise, was the most efficient way to increase BDNF compared to one-day fasting. 4-5 fold increase (396 pg L-1 ～1170pg L-1) compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L)-1 ～390pgL-1).
The cause of these differences is not yet known and further research is needed to understand the mechanisms involved. .
A brain substrate switch is when the brain switches from one preferred fuel source to another to ensure that the body’s energy needs are met, for example, metabolizing lactate instead of glucose during exercise. The brain shift from glucose consumption to lactate initiates a pathway that leads to elevated levels of BDNF in the blood.
The observed increase in BDNF during exercise may be due to an increase in the number of platelets (the smallest blood cells) that store large amounts of BDNF. The concentration of circulating platelets in the blood is more affected by exercise than by fasting, increasing by 20%.
Twelve physically active participants (6 males, 6 females, ages 18-56) participated in the study. A balanced proportion of male and female participants was intended to better represent the population rather than to show gender differences.
Further research is underway to delve deeper into the effects of calorie restriction and exercise to distinguish effects on BDNF from cognitive benefits.
Travis Gibbons says: I am interested in whether exercising vigorously at the beginning of the fast accelerates the beneficial effects of the fast.
“Fasting and exercise have rarely been studied together. We believe that the combined use of fasting and exercise can optimize BDNF production in the human brain.”
About this exercise and dementia research news
author: press office
sauce: Physiological Society
contact: Press Office – Physiological Society
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See also
Original research: closed access.
“Fasting for 20 hours does not affect exercise-induced increases in circulating BDNF in humans,” Travis Gibbons et al. Journal of Physiology
overview
Fasting for 20 hours does not affect exercise-induced increases in circulating BDNF in humans
Intermittent fasting and exercise protect neurons against age-related cognitive decline. The link between these two seemingly disparate stressors is the ability to divert the brain away from glucose metabolism alone. This brain substrate switch is involved in the upregulation of brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie these neuroprotective effects.
We investigated the single and interactive effects of (1) fasting for 20 hours, (2) light exercise for 90 minutes, and (3) high-intensity exercise on peripheral venous BDNF in 12 volunteers.
A follow-up study isolated the effects of cerebrovascular shear stress on circulating BDNF. Fasting for 20 hours decreased glucose and increased ketones (P. ≤ 0.0157) but did not affect BDNF (P. ≥ 0.4637). By light cycling at 25% of peak oxygen uptake (${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$), serum BDNF was increased by 6 ± 8% (unrelated to feeding or fasting) and was mediated by a 7 ± 6% increase in platelets (P. < 0.0001).
Plasma BDNF increased from 336 pg l-1 [46,626] ~390pgl-1 [127,653] 90 minutes of light cycling (P. = 0.0128). Six 40-s intervals at 100% of ${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$ also resulted in plasma and serum BDNF Increased BDNF ratio per platelet 4-5 times higher than light exercise (P. ≤ 0.0044). Plasma BDNF correlated with circulating lactate during high-intensity intervals (r = 0.47, P. = 0.0057), but not during light exercise (P. = 0.7407).
Changes in cerebral shear stress – naturally occurring during exercise or experimentally induced with stimulated CO2 – Does not support changes in BDNF (P. ≥ 0.2730).
The BDNF response to low-intensity exercise is mediated by an increase in circulating platelets, and either the duration of exercise or, particularly, the intensity of exercise must be increased to release free BDNF.
