# Six minutes of daily high-intensity exercise can delay the onset of Alzheimer’s disease

summary: 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 production of BDNF, a protein involved in memory, learning and brain plasticity, which can protect the brain from age-related cognitive decline.

Source: Physiological association

Six minutes of high-intensity exercise can extend the life of a healthy brain and delay the onset of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s.

New research has been published in Journal of Physiology He shows that a short but intense bout of cycling increases production of a specialized protein essential for brain formation, learning and memory, and can protect the brain against age-related cognitive decline.

This insight into exercise is part of the drive to develop accessible, equitable, and affordable non-drug approaches 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 nerve cells.

Animal studies have shown that increased availability of BDNF promotes the formation and storage of memories, enhances learning and enhances overall cognitive performance. These key roles and its pronounced 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 the need to explore non-drug approaches that could preserve brain capacity that humans could use to increase BDNF naturally to aid healthy aging.”

To separate the effect of fasting and exercise on BDNF production, researchers from the University of Otago, New Zealand, compared the following factors to examine the isolated and interaction effects:

• Fasting 20 hours
• Light exercise (90 minutes of low-intensity cycling)
• High-intensity exercise (a bout of vigorous cycling for six minutes)
• Combine fasting and exercise

They found that short but vigorous exercise was the most effective way to increase BDNF compared to a single day of fasting with or without a long session of light exercise. BDNF increased four to fivefold (396 pg l-1 up to 1170 p-1) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg/L-1 to 390 p-1).

The reason for these differences is not yet known, and more research is needed to understand the mechanisms involved. One hypothesis relates to the cerebral substrate switch and glucose metabolism, which is the brain’s primary fuel source.

Cerebral substrate switching occurs when the brain changes 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 brain’s transition from glucose to lactate initiates pathways that lead to higher levels of BDNF in the blood.

The noticeable increase in BDNF during exercise could be due to an increase in the number of platelets (the smallest blood cells), which store large amounts of BDNF. The platelet concentration in the blood is more affected by exercise than by fasting and increases by 20%.

The study involved 12 physically active participants (six males and six females, ages 18 to 56). The balanced ratio of male and female participants was to provide a better representation of the population rather than pointing out gender differences.

More research is being done to delve deeper into the effects of caloric restriction and exercise to discern the effect on BDNF and the cognitive benefits.

Travis Gibbons noted, “We are now studying how fasting for longer periods, say up to three days, affects BDNF. We are curious as to whether strenuous exercise at the onset of the fast accelerates the beneficial effects of fasting.”

Fasting and exercise are rarely studied together. We believe that fasting and exercise can be used in combination to improve BDNF production in the human brain.”

author: press office
Source: Physiological association
Contact: Press Office – Physiological Society
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Fasting for 20 hours does not affect exercise-induced increases in circulating BDNF in humansBy Travis Gibbons, et al. Journal of Physiology

Summary

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

Intermittent fasting and exercise provide neuroprotection against age-related cognitive decline. The link between these two seemingly different precursors is their ability to steer the brain away from metabolizing glucose exclusively. This brain switch has been linked in the regulation 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 interactional effects of (1) 20-hour 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 effect of cerebral vascular shear stress on circulating BDNF. Fasting for 20 hours decreases glucose and increases ketones (s ≤ 0.0157) but no effect on BDNF (s yen 0.4637). Light cycling at 25% of peak oxygen uptake (${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{peak}}}$) increased BDNF in serum by 6 ± 8% (regardless of feeding or fasting) and a 7 ± 6% increase in platelets was mediated (s <0.0001).

Plasma BDNF was increased by 336 pg l-1 [46,626] to 390 pg L-1 [127,653] 90 minutes of light cyclings = 0.0128). Six 40-second periods of 100% of ${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{Peak}}}$ increase plasma and serum BDNF, also because BDNF per platelet ratio is 4 to 5 times higher compared to light exercise (s Japanese yen 0.0044). Plasma BDNF has been associated with circulating lactate during periods of high intensity (s = 0.47, s = 0.0057), but not during light exercise (s = 0.7407).

Changes in cerebral shear stress – whether naturally occurring during exercise or experimentally induced with inspiratory CO2 – does not comply with changes in BDNF (s 0.2730).

BDNF responses to low-intensity exercise are mediated by increased platelets, and increasing exercise duration or intensity in particular is required to release free BDNF.