Ozva AdminResume: Researchers report that six minutes of high-intensity exercise on a regular basis 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, which could protect the brain from age-related cognitive decline.
Font: The Physiological Society
Six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease.
New research published in The Journal of Physiology shows that a brief but intense cycling session increases the production of a specialized protein that is essential for brain formation, learning and memory, and could protect the brain from age-related cognitive decline.
This information about exercise is part of the drive to develop accessible, equitable, and affordable non-drug approaches that anyone can take 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 the survival of neurons.
Animal studies have shown that increasing the availability of BDNF encourages the formation and storage of memories, enhances learning, and generally increases cognitive performance. These key functions and its apparent neuroprotective qualities have led to interest in BDNF for aging research.
Lead author Travis Gibbons, from the University of Otago, New Zealand, stated: “BDNF has shown great promise in animal models, but pharmaceutical interventions have so far failed to safely harness the protective power of BDNF in humans.
“We saw a need to explore non-drug approaches that can preserve the brain’s ability that humans can use to naturally increase BDNF to help with healthy aging.”
To separate the influence of fasting and exercise on BDNF production, researchers at the University of Otago, New Zealand, compared the following factors to study isolated and interactive effects:
- 20 hour fast
- Light exercise (90 minute low intensity cycling)
- High intensity exercise (six minutes of vigorous cycling)
- Combined fasting and exercise
They found that brief but vigorous exercise was the most efficient way to raise BDNF compared to a fasting day with or without a prolonged bout of light exercise. BDNF increased four to five fold (396 pg L-one up to 1170 in. L-one) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-one up to 390 in. L-one).
The cause of these differences is not yet known and more research is needed to understand the mechanisms involved. One hypothesis is related to the change in brain substrate and the metabolism of glucose, the main source of fuel for the brain.
Brain substrate switching is when the brain switches from its preferred fuel source to another to ensure that the body’s energy demands are met, for example, metabolizing lactate instead of glucose during exercise. The transition of the brain from consuming glucose to lactate initiates pathways that result in elevated levels of BDNF in the blood.
The increase in BDNF observed during exercise could be due to the increased number of platelets (the smallest blood cells), which store large amounts of BDNF. The concentration of platelets circulating in the blood is more influenced by exercise than by fasting and increases by 20%.
Twelve physically active participants (six men, six women aged 18-56) participated in the study. The balanced ratio of male and female participants was to provide a better representation of the population rather than indicate gender differences.
Further research is ongoing to delve deeper into the effects of caloric restriction and exercise to distinguish the influence on BDNF and cognitive benefits.
Travis Gibbons noted: “We are now studying how fasting for longer periods of time, for example up to three days, influences BDNF. We are curious if vigorous exercise at the beginning of a fast accelerates the beneficial effects of the fast.
“Fasting and exercise are rarely studied together. We believe that fasting and exercise can be used together to optimize BDNF production in the human brain.”
About this exercise and dementia research news
Author: press office
Font: The Physiological Society
Contact: Press Office – The Physiological Society
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See also
original research: closed access.
“Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans.” by Travis Gibbons et al. physiology journal
Resume
Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans.
Intermittent fasting and exercise provide neuroprotection against age-related cognitive decline. One link between these two seemingly distinct stressors is their ability to steer the brain away from glucose-only metabolism. This brain substrate switch has been implicated in the upregulation of 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) a 20-h fast, (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. The 20-h fast decreased glucose and increased ketones (P ≤ 0.0157) but had no effect on BDNF (P ≥0.4637). Light cycles at 25% of maximal oxygen uptake (${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$) increased BDNF serum by 6 ± 8% (regardless of being fed or fasting) and was mediated by an increase in platelets of 7 ± 6% (P <0.0001).
Plasma BDNF increased from 336 pg l−1 [46,626] at 390 hp l−1 [127,653] for 90 minutes of light cycling (P = 0.0128). Six 40-s intervals at 100% ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}}$ also increased plasma and serum BDNF as the ratio of BDNF per platelet 4 to 5 times more than light exercise (P ≤0.0044). Plasma BDNF was 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, either naturally occurring during exercise or experimentally induced with inspired CO2 – did not correspond to changes in BDNF (P ≥0.2730).
BDNF responses to low-intensity exercise are mediated by increased circulating platelets, and increasing exercise duration or intensity is required to release free BDNF.
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