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 short but intense bout of cycling increases the production of a
specialised protein that is essential for brain formation, learning and memory,
and could protect the brain from age-related cognitive decline. This insight on
exercise is part of the drive to develop accessible, equitable and affordable
non-pharmacological approaches that anyone can adopt to promote healthy ageing.
The specialised protein named
brain-derived neurotrophic factor (BDNF) promotes neuroplasticity (the ability
of the brain 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 overall boosts
cognitive performance. These key roles and its apparent neuroprotective
qualities have led to the interest in BDNF for ageing research.
Lead author Travis Gibbons from
University of Otago, New Zealand said: “BDNF has shown great promise in animal
models, but pharmaceutical interventions have thus far failed to safely harness
the protective power of BDNF in humans. We saw the need to explore
non-pharmacological approaches that can preserve the brain’s capacity which
humans can use to naturally increase BDNF to help with healthy ageing.”
To tease apart the influence of fasting
and exercise on BDNF production the researchers, from the University of Otago,
New Zealand, compared the following factors to study the isolated
and interactive effects:
·
Fasting for 20 hours,
·
Light
exercise (90-minute low intensity cycling),
·
High-intensity
exercise (six-minute bout of vigorous cycling),
·
Combined fasting and exercise.
They found that brief but vigorous exercise was the most efficient way
to increase BDNF compared to one day of fasting with or without a lengthy
session of light exercise. BDNF
increased by four to five-fold (396 pg L-1 to 1170 pg L-1) more compared to fasting (no change in BDNF
concentration) or prolonged activity (slight increase in BDNF concentration,
336 pg L-1 to 390 pg L-1).
The cause for these differences is not
yet known and more research is needed to understand the mechanisms involved.
One hypothesis is related to the cerebral substrate switch and glucose
metabolism, the brain’s primary fuel source. The cerebral substrate switch is
when the brain switches its favoured fuel source for another to ensure the
body’s energy demands are met, for example metabolising lactate rather than glucose
during exercise. The brain’s transition from consuming glucose to lactate
initiates pathways that result in elevated levels of BDNF in the blood.
The observed increase in BDNF during
exercise could be due to the increased number of platelets (the smallest blood
cell) which store large amounts of BDNF. The concentration of platelets
circulating in the blood is more heavily influenced by exercise than fasting
and increases by 20%.
12 physically active participants (six
males, six females aged between 18 and 56 years) took part in the study. The
balanced ratio of male and female participants was to provide a better
representation of the population rather than indicate sex differences.
Further research is underway to delve
deeper into the effects of calorie restriction and exercise to distinguish the
influence on BDNF and the cognitive benefits.
Travis Gibbons said: “We are now studying how fasting for longer durations, for example up to three days, influences BDNF. We are curious whether exercising hard at the start of a fast accelerates the beneficial effects of fasting. Fasting and exercise are rarely studied together. We think fasting and exercise can be used in conjunction to optimise BDNF production in the human brain.”
Journal article: https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP283582
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