Muscle hypertrophy has its place in almost every competitive sport.
Gaining muscle can be beneficial for many groups of people ranging from the world’s most elite athletes to the general population. For Bodybuilders, it’s the name of the game.
What is driving muscle growth? As of late, this question has been up for debate and the internet is nothing short of saturated on the subject. I’m going to illustrate some of the basic physiological events that occur during and post-training and discuss its implications for progressive overload.
Note: we are focusing primarily on “myofibrillar” hypertrophy in this article, not sarcoplasmic.
A Brief Overview of Skeletal Muscle Anatomy
Before we dive into the main topic, we must cover the basic anatomy of skeletal muscle and understand how it functions based on it’s structure. Imagine you have a package of plastic straws all bound together in the shape of a cylinder. That would give you a general idea of the structure of skeletal muscle.
Skeletal muscle is made up of long cylindrical cells called muscle fibers. Muscle fibers are filled with several myofibrils, and myofibrils contain several threadlike structures called myofilaments. These myofilaments are composed of two varieties of contractile proteins: Actin and Myosin (“thick” and “thin” filaments). These two proteins work together and are key components in the process of muscle contraction.
Inherently, your brain communicates with your muscular system via the nervous system to “excite” the muscle through an electrical stimulation and action potentials. The nerve impulse causes a release in calcium, which in turn binds to the myofilaments, initiating the muscle contraction. In short, calcium “allows” Actin and Myosin to bind together (termed cross-bridging). The two will pull on each other, shortening the sarcomere. This is known as the “Sliding Filament Theory.”
Other molecules bound to the myosin head (such as phosphate and ADP) are released in this process. ATP (Adenosine Triphosphate) later bonds to the myosin head, allowing separation of the filaments to move back to a relaxed position, or lengthen, and repeat the process.
(Marieb & Smith, 2019)
This process happens every single time we move.
“Muscle hypertrophy” refers to enlargement resulting from training, primarily owing to an increase in the cross-sectional area (CSA) of the existing muscle fibers. With training, cross-sectional fiber area increases (hypertrophy) in direct proportion to the increases in myofibrillar size and number – an increase in the muscle fiber CSA due to an increase in predominantly actin and myosin (Haff & Triplett, 2016).
Now that we have a baseline of information, let’s move forward and discuss what “turns on” growth.
Why Do Muscles Grow? – The Physiology Behind it All
When a muscle experiences any magnitude of tension, a certain amount of muscle fibers are recruited to handle the force demand. As the tension becomes greater and greater (increases in force demands), more muscle fibers are recruited to overcome the stressor. In the world of Exercise Physiology, this concept is known as the Size Principle (Henneman 1957).
On the fiber level, there are specific types of fibers designed to handle specific amounts of tension for different durations of time. There are several muscle fiber types, but for simplicity’s sake, we will focus on the two largest categories: Type I and Type II. Type I fibers are considered the “Slow Twitch” fibers. They are extremely fatigue resistant, but only capable of handling low amounts of force (bouts of effort common in endurance athletes). Type II fibers are the “Fast Twitch” fibers with nearly the opposite function. They are responsible for high outputs of force but fatigue fairly quickly (Haff & Triplett, 2016). The Size Principle demonstrates a recruitment process of these fibers when put under load. Initially, Type I fibers are recruited when met with a stressor. If the demand is beyond the capability of those fibers, the larger, Type II (high-threshold fibers) are called in to fill the gap and meet the demand. If that stressor was great enough, it will force the body to adapt so that the next time it is met with that demand, it is better prepared for it. But how does that happen?
Once high-threshold fibers (the ones with the greatest growth potential) are exposed to high enough levels of tension for a period of time, mTOR (mechanistic target of rapamycin) is triggered causing a slew of different pathways including mRNA Translation (also known as Protein Synthesis) (Iadevaia et al. 2012). When the magnitude of Muscle Protein Synthesis is great enough, we get a net positive protein balance where Muscle Protein Synthesis exceeds Muscle Protein Breakdown. This process, termed Protein Turnover, results in what we know as Muscle Hypertrophy and consists of an increase in cross-sectional area of the muscle itself, and an increase of proteins within the muscle, specifically Actin and Myosin (the main contractile proteins) (Pikosky et al. 2006). The end result being a greater capability of force production and a larger muscle (Haff & Triplett, 2016).
Muscle Protein Synthesis > Muscle Protein Breakdown
Mechanical Tension Defined
In 2010, a meta-analysis by Schoenfeld hypothesized three contributors to hypertrophy – Mechanical Tension, Metabolic Stress, and Muscle Damage. Since then, mechanical tension has been thought of as the largest contributor to growth with metabolic stress having a smaller role and muscle damage being a byproduct to a stretch under load and general hard training. Mechanical tension will be primarily examined in this entry (with my thoughts on the other two mechanisms to come in a later post).
Tension is the stress, or force, placed on your musculature when performing an exercise. The muscle itself must generate enough force to overcome the demand the weight places on the body. The muscles contract, pulling on the skeletal structure, and the weight is moved. Thus, mechanical tension is ‘driving’ the initial pathways that eventually result in muscle hypertrophy.
In the literature, the way tension is quantified is the product of the number of repetitions, number of sets, and the load (also termed “Volume-Load” or “Tonnage”). This is a fine explanation on paper, but misses a few key components.
As mentioned before, to optimize your hypertrophic potential, it is necessary to expose high-threshold motor units to tension – happening only at a close proximity to failure. This will be the most significant contributor to muscle growth, but that’s not the entire picture.
So should we go into the gym and just perform some heavy singles and go home? Not so fast, although absolute intensity is highest in a one rep max and would result in full recruitment from the get go, the duration of exposure is insufficient as the muscle only experiences a single contraction. [study on 1RM insufficient for hypertrophy]
What does this tell us? It means that the magnitude of tension is only one component and by definition isn’t sufficient on its own. The duration of exposure (time), or the number of repetitions, is the second component.
Force x Time = Impulse
In Physics, the magnitude of the load (a force) multiplied by the duration of exposure (time experiencing that force) is termed Impulse. This is how we conceptualize volume, tonnage, or the totality of tension placed on the muscle. Based on the equation, we can see Impulse on a muscle will be greater when a set is taken closer to failure, but a similar level can be achieved with a wide range of loads and repetitions. In simple terms, greater impulses over time will result in larger muscles.
Essentially, the Impulse within a single set needs to be high enough to maximize that set’s potential to produce growth. Then, there needs to be a sufficient sum total of sets with a similar quality of effort over the course of a week to produce noticeable growth. This leads us back to our original definition – a heavy enough load that will cause fatigue performed with a high enough effort done an adequate amount of times per week.
Eventually, that total stimulus required to trigger the mTOR pathway will increase as an adaptive response to training…
We are adaptive creatures, and as previously mentioned, we need a sufficient stimulus that warrants an adaptation. The traditional definition of progressive overload reads something like, “increasing the stress on the body during exercise over time.” This is a fine explanation, but is often misinterpreted in practice. We have a chicken or the egg scenario here.
Your ability to add weight to the bar is the observation that overload has occurred and not a requirement to “induce” progressive overload (credit to Brian Minor). Being able to do more reps or lift more weight tells us what we have been doing previously was enough to elicit an adaptive response.
Yes, over time we want to be able to observe a strength increase on our lifts, but “beating the log book” is not required to induce overload. For example, let’s take an individual who is doing 20 sets per a given muscle group per week where they only need 10 sets per week to induce an adaptation (basically, they’re doing more than enough ‘total work’). Over several weeks, a load increase wouldn’t be necessary. Even if that person performed the same amount of reps and allowed RPE’s to fall (RPE 5 being as low as practically possible), that would be a sufficient overload. Conversely, let’s take another person doing 5 weekly sets per a given muscle group where they really need 10 sets of total work. In most cases, that person would plateau. But even a strength increase week to week would not be enough to induce an adaptation.
There is an inverted U shaped curve illustrating the response to dosages of volume (numbers will vary person to person). The main points on that curve are Maintenance Volume: the amount of volume needed to maintain muscle mass, Minimum Effective Volume: the least amount of volume needed to progress, Maximum Adaptive Volume: the very tip of the curve, where you see your best progress and are still able to recover chronically, and Maximum Recoverable Volume: the most amount of work you can do and still recover (right before the downward slope of the curve). This concept applies to all sports, and many other areas outside of the gym.
In order to see progress, you need to be training somewhere between MEV and MRV. Because we have this productive range of volumes to work with, that tells us that “beating the log book” session to session is simply not required. If it was, then this range wouldn’t exist. It would just be the amount of work you did last session and above.
But again, we should still seek to see strength increases in the moderate rep ranges over the course of a training career.
The Relationship Between Muscle Cross-Sectional Area and Force Output
Now, it’s important to note that there are many factors that can contribute to strength gains. Muscle size, neural adaptations, tendon stiffness, biomechanics, and several other mechanisms could contribute to an increase in strength (Jones et al. 2008). The size of the muscle is one of the largest contributors to strength and will be our primary focus here.
The relationship between muscle cross-sectional area and force output has been studied over and over in the academic setting. Fukunaga et al. (2001) examined the relationship between muscle cross-sectional area and joint torque. They nearly found a perfect correlation (r = 0.927) for the biceps and (r = 0.924) triceps. There aren’t too many variables so highly correlated in any field of research. In fact, a correlation this high is usually only seen in theory and almost never in practice.
If this is the case, why do we see 160 lb Chinese Olympic Weightlifters squat 600 lbs for multiple reps seemingly effortlessly?
Again, strength is multifactorial. There are many other adaptations that result from training to get strong at a specific movement. Certainly, they are not lacking muscularity, but strength athletes are extremely proficient at their movement, a skill in itself.
How does that apply to us? We can infer a larger muscle contributes to strength more so than strength’s contribution to a larger muscle. A larger muscle has the potential to be a stronger muscle, but is not necessarily the “strongest” unless an athlete undergoes training specific to maximize strength adaptations (Campos et al. 2002).
The takeaway: if your biceps have grown an inch, odds are you can curl more than you did. But due to the principle of specificity, genetics, and the like, there may be stronger people who carry less mass. Even then, one can almost certainly say even strength athletes get bigger one year in as strength increases.
But, I’m not able to do more reps session to session … Am I still growing?
Our “scope” per se used to measure progress is only so good. And what I mean by that is, there’s a very good chance you have improved, but expressing that improvement is limited by the fractional increases available to us.
A 5 lb increase on a 200 lb bench press would be a 2.5% improvement. On the same note, adding a single rep to a set of 8 would be a 12.5% improvement. Come the following session, if you only improved 2%, that’s not quite enough to show any sort of improvement. In this case, the time table to see adaptations is just longer, and we can’t make observations smaller than a certain percentage in practice.
Often times, what seems like a plateau may just be microscopic progress and could just require patience and consistency.
In summary, training at a high enough effort with an adequate amount of volume causes a disruption in homeostasis that results in the development of larger muscles and more contractile proteins. This adaptation results in a greater ability to produce force. This implies the sequence of adding external load to a movement comes following the adaptation and development of additional muscle tissue. Beating the log book is not required for a session to be overloading as there are a range of effective volumes useful to us. Our ability to observe progress is limited to the smallest weight increment available or by the percentage increase adding a single rep. Over time, progress will seemingly slow due to training age, volume requirements, and the small rate at which you actually progress session to session.
- Marieb, E. N., Smith, L. A., & Zao, P. Z. (2019). Human anatomy & physiology laboratory manual. New York, NY: Pearson.
- Haff, G., & Triplett, N. T. (2016). Essentials of strength training and conditioning. Champaign, IL: Human Kinetics.
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- Iadevaia V., Wang X., Yao Z., Foster L.J., Proud C.G. (2012) Evaluation of mTOR-Regulated mRNA Translation. In: Weichhart T. (eds) mTOR. Methods in Molecular Biology (Methods and Protocols), vol 821. Humana Press
- Matthew A. Pikosky, Patricia C. Gaine, William F. Martin, Kimberly C. Grabarz, Arny A. Ferrando, Robert R. Wolfe, Nancy R. Rodriguez, Aerobic Exercise Training Increases Skeletal Muscle Protein Turnover in Healthy Adults at Rest, The Journal of Nutrition, Volume 136, Issue 2, February 2006, Pages 379–383, https://doi.org/10.1093/jn/136.2.379
- Schoenfeld, Brad. (2010). The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training. Journal of strength and conditioning research / National Strength & Conditioning Association. 24. 2857-72. 10.1519/JSC.0b013e3181e840f3.
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- Campos, G.E., Luecke, T.J., Wendeln, H.K. et al. Eur J Appl Physiol (2002) 88: 50. https://doi.org/10.1007/s00421-002-0681-6
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- Fukunaga, T., M. Miyatani, M. Tachi, M. Kouzaki, Y. Kawakami, and H. Kanehisa. 2001. “Muscle Volume Is a Major Determinant of Joint Torque in Humans.” Acta Physiologica Scandinavica 172 (4): 249–55.
- Henneman, E. 1957. “Relation between Size of Neurons and Their Susceptibility to Discharge.” Science 126 (3287): 1345–47.
- Iadevaia, Valentina, Xuemin Wang, Zhong Yao, Leonard J. Foster, and Christopher G. Proud. 2012. “Evaluation of mTOR-Regulated mRNA Translation.” Methods in Molecular Biology 821: 171–85.
- Jones, Eric J., Phil A. Bishop, Amanda K. Woods, and James M. Green. 2008. “Cross-Sectional Area and Muscular Strength: A Brief Review.” Sports Medicine 38 (12): 987–94.
- Pikosky, Matthew A., Patricia C. Gaine, William F. Martin, Kimberly C. Grabarz, Arny A. Ferrando, Robert R. Wolfe, and Nancy R. Rodriguez. 2006. “Aerobic Exercise Training Increases Skeletal Muscle Protein Turnover in Healthy Adults at Rest.” The Journal of Nutrition 136 (2): 379–83.