The Expiration Date on Your Muscle Gains

A new muscle study tells us how training makes us strong- and for how long the benefit sticks around.

PC: Bradley Marshall

The evidence has been compounding for decades, and it hasn’t slowed down. Muscles matter. Human muscle mass has been shown to play a massive role not just in strength in the gym, but in healthy aging, prediction of lifespan, and regulation of key features of metabolism, like blood sugar. The World Health Organization guidelines have underscored their recommendation that we all adhere to a regular strength routine in order to make sure our best days remain ahead of us. 

What a new study in Nature offers is greater clarity as to whether or not the New Year’s resolution we made in January and forgot about in February, to do more strength training, will still have done us any good by the time we make it to December.

Maithreyan Kuppusamy, Martin Matijass, and colleagues at the Institute of Cardiovascular Research and Sports Medicine, in Cologne, Germany wanted to know how muscle changes when we strength train. Also, how long do those adaptations stick around if we fall off the wagon?

How we gain strength without size

Most of us know that our muscles feel beat up after the first lifting session in a long time, and some of that soreness is attributed to muscle damage. We break the tissue down by working it hard, and hopefully it will grow back stronger and more prepared to meet the next challenge. The body has a few ways of helping that muscle to grow back. One, which gets most of the attention, is hypertrophy. Muscles get larger because of hypertrophy, but it’s not the only way that they get stronger. As the authors point out, not too much hypertrophy happens in the first six or eight weeks of a strength program.

This is where Kuppusamy and Matijass pick up. They had eight volunteers take on a strength routine for six weeks. They tested the strength and chemical composition of their muscle fibers before and after the program, and then tested them again after three weeks of total rest to see if any of those gains stuck around.

Muscle cells get stronger, but not for long

Cells have many components, but for the sake of this study, those components really fell into one of two buckets: one bucket was for cellular machinery attached to the cytoskeleton (skeleton of the muscle cell), and the other was for everything else. 

When most of us talk about "muscle damage", we’re almost saying the same thing as "damage to the cytoskeleton of a muscle cell". Other molecules tend to get stuck around a damage site. Then, a normal process of cellular recycling, called CASA, kicks off. The damaged tissue gets broken down in the CASA process, and the pieces are used to rebuild healthy muscle tissue.

"It looks like the strength training routine we stopped doing in February has probably lost most of its physical benefit by March."

The team took a sample of muscle tissue out of each volunteer’s leg right after an overloading strength session– right after the damage was done, but before CASA could clean up the mess like usual. The researchers did this before any training regimen, then again after six weeks of resistance exercise training, and again after three weeks of rest and recovery. Then they looked at the sample to see what enzymes were getting stuck in damaged tissue, and in what quantity. Previous work showed that more enzymes at the damage site mean that more muscle damage occurred. They found ten enzymes that were involved, and a similar quantity of them after the three-week rest phase as before any training had been done.

That tells us about the volume of repair molecules involved, but it doesn’t tell us who the ringleaders are. Maybe there’s one enzyme that sets the stage for CASA, and the other proteins are just following the leader. To find out, the team used mouse muscle cells and-- through chemical manipulation with a substance called Bafilomycin A1-- suppressed one of each of those ten proteins at a time to see if CASA was still happening. What was new and surprising was that just two of the ten proteins had outsized control over the process: one called PDZ and LIM domain protein 3 (PDLIM3), and another called Perilipin-5 (PLIN5). PLIN stands out in particular, because it relies on a lipid droplet (fat) to get around. Meaning, cellular fat stores have a role in CASA-based muscle healing.

What have we gained?

The implications of the paper run in a few directions. For one, it looks like the strength training routine we stopped doing in February has probably lost most of its physical benefit by March. We’re likely better off keeping up a cadence of semi-regular strength work– at least once a week or so. 

Second, understanding the molecular pathways that underlie strength training and detraining expose new questions. Some molecules play much larger roles in these sorts of tissue changes than anyone had thought. Fat droplets deliver machinery to the sites of muscle injury. Some protein levels drop back off after a period of de-training while others don’t. Why?

"Human muscle mass plays a massive role not just in strength in the gym, but in healthy aging, prediction of lifespan, and regulation of key features of metabolism, like blood sugar."

Finally, there are some other implications to consider if muscle fiber activity has the potential to add strength without adding mass, in the way that hypertrophy does. In endurance sports, that’s exactly what athletes are looking for– more strength without any additional weight to carry. Runners in particular are known to subject their muscles to a lot of damage through the eccentric contractions that occur with each step. Could the special cell signaling described by Kuppusamy and Matijass hold some key to improving tissue durability and long distance performance? 

The study focused on resistance training rather than endurance training, so it’s hard to know for sure. In any case, it’s a step forward in understanding what our muscles are doing for us daily. Just knowing is a step towards influencing it in favor of better health and performance.

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