Can 6 Minutes of Intense Cycling Put the Brakes on Alzheimer’s?
Short bouts of intense exercise may help protect the brain from age-related cognitive decline by increasing production of a key protein involved in neuroplasticity, learning, and memory, new research suggests.
In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.
However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago, New Zealand, and postdoctoral fellow at the University of British Columbia-Okanagan.
“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Gibbons told Medscape Medical News.
The findings were published online January 11 in The Journal of Physiology.
Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.
To tease apart the influence of fasting and exercise on BDNF production, Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20 to 40 years.
In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.
Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.
Fasting for 20 hours led to aninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.
Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.
In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
“My leading theory is that during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Gibbons noted.
“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.
However, “Whether this translates to ‘warding off dementia’ is not clear,” Gibbons added.
The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.
The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.
“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.
Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.
J Physiol. Published online January 11, 2023. Abstract
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