Sarcoplasmic vs Myofibrillar Hypertrophy: Bodybuilding Myth vs Cellular Reality

Is bodybuilder muscle just water and sarcoplasm, while powerlifter muscle is “dense”? Not in any way the research can prove. Sarcoplasmic vs myofibrillar hypertrophy is a real topic in muscle biology, but the gym version of it (high reps for fluff, heavy singles for density) has never been demonstrated in a trial.

Here is what the biopsies and electron microscopy studies actually show, where they disagree, and what to do with your training. This is a deep-dive inside our complete guide to muscle hypertrophy for natural lifters, so start there if you want the full picture.

What do sarcoplasmic and myofibrillar mean?

A muscle fiber is a long cell. Inside it you have two broad compartments.

• Myofibrillar: the contractile machinery. Actin, myosin and the other proteins arranged in sarcomeres, bundled into myofibrils. This is the part that shortens and produces force.
• Sarcoplasmic: everything else inside the cell. Fluid, glycogen, enzymes for energy production, mitochondria, the sarcoplasmic reticulum. Often called “non-contractile,” though that is slightly misleading because these parts keep the contractile machinery running.

The popular claim is that you can grow one without the other. Train in the 8-15 rep range and you get “sarcoplasmic” size. Lift heavy for fives and you get “myofibrillar” size. Neat story. The problem is that no one has run a trial showing a rep range does that.

Is sarcoplasmic hypertrophy real?

This is where it gets interesting, because there is real data behind the debate. It is just thinner than forum posts make it sound.

The 6-week biopsy study

In 2019, a research group at Auburn University had 30 previously trained men (average 5 years of training) do 6 weeks of high-volume resistance training with biopsies of the vastus lateralis before, at week 3 and at week 6. They then looked closer at 15 men whose fibers clearly grew (Haun et al., 2019).

In those 15 responders:

• Mean fiber cross-sectional area rose 23%.
• Muscle glycogen concentration did not change.
• Citrate synthase activity, a marker of mitochondrial volume, fell 24%.
• Actin and myosin concentrations fell roughly 30%, though the statistical tests only approached significance (p = 0.052 and 0.055).
• Proteins tied to glycolysis and other energy pathways went up in the sarcoplasmic fraction.

Eight days after the last session, seven of the participants were biopsied again. Sarcoplasmic protein concentration was still higher than baseline and actin and myosin were still lower.

The authors read this as sarcoplasmic expansion: the fiber got bigger, and the contractile proteins became more diluted. Reasonable reading. It also comes with caveats: only 15 men, borderline p-values in the main analysis, one program, and commercial funding among the supporters (Impedimed, plus a gift in kind through a coaching company, both disclosed in the paper).

The review that reframes the whole question

The same lab, with Brad Schoenfeld and others, wrote a critical review the same year. It points out that the textbook model assumes fiber growth comes with proportional growth in myofibrillar protein, but that there is “ample evidence” that myofibrillar concentration may be diluted by sarcoplasmic expansion as fibers grow. It also notes that changes at the whole-muscle, fiber and molecular levels are often poorly correlated with one another (Haun et al., 2019).

Read that twice. The honest conclusion is not “sarcoplasmic hypertrophy is the main thing.” It is “our measurements of what happens inside the fiber are noisy, and the neat model is shakier than the textbooks suggest.”

Does the evidence agree? No.

Conflicting results deserve a fair hearing, so here they are.

Study A, high volume (2019). Trained men, 6 weeks, high volume. Fiber area up, actin and myosin concentration down, sarcoplasmic proteins up (Haun et al., 2019).

Study B, high load, low volume (2020). Fifteen recreationally trained men did full-body, low-volume training at 68-90% of 1RM for 10 weeks. Type II fiber area and squat strength rose. But sarcoplasmic protein concentration and muscle tissue percent fluid did not change, myosin heavy chain trended slightly down (-2.9%, p = 0.069) and actin dropped about 3.2%. Only 13 sarcoplasmic proteins changed, and metabolism-related proteins were not affected (Vann et al., 2020). Odd detail: whole-body fat-free mass decreased in that study, which tells you how messy these outcomes can be.

Study C, 12 weeks in untrained men (2018). Researchers split young men by how much muscle they gained. Myofibrillar and sarcoplasmic protein concentrations did not differ between high and low responders, before or after training. Citrate synthase fell over time across both groups, and high responders had higher citrate synthase activity overall (Roberts et al., 2018).

Why might they differ? Different training volumes, different populations (trained versus untrained), different measurement methods, small samples, and the simple fact that biopsy results from one spot in one muscle are noisy. A cautious reading: sarcoplasmic expansion can probably happen, particularly with high-volume work in trained people, but the size and consistency of the effect is not established, and heavy lower-volume training looks less likely to produce it.

Do bodybuilders and powerlifters have different muscle density?

This is the part that fuels most of the arguments, so let’s be exact about what the old data say.

In 1982, MacDougall and colleagues took triceps biopsies from two international-level powerlifters and five elite bodybuilders, plus five volunteers measured before and after 6 months of arm training. Fiber areas in the elite group were not significantly different from the trained controls, despite far bigger arms and strength, which suggests the elite group simply had more fibers. Myofibrillar volume density was significantly lower and cytoplasmic volume density higher in the elite group than in the trained controls. The authors also noted more structural abnormalities in the elite group and said these might be associated with anabolic steroid use (MacDougall et al., 1982).

Three things matter here:

1. The powerlifters and bodybuilders were analyzed as one elite group. Seven people. You cannot read off “bodybuilders are less dense than powerlifters” from that paper.
2. Possible steroid use is flagged by the authors, so this may not describe natural lifters.
3. It is a snapshot of people with extreme muscle, not a trial of what a rep range does.

In another small data point, a 2020 pilot of 18 men (6 per group) found total myofibrillar protein per mg of muscle was higher in trained men than in older untrained men, but not significantly different from younger untrained men. Actin and myosin abundance per mg was higher in the trained men than in both untrained groups. The authors described the packing difference as modest (about 9%) and called the results preliminary, given the small groups (Vann et al., 2020). So if there is a “density” difference between trained and untrained muscle, the best available data say it is modest.

None of this proves bodybuilders and powerlifters build different tissue. What it tells you: elite people differ in many ways, and the cleanest explanation for very large muscles may be fiber number and total volume of tissue, not a fancy fiber recipe.

What about glycogen and mitochondria?

These are the usual suspects for “non-contractile growth.”

Glycogen. It binds water, so more glycogen can mean a fuller-looking muscle, which is why a high-carb day can change how you look in the mirror. In the 6-week high-volume study, though, muscle glycogen concentration did not change (Haun et al., 2019). So glycogen did not explain the fiber growth in that trial. The short-term swelling you feel mid-workout is a different thing; we cover it in gym pump vs true muscle hypertrophy.

Mitochondria. Older work found that 6 months of heavy training in six men reduced mitochondrial volume density by 26% and the effect correlated with fast-twitch fiber growth (r = 0.845). The authors concluded this was dilution from larger myofibrils, not a loss of mitochondria (MacDougall et al., 1979). Newer trials found falling citrate synthase activity too, in the 6-week study (24% drop) and in the 12-week study. Mitochondrial markers per unit of muscle fall as fibers grow. That does not mean you lose conditioning. It means a bigger fiber has to build more machinery just to keep the same density.

Does this change how you should train?

Short answer: not much.

If sarcoplasmic expansion is real, it is not something you can aim at. If myofibrillar growth is the main driver, it is not something you can isolate. Either way, the practical levers are the same ones that drive growth in general.

Heavy and light loads grow muscle similarly. A meta-analysis of 21 trials with sets taken to failure found hypertrophy was similar between low-load (60% 1RM or less) and high-load training, while 1RM strength favored heavy loads (Schoenfeld et al., 2017). A later review argued that muscular adaptations can be obtained across a wide range of loading zones, challenging the idea of a strict “hypertrophy rep range” (Schoenfeld et al., 2021). If you want the deeper breakdown, see high-load vs low-load hypertrophy.

Here is how to apply it:

• Use a mix. Heavy compounds around 5-10 reps for strength and some lighter, higher-rep isolation work for muscle and joint comfort.
• Take sets close to failure. Reps far from failure with light loads are where “pump work” stops being productive.
• Progress something. More reps, a little more weight, better control. Our training volume calculator helps you check how many hard sets per muscle you are actually doing each week.
• Do not turn this into a program design question. A balanced split like the ones on our free plans page already covers a sensible spread of ranges.

Why does the myth stick around?

Three reasons, all understandable.

First, elite bodybuilders and elite powerlifters really do look and perform differently. That is easy to read as different tissue, when selection, genetics, body composition, drug use and training goals all differ too.

Second, strength-to-size ratio varies between people. Neural factors, tendon insertions and limb length, and technique shape strength, so “strong for his size” is not evidence for dense fibers. That connects to how fast and slow fibers respond to training and to what actually drives growth, which we cover in mechanical tension vs muscle damage.

Third, the biology is not fully settled, so each side can quote a paper. That is exactly why a cautious reading helps. Newer biopsy work suggests concentration of contractile protein can fall as fibers grow in some situations. What has not been shown is that this matters for strength, long-term health or how you should program.

If you are curious how growth gets laid down at the nuclear level, satellite cells and myonuclear addition is the natural next read.

Limits of the evidence

Be honest about what we do not know.

• Small samples. The key biopsy studies had 15 to 30 participants, and the electron microscopy study had seven elite lifters.
• Narrow populations. Mostly young, college-aged men. Very little in women, older adults or advanced natural bodybuilders.
• Short durations. 6 to 12 weeks is not years of training.
• Measurement noise. A biopsy is a tiny sample from one muscle, and concentration measures can shift with how the tissue is processed.
• No direct test. No trial has randomized people to “sarcoplasmic” and “myofibrillar” programs and tracked strength and size outcomes.

If you are on medication, have a muscle or kidney condition, or notice unusual swelling, pain or dark urine after training, check with a doctor. None of this article is medical advice.

The bottom line

Muscle growth is not a choice between fluid and protein. Fibers grow, and they probably change in more than one way when they do. In some trained men doing high-volume work, contractile protein concentration appeared to dilute. In others, with heavier work, it barely moved. And no study shows that you can steer which one happens with a rep range.

So lift hard, close to failure, across a mix of loads. Add reps or weight over time. Eat enough protein, around the amounts in our protein calculator, and sleep. The cell biology debate is fascinating. Your next set is more important.