New York, Jun 16 (IANS): Finding it hard to exercise daily? How about popping a pill that could help replace your workouts? Science is closer to that goal, with researchers identifying a molecule in the blood that is produced during exercise.

This may be particularly helpful for older or frail people who cannot exercise enough, and taking the medication can help them slow down osteoporosis, heart disease or other conditions.

According to researchers at Baylor College of Medicine and Stanford University the drug molecule could effectively reduce food intake and obesity in mice.

The findings, detailed in the journal Nature, also improves understanding of the physiological processes that underlie the interplay between exercise and hunger.

"Regular exercise has been proven to help weight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese," said Dr. Yong Xu, professor of paediatrics, nutrition and molecular and cellular biology at Baylor.

"If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health," Xu added.

The team conducted comprehensive analyses of blood plasma compounds from mice following intense treadmill running. The most significantly induced molecule was a modified amino acid called Lac-Phe. It is synthesised from lactate (a byproduct of strenuous exercise that is responsible for the burning sensation in muscles) and phenylalanine (an amino acid that is one of the building blocks of proteins).

In mice with diet-induced obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by about 50 per cent compared to control mice over a period of 12 hours without affecting their movement or energy expenditure.

When administered to the mice for 10 days, Lac-Phe reduced cumulative food intake and body weight (owing to loss of body fat) and improved glucose tolerance.

The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight on an exercise regime as a control group on the same exercise plan.

Interestingly, the team also found robust elevations in plasma Lac-Phe levels following physical activity in racehorses and humans. Data from a human exercise cohort showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.

The team next aims to find how Lac-Phe mediates its effects in the body, including the brain.