Exercise Lowers Brain Glutamate, May Reduce Toxicity

Scientists at the University of Guelph in Canada, have concluded in a recent study, that exercise can increase the use of the neurotransmitter glutamate in the brain, potentially lowering toxicity associated with excessive levels of the compound in neurodegenerative conditions such as Huntington’s disease.

Glutamate is one of the brain’s most frequently employed signaling molecules, but its abundance requires strict control of the levels present outside cells. When a glutamate neuron signals, releasing glutamate to excite another nerve cell in the process, the neurotransmitter needs to be rapidly cleared from the neuronal connection, called synapse, to allow new signals to be transmitted.

Glutamate present in too high levels becomes toxic to cells, and a failure to adequately control release or reuptake of the neurotransmitter is contributing to numerous disease states. Mitochondria — our cellular powerhouses — use glutamate, which is an amino acid, in their oxidative energy-producing processes.

Until recently, no one had investigated whether brain mitochondria might react to the increased energy demands during exercise by using more of the neurotransmitter.

“As we all know, exercise is healthy for the rest of the body and our study suggests that exercise may present an excellent option for reducing the severity of brain disorders,”  said Dr. Eric Herbst, the lead author of the study, in a press release.

The study, “Exercise increases mitochondrial glutamate oxidation in the mouse cerebral cortex,”  published in Applied Physiology, Nutrition, and Metabolism, allowed mice to run for 45 minutes on a treadmill before their brains were examined. Researchers noted that brain mitochondria used more glutamate after the exercise, without altering the use of pyruvate, another mitochondrial nutrient.

“Taking into account that there are no cures for neurodegenerative diseases where glutamate is implicated, this study offers another example of the benefits of exercise for our brains,” continued Dr. Herbst. “In short, these findings offer another reason to exercise with the aim of either preventing or slowing the neurodegeneration caused by these disorders.”

The identification of mechanisms behind this selective increase in mitochondrial glutamate metabolism might give researchers in other fields important insight for ways to lower excessive brain glutamate and hinder its toxicity.

Exactly how these findings are applicable to people with neurodegenerative diseases, such as Huntington’s, needs further investigation.