Hypertrophy and hyperplasia are two prolix words that refer to how muscles grow.
Specifically, hypertrophy occurs when muscle cells get bigger, and hyperplasia occurs when the number of muscle cells increases.
Countless studies show that hypertrophy occurs in humans, normally as a result of lifting weights. Hyperplasia has proven to be a bit of a physiological chimera, though, with debate ongoing about whether it exists or not.
Hyperplasia truthers contend that hypertrophy and hyperplasia both contribute to muscle growth, and if you want to build as much muscle as possible, you should train to target both.
Hyperplasia deniers disagree. They say that hyperplasia is a myth based on questionable animal research that’s neither safe nor practical to extrapolate to humans, or that if it does occur, it’s too insignificant to matter. If you want to get jacked, they say, just focus on training for hypertrophy.
In this article, you’ll learn the difference between hypertrophy and hyperplasia, what science says about both, and what may or may not work for increasing both.
Muscle hypertrophy is the scientific term for an increase in muscle cell size.
(Hyper means “over” or “more,” and trophy means “growth,” so muscle hypertrophy literally means the growth of muscle cells.)
Technically, muscle hypertrophy can be achieved by increasing any of the three main components of muscle tissue—water, glycogen, or protein—though weightlifters are normally most interested in increasing the amount of protein in muscle (also known as myofibrillar hypertrophy).
Muscle hyperplasia refers to the formation of new muscle cells (plasia means “growth”).
Increasing the number of muscle cells in a muscle increases its total size the same way that increasing the size of individual muscle cells does.
While there’s no doubt about muscle hypertrophy’s contribution to overall muscle growth, many claim that muscle hyperplasia doesn’t occur at all in humans, and any increase in muscle size is solely due to an increase in the size of individual muscle fibers (hypertrophy).
Of course, all of these studies are on animals. More to the point, they required strange and in some cases cruel and unusual protocols to elicit muscle hyperplasia that simply aren’t workable in humans.
For example . . .
- In one study, scientists found that they could cause a 294% increase in muscle size due to hyperplasia when they attached progressively heavier weights to a bird’s wing for 28 consecutive days.
- In another, researchers found that they could cause hyperplasia in rats by cutting them open and partially destroying some of their muscle tissue, then letting it heal.
- And in yet another, scientists found that hyperplasia occurred in salmon as they developed during adolescence.
This makes it difficult to draw any firm conclusions about what actually causes hyperplasia, and even more difficult to see how you or I could use any of this information to cause hyperplasia in our muscles.
While there are a handful of human studies on muscle hyperplasia, they’re plagued with methodological issues.
For instance, multiple studies show that bodybuilders have significantly more total muscle cells than people who don’t exercise regularly. This has led some people to suggest that years of heavy, high-volume weightlifting may cause muscle hyperplasia.
There are several problems with this line of thinking, though . . .
- We have no idea how many muscle cells everyone had before the study. It’s possible (and perhaps likely) that the bodybuilders in these studies were just born with more muscle cells than the sedentary people.
- The studies didn’t directly measure or demonstrate muscle hyperplasia. Instead, they just found a correlation between bigger muscles and more muscle cells. Muscle hyperplasia may or may not have caused this to occur.
- Most other studies have found that bodybuilders and sedentary people have the same number of muscle cells. This would indicate that most bodybuilders have bigger muscles through growing their existing muscle cells (hypertrophy), not adding new ones.
It’s also worth bringing up the ever-present elephant in the room: steroids could’ve helped the bodybuilders in these studies to grow new muscle cells, since research shows that steroid users have significantly more muscle cells than natties.
(It might also help explain why people who’ve used steroids tend to keep at least some of their chemically enhanced gains years after they stop taking drugs.)
There’s one other study that looked at hyperplasia in humans that didn’t use bodybuilders as participants.
In it, researchers at the University of Umeå autopsied the left and right anterior tibialis muscles (the muscles that lie close to your shin bones) of seven previously healthy right-handed men with an average age of 23.
They used this method because . . .
- Everyone uses their body asymmetrically (around 90% of us have a right-side bias) which causes muscles on each side of the body to develop differently.
- For most people, this results in the muscles of their non-dominant leg being larger and stronger than the muscles of their dominant leg (which is counterintuitive, but true).
- The lower-leg muscles are used in many daily activities. Thus, any differences in how these muscles develop should be more pronounced than in other, lesser used muscles (like the biceps).
The results of the biopsies showed that there were 10% more muscle fibers on average in the left muscle than the right, which the researchers believed was best explained by hyperplasia.
And this all seems plausible . . . until you realize just how shonky muscle biopsies can be.
For example, one study that used muscle biopsies to measure fiber type composition found that “duplicate” biopsies were up to 12% different from one another (probably due to measurement error). What’s more, muscle fibers don’t run from one end of a muscle to the other, which means you can get very different results if the biopsies are taken at different points along the same muscle.
Even if you take the results at face value, they suggest you’re only likely to experience a ~10% in muscle growth after ~23 years of almost continuous training.
Basically, if hyperplasia does exist, it likely takes a long time to occur, and only contributes a whit to the size and strength of your muscles.
So, where does that leave us?
We know that hyperplasia occurs in animals, though how it happens seems to differ depending on the species and the protocols used to cause it.
Whether it occurs in humans is still an open question.
The two most plausible ways to cause hyperplasia are:
- To take steroids (although it’s still not clear how effective this really is).
- To stress a muscle for several hours every day for years (and possibly decades), which may be enough to boost muscle hyperplasia by a few percentage points . . . maybe.
In other words, there are no guaranteed ways to cause hyperplasia, and even the most promising methods are likely to fall flat.
The best way to trigger hypertrophy is to lift weights.
Specifically, you should . . .
- Spend the majority of your time in the gym training with weights that are around 75-to-85% of your one-rep max, or that allow you to do about 4-to-10 reps before reaching muscular failure (the point at which you can’t move the weight despite giving your maximal effort).
- Do 10-to-20 sets per muscle group per week.
Training like this creates enough tension in your muscle fibers to activate specialized proteins in muscle cells, and kicks off a cascade of genetic and hormonal signals that stimulate the body to build new muscle tissue.
These signals increase an enzyme in the body known as mammalian target of rapamycin, or mTOR, which boosts protein synthesis, and voila, you’ve caused hypertrophy.
It’s possible that hyperplasia can occur in humans, but it’s not at all clear if we can cause it.
If it does occur, it’s probably just a side effect of lifting weights properly rather than something you can trigger with “special” diet or training techniques.
That hasn’t stopped people trying to develop training protocols that cause hyperplasia, of course.
Since the largest increase in muscle fiber number occurred in animal studies that used extreme weighted stretching, some fitness gurus claim you can do the same thing on a smaller scale.
Usually, they recommend stretching in between sets and using high-reps and light weights in an attempt to mimic the protocols used in animal studies.
And while at least one study has shown that stretching alone can cause muscle growth in humans (albeit through hypertrophy), and several others have found an association between weighted stretching and an increase in anabolic hormones in the body, none have found that weighted stretching causes hyperplasia in humans.
Of course, this idea doesn’t pass the smell test, either. Even if you really took this advice to heart and stretched for say, 20 minutes per day and did 20 high-rep, low-weight sets per day for a muscle group (and let’s assume you didn’t get injured in the process), this is still nowhere close to loading a muscle with weight for 28 days straight.
This is like assuming that because water can erode rock, you can cut through a boulder with a garden hose.
Thus, until we know more about hyperplasia in humans, it’s probably sensible to stick with training techniques that have been shown time and again to increase muscle size. Lifting heavy weights, doing the right amount of volume, getting enough rest, and all of the other “unsexy” stuff that really moves the needle.
+ Scientific References
- BJ, S. (2010). The mechanisms of muscle hypertrophy and their application to resistance training. Journal of Strength and Conditioning Research, 24(10), 2857–2872. https://doi.org/10.1519/JSC.0B013E3181E840F3
- SE, A., PK, W., ME, D., & WJ, G. (1989). Regionalized adaptations and muscle fiber proliferation in stretch-induced enlargement. Journal of Applied Physiology (Bethesda, Md. : 1985), 66(2), 771–781. https://doi.org/10.1152/JAPPL.19220.127.116.111
- JA, C., & FW, B. (1998). Myogenin mRNA is elevated during rapid, slow, and maintenance phases of stretch-induced hypertrophy in chicken slow-tonic muscle. Pflugers Archiv : European Journal of Physiology, 435(6), 850–858. https://doi.org/10.1007/S004240050593
- D, D. J., V, J., & W, H. (2015). Intermittent stretch training of rabbit plantarflexor muscles increases soleus mass and serial sarcomere number. Journal of Applied Physiology (Bethesda, Md. : 1985), 118(12), 1467–1473. https://doi.org/10.1152/JAPPLPHYSIOL.00515.2014
- M, N., A, Y., S, N., T, N., T, Y., M, I., K, M., H, O., & S, N. (2002). A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle. Biochemical and Biophysical Research Communications, 293(1), 247–251. https://doi.org/10.1016/S0006-291X(02)00209-7
- PD, G., BF, T., RL, M., & M, R. (1981). Muscular enlargement and number of fibers in skeletal muscles of rats. Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology, 50(5), 936–943. https://doi.org/10.1152/JAPPL.1918.104.22.1686
- W, G., GC, E., & F, B.-P. (1977). Skeletal muscle fiber splitting induced by weight-lifting exercise in cats. Acta Physiologica Scandinavica, 99(1), 105–109. https://doi.org/10.1111/J.1748-1716.1977.TB10358.X
- Higgins, P. J., & Thorpe, J. E. (1990). Hyperplasia and hypertrophy in the growth of skeletal muscle in juvenile Atlantic salmon, Salmo salar L. Journal of Fish Biology, 37(4), 505–519. https://doi.org/10.1111/J.1095-8649.1990.TB05884.X
- J Antonio, & W J Gonyea. (n.d.). Muscle fiber splitting in stretch-enlarged avian muscle - PubMed. Retrieved September 7, 2021, from https://pubmed.ncbi.nlm.nih.gov/7968431/
- D’Antona, G., Lanfranconi, F., Pellegrino, M. A., Brocca, L., Adami, R., Rossi, R., Moro, G., Miotti, D., Canepari, M., & Bottinelli, R. (2006). Skeletal muscle hypertrophy and structure and function of skeletal muscle fibres in male body builders. The Journal of Physiology, 570(Pt 3), 611. https://doi.org/10.1113/JPHYSIOL.2005.101642
- L, L., & PA, T. (1986). Motor unit fibre density in extremely hypertrophied skeletal muscles in man. Electrophysiological signs of muscle fibre hyperplasia. European Journal of Applied Physiology and Occupational Physiology, 55(2), 130–136. https://doi.org/10.1007/BF00714994
- SE, A., WH, G., WJ, G., & J, S.-G. (1989). Contrasts in muscle and myofibers of elite male and female bodybuilders. Journal of Applied Physiology (Bethesda, Md. : 1985), 67(1), 24–31. https://doi.org/10.1152/JAPPL.1922.214.171.124
- JD, M., DG, S., SE, A., & JR, S. (1984). Muscle fiber number in biceps brachii in bodybuilders and control subjects. Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology, 57(5), 1399–1403. https://doi.org/10.1152/JAPPL.19126.96.36.1999
- T, H., E, J., & B, S. (1978). Cross-sectional area of the thigh muscle in man measured by computed tomography. Scandinavian Journal of Clinical and Laboratory Investigation, 38(4), 355–360. https://doi.org/10.3109/00365517809108434
- P, S., ER, F., P, N., & A, T. (1981). The relationship between the mean muscle fibre area and the muscle cross-sectional area of the thigh in subjects with large differences in thigh girth. Acta Physiologica Scandinavica, 113(4), 537–539. https://doi.org/10.1111/J.1748-1716.1981.TB06934.X
- F, K., A, E., S, H., & LE, T. (1999). Effects of anabolic steroids on the muscle cells of strength-trained athletes. Medicine and Science in Sports and Exercise, 31(11), 1528–1534. https://doi.org/10.1097/00005768-199911000-00006
- Yu, J.-G., Bonnerud, P., Eriksson, A., Stål, P. S., Tegner, Y., & Malm, C. (2014). Effects of Long Term Supplementation of Anabolic Androgen Steroids on Human Skeletal Muscle. PLoS ONE, 9(9), 105330. https://doi.org/10.1371/JOURNAL.PONE.0105330
- M, S., J, L., A, E., & CC, T. (1991). Evidence of fibre hyperplasia in human skeletal muscles from healthy young men? A left-right comparison of the fibre number in whole anterior tibialis muscles. European Journal of Applied Physiology and Occupational Physiology, 62(5), 301–304. https://doi.org/10.1007/BF00634963
- L, B., & HG, B. (1963). Lateral dominance and right-left awareness in normal children. Child Development, 34, 257–270. https://doi.org/10.1111/J.1467-8624.1963.TB05137.X
- AR, F.-M., L, G., & Y, B. (1980). Isokinetic and static plantar flexion characteristics. European Journal of Applied Physiology and Occupational Physiology, 45(2–3), 221–234. https://doi.org/10.1007/BF00421330
- NA, T., & JG, W. (1986). Exercise-induced skeletal muscle growth. Hypertrophy or hyperplasia? Sports Medicine (Auckland, N.Z.), 3(3), 190–200. https://doi.org/10.2165/00007256-198603030-00003
- E, B., & B, E. (1982). The needle biopsy technique for fibre type determination in human skeletal muscle--a methodological study. Acta Physiologica Scandinavica, 116(4), 437–442. https://doi.org/10.1111/J.1748-1716.1982.TB07163.X
- J, L., K, H.-L., & M, S. (1983). Distribution of different fibre types in human skeletal muscles. 2. A study of cross-sections of whole m. vastus lateralis. Acta Physiologica Scandinavica, 117(1), 115–122. https://doi.org/10.1111/J.1748-1716.1983.TB07185.X
- E R Helms, P J Fitschen, A A Aragon, J Cronin, & B J Schoenfeld. (n.d.). Recommendations for natural bodybuilding contest preparation: resistance and cardiovascular training - PubMed. Retrieved September 7, 2021, from https://pubmed.ncbi.nlm.nih.gov/24998610/
- BJ, S., D, O., & JW, K. (2017). Dose-response relationship between weekly resistance training volume and increases in muscle mass: A systematic review and meta-analysis. Journal of Sports Sciences, 35(11), 1073–1082. https://doi.org/10.1080/02640414.2016.1210197
- A L Goldberg, J D Etlinger, D F Goldspink, & C Jablecki. (n.d.). Mechanism of work-induced hypertrophy of skeletal muscle - PubMed. Retrieved September 7, 2021, from https://pubmed.ncbi.nlm.nih.gov/128681/
- Graham, Z. A., Gallagher, P. M., & Cardozo, C. P. (2015). Focal adhesion kinase and its role in skeletal muscle. Journal of Muscle Research and Cell Motility, 36(0), 305. https://doi.org/10.1007/S10974-015-9415-3
- Yoon, M.-S. (2017). mTOR as a Key Regulator in Maintaining Skeletal Muscle Mass. Frontiers in Physiology, 8(OCT), 788. https://doi.org/10.3389/FPHYS.2017.00788
- CL, S., BDH, K., MR, B., GR, J., & JM, J. (2017). Stretch training induces unequal adaptation in muscle fascicles and thickness in medial and lateral gastrocnemii. Scandinavian Journal of Medicine & Science in Sports, 27(12), 1597–1604. https://doi.org/10.1111/SMS.12822
- GR, M., DW, W., & K, B. (2015). The molecular basis for load-induced skeletal muscle hypertrophy. Calcified Tissue International, 96(3), 196–210. https://doi.org/10.1007/S00223-014-9925-9
- G, M., CI, M., A, B., K, W., & GL, O. (2014). Muscular adaptations and insulin-like growth factor-1 responses to resistance training are stretch-mediated. Muscle & Nerve, 49(1), 108–119. https://doi.org/10.1002/MUS.23884