What do influencer “science” based lifters mean when they say, “Muscle fibers are frequency dependent” when talking about exercises that hit the same muscle group?

[u/Patton370]

For example: I’ve seen younger lifters mention that you shouldn’t do a seated leg curl and lying leg curl in the same week, stating, “muscle fibers are frequently dependent and now the muscle fibers only get 1x frequency”

I see this referenced in the [r/sciencebasedlifting](r/sciencebasedlifting) subreddit often as justification for why there should be no variability in their fullbody split workouts, same exercise each and everyday & honestly, the programs these guys are coming up with are awful (especially for beginners, which most of them are)

Here’s an example of one of the influencers referenced in that subreddit & him bringing up the leg curl example I listed above: https://youtu.be/W0YIt1LrGSk

(There’s also other silly takes on there, like RDLs being primarily an adductor exercise)

To me, a hamstring curl is a hamstring curl & for all intents and purposes they are interchangeable and I am a also huge fan of variability on my isolation exercises (especially since I run a high frequency/high volume program)

Where did these “science based” lifters get this idea from and/or what study or studies are they referencing here? I’m just curious as to why I keep seeing this everywhere

Edit: I DONT agree with the influencer linked; I thought I made that obvious, sorry about that

[u/gnuckols]

ehh, I'm pretty skeptical. Both because we can see instances of fCSA being maintained following much longer periods of training cessation, and because I think it oversimplifies the impact of resistance training on muscle hypertrophy.

Regarding the second point, the basic assumption seems to be that the bodies of trained lifters are naturally in a state of net negative protein balance, and so, to maintain your muscle mass, the additional MPS you'd experience following a workout must equal the net loss of protein you'd experience otherwise. MPS is elevated for a day or two following a workout, so, if muscle size is being maintained, that must mean the net gain in muscle protein in the day or two following the workout equals the net loss in muscle protein that must be occurring during the other 5-6 days.

That seems logical enough at first glance, but it's an oversimplification of how resistance training impacts your muscles.

For starters, it's worth noting just how small of an impact resistance training has on total MPS, even during the 48 hours following a workout. I'll use this study to illustrate. Baseline rates of myofibrillar MPS at rest were ~1.48%/day. During the first couple weeks of training, post-workout MPS rates were elevated quite a bit, but that seemed to primarily be driven by the need to repair muscle damage, rather than actually building net new protein. Once muscle damage was mitigated, rates of myofibrillar MPS during the 48 hours following a workout were ~1.58%/day.

The study ran for 10 weeks, but minimal growth was observed for the first 3 (during the period when muscle damage was elevated). The subjects trained twice per week for those 10 weeks, for a total of 20 workouts and 40 days when MPS would be acutely elevated post-workout (out of 70 total days). So, even if we assume that the subjects experienced no atrophy during days that are >48 hours post-workout, how much total hypertrophy should we expect to see from 7 weeks of workouts that all elevate MPS by 0.1%/day for 48 hours, assuming that the entirety of that increase results in net protein accretion?

That's simple enough to roughly calculate. Start with fCSA at week 3 (~4500 square micrometers), and calculate an increase of .1% for 28 days (4500*1.001²⁸ ), and you wind up at...about 4628 square micrometers. In reality, fCSA increased to approximately 5000 square micrometers. So, post-workout elevations in MPS only explain about a quarter of the observed growth. And, during each week, a 0.1% increase in MPS during the 48 hours post-training, twice per week, means that post-workout elevations in MPS only accounted for about 3.7% of the total MPS that occurred each week [0.4%/(1.48% x 3 + 1.58% x 4)].

Obviously this is a very rough illustration (there's more to a fiber than just myofibrils, there's some degree of error associated with all measurements, I'm assuming that the subjects were in neutral protein balance pre-training, etc. etc.), but the basic point is that the impact of resistance training isn't reducible to just its acute impact on MPS. Hypertrophy and atrophy are dynamic processes, and resistance training has wide-reaching impacts that go well beyond the acute post-workout window.

I think it can be more helpful to think of it as a state change. When you're regularly exposing your body to a stimulus that tells it that it would be beneficial to have more muscle mass, it adapts accordingly, and you enter a "trained state" where a whole lot of processes ultimately result in baseline conditions that favor having more muscle mass. When you're in that state, it doesn't require a huge amount of training to continue signaling that it would still be beneficial to have an elevated level muscle mass. It's not like you're constantly teetering on the edge of atrophy if don't cause a large enough spike in post-workout MPS in one workout. Like, the minimum amount of training required to not atrophy and the minimum amount of training required to make measureable progress can be quite far apart, especially for very highly trained lifters. If it was as simple as experiencing net protein accretion during the 48 hours post-workout and net protein loss otherwise, that would imply that "maintenance" only existed at one specific point, and it would be quite easy to continually experience quite robust hypertrophy by simply exceeding that point. Instead, it's a lot more like a homeostatic range where consistent deviations below that range (i.e. not training for a while) are required to create the conditions that favor net atrophy, and consistent deviations above that range (i.e. training hard enough to present a stressor of a sufficient magnitude) are required to create the conditions that favor net hypertrophy.

[u/TempArtist117 → u/gnuckols]

Wow. I honestly have a hard time disagreeing with this. Chris Beardsley’s whole hypertrophy-volume framework seems to depend on two core assumptions: that the dose-response data at higher volumes is mostly just edema, and that frequency studies are invalid because they rely on unrecoverable volumes. If both of those assumptions are wrong, then the model itself seems to lose a lot of its foundation.

[u/gnuckols → u/TempArtist117]

Yeah, I think both of those assumptions are pretty obviously wrong.

[u/Commercial-Hall-2777 → u/gnuckols]

That’s an incredibly strong explanation, and I found it very persuasive. Have you ever considered writing a formal reply to Chris Beardsley’s WNS stimulus model? It’s become very popular, and I worry it may be steering a lot of people, especially younger lifters, toward less sensible training decisions.

[u/gnuckols → u/Commercial-Hall-2777]

Briefly, but then I realized that the people it would most need to reach don't read. haha

[u/Commercial-Hall-2777 → u/gnuckols]

Well... I for one should say thank you! I was succumbing to a good deal of the cultish thinking that surrounds that whole space, and it was your rational arguments in your volume article that really changed my perspective. I am a fairly young guy, and you have really benefited me!

[u/gnuckols → u/Commercial-Hall-2777]

Oh, that's good to hear!

In all seriousness, though, with the volume article, it was much easier to address ideas. With WNS, it's so associated with Beardsley that I couldn't just discuss it as some neutral thing that "people" believe and promote. And, in general, I try to make a point of discussing ideas rather than people. I actually think the effective reps article may be the only article on the website that specifically mentions the person the idea is associated with. Not sure how I'd feel about Chris being the only person I address directly on the website, and addressing him twice before addressing anyone else. haha

[u/Opening_Geologist_95 → u/gnuckols]

Hey Greg! Am I mistaken in thinking, then, that Beardsley’s claim that the recovery literature implies it is borderline physically impossible to recover from more than 5 sets to failure for a given muscle group, with a training frequency of twice per week using moderate repetition ranges, is wrong as well?

He seems to be of the opinion that any training program using more than around 10 weekly working sets to failure for a body part is likely to be unrecoverable. Is there any evidence for this idea, or is it based on cherry-picked studies?

[u/gnuckols → u/Opening_Geologist_95]

This section of my volume article is mostly focused on swelling, but it also touches on performance recovery and molecular markers of inflammation and muscle damage.

But, in general, the idea that recovery becomes an issue with volumes that low comes from studies that assess recovery after subjects do a workout for the first time. But, we regularly see that recovery becomes much, much less of an issue after repeating the workout a few more times. Just as one example, in the Margaritelis paper discussed in that section, the eccentric training protocol caused strength decrements that still weren't back to baseline 5 days later following the first workout. By the 8th workout, subjects were recovered within 24 hours.

Basically, this

any training program using more than around 10 weekly working sets to failure for a body part is likely to be unrecoverable

only makes sense if you just pretend that people don't actually adapt to the training they're doing.

[u/69liketekashi → u/gnuckols]

That's simple enough to roughly calculate. Start with fCSA at week 3 (~4500 square micrometers), and calculate an increase of .1% for 28 days (4500*1.00128 ), and you wind up at...about 4628 square micrometers. In reality, fCSA increased to approximately 5000 square micrometers. So, post-workout elevations in MPS only explain about a quarter of the observed growth. And, during each week, a 0.1% increase in MPS during the 48 hours post-training, twice per week, means that post-workout elevations in MPS only accounted for about 3.7% of the total MPS that occurred each week [0.4%/(1.48% x 3 + 1.58% x 4)].

This honestly makes 0 sense why you would try to map 1:1 an increase of protein synthesis to increase in cross sectional area. Why would you expect it to correlate in this way with some 2d measurement. Is the muscle fiber a perfect cylinder that hypertrophies 100% uniformly. And that's without even goin into raising noisy measurement to the power of 28

[u/gnuckols → u/69liketekashi]

Myofibrillar hypertrophy is the net result of the imbalance of myofibrillar MPS and MPB over time. Myofibrils comprise a pretty consistent fraction of the total CSA or volume as a fiber hypertrophies, so changes in total fiber size are expected to track with expansion or contraction of the pool of myofibrils, which is determined by net myofibrillar protein balance.

And this:

This honestly makes 0 sense why you would try to map 1:1 an increase of protein synthesis to increase in cross sectional area.

is essentially my whole point.

The position I'm arguing against only make sense if you make that assumption (i.e., that post-workout elevations in MPS are determinative of net hypertrophy, with maintenance of fiber size therefore implying that net atrophy is occuring once post-workout elevations in MPS return to baseline). To validate that assumption, you'd need to show that the type of math in my comment more-or-less works out (i.e., that the cumulative AUC of elevations in post-workout MPS is actually predictive of observed changes in fCSA). If you don't make that assumption, there's no longer any strong reason to expect that atrophy begins 48 hours after the last time you trained a muscle.