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 and Parkinson’s disease.
New research shows that a short but intense bout of cycling increases the production of a specialised protein 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 their apparent neuroprotective qualities have led to the interest in BDNF for ageing research.
Lead author Travis Gibbons from the University of Otago, New Zealand, said: “BDNF has shown great promise in animal models, but pharmaceutical interventions have thus far failed to harness the protective power of BDNF in humans safely. We saw the need to explore non-pharmacological approaches that can preserve the brain’s capacity, which humans can use to increase BDNF to help with healthy ageing naturally.”
To tease apart the influence of fasting and exercise on BDNF production, 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 (a 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 more than fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration).
The cause for these differences is unknown, and more research is needed to understand the mechanisms involved. One hypothesis relates 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) that 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 and six females aged 18 and 56) participated in the study. The balanced ratio of male and female participants was to represent the population better 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 optimise BDNF production in the human brain.”
