High Reps and Hypertrophy: What’s The Relationship?

Recently, I posted a few thoughts on high rep sets (8+) of the main lifts in powerlifting — squat, bench press, and deadlift — in the caption of a meme that seemed to ruffle some feathers. Nothing new, I tend to be opinionated and outspoken, and I like asking questions and challenging dogma. Neither the meme nor the caption was directed at anyone in particular, just the idea that high rep sets of squat, bench press, and deadlift, are probably not the best use of a lifter’s time. This led to some interesting discussions and colorful comments. One being that my sentiment is scientifically inaccurate and ignores history, and law, and how things have been done for 60+ years. But am I?

It is widely accepted, or assumed might be a better word, that a bigger muscle has the potential to be a stronger one, thus, training with an emphasis on hypertrophy is a popular approach in some circles of powerlifting and has been for a long time. Coaches have been successful in using traditional periodization models with hypertrophy blocks and sets of 8+ since before I was even alive. However, researchers and practitioners have also been challenging the idea that a bigger muscle is a stronger muscle for 60+ years.

To give historical context, I refer to a 2019 paper by Jeremy Leonekke and colleagues titled ‘Exercise-Induced Changes in Muscle Size do not Contribute to Exercise-Induced Changes in Muscle Strength’ where the authors give a brief overview of the science challenging the relationship between muscle size and strength, dating back to the 1930s.

“In the previous century, there seemed to be much skepticism regarding the role that exercise-induced changes in muscle size played with exercise-induced changes in muscle strength. In 1939, Schneider suggested that “Casual observation is sufficient to prove that muscles do not make a similar gain in size.” In 1952, Rasch echoed his own skepticism of changes in muscle size and changes in muscle strength (among other things) in a paper titled “The Problem of Muscle Hypertrophy.” In 1963 and 1976, it was written by Morehouse and Miller that “It has not been proved that hypertrophy is necessarily a desirable reaction. Some students are of the opinion that it may be simply a by-product of training, perhaps a noxious one.” Following this point in time, the narrative began to be consistently told in a different manner. To illustrate, Brooks and Fahey suggested in 1985 that “Muscles are strengthened by increasing their size and by enhancing the recruitment and firing rates of their motor units. It appears that both of these processes are involved in the adaptive response to resistance exercise.”

What happened to change how the story was told? Evidence that muscle hypertrophy may be related to changes in maximum strength was provided early on by Ikai and Fukunaga in 1970. They had five individuals’ exercise one arm with isometric contractions while the other arm served as a non-exercise control. Following 100 days of exercise, both arms increased strength (trained arm: 115 kp vs. untrained arm: 37 kp) but only the arm that exercised observed a change in muscle size. These authors suggested that increases in muscle cross-sectional area and nerve discharge are the two primary factors leading to exercise-induced increases in strength.

Interestingly, the original work that most textbooks cite as evidence for the time course of changes in muscle strength is the study completed by Moritani and deVries. This was an 8-week study in which five individuals did bicep curls in one arm and had the other arm serve as a non-exercise control. The outcomes of interest were changes in amplitude (measured by surface electromyography [EMG]) and arm circumference. The authors took a downward shift in the EMG amplitude relative to an absolute force measurement as evidence that growth had taken place. Of note, muscle growth was not actually measured. Following 2 weeks of training, there was an increase in strength but the authors reported no downward shift in EMG amplitude relative to absolute force. The authors concluded that this lack of shift indicated that the immediate increase in strength was neural in origin. Following 8 weeks of exercise, both arms saw an increase in strength (trained arm: 21 lb vs. untrained arm: 13 lb) but only the arm that exercised observed a downward shift in the EMG measurement. The conclusion of this study was “After the first 3–5 weeks, muscle hypertrophy becomes the dominant factor in strength gain.”

Though there are numerous studies showing that muscle hypertrophy occurs alongside changes in strength, this alone is insufficient to inform us on the importance of muscle growth for increasing strength. One point to consider when evaluating the classic studies used as support for this “neural first, followed by hypertrophy” narrative is what would have occurred had both arms exercised but one was designed to minimize growth? We have been working with a model where we are able to produce changes in strength without producing changes in muscle growth. Though this is not without its own set of limitations, this model may provide some insight into how important a change in muscle size is for a change in muscle strength.”

The paper goes on to conclude that, “We have attempted to test the causal relationship by creating studies designed to produce differential results on one dependent variable (muscle size) and test how this in turn impacts the other dependent variable (muscle strength). While we appreciate that there are some limitations to our research, the fact remains that there is still no available evidence supporting the claim that changes in muscle size lead to changes in voluntary strength. Our hope is that through appropriately designed studies, we and others will be able to better address this research question in the years to come.”

There is also a reply to Taber et al. 2019 that I think is a bit of a cherry on top, “The authors find the question of “Does hypertrophy contribute to strength gain?” less interesting than, “To what extent and under what circumstances does hypertrophy contribute to strength gain?” However, this question assumes that a change in muscle size contributes to a change in muscle strength. This is the same issue with the authors’ proposed hypothetical figure and the majority of literature on this topic. Aside from the theoretical reason for why a change in muscle size should contribute to a change in muscle strength, the authors present no experimental evidence demonstrating that a change in one contributes to a change in the other. Their position is that there is a contributory-causal relationship but are unable to provide the type of evidence required to make that claim, as their argument rests on correlations across time. It cannot be said that a result provides evidence for a claim if little has been done to rule out ways that the claim may be false. The claim must be tested through experiments whereby muscle growth is manipulated across groups to determine the impact of that manipulation on changes in strength.”

For more, I highly recommend checking out the paper for yourself, as well as other work by Dr. Leonekke and colleages. He even did a podcast with my coach which I recommend that as well.

So, we’ve been questioning the relationship between muscle size and strength since the 30s and still don’t have a clear cut answer, but I’m ignoring history and science? Hmmm…

My argument was also not that hypertrophy isn’t important, rather that hypertrophy can be achieved through a variety of rep ranges outside the ol’ 8–12. And also, that powerlifters are not bodybuilders, therefore trying to maximize hypertrophy within the program by utilizing high rep sets of the main lifts might not be in a powerlifter’s best interest. Just like trying to maximize strength by programming heavy singles might not be in a bodybuilder’s best interest. It’s just a matter of what takes priority, and what the goal of the training is. That’s not to say that a powerlifter wouldn’t ever benefit from spending time away from lifting heavy to focus on building muscle, just depends on the context. However, I still don’t think it’s super important to do so.

According to Travis et al., altering the structural component of the muscle is often the aim of hypertrophic training, yet not all hypertrophy is equal; such alterations are dependent upon how the muscle adapts to the training stimuli and overall training stress. When comparing bodybuilders to strength and power athletes such as powerlifters, weightlifters, and throwers, while muscle size may be similar, the ability to produce force and power is often inequivalent.

As such, the term “hypertrophy” is often used as a general expression of muscle enlargement. However, there are several forms of hypertrophic outcomes that are possible, which include:

• Structural Skeletal Muscle Hypertrophy: skeletal muscle hypertrophy is often referred to as a conformational increase to the observed anatomical structure of the muscle tissue, and is often assessed by measuring muscle size via mCSA and muscle thickness (MT) and architectural components (i.e., pennation angle, fascicle length).
• Myoplasticity and Fiber Type Flux Hypertrophy: myoplasticity has been defined as the capacity of skeletal muscle to alter its structural and enzymatic protein content according to changes in use and the environment (i.e., the training stressor); the effects are predominantly a result of changes in gene expression. It is evident that regardless of training for hypertrophy or strength, if the training volume is increased enough and the intensity is prescribed appropriately, the physiological response may result in hypertrophic adaptations associated with fiber type mutations. Skeletal muscle in humans is predominately characterized based on MHC isoforms, as previously discussed, categorized as type I, II, and IIX, along with intermediate hybrid muscle fibers such as I/IIA, IIA/IIX, and I/IIA/IIX, with each displaying specific and unique morphological, biochemical, metabolic, and contractile proprieties. Regardless of pure or hybrid isoforms, type II fiber content appears to influence whole muscle function, and often correlates strongly with athletic performance associated with force, velocity, and power production.
• Sarcoplasmic and Myofibrillar Hypertrophy: sarcoplasmic hypertrophy has been defined as the chronic increase in the volume of the sarcolemma and related constituents such as the mitochondria, sarcoplasmic reticulum, t-tubules, and sarcoplasmic enzymes (i.e., noncontractile elements). Conversely, myofibrillar hypertrophy has been defined as the increase in the size or number of myofibrils accompanied by an increase in sarcomere number or protein abundance related to contractile force generation. This has been demonstrated with bodybuilders as well as strength and power athletes. It is important to make a distinction between these two modes of hypertrophy, as these variable changes may appear to be of a similar change in muscle hypertrophy via ultrasound (i.e., cellular swelling); however, the function within the muscle is likely different between these two separate alterations as a result of the training stimuli.
• Selective Regional and Indiscriminate Hypertrophy: due to the ability to alter the architecture, morphology, and fiber type of a given muscle, careful consideration should be given to the development of hypertrophy within a target muscle and across target muscle groups. By examining various athletes’ hypertrophic development in different regions of a muscle, it is evident that across sports, there is a differential need for specific regional hypertrophy to accomplish a sporting task. In sports where relative strength is critical for success, there is a possibility that indiscriminate hypertrophy, where whole muscle growth is realized, may be detrimental for performance. As highlighted in a recent review by Zabaleta-Korta, there is ample evidence suggesting that regional growth of the quadriceps musculature is highly dependent on the exercises prescribed. For example, a sprinter developing distal hypertrophy of the quadricep would likely diminish sprint times due to changing the athlete’s sprinting technique from additional muscle at the knee as a result of indiscriminate growth. Conversely, if the sprinter obtains regional growth at the proximal region of the quadriceps near the hip musculature, sprinting performance could be improved further. The different outcomes in hypertrophy could very well be related to the exercise prescribed and how each repetition is executed (e.g., range of motion, tempo).

These potential outcomes should be considered when prescribing training volume (i.e., product of sets × reps × load) and intensity (i.e., percentage of 1-repetition-maximum [% of 1RM]) to drive the desired hypertrophic adaptation rather than settling for a general hypertrophic change determined by gross muscle measurements. Additionally, it is vital to point out that hypertrophy and strength are not completely separate phenomena, although this is a controversial topic. However, despite the literature supporting or opposing these views, it is proposed that hypertrophy and strength should be sequentially accentuated so that one training adaptation can potentiate the next (e.g., train to induce hypertrophic increases in preferred muscle fiber size → increase force and power production of the now larger muscle fiber). Therefore, with evidence indicating that preferential hypertrophic adaptations are indeed possible, it may be advantageous for strength and power athletes to increase type II muscle fiber content rather than type I content to improve the associated contractile machinery of type II fibers to potentiate sport performances (Travis et al. 2020).

Training intensity (%1RM) alone appears to be a key factor in fiber type alterations relative to mechanical stress dictating the extent of cellular transformation, disruption, and fiber type II/I content. For a bodybuilder who is concerned with muscle symmetry and shape, training volume would likely be the primary training stimulus rather than high-load, high-intensity training aimed at specifically stimulating type II fiber content for strength or power purposes. Considering that bodybuilders can gain a similar amount of mCSA compared to powerlifters and weightlifters, bodybuilders are typically not considered strong compared to strength and power athletes; this may be attributed to a smaller II/I fCSA ratio. For powerlifters and weightlifters who often train with high intensity (i.e., ≥85% 1RM), low repetitions (i.e., ≤5 repetitions per set) using compound competition movements (i.e., back squat, bench press, deadlift, snatch, clean and jerk), these athletes display 20% greater type II fCSA compared to bodybuilders. Bodybuilders tend to train with low intensity (i.e., ≤70%) and high repetitions (≥10 repetitions per set), which may explain why strength and power athletes have muscle fiber diameters twice as large as type I fibers compared to bodybuilders. In a review of the literature by Sale, indirect evidence was provided for this idea, suggesting that subjects who performed back squats with higher loads showed greater strength gains compared to groups performing movements that only recruited similar musculature with lower loads using leg presses and performing knee extensions. This adaptation was attributed to higher threshold motor unit recruitment and the activation of target muscle fibers (Travis et al. 2020).

To target specific fibers and higher threshold motor units, it appears that using higher loads (≥80% 1RM) is warranted for strength and power athletes [Mangine, and Fry]. However, while this threshold is only theoretical, there is likely an intensity continuum that can be used to promote the desired hypertrophic outcome. Considering that muscle force reflects the number of cross-bridges working in parallel, the maximum force developed is related to the fCSA of the specific muscle fiber type targeted. Depending on the number of MHC cross-bridges working in parallel to interact with the actin filaments, the force required to overcome the training stimulus can then be generated at the ultrastructural level. For instance, depending on the training stimuli, protein secretion and MHC adaptations may be different for high-load, low-volume training (e.g., peaking periods) compared to low-load, high-volume training (e.g., preparatory or accumulation periods) [Ogborn & Schoenfeld]. For example, as pointed out by Ogborn and Schoenfeld, type II muscle fibers have displayed superior growth after high-intensity strength training, yet bodybuilders display greater growth of type I fibers compared to powerlifters as a result of training with high repetitions and lower loads, as pointed out by Fry. It should be noted that the athletes who require great levels of muscular force and power (i.e., powerlifters, weightlifters) are the ones who also possess the greatest content of the fibers capable of producing the greatest force and power.

Rather than achieving maximum hypertrophy, optimal hypertrophy should be acquired relative to (A) increasing sarcomeres in parallel and/or in series relative to predominant competition tasks, (B) increasing the type II/I fCSA ratio, (C) enhancing type II myofibril utility, and (D) accruing select regional areas of hypertrophy to improve the function of type II molecular motors relative to competition tasks. For athletes, the purpose of using specific yet varied training stimuli is to elicit biological changes that could improve performance for a specific sporting task. When considering task-specific hypertrophy for strength and power athletes, heavy loading (80–95% 1RM) while using low repetitions (e.g., 5 repetitions per set) during a hypertrophic emphasis may have greater effects on type II muscular adaptations for strength and power compared to lighter loading. Interestingly, the literature opposed to these ideas has not demonstrated that low-load, high repetition training is more advantageous for improving force production and power output (Travis et al. 2020).

I understand that traditional periodization models have been around for a long time, and if they didn’t work, they wouldn’t still be around today. Everything “works.” We can train in a variety of ways and get stronger, there is no specific evidence that says “this is the one best way to program for one repetition maximum testing!” We have the experience and anecdote of the generations before us, we have academic research and texts from the past century that are constantly evolving and being updated. It’s okay to have different ideas and perspectives but we shouldn’t be married to any single one, and be open to gaining new insights and knowledge. Even the authors in the Travis et al. paper state that they do not agree with Dr. Leonekke and colleagues but referenced their article multiple times, because you can’t just ignore what you don’t like. You have to consider all angles. There is room for disagreement and discussion. This isn’t about being right, it’s about being less wrong as time goes on, and not holding onto old ideas for dear life.