I’m often asked what the differences are between hypertrophy and hyperplasia. It’s a fair question since you have to fully understand muscle structure and muscle adaptation to see the whole picture. Hopefully this will clear up the difference.
Skeletal muscle is the largest organ in the body. It is primarily characterized by its mechanical activity which is required for posture and movement. Importantly, muscle has adaptive potential, which means it is capable of modifying its structure in response to a stimulus.
The four main principles of training are overload, specificity, reversibility and individuality. In this post I’ll focus on overload which means a muscle must be worked against a load that is greater than normal. Resistance exercise is a very good way to induce muscles to grow via overload.
To understand the changes that occur due to training it is necessary to know some basic muscle anatomy.
You may have seen this image before. Now, what I want to focus on is the muscle fiber. To be clear – a muscle fiber is a muscle cell. They are one in the same. Muscle fibers are unique because they are multinucleated and striated. This means that each muscle cell can have more than one nucleus. Each nucleus is responsible for controlling a finite volume of sarcoplasm, this is termed the myonuclear domain. The striations mentioned here are due to the alternating of light and dark bands (myosin/actin) and are not the same striations that you see on people with very low body fat.
If you look inside a muscle fiber you can see the myofibrils. They look like small cylinders. Notice how many myofibrils are packed into a muscle fiber. Here’s a closer look where you can really see them:
There is also another level inside the myofibril – these are myofilaments which are made up of actin and myosin. These are the basic structures that allow muscle to contract.
When thinking of hypertrophy and hyperplasia we are working on the level of muscle fibers.
Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells (muscle fibers).
Hyperplasia is an increase in the number of muscle fibers due to some type of stimulus. In most discussions that stimulus is exercise. Specifically, resistance exercise.
The theory of muscle hyperplasia was first published in the 70s by Dr. Gonyea (3). His first experiment used cats that were trained to lift weights with their right forelimb to receive food. After extended training, muscle fibers were counted and found to have an increase in number due to this training. This increase was reportedly due to muscle fiber splitting. This means that one muscle fiber split into two (see left below).
The most convincing data for hyperplasia occurs in animal models. Some of the first models used chronic stretching to cause increases in muscle. Basically, they stretched a muscle by attaching a weight to it. This would be equivalent to holding dumbbells at your side in order to stretch the muscles in your arms. One study showed that 30 days of chronic stretch (with no rest) caused a 172% increase in muscle mass and a 50-70% increase in muscle fiber number (6). Obviously, you’re not going to throw this type of exercise into your training program. Though it does raise some interesting questions. Mainly – How did this occur?!
This leads us to Dr. Jose Antonio. He is a modern pioneer in the study of hyperplasia. His theory is that large fibers can split into two or more smaller fibers (6, 12, 13). He completed a study in the early 90s that used a progressive overload stretch in birds. Interestingly, this study reported a 334% increase in muscle mass as well as a 90% increase in muscle fiber number. This is the largest increase in hypertrophy recorded in any animal or human study. That includes the use of testosterone.
There are a few other studies that support this theory. The main problem with human studies of hyperplasia is that a muscle is made up of hundreds of thousands of muscle fibers. Therefore, the most direct way to see if there is an increase in muscle fibers is to count them. As Jalen Rose would say – NOT GON’ BE ABLE TO DO IT. For example, one study by Sjostrom et al. found that the tibialis anterior had over 150,000 fibers. Can you imagine counting that many fibers? Surely your eyes would cross and the errors would compound.
However, there are a few studies that have reported elite bodybuilders have more fibers per motor unit than controls. This indicates that there might be a case of hyperplasia with long-term training (2). The problem with bodybuilders is that they are often taking some sort of PEDs, which may confound results due to the physiological changes that are induced. Research has a lot of limitations – this is just one of them.
Through human development, from birth until adulthood, muscle size increases drastically. During hypertrophy there is no change in the number of muscle fibers. Instead, the whole muscle fiber gets larger. Muscle is always trying to adapt its structural and functional properties to the demand of use.
We often push the limits to stress our muscle fibers so much that the fiber suffers damage. One way hypertrophy occurs is through satellite cells. Once activated, satellite cells proliferate and migrate to the site of muscle damage. Then they fuse to the damaged muscle cell and help repair and increase growth of muscle tissue. There is some debate in the muscle field whether or not they are required for hypertrophy, but they do play a role.
Satellite cell pathway (JAP)
There are three models of hypertrophy used including: compensatory hypertrophy, stretch-induced hypertrophy, and weight lifting. Factors such as genetics, age, and gender have been shown to play a role in hypertrophy in response to training. This can affect both the rate and the increase in muscle mass (14). A full review of muscle hypertrophy can be found here by Brad Schoenfeld.
Sidenote: An increase in muscle size could be done in two ways: sarcoplasmic hypertrophy or myofibrillar hypertrophy. Wrong. That’s broscience. There are no examples of sarcoplasmic hypertrophy in any studies in humans. In fact, Claaseen et al (Journal of Physiology, 1989, 409: 491-495) showed that the linear distance between myofilaments did not change with training. The occasional example of a difference between hypertrophy and strength gain (9) is not due to a sarcoplasmic hypertrophy in the low-load ranges with high reps (i.e., 3-4 sets of 12-15 reps). Rather, it is a neuromuscular training-zone specific strength response in the low vs. the high load groups. The nervous system is a huge component when training.
Hypertrophy is a multidimensional process which involves the interaction of satellite cells, the immune system, hormones and growth factors with muscle fibers. The explanation of the mechanisms of muscle hypertrophy are all over the internet, so I’ll spare you the extra 1000 words trying to explain it further.
Some of the argument against hyperplasia is the structure of human muscle compared to animal muscle. For example, cats have up to eleven fiber types but humans only have three main types plus two types that are transitional. The main reason for using animal models in research is that human biopsies are often required to study muscle tissue. If you’ve ever had a biopsy you know that it hurts like hell. This makes it difficult to recruit subjects for experiments. It’s also unethical to do some procedures on humans that scientists can do on animals.
One study was done in 5 elite male bodybuilders, 7 intermediate caliber bodybuilders, and 13 age-matched controls. This study looked at muscle fiber numbers in the biceps via biopsy. There was a wide range in the number of fibers in biceps (172,085–418,884), but despite these differences in muscle size there was no significant difference in the number of fibers between groups. Also, the proportion of muscle comprised of connective and other non-contractile tissue was the same for all groups. The researchers concluded that the training directed toward achieving maximum muscle size does not result in an increase in fiber numbers (11). There are several studies which show no change in fiber number despite significant increases in muscle mass (15, 16, 17).
I think more experiments are needed before a definitive answer can be provided. Hyperplasia is not yet substantiated, and new fibers, if present, could be the result of satellite cells causing fibers to regenerate. I don’t believe that there is enough evidence to say that muscle fibers split. I don’t think we’ll see any new studies soon since the indication is that hyperplasia doesn’t occur due to normal exercise training. It only occurs during chronic – non physiological training.
A closer look at publication trends show the number of hyperplasia is very low. You can see belowat it averages about ~25 publications per year. Further below, if you look at the results from skeletal muscle hypertrophy publications you can see it is much higher with steady increases over the past decade. This is another indicator that science has focused on hypertrophy rather than hyperplasia.
PS – If you want to try a different style of training or are convinced that you can elicit hyperplasia then you may want to watch Dr. Wilson’s intraset stretching videos. There was also a recent article on T-Nation about it. If nothing else you’ll weaken your muscle so that you can induce more damage, which could cause a better muscle adaptation.
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- MacDougall. J.D., et al. 1984. Muscle fiber number in biceps brachii bodybuilders and control subjects. Journal of Applied Physiology: Respiratory, Environment and Exercise Physiology 57:1399-1403.
- Gonyea, W. Acta Physiol Scand. 1977 Jan;99(1):105-9.
- Craig, BW. 2001 Hyperplasia: Scientific fact or fiction? NSCA 23:42-44.
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- Tamaki T, Uchiyama S, Nakano S: A weight-lifting exercise model for inducing hypertrophy in the hindlimb muscles of rats. Med Sci Sports Exerc 1992, 24:881-886.
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- Gollnick PD, Parsons D, Riedy M, Moore RL: Fiber number and size in overloaded chicken anterior latissimus dorsi muscle. J Appl Physiol Respir Environ Exerc Physiol 1983, 54:1292-1297.
- Timson BF, Bowlin BK, Dudenhoeffer GA, George JB: Fiber number, area, and composition of mouse soleus muscle following enlargement. J Appl Physiol (1985) 1985, 58:619-624.
- McCall GE, Byrnes WC, Dickinson A, Pattany PM, Fleck SJ: Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training. J Appl Physiol (1985) 1996, 81:2004-2012.