Exercise in a pill is still the stuff of science fiction

Thursday July 18 2013

"Could we one day get our daily dose of exercise from a pill?" the Mail Online asks, going on to say that, "scientists believe we could be closer to developing a drug that gives us the benefits of exercising without moving a muscle."

As regular readers may expect, the truth behind this headline is far less ground-breaking than the news would have you believe.

The research in question did not involve the creation of a drug to replace exercise, but instead looked at how a protein called Rev-erb-α affects the muscles and exercise capacity of mice.

The researchers discovered the molecular mechanisms that link this protein to the "power plant" of cells, the mitochondria. They found that mice unable to produce the protein cannot run as far or for as long as normal mice. However, when lots of this protein is produced, or when a drug is given that enhances the function of this protein, mice are able to run longer and further – you might say that the protein can create "marathon mice".

Researchers suggest that developing a drug to increase Rev-erb-α could help people with skeletal muscle diseases that reduce their ability to exercise.

The quest for a quick fix continues, but the old-fashioned method of getting up and moving is still the best way to reap the benefits of exercise.

Where did the story come from?

The study was carried out by researchers from the Pasteur Institute in France, The Scripps Research Institute in the US, and other organisations throughout Europe. It was directly funded by the Marie Curie Foundation, the European Commission, and other foundations and governmental organisations. The study was also funded by unrestricted research grants from research institutes and pharmaceutical companies, including AstraZeneca, Merck and Lilly.

It was published in the peer-reviewed journal Nature. The findings were publicised in a measured and well written press release from The Scripps Research Institute.

The Mail Online's headline was misleading. It suggested we will one day be able to take exercise in pill form, which is not quite reflective of the research. The study did not look at or seek to develop a drug that replaces exercise – the claim that it did is pure fantasy.

While a drug to replace exercise is not on the horizon, the researchers state that this research may make it possible to develop a drug to help people who have skeletal muscle disorders, who are less able to exercise.

What kind of research was this?

This was a laboratory and animal study that investigated a protein called Rev-erb-α in mice. It looked at the role of Rev-erb-α in metabolism and the ability of muscles to use oxygen.

This study examined the role of Rev-erb-α in overall functioning by measuring mouse performance on a treadmill. It also looked at the molecular function of the protein, specifically its relationship with the functioning of mitochondria in skeletal muscles.

Mitochondria are structures within most cells that are responsible for producing the bulk of a cell's chemical energy (known as ATP). These structures are sometimes called cells' "power plants" because of their essential role in energy production.

As an animal study, we cannot assume the same results would be seen in people. Despite exciting headlines suggesting that an exercise pill is on its way, this study really looks into the molecular mechanisms and functions of this protein.

While this is essential information to have before the development of any pill, it is still early days and it is unclear if any therapies and drugs will result from this research.

What did the research involve?

The research involved a series of experiments designed to investigate the function and mechanisms of the action of the protein Rev-erb-α.

The researchers first examined the role of Rev-erb-α in the ability of skeletal muscles to use oxygen and its influence on exercise capacity (skeletal muscles are a type of muscle we use to control the movement of our bones).

To do this, the researchers assessed the exercise capacity of mice genetically engineered to be unable to produce Rev-erb-α (known as "knockout" mice) and compared them with typical unengineered mice (known as "wild type" mice).

They then assessed the ability of Rev-erb-α to increase the number of new mitochondria produced in skeletal muscle. To do this, researchers examined the levels of molecules needed to generate mitochondria and compared them between knockout and wild type mice.

The researchers finally looked at the influence of Rev-erb-α on the functioning of the mitochondria within the skeletal muscle cells. To do this, they treated mice with a molecule that enhances the activity of Rev-erb-α and then assessed the exercise capacity of the mice.

What were the basic results?

The researchers found that prior to exercise, the mice's resting oxygen consumption was similar in both the wild and the knockout mice. However, the knockout mice had a significantly lower aerobic capacity during a treadmill test (60% lower at the point of exhaustion).

The knockout mice also ran for less time and distance during endurance tests, which indicates an inability to sustain long-term exercise.

When looking at the role of Rev-erb-α in the production of new mitochondria, the researchers found Rev-erb-α is likely to regulate the generation of new mitochondria in skeletal muscles by influencing the process by which other molecules and proteins interact to generate new mitochondria.

Researchers found that mice had improved exercise capacity and mitochondrial function when they caused the mice to produce too much Rev-erb-α or enhanced the activity of Rev-erb-α by treating mice with a drug.

How did the researchers interpret the results?

Researchers say that the results of their experiments indicate that Rev-erb-α is a major regulator of skeletal muscle mitochondria, and that activation of this protein by a drug "may be a promising approach for the treatment of skeletal muscle diseases with compromised exercise capacity".


This research suggests that a specific protein plays an important role in the ability of muscles to produce energy and use oxygen.

It is tempting (especially for journalists) to extrapolate this study's results both to people and to future applications. However, at this stage the research does not suggest that we will ever be able to take a pill instead of taking exercise. While it found that overexpression of Rev-erb-α allowed the mice to do more exercise, it did not actually replace exercise.

The author's conclusions that a future drug could one day be a treatment option for individuals with reduced exercise capacity caused by skeletal muscle diseases is a more realistic possibility.

The idea that people generally will no longer require exercise and instead will be able to just take a pill is a fantasy that is simply not supported by this research.

Unless a new wonder drug is discovered that will allow us to skip going for a walk or a swim, it is still recommended that we get at least 30 minutes of moderate-intensity exercise a day for at least five days a week.

The NHS Choices Fitness hub has a variety of options and suggestions on how to reach this 150 minutes per week target, as well as tips on ways to get started with an exercise regime if you are currently not very active.

Analysis by Bazian
Edited by NHS Choices