ATP could bring your breath back

Scientists have pinpointed the molecular trigger that tells the body to breathe more quickly and deeply when our metabolism increases, such as when we exercise.

Their findings, published in the latest issue of Nature , could shed light on ways to boost breathing, for example for Olympic athletes, along with better understanding common respiratory disorders such as sleep apnoea, sudden infant death syndrome and Ondine's curse, a rare breathing disorder where patients who fall asleep stop breathing and die.

The team of scientists from University College London (UCL) and University of Warwick have discovered that adenosine triphosphate (ATP) - a molecule known to be the intracellular energy 'currency' - is released from key areas of the brain when blood levels of carbon dioxide (CO2) rise.

Dr Alexander Gourine from UCL's Department of Physiology says: "Whether you are sprinting for an Olympic medal or simply running for the bus, your body has to increase your breathing to ensure you are absorbing enough oxygen to fuel your muscles and exhale extra CO2 for the duration of your sprint.

"While the broad control mechanism for breathing has been known for many years, we have discovered how this works at the molecular level. The release of a key chemical from the brain effectively matches your breathing to your metabolism and activity. In other words, extracellular ATP in the brain optimises your breathing to boost maximum performance.

"Our findings could potentially be used to help identify ways of stimulating respiration, particularly for breathing disorders such as chronic airway disease, sleep apnoea and Ondine's curse - a rare breathing disorder where patients who fall asleep stop breathing and die. It could also be of relevance to sudden infant death syndrome - the leading cause of death in infants between 1 month and 1 year of age in the industrial world."

When our metabolism increases, for example when we start to exercise, we may experience an increase in CO 2 levels in the blood, where the body is taking oxygen out of the bloodstream and releasing CO 2 as a waste gas. In this study, this rise was found to trigger the immediate release of ATP from CO 2 sensitive regions of the brain, which in turn regulated the body's breathing to maintain blood CO 2 at adequate levels. Blocking ATP receptors at these sites was found to diminish the chemosensory control of breathing, which prevented the body from increasing respiration sufficiently to meet the needs of the metabolism.

Notes for Editors

For more information or to set up an interview, please contact J enny Gimpel at the UCL Media Relations Office on +44 (0)20 7679 9739, Out of Hours: +44 (0)7917 271364 or e-mail j.gimpel@ucl.ac.uk.

'ATP is a mediator of chemosensory transduction in the central nervous system' by Alexander Gourine, Enrique Llaudet, Nicholas Dale and Michael Spyer, is embargoed to 18:00 London time ( 13:00 US Eastern) Wednesday 6 J uly 2005 and is published in Nature on 7 July 2005 .