When we talk about strength training in middle age, and beyond, the focus is slowing down muscle loss. If we keep our muscles, we won’t fall over and end up permanently disabled.

In this way, strength training helps us maintain a higher quality of life. We’re not left in the corner with an old movie playing on the box.

The other claim is that strength training improves our longevity.  Primarily, again, if we don’t fall over, we don’t die prematurely. But it’s not the whole story.

Research says that 30 to 60 minutes of strength training a week is associated with a 10 to 20 per cent drop in the risk of mortality, cardiovascular disease and cancer.

How might strength training work against heart disease and cancer? This takes a little teasing out.

Ageing caused by cellular garbage?

One theory describes ageing as the lifelong accumulation of various types of molecular and cellular damage.

This cellular garbage is in part caused by toxic by-products of metabolism, and by inefficient repair and clean-up systems.

It’s one theory. It may be wholly or partly right.

However, the accumulation of defective cellular material is implicated in disorders such as Alzheimer’s, Parkinson’s disease and ALS. In these instances, the garbage (such as amyloid plaque) blocks neurons from transmitting signals.

But this is a full-body issue – notably muscles and nerves, not just the brain.

According to researchers from the University of Bonn Institute of Cell Biology, muscles and nerves “are long-lasting, high-performance organs whose cellular components are subject to constant wear and tear”.

The good news: They are served by a fairly efficient clearing system.

There’s a protein called BAG3 that “plays a critical role in the elimination of damaged components”.

BAG3 identifies these broken parts and ensures that they are enclosed by cellular membranes to form an “autophagosome”.

Autophagosomes “are like a garbage bag in which cellular waste is collected for later shredding and recycling”.

But BAG3, the cellular garbage collector, needs a mechanical force to activate it.

That’s where strength training comes in

A new study found that lifting weights activates this cellular waste disposal in the muscles, including the heart.

The researchers say this prevents heart failure and nerve diseases.

The findings “could form the basis for new therapies for heart failure and nerve diseases, and even afford benefits for manned space missions”.

The research was led by Professor Jörg Höhfeld.

Höhfeld said when the BAG3 clean-up system is damaged, the consequences are quick and catastrophic.

“Impairment of the BAG3 system does indeed cause swiftly progressing muscle weakness in children, as well as heart failure –one of the most common causes of death in industrialised Western nations,” he said.

The study also involved sports physiologists from the German Sport University Cologne and the University of Hildesheim.

Professor Sebastian Gehlert, of Hildesheim, said the research had revealed “what intensity level of strength training it takes to activate the BAG3 system”.

This was useful because physiologists “can optimise training programs for top athletes and help physical therapy patients build muscle better”.

Gehlert is making use of these findings to support members of the German Olympic team.

Experiments in space

The study was partly funded by the German Space Agency because of its relevance to manned space missions.

Höhfeld said: “BAG3 is activated under mechanical force. But what happens if mechanical stimulation does not take place?”

This would be the case for astronauts living in a weightless environment, or immobilised intensive care patients on ventilation.

In such cases, the lack of mechanical stimulation rapidly leads to muscle atrophy, the cause of which Höhfeld ascribes at least in part to the non-activation of BAG3.

Drugs developed to activate BAG3 might help in such situations, he said.

Höhfeld’s team is now preparing experiments to be conducted on board the International Space Station.

BAG3 research, he said, could in fact help us reach Mars one day.