Just 1 hour on treadmill can boost metabolism for 2 days

A single workout session consisting of three 20-minute treadmill runs could activate neurons that are important regulators of blood glucose levels and energy balance as well as influence metabolism for up to two days, says a study over mice.

The findings showed that a single bout of exercise for mice could boost the activity of energy-burning neurons and inhibit the counterpart one for up to two days and those changes can last longer with more training.

“It doesn’t take much exercise to alter the activity of these neurons,” said  a neuroscientist.

“The study predicts that getting out and exercising even once in a semi-intense manner can reap benefits that can last for days, in particular with respect to glucose metabolism,” he added.

Further, a single workout consisting of three 20-minute treadmill runs caused a decrease in appetite that lasted up to six hours.

“This result may explain at the neural circuit level why many people don’t feel hungry immediately after exercise,” he said.

For the study,  the team measured the effects of short- and long-term exercise on two types of neurons that comprise the melanocortin brain circuit. Both humans and mice have this circuit.

One of the neuron types is associated with reduced appetite, lower blood glucose levels, and higher energy burning when activated while the other type increases appetite and diminishes metabolism when activated.

The study also provides avenue to research potential treatments to improve glucose metabolism in patients with conditions such as diabetes.

“It is possible that activating melanocortin neurons may hold therapeutic benefits for patients one day, especially for diabetics who need improved blood-glucose regulation,” he said.

“This research is not just for improving fitness. A better understanding of neural links to exercise can potentially help a number of conditions affected by glucose regulation,” he noted.

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New brain implant to treat people with memory loss

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 Researchers have developed a brain implant that translates short term memories into longer-term ones and may help dementia sufferers and brain-damaged patients retain their memory. 

 

Researchers at the University of Southern California and Wake Forest Baptist Medical Center said the prosthesis, which includes a small array of electrodes implanted into the brain, has performed well in laboratory testing in animals and is currently being evaluated in human patients.

Designed originally at USC and tested at Wake Forest Baptist, the device builds on decades of research by Ted Berger and relies on a new algorithm created by Dong Song, both of the USC Viterbi School of Engineering.

The development also builds on more than a decade of collaboration with Sam Deadwyler and Robert Hampson of the Department of Physiology & Pharmacology of Wake Forest Baptist who have collected the neural data used to construct the models and algorithms.

When brain receives the sensory input, it creates a memory in the form of a complex electrical signal that travels through multiple regions of the hippocampus, the memory centre of the brain.
At each region, the signal is re-encoded until it reaches the final region as a wholly different signal that is sent off for long-term storage. If there's damage at any region that prevents this translation, then there is the possibility that long-term memory will not be formed.

That's why an individual with hippocampal damage (for example, due to Alzheimer's disease) can recall events from a long time ago - things that were already translated into long-term memories before the brain damage occurred - but have difficulty forming new long-term memories.

Song and Berger found a way to accurately mimic how a memory is translated from short-term memory into long-term memory, using data obtained by Deadwyler and Hampson, first from animals, and then from humans.

Their prosthesis is designed to bypass a damaged hippocampal section and provide the next region with the correctly translated memory.

In experiments, Hampson and Deadwyler read the electrical signals created during memory formation at two regions of the hippocampus in patients who had electrodes implanted in their hippocampi to treat chronic seizures.
 
The information was then sent to Song and Berger to construct the model.

The team then fed those signals into the model and read how the signals generated from the first region of the hippocampus were translated into signals generated by the second region of the hippocampus.

In hundreds of trials conducted with nine patients, the algorithm accurately predicted how the signals would be translated with about 90 per cent accuracy.

"Being able to predict neural signals with the USC model suggests that it can be used to design a device to support or replace the function of a damaged part of the brain," Hampson said.