Author’s note:

This article is due for a major overhaul. There are a couple things in here I don’t entirely agree with anymore. Mainly pay attention to the mechanistic stuff (the importance of myonuclei and satellite cells), and its implications for “muscle memory.” Based on some more recent research, I’m less confident about time off resulting in enhanced hypertrophy once you resume training (though I think the mechanism is still plausible, and I’d still like to see it tested on well-trained lifters).

What you’re getting yourself into

~8600 words, 15-30 minute read time

Key points

1. Myonuclei are the “control centers” of a muscle fiber.

2. Muscle size is ultimately determined by how many myonuclei a muscle fiber has; there is a maximum area they can “oversee,” and once they reach that limit, you stop growing unless you can add more.

3. The primary way to gain more myonuclei is through reasonable amounts of muscle damage.

4. Over time, it becomes harder to damage your muscles due to the Repeated Bouts Effect.

5. This article discusses how to make your muscles more susceptible to muscle damage, and thus the addition of myonuclei and ultimately more growth.

6. Myonuclei-related factors help explain “muscle memory,” the effectiveness of steroids, why men generally have an easier time gaining muscle, the difference between genetic freaks and everyone else, and a bunch of other neat stuff.

W

hile the title of the article is “Grow Like a New Lifter Again?” it discusses much more than that. It’s fundamentally about why your muscles grow in the first place, why they stop growing, the most important factor for long-term muscle growth, why new lifters grow so quickly, how to partially re-create those circumstances, muscle loss, and when muscle loss can actually help you.

By the way, the answer to the question posed in the title is yes!

Probably.

Sort of.

Isn’t that the type of emphatic statement that makes you fired up to read an article? Good! Let’s dive in.

This article is a change of pace from what I usually write. Typically, I don’t put pen to paper (or fingers to keys, in this case) unless I’m very confident about what I have to say, because I have the annoying habit of including disclaimers about things I’m unsure of, so articles I write concerning topics I’m less confident about can become an almost unreadable array of “probablies,” “maybes,” and “perhapses.”

However, in this case, I’m excited enough about this subject to forge on ahead, and I’m not aware of any research currently in progress to directly shed any more light on it, so now is as good of a time as any. From the outset, though, I want you to know I’m approaching the second part of this article with the perspective of “this seems plausible enough, and would certainly explain a lot,” not, “THIS IS ABSOLUTELY WHAT’S GOING ON.” The first part is definitely solid, though, and is still crucial information to learn if you want to understand how your muscles grow.

Let’s start by laying a foundation.

Most cells in your body have a single nucleus that oversees most of the important functions of the cell. Your muscle fibers, on the other hand, are exceptionally large single cells that have multiple muscle nuclei (called myonuclei). The myonuclei come from satellite cells – cells that surround the muscle fibers that can fuse with muscle fibers to repair them after exercise, and donate their nuclei. Those nuclei are crucial for synthesizing the protein that makes muscles grow, regulating the local hormonal environment, and generally ordering the goings-on of the muscle fiber.

Each myonucleus can “oversee” a certain volume of sarcoplasm (the contents of a muscle fiber). The volume of sarcoplasm it oversees is called its myonuclear domain. There is a limit to how much sarcoplasm each myonucleus can oversee – a limit on its myonulcear domain. Once you reach this limit, the only way to continue getting bigger is to add more myonuclei to the muscle fibers.

When you lose muscle, those myonuclei stick around for a long time. We don’t know exactly HOW long, but it’s well-understood that you lose them at a much slower rate than contractile protein itself. They’ll all be there for a matter of weeks, you’ll lose none or very few in a matter of months, and an elevated number will stick around for a matter of years, assuming nothing drastic happens.

For example, a few studies show a loss of myonuclei within a matter of weeks or months with complete unloading (hind limb suspension in rodents, relatively weightlessness or microgravity conditions, denervation, or spinal transection), though even in extreme circumstances like these, they’re still lost much slower than muscle mass is; however, in one study, powerlifters who had previously used steroids (which elevate myonuclei number) but had been off drugs for an average of 4.5 years still had elevated numbers of myonuclei in their traps compared to powerlifters who’d never used steroids. Three of them didn’t even lift anymore. This wasn’t the case in the vastus lateralis (a quad muscle), but that’s to be expected, since we know steroids affect the traps (and probably all shoulder girdle muscles) more than they do the quads. Check out this review for a more in-depth look.

Myonuclei are the primary reason for the phenomenon of “muscle memory” – why you can regain lost muscle much faster than you can build muscle in the first place. It may take several months to build 10lbs of muscle, and if you’re out of the gym for 3 months, it’s very likely that you’ll lose the bulk of that new muscle you built. However, most people find it doesn’t take very long – generally a month or less (and certainly less time than they were away from the gym for) – to gain all of that muscle back.

This isn’t overly surprising. It’s the myonuclei themselves that regulate the process of protein synthesis. If you have more myonuclei per unit volume of sarcoplasm (if the myonuclear domain is smaller), they can ramp up protein synthesis to get back to their myonuclear domain limits pretty quickly, meaning voila, all of your old muscle comes back in a hurry.

Let’s discuss a few more little tidbits about myonuclei before we carry on, just to make sure we’re on sure footing (and because it’s pretty freaking cool):

As we’d expect, myonuclear addition precedes muscle hypertrophy. People get overly focused on protein synthesis itself, and don’t pay enough attention to what’s actually directing it. Since muscle size is ultimately limited by myonuclear domain, you need to continually add myonuclei to your muscle fibers to continue growing (how to do that is the topic of this article). If you don’t, you’ll build muscle up to the point that you max out your myonuclear domain, and not be able to grow any more.

Genetic freaks are the ones that can grow a larger satellite cell pool, activate them more effectively, and get more myonuclei from them. In the linked study, the satellite cell pool at the end of the study for extreme responders was roughly twice the size of moderate responders, and three times the size of nonresponders. There are probably other factors in play, but factors affecting satellite cell pool and myonuclear addition seem to be the most important ones.

NSAIDs (like Advil, Aleve, Motrin, etc.) decrease long-term (but maybe not short-term) muscle growth, in all likelihood. How? By suppressing satellite proliferation and differentiation. Solid overview here (yes, it’s T-Nation, but it’s also Dr. Brad Schoenfeld, and I haven’t found a better summary anywhere else).

Basically any type of resistance exercise (with or without muscle damage) can expand the satellite cell pool (as long as you aren’t taking anti-inflammatories), but training that causes relatively high degrees of muscle damage is what works best for actually getting those satellite cells to differentiate into muscle stem cells (myoblasts) and donate their nuclei to the muscle fiber. To quote a 2012 review:

Satellite cells are activated by various types of exercise, both damaging and apparently non-damaging exercise. Thus, the threshold for satellite cell activation is rather low, and the satellite cell response does not seem to be directly related to muscle damage markers. However, only if the initial muscle damage induces a necrotic process in segments of myofibres will the satellite cells leave their position and migrate to the area of damage as (differentiated) myoblasts.*

*There’s a caveat to this at the end of the article

The authors of that review also advise that a prolonged decrease in strength of 4 days or more is a more reliable indicator of sufficient muscle damage than soreness (DOMS). The contrarian in me is greatly pleased by this idea, since it seems like most people are praising increased training frequency as the be-all-end-all for strength and hypertrophy, and obviously it’s hard to mix prolonged performance decrements and training a lift 4 times per week. Later on, I’ll discuss how the two can fit together.

In summary: Muscles have multiple nuclei, which can only control a given area inside the muscle. When you bump up against that limit, if you don’t add more nuclei, you stop getting bigger. Those nuclei come from the satellite cells that surround your muscle fibers, and people who grow faster are the ones whose satellite cell pool expands larger/faster than other peoples’. Just about any type of resistance training can expand the satellite cell pool, but that expansion is limited by anti-inflammatory drugs (since their activation is tied to inflammation), and they generally only fuse to muscle fibers if the muscle is significantly damaged, which is best assessed by strength being depressed for 4 or more days – soreness is one indicator, but not as reliable of an indicator.

Alright. That’s what we know. Now for some implications/applications before moving on to the more exciting stuff.

1) Muscle loss during weight loss

If it’s important that you maximize muscle size or performance right at the end of a cut, then you’re absolutely better off with a small deficit, cutting slowly. In fact, it’s been shown that even trained athletes can gain muscle and improve performance in a small deficit (losing 0.7% of their bodyweight each week). When I’ve brought up this study before, I’ve gotten some blowback about it, so I asked Dr. Brad Schoenfeld to make sure it wasn’t just an anomalous research finding. His response: “The review by Helms cites some of the studies. Stu Phillips also published a study showing recomposition. I’ve seen this in my lab time and again; it’s not even arguable.”

So there’s that.

However, if you’re someone who doesn’t particularly like dieting that slowly, a larger deficit probably won’t hurt you much in the long run. Yes, you’ll lose some muscle/strength, but if you don’t have a powerlifting competition or a bodybuilding show at the end of your diet, it doesn’t really matter. As you lose muscle, those myonuclei will hang around, and you’ll have no issue getting your old muscle back pretty quickly.

With that being said, don’t think I’m advocating crash diets. I’m definitely not. I’m just pointing out that while large deficits certainly have their drawbacks, they may not negatively impact muscle mass in the long run as much as we once thought.

2) Time away from the gym

It’s absolutely not worth worrying about. Afraid to take a week off for vacation? Don’t be.

Depending on training status, it takes 2-4 weeks to have measurable decreases in muscle size and strength. Studies investigating rate of strength loss usually use simple movements (like knee extension, measuring maximum moment or something of that nature), so it’s possible that your lifts will be down after a couple of weeks out of the gym, but that’s more a symptom of rusty motor patterns than actual strength loss. That performance will come back within 2-3 sessions practicing the lifts again.

Want to take a vacation? Don’t worry about training. Need to take time off to study for finals? That’s fine. Family emergency? Come on now. Priorities.

Any muscle you DO lose in that time span will all come back in a hurry. Those myonuclei aren’t going anywhere, and they’ll be more than happy to ramp up protein synthesis to get your muscles back to their old size post haste.

Additionally, there’s good reason to believe they’ll actually help you come back bigger and stronger than before. More on that later.

3) Training around injury

Take your time. Go to a physical therapist and get on a rehab program. If you lose some muscle, so what? It’ll come right back.

If it’s more of a minor, chronic thing, then don’t do anything that causes pain. I’d still recommend going to a physical therapist and getting some exercises that will help fix the issue. In the meantime, take it easy and do the lifts that are still comfortable. Then if, for example, you have elbow pain while benching, cut back on the bench work and see if you can find exercises that stimulate your pecs, triceps, and shoulders that don’t cause pain.

Conservative approaches pay off. Don’t risk turning a small annoyance into a long-term headache. Do what you can to mitigate muscle loss, but if you lose some mass and strength while dealing with an injury, again, it’s not worth being concerned about. Even with 3 weeks of complete immobilization (which will cause a much larger loss in muscle and strength than just not lifting, since those muscles will still be stimulated by day-to-day activities), it only takes 2-4 weeks to get your strength and muscle back, likely much less without a cast. However, a serious muscle, tendon, or ligament tear generally takes 12 weeks or longer to recover from. Playing it safe in the short run pays off big in the long run.

Okay. Now to the part that’s both more speculative and more fun.

Detraining and rebounding

Let’s think through this for a moment. You need to continue gaining more myonuclei if you want to keep getting bigger, because the amount of muscle you can have per myonucleus is limited. The best way to do that is to do exercise that causes significant muscle damage. Now, we’re not talking rhabdo. We want the type of training in which your muscles take at least 4-5 days to be fully recovered. The authors of that review go as far as to say exercise that causes significant muscle damage is the only way to get those myoblasts to fuse with the muscle fiber, thus donating their nuclei. I’m skeptical of absolutes in biology, but we can probably at least conclude that it’s important.

Unfortunately, this pesky thing called “The Repeated Bouts Effect” (RBE) kicks in, whereby your muscles aren’t damaged nearly as easily. Less damage, less myonuclei accrual, less potential for future growth. (The precise ways your muscles adapt to resist damage aren’t overly important to us right now. There are quite a few. If you’re curious, read the review linked above.)

That makes newbie gains make more sense, right?

There IS simply a decrease in muscle protein synthesis over time as well, but my hunch is that the root cause is the same: decreased muscle damage due to the RBE, affecting both satellite cell response/myonuclei accretion and intracellular signaling (probably via the inflammation that goes along with muscle damage affecting local IGF-1 response).

So, now for the speculation. Can we recreate these conditions? Is it possible to make quasi-newbie gains again? I’m talking specifically about muscle gains, not strength; strength is largely due to neural adaptations. Also note that I said “quasi-newbie gains,” as I don’t think it would be possible to totally recreate the factors you have going for you on your first day in the gym.

All that being said: Yes, I think you can.

How? By taking time off to re-sensitize your muscles to training, undoing many of the adaptations that result in the RBE. After that, your muscles will be more susceptible to damage, more prone to accumulating new myonuclei, and primed for greater total hypertrophy.

When you’re a new lifter, your myonuclear domain is smaller (meaning you have potential to grow without adding new myonuclei). Your muscles are more susceptible to damage, and thus more susceptible to the addition of more myonuclei, which are required for increased long-term growth.

When you’re an experienced lifter who’s taken time off, your myonuclear domain is smaller, and your muscles are more susceptible to damage (since RBE-inducing adaptions decrease with time away from training), and thus more susceptible to the addition of more myonuclei, which are required for increased long-term growth.

To flesh this out a bit more, let’s start with the research, move on to the theoretical rationale, and go over some examples of how this looks in practice.

Starting with the research:

1) This study showed that alternating 6 weeks of training with 3 weeks off for 24 weeks (train 6, off 3, train 6, off 3, train 6) produced the same strength and mass gains as training for 24 weeks straight.

The fact that you’re getting the same results with just 3/4 the time spent training is neat enough, but I have a hunch that it may have actually produced better results if the study was conducted on trained lifters instead of untrained lifters because of the mechanism I’m proposing (ameliorating the RBE, setting the stage for more muscle damage, myonuclei accumulation, and ultimately larger gains). That mechanism wouldn’t apply as strongly to new lifters whose muscles hadn’t had as much time under load.

The volume a high-level lifter handles would crush a newbie; thus, those adaptations that result in the RBE must have occurred to a much greater degree so their muscles can handle the increased level of training volume. Furthermore, I think it would be primarily useful to break through a strength/mass plateau (when you’d reached maximal myonuclear domain size, and weren’t experiencing enough muscle damage to add new ones), and the untrained lifters in this study increased strength steadily over the course of the study, meaning they weren’t yet in a position to maximally benefit from this type of strategy. At the very least, we have evidence that in some contexts, taking time off is just as good as training with no breaks.

2) This study (by the same authors) found basically the same thing, over 15 weeks, with one group training for 15 weeks straight, and one group taking 3 weeks off in between two 6-week training blocks.

Strength and muscle gains at the end of the 15 weeks were similar, but in the group training continuously, strength and mass gains started to slow down during the last 6 weeks of training, whereas the strength and muscle gains during each 6-week training block were the same in the group that took 3 weeks off – two blocks of newbie gains.

3) This study shows that it only takes 12 days without resistance training to restore mTOR (the primary hypertrophy pathway) signaling to newbie levels.

Yes, it’s in rodents. Of course, rodent metabolism is faster than ours, so it’s hard to say how long 12 rodent days translate to in human days for the same physiological effect. My hunch is that it’s not MUCH longer than 12 days – maybe a month or so at most – because while every other tissue in rodents has a considerably higher metabolic rate (7-10 times or so), it’s actually pretty similar in skeletal muscles, largely because in other tissues, metabolic rate is supply-driven, and in muscle tissues, it’s demand-driven. (If that piques your interest, I’d strongly recommend this book.) Either way, the details are unimportant: Hypertrophy signalling pathways can ramp back up to newbie levels after a not-too-terribly-long time away from resistance training.

I came across quite a few other studies (and my friend Andrew Vigotsky hooked me up with several more), but they weren’t overly relevant. Most of them involved rehabbing serious injuries or detraining periods of 3 months or more (up to a year).

Ultimately, the research we have is promising, but far from conclusive. We don’t have any studies on well-trained lifters, who are the ones more affected by the RBE, but it is cool that taking time off is at least as good as continuous training for new lifters – the ones who shouldn’t need any extra bump to get over strength/mass plateaus. And, of course, none of these studies actually looked at myonuclei accrual, so they don’t say anything about the proposed mechanism.

Now, let’s move beyond the published research and look at biological rationale and plausibility.

Biological rationale and plausibility

Why do your muscles grow in the first place? Keep in mind, this isn’t a “how” question (if it was, then we’d just be talking about the fairly well-understood causes of muscle hypertrophy). It’s a “why” question. “Why” questions are always a bit opaque, and applying a higher purpose-driven function to biological systems is more a matter of plausibility than truth. You can never prove it. It’s just a question of what explanation makes the most sense of the phenomena you’re looking at, and can then be used to make further predictions about other phenomena.

I think the answer to “why do muscles grow in the first place?” is the fairly non-controversial one: “As a defense mechanism.”

This makes sense. Your muscles’ primary job is to help you acquire food so you survive and pass on your genes, and, in the case of humans, stay alive and function long enough to pass on wisdom and social norms to future generations. They don’t do that very well if they’re seriously injured, so their adaptations primarily exist as protective functions. This is true of both aerobic and hypertrophic adaptations.

In the case of aerobic adaptations, you mobilize and use fuel stores more effectively to maintain muscle function (so you don’t conk out due to exhaustion during the middle of a hunt or a fight), and your mitochondria grow, multiply, and produce more aerobic enzymes to use that fuel more efficiently and protect your muscles from free radical damage. Muscles that fatigue easily or are damaged excessively by free radicals are less able to carry out their functions, so they adapt in a protective manner. You care about running farther and faster. They care about mitigating damage and keeping you from fatiguing, and thus dying.

In the case of muscle growth, similar protective mechanisms are in play. There’s the old mantra that when you lift, you tear your muscles down, so they build themselves back up stronger so a similar stressor they meet in the future won’t be as threatening. That’s a (partially true) explanation describing muscle growth as a protective mechanism. But it’s only half the story.

The other half is the adaptations that cause the repeated bouts effect. All of those adaptations are fundamentally protective. A bigger, stronger muscle that’s just as susceptible to damage doesn’t make much sense, after all. When you exposed it to heavier loads, if it could produce even more force without other protective mechanisms keeping it safe, it would be even more prone to injury, and thus incapable of carrying out its purpose.

So then the question becomes: “Why don’t my muscles continue getting bigger and bigger, with those RBE-inducing adaptations keeping pace? Then they could keep producing more force (making them more capable of comfortably dealing with any threats in the environment: needing to lift and move heavy things, strolling into battle like Gregor Clegane, etc.), while still being protected from damage.”

Energy. Extra muscle isn’t very “costly” at rest, receiving very little blood flow and only burning about 13kcal/kg per day, so if you gained 10kg (22lbs) of muscle, you’d only need about 130 extra calories per day to fuel it at rest. However, it is very “costly” during exercise; if you’re 50% bigger, you burn 50% more energy for everything you do. And if aerobic adaptations (increased mitochondria, increased capillary density, etc.) don’t keep pace, you’ll fatigue much easier. If you’re active for several hours per day hunting/fighting/doing other human stuff, then the energetic cost of that extra mass really adds up, meaning you’ll be more likely to die (and your genes along with you) when the next famine comes. There were clear disadvantages to being “too big,” but not clear advantages. You didn’t need to be the biggest, strongest human on the planet; you just needed the capacity to be stronger than “the next guy,” who was pretty similar to you until cheap travel and globalization mixed all of our little clans together.

There are also clear advantages for your muscles to shrink but retain their myonuclei when you stop training. You don’t have to keep all that extra metabolically costly tissue hanging around when you aren’t using it, but you retain the ability to get it all back rapidly when the need arises. You also lose many of the adaptations that result in the RBE. The “to what degree” isn’t clear, and the “how soon” isn’t clear (and they probably vary person to person), but it’s clear that it happens. You know how, after a layoff, your recovery times are much longer and you get so much sorer after a training session you’d have had no issues with previously? Some of those RBE-inducing adaptations have clearly gone away.

In fact, having a maximum myonuclear domain is a protective adaptation as well. It’s thought that myostatin, that pesky hormone that keeps you from getting jacked beyond belief, mainly functions to keep your muscle working properly by constraining the maximum myonuclear domain size.

You can think of each myonucleus as a wifi router. If you’re within range of it, your devices can send and receive information, and everything works smoothly. Take your devices too far away from the wifi router, and they still have the capability to do everything they could before, but without the wifi router to send and receive information, you can’t do anything except play Solitaire. If your myonuclear domains expand too much, then some of the contents of the muscle fiber are too far away from the wifi router, so while they still have the same potential for functionality, without the nucleus to organize it all (making sure proteins and signaling molecules get sent where they should, overseeing organization and repair of cellular structures, etc.), they stop working properly. Myostatin limits muscle hypertrophy to constrain the myonuclear domain so everything works right. Without it, muscles can get much, much larger, but they also become weaker and less functional.

So, here’s the general lay of the land:

Muscles get bigger and stronger as a protective mechanism, but they also adapt in other ways for protection, causing the repeated bouts effect, which makes muscles less susceptible to damage. When the muscles are damaged, myoblasts (which started as satellite cells) go to the area to repair the damage, and also donate their myonuclei to the fiber. The muscle can grow freely until you reach the myonuclear domain limit, at which point hypertrophy shuts down (likely regulated by myostatin) as another protective mechanism to keep the muscles functioning properly. When you stop training, you lose muscle mass to cut metabolic cost, but those myonuclei stick around so you can quickly get all your old muscle mass back quickly. RBE-inducing adaptations also go with time off, making your muscles more susceptible to damage again. Muscle damage is what causes the fusing of more myoblasts and the accrual of new myonuclei.

So, does that set the stage for enhanced growth after a layoff from training, above that which would have been possible with continuous training? If so, it would particularly apply to people who had spent plenty of time training already, and who are at a strength/size plateau.

The thing is, we don’t know for sure. I think there’s a strong theoretical case, but all of the studies conducted thus far using protocols that would bring about these circumstances have been conducted on untrained lifters. The results of those studies are promising (results matching those of continuous training, in a population I’d have assumed would do better with continuous training, since they weren’t yet at a plateau), but they don’t give us any definite answers.

So now that we’ve seen the (quite pauce) literature and have looked at the theoretical rationale, let’s move on to observational evidence.

Observational Evidence

This is what got me interested in this idea in the first place.

One of the more common questions I get asked is some variant of, “X lift was plateaued. I took time off for (insert reason here). When I came back, I got back on the same training program but started hitting PRs again in (insert time frame here. Usually 4-8 weeks or so). What’s going on here?”

Some of my biggest personal records have come very soon after a layoff. Both of my best benches came within 8 weeks of taking time away from the gym, or dialing my training way back. My 1885 total at 242 was the product of a training cycle that started after 4 very easy weeks of training (I think I got in 3 sessions in 4 weeks) over the holidays, incidentally after plateauing hard for the prior 3 months. The best deadlift session of my life followed on the heels of 10 weeks almost entirely off due to a particularly bad run of the exertion headaches that limit me from time to time. Most recently, I hit an all-time PR paused squat at one of my seminars in Malaysia after being afraid I was going to make a fool of myself due to minimal training and working around the clock for a month leading up to the launch of The Art and Science of Lifting.

If you’ve ever coached athletes during an offseason, especially if they’ve been slacking since the end of their competitive season, I’m sure you’ve seen this as well: insane progress in a short period of time. They don’t just quickly recover the strength they lose during their competitive season; they also gain a considerable amount of strength and muscle over their previous peak in a very short time span (this is especially true of sports that require a lot of strength training, like American Football).

Of course, there are alternate explanations for all of those things. Maybe the people sharing their experiences with me were just overtrained before. Maybe I’m just weird (I am, but that’s beside the point). And of course, when you’re dealing with high-level football players, you’re dealing with people who have exceptionally good genetics, and it’s impossible to know how much bigger or stronger they would have gotten under other circumstances. However, it was enough to set me down this line of thinking.

But do any good strength athletes or bodybuilders actually do this?

Do they take time off to get bigger and stronger?

Yes.

John Meadows, recently minted IFBB pro, takes 2-3 weeks of easy training after every show, followed by 3 weeks off entirely. There are also stories of Kevin Levrone taking 6+ months off at a time while he racked up the most IFBB heavyweight pro wins in the 1990s (he was the lead singer of a relatively successful rock band, and took time off serious training while they were touring), but I wasn’t able to verify the veracity of those stories.

Ed Coan, the greatest powerlifter of all time, took two weeks off after every meet, which seems to have been the common practice of the day.

Ilya Ilin took multiple months off lifting entirely after his 2012 Olympic gold medal, mostly sticking to rowing and swimming for his training. He eventually got below 90kg (he competed at 94kg, generally weighing over 100kg during the training cycle leading up to London) before blowing up to a top bodyweight around 115kg (considerably over his previous peak weight) en route to his world championship at 105kg.

To recap: research is promising but doesn’t directly address this approach, there’s a convincing theoretical rationale for periodically taking time away from training to boost long-term muscle gains (in my opinion), plenty of interesting anecdotes support it, and some super top-level guys in a variety of sports do it.

So, here’s the deal. I think this idea is very interesting, quite compelling, and probably works. I’m not saying it’s THE SECRET or ONE WEIRD TRICK, but I think this is a viable strategy that can help people get past plateaus and set them up for more long-term growth by partially recreating newbie-like conditions. I think it works (with the potential for pretty meaningful payoff), I’m not sure it works, and I think worst-case-scenario is that taking some time off occasionally won’t really affect your overall rate of progress either positively or negatively.

And as a general rule, if something might help, and it doesn’t hurt, it’s definitely worth a shot!

Putting it into practice

“But wait a second,” you might be saying, “I thought you generally favored increased training frequencies for muscle and strength gains?”

I do. And here’s how it fits together:

High frequency training works for two major reasons:

You get more frequent practice with the movements you’re trying to master, increasing the rate of motor learning. The muscles are stimulated more frequently, leading to more spikes in muscle protein synthesis across the week, ultimately leading to greater muscle gains. This is especially important for more experienced lifters, because muscle protein synthesis returns to baseline within a day or so (usually two days at most), whereas it stays elevated for a longer period of time in new lifters.

For a more in-depth look at these factors and the literature that supports them, snag a free copy of The Bulgarian Manual where the research surrounding these issues is discussed in a fair amount of depth.

For short-term strength and mass gains, those two factors are exactly what you want. You can master the movements faster and build more muscle.

But what about for long-term strength and mass gains? You need more myonuclei to get bigger. And you need more muscle to get stronger (in the long run). That means more muscle damage, which means you can’t train as frequently, at least for a period of time.

So, here are a few rough outlines you could use to take advantage of both approaches:

Take 2-4 weeks off lifting, but still be active during that time (active rest beats time completely off). In your first week back, use a body-part split, training each muscle or lift once per week, keeping things pretty reasonable – 2-4 sets of 5-12 reps for 2-3 exercises per muscle group, taking all lifts through a full range of motion. In your second week back, take things up a notch so you get equally sore again. Use things like slow or overloaded eccentrics (the eccentric portion of the rep – lowering the weight –causes much more damage than the concentric portion – actually lifting the weight), drop sets, rest-paused sets, weighted stretching, etc. In your third week back, keep the same split, and, to paraphrase Spinal Tap, kick those intensity techniques up to 11. Take a deload week after that (not a week off, but a week of easy training) to recover. Follow that up with a block of higher frequency, training each muscle or movement 3+ times per week. Use one of the DUP approaches floating around or an even higher frequency approach like the Bulgarian Method. After your strength and/or mass gains plateau (probably 6-10 weeks), take another 2-4 weeks of active rest away from strength training, and then start over again.

Simply cycle higher and lower frequency blocks. This is for people who can’t stand to take time away from the gym. Run a block of higher frequency training, during which you’re focusing on progressively adding more weight to the bar. When you plateau, take a deload week (not entirely off, but a week of easy training – lower volume, slightly lower intensity). Follow that up with a 3-6 week block of training each muscle/movement once per week. During this block, you’re less concerned with adding more weight, and more concerned with making each week progressively more difficult. A vanilla approach would just be adding an extra set or two for each muscle each week. Or, if you want to progressively add more advanced techniques (listed above) each week, that’s cool too. Once you’re right at the limit of what you can recover from, take an easy week, and dive back in to a high frequency block.

Cycle frequency for each muscle/movement. For a powerlifter, that means training one lift once per week with high volume and some pretty gnarly accessory work, one lift with higher frequency approach, and just doing the minimum required to maintain one lift. Do that for 4-6 weeks. If you need to, take an easy week after that block. Then, for the next 4-6 weeks, train another lift hard once per week, another lift with higher frequency, and just maintain the other.

Take 2-4 weeks of active rest away from training 1-4 times per year. Train however your normally would the rest of the time. You should be pretty darn sore your first couple of weeks back after each layoff. Perfect. That’s setting the stage for future growth. This is the “I don’t like to complicate stuff too much” strategy.

As a general note, since all of those approaches are aimed at promoting muscle growth, I’m assuming a caloric surplus. After a few rounds, if you need to cut, just focus on maintaining training volume and intensity as well as you can, and don’t try to do anything too fancy.

Further caveats and implications (AKA the cool stuff that doesn’t fit anywhere else in the article):

During your time off, don’t be a slug. Playing sports, doing some aerobic work, etc., is fine. Preferable, even. Staying active will help you lose less muscle and strength and build your general work capacity, while still increasing your responsiveness to subsequent strength training. DON’T use this as an excuse to be lazy. Stay active, but stay active by engaging in activities other than lifting. This is active rest with a purpose, not total rest for the sake of sloth. This would all help explain the rebound people report when coming off a layoff or finishing up a diet, quickly shooting past their prior strength/muscle peak. In either case, there’s likely going to be some muscle loss and decreases in RBE-related adaptations. In the case of the layoff, you lose muscle because you aren’t training, and it’s desensitized to loading because… you haven’t been loading it. In the case of a diet, you’ve likely lost a bit of muscle (especially if you’re getting really lean), and had to dial back training volume a bit, leading to a partial decrease in RBE-related adaptations. Also, when coming out of a diet, you’re at a metabolic advantage for gaining muscle mass. In both of those circumstances, you’re primed to not just regain lost muscle, but also add more muscle over your previous peak. Just to make this point clear, in the short term, muscle damage and the accrual of more myonuclei is neither necessary nor sufficient for muscle growth. Your muscles can grow just fine up to their myonuclear domain limits without any significant muscle damage. In the long run, muscle damage is likely necessary, but not sufficient. For example, downhill running causes a ton of muscle damage, but you don’t see trail runners with 32 inch quads. To reap the growth-promoting benefits, we’re mainly talking about reasonable levels of muscle damage in the context of lifting, not extreme wanton muscle damage for its own sake. There’s likely a limit for how long of a layoff is beneficial. The studies linked above used 12 days (for rodents) and 3 weeks. My hunch is that 2-4 weeks is probably the sweet spot, based on those studies and my own observations. With a longer layoff, you’ll likely end up losing some myonuclei so that the “rebound” just gets you back to your previous level; that was the general finding of the studies I mentioned with layoffs lasting 3-12 months. This is not referring to normal deloading. With a deload, your goal is to do as little as you can to maintain performance while diminishing fatigue, meaning minimizing muscle loss and likely increasing in strength (with fatigue diminished). The goal here is different: It’s to get rid of RBE-related adaptations to make your muscles easier to damage. Simply taking time away from the gym (or, if you just can’t bear to stay away from the gym, decreasing training stress substantially) and engaging in other activities will accomplish this, but will also lead to short-term decreases in muscle mass and strength. As a caveat to “only muscle damage causes myonuclear addition,” it’s also been shown that differentiated satellite cells will donate their nuclei when prompted by local growth factors like IGF-1 (local IGF-1 much more so than systemic IGF-1). While that’s not an overly important distinction, it is one worth pointing out. Muscle damage and overload are the two factors that increase the expression of myonuclear IGF-1 (and its variants) the most, as well as the release of IGF-1 and other growth factors by local immune cells. The studies linking this local IGF-1 expression to overload didn’t also measure muscle damage so it seems likely that the overload caused muscle damage, and that muscle damage is still the factor playing the primary role, with IGF-1 and its variants simply being the messengers that make the magic happen. When I referred to genetic freaks being the ones with larger satellite cell responses and an easier time gaining new myonuclei, keep in mind that I’m referring to rate of muscle growth, relative to your starting point. Interestingly, elite bodybuilders’ muscle fibers are about the same size as normal people who have just been lifting for 6 months. The obvious implication – the people who end up huge had more muscle fibers to begin with, OR gained more muscle fibers along the way (skeletal muscle hyperplasia, in addition to hypertrophy). If the difference between elite bodybuilders and the rest of us has to do (partially – I think a difference in total muscle fibers to start with is likely) with gaining more muscle fibers, how do you do that? The two main theories revolve around satellite cells (becoming myoblasts which fuse together to make a new muscle fiber instead of fusing to an existing muscle fiber) and damage-mediated responses (fibers splitting as a result of damage). So if you DO need to gain more muscle fibers to keep growing – a position that’s still somewhat controversial, at least in humans – causing muscle damage is probably the best way to do it. This would also help explain why Type II muscle fibers are more prone to growth than Type I fibers; they’re more easily damaged when training. I also think this may help explain people who report big gains in size and strength when, paradoxically, switching to lower volume, lower frequency approaches. The link between volume and hypertrophy is very clear in research, but it could be that people who train with high volumes and frequencies for a prolonged period of time simply build up so many RBE-inducing adaptations that it becomes hard to continue growing. By dialing back their workload, their muscle become more sensitive to loading again (though they’d still need to apply overload after initially scaling back training volume). It’s worth pointing out again that soreness and muscle damage aren’t perfectly correlated, and that strength decrements lasting 4 days or longer are a better indicator. However, as a quick and dirty way to assess muscle damage, being pretty sore for 2-3 days after a workout works well enough. It’s well-understood that progressive overload is key for long-term strength and size gains. However, logically, if you added more weight or volume indefinitely, you’d get to the point that training became your full-time job. Taking time away to re-sensitize your muscles to the effects of training breaks this vicious cycle. This will probably help you grow more after your break, and the worst case scenario is that you can resume training with lower volume and keep applying overload without having to resort to astronomical workloads. This is in line with the basics of periodization: You want to overload and improve some factors while allowing others to become relatively detrained, so that when you focus on them again, you’ll be able to improve them beyond their previous levels. In most sports, strength and muscle mass are just one part of the equation, and so it’s okay for them to become relatively detrained when you’re focusing more on aerobic adaptations, skill development, etc. However, in strength sports or bodybuilding, you’re really only trying to accomplish three things: build skill with the lifts, build mass, and increase strength. You do all three of those things by lifting heavy stuff repeatedly, so none of those factors are ever truly detrained. Therefore, taking time off, or spending dedicated blocks focusing on aerobic factors (like Ilya Ilin) to allow for some detraining of the muscles can be seen as an integral part of a long-term periodized training plan. Even when we say “overload causes muscle growth” we have to ask “how?” Addition of new myonuclei is the only way we know of currently (except for a couple of studies in mice with no satellite cells, but these are very rare exceptions to the rule) once your muscles reach their myonuclear domain limits. The recently maligned “tear your muscles down and build them back up” mantra of muscle growth actually seems to ring true, at least in the long run. You don’t necessarily have to cause lots of (or any!) muscle damage every workout to grow (as the success of higher frequency, lower volume-per-session programs has shown), but periodically causing muscle damage does seem to be a key to growth long-term. I think this is also a reason why new exercises are often effective at helping people get through size/strength plateaus. There’s nothing magical about the exercise itself, but new exercises are often sufficient to cause muscle damage because the body isn’t as adapted to them. Range of motion plays an important role as well, and probably helps explain why full-ROM lifting (probably due to the portion of the lift where the muscles are under the greatest stretch) generally causes more hypertrophy than partial ROM, even when equated for total work done or when higher loads are used for partial range of motion. Greater ranges of motion generally cause more muscle damage and (therefore?) IGF-1 release. The reason I stress that this is more important for more advanced lifters is that muscle growth of up to 15% (pretty solid gains for a new lifter) can come without addition of new myonuclei, 15-27% is a bit of a gray zone, and gains of more than 27% require the addition of new myonuclei, as your muscles max out their myonuclear domains. So, once you’ve already put on some size, these strategies become increasingly useful to put on even more. If you’re not taking time off occasionally, you need to make sure your program has periods of lower frequency training where you can focus on generating more muscle damage. They don’t have to be the focal point of your training, but they should probably be included. You may recognize this as being very similar to the old idea of “strategic deconditioning.” It is. If you’re already familiar with it, this article just provides some insight into why it works and how to incorporate it. This may be one reason why many studies show men and women attaining similar hypertrophy in the short term (relative to initial lean body mass. Several of those studies are presented in the linked article, though I disagree with the conclusion that long-term muscular potential is the same. That’s the subject for another article, though), but men wind up gaining more muscle (relative to initial lean body mass) in the long run. Women experience less muscle damage from training, largely because estrogen is protective against muscle damage. Why do anabolic steroids work so well? Because they work by this same mechanism – expanding the satellite cell pool helping muscle fibers gain more nuclei, faster. Just to re-iterate a point I made in this article: myonuclei-related factors are a major reason why steroid use gives people a long-term advantage in sports, even after they stop using. Even after they go off steroids, those myonuclei hang around for years afterward, leaving them with a muscular advantage that lasts for years after their last cycle.

I don’t want you to walk away from this thinking that extended rests are the holy grail for long-term progress. The key points had to do with how your muscles grow in the long run by adding more myonuclei, rethinking the role of muscle damage as one of the integral players in long-term (though maybe not short-term) muscle growth, and moving away from the simple stimulus/response paradigm when thinking about training effects.

The response you get from training is not just a direct result of the training stress. It’s an interaction between the training stress and how responsive you are to that stress. Overload is necessary because that responsiveness decreases over time. To continue making progress, strategies to increase responsiveness should be considered just as strongly as strategies to increase the training stress. Time away from training is one way to accomplish that (and probably the most robust way), but other things you should already be doing play a role as well – sleeping more, managing other stressors outside the gym, and including some variety in your training.

At the very least, if you’re not sold on the idea of taking time off, you should at least include periods of lower frequency and higher variation in your training. Some of the RBE-inducing adaptations are general, and others are more specific to the specific movements being done and the training parameters used. Cycle in different exercises, change your loading schemes, and use techniques aimed at causing more muscle damage from time to time (slow or overloaded eccentrics especially). This will cause more muscle damage than just increasing training volume in the same general intensity ranges for the same lifts. It’s a matter of including enough novelty to avoid staleness and provoke an adaptive response, not pure “muscle confusion.” Alternately/additionally, even if you don’t want to take time entirely off, dialing back your training volume/intensity for a month or so from time to time would probably be sufficient to hold on to your strength and size gains in the short term, while also making you more prone to muscle damage and subsequent muscle growth when you ramp training volume and intensity back up.

That’s about it. I’m sure I’ll get mixed reactions to this article ranging from “we’ve known about this forever” to “he’s saying the ONE WEIRD TRICK to more gains is by doing less. What is this, a late night infomercial?”

For the former group, we’ve suspected this for a long time, so it’s cool that we now have insight into some plausible mechanisms for why it could work. For the latter group, you’re partially right and partially wrong. The idea of “tricking” your muscles into getting larger (since there are selection pressures against growth past a certain point. And no, I’m not saying this is a trick for unlimited growth. There’s obviously a limit somewhere), and doing so by periods NOT training does sound like too-good-too-be-true salesmanship, but I’ll point out two things. 1) nowhere did I say “this is 100% for sure what’s happening,” 2) I suggested other ways to accomplish the same outcome, and 3) it sounds too good to be true until you realize that the crux of why it might work is increased muscle damage. The brief time away from training isn’t sloth. It’s the calm before the storm.

Don’t be afraid of muscle damage. Being sore from time to time is important – perhaps even necessary – for long-term muscle growth. Though their are clear benefits to higher-frequency approaches in the short-term, lower frequency approaches that let you cause some more muscle damage each session are likely beneficial in the long run by letting you gain more myonuclei, raising the ceiling on how much more you can grow. You can, and should, combine both approaches to maximize long-term results.

Edit: I just want to make a few things clear, that I don’t think were expressed well enough at the time of initial publication. Thanks to Eric Helms for pointing out these shortcomings to ensure people weren’t getting the wrong takeaways from this article:

1) The repeated bouts effect isn’t all bad. With less damage and faster recovery times, you’re able to train harder, more frequently, and get in more quality practice with the lifts you’re trying to master.

2) I don’t want people to walk away from this thinking that taking time off is some holy grail for long-term mass gain. I purposefully made sure to hammer home the point that that part of the article was speculative. The basic physiology (long-term hypertrophy being dependent on the addition of new myonuclei, primarily via muscle damage, allowing for more total growth) was the important part. In terms of how to achieve that, time off is listed fourth on the infographic (after overload, novelty, and eccentric stress) for a reason – the four ways to achieve that muscle damage are listed roughly in order of importance.

3) I also don’t want you to get the idea that muscle damage is the only important factor for hypertrophy. It’s a matter of the time scale. In the short-term, overload (mainly training volume) is both necessary and sufficient for muscle growth, and damage is neither necessary nor sufficient. In the long-run, overload is necessary but not sufficient (if sufficient muscle damage isn’t taking place), and the same applies to muscle damage (it needs to happen, but it’s not going to cause growth by itself without sufficient training volume). Ultimately, training volume is still the most important factor. Increasing volume will generally be enough to cause muscle damage as well, but the other options are still worth keeping in mind if you get to a point that further increasing training volume becomes either impossible or unfeasible due to issues with recovery or time constraints.

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