How does mechanical tension cause muscle growth when bar speed is maximal on every rep in the set?

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According to the stimulating reps hypothesis of muscle growth, hypertrophy is stimulated when the muscle fibers controlled by high-threshold motor units experience a sufficiently high level of mechanical tension. This mechanical tension is primarily the result of the force-velocity relationship (although the passive element of the length-tension relationship can also affect muscle fiber force production if range of motion is altered or when force is exerted during eccentric contractions).

Consequently, we observe hypertrophy after any workout in which effort is high (since effort determines motor unit recruitment) and bar speed is slow (since slow speeds permit muscle fibers to produce high forces, which produce the high levels of mechanical tension). This combination of variables commonly occurs during heavy strength training workouts, but it can also occur in the final reps of a set when using light loads and training to failure (since bar speed reduces over the set, while effort levels increase). These final reps of the set that cause hypertrophy are called “stimulating reps” which is where the hypothesis gets its name from.

The model is very powerful, because it provides a simple explanation for why strength training with the same number of sets of any load between 5RM and 30RM causes the same hypertrophy (each set involves the same number of reps with a high effort and a low bar speed, and therefore the same number of stimulating reps). Alternative hypotheses (such as those involving metabolic stress and/or muscle damage) require different mechanisms to stimulate hypertrophy during training with heavy loads or light loads, but somehow the muscle growth is expected to be equal when training with all loads, despite being achieved by different mechanisms, which is quite difficult to believe.

In this model, hypertrophy does not occur after a workout in which only the muscle fibers that are controlled by low-threshold motor units experience high levels of mechanical tension due to slow movement speeds (when effort is low). In fact, the muscle fibers of low-threshold motor units do not grow at all after exercise, because they are already regularly being stimulated at slow speeds (and therefore high forces) during the activities of daily life. They have already reached their maximum possible size, and cannot grow more from yet another bout of exercise. This explains why walking around all day will not produce muscle growth, even though some muscle fibers are producing very high forces.

Similarly, in this model, hypertrophy does not occur after a workout in which the muscle fibers that are controlled by high-threshold motor units experience low levels of mechanical tension (when velocity is high). This explains why maximal effort throwing and jumping practice do not produce any muscle growth, even though they involve very high levels of motor unit recruitment (although plyometrics might well stimulate hypertrophy, if the jumps involve a meaningful landing phase in which eccentric force is produced).

What about peripheral fatigue?

The stimulating reps model has been criticized on the basis that peripheral fatigue incurred early on during a set of strength training exercise might reduce the force exerted by the muscle fibers of high-threshold motor units, and thereby reduce the mechanical tension that they experience.

During bodybuilding training, this criticism does not apply, since the muscle fibers of high-threshold motor units are not active at the start of the set (since effort levels are low). Therefore, they cannot be fatigued until the end of the set (which is when the reps are stimulating anyway).

During athletic (or velocity-based) training in which individuals perform each rep of a set with maximal effort, the criticism does apply. In this type of training, a maximal effort is used in each rep. This means that high-threshold motor units are recruited from the very first rep, and can therefore be fatigued from the very start of the set. In fact, if we take a very simplistic model of peripheral fatigue and then follow the model through, we might predict that this type of training would lead to the muscle fibers controlled by those motor units never experiencing high levels of mechanical tension. They would move too fast to experience high mechanical tension at the beginning of the set, but would be too fatigued to produce high mechanical tension at the end of the set. We might predict that minimal hypertrophy would occur after training in this way (irrespective of the proximity to failure).

This contradicts the findings in the literature, which consistently show greater muscle growth when doing this type of training and stopping each set closer to failure instead of further away from failure (by using bar speed thresholds). Clearly, either the stimulating reps model is incorrect (as currently stated), or the very simplistic model of peripheral fatigue is incorrect.

What are the mechanisms of fatigue?

Fatigue is a temporary and reversible reduction in the ability to produce muscle force. It occurs because of many changes inside the muscle itself (called “peripheral” fatigue) and because of changes inside the brain and spinal cord (called “central nervous system” fatigue).

Both peripheral fatigue and central nervous system (CNS) fatigue occur during all types of exercise. Yet, peripheral fatigue is the dominant type of fatigue during strength training, while CNS fatigue contributes to the same extent as peripheral fatigue during aerobic exercise. We can probably ignore CNS fatigue for the purposes of this analysis.

Crucially, peripheral fatigue has multiple aspects, which are very important to understand if we want to see how the mechanical tension produced by single muscle fibers is affected during a strength training set.

Peripheral fatigue is caused by [1] an impairment of actin-myosin crossbridge function due to metabolite (phosphate and hydrogen ion) accumulation, [2] a reduction in the sensitivity of myofibrils to the presence of calcium ions, likely due to the production of reactive oxygen species, [3] excitation-contraction coupling failure due to sustained exposure to phosphates and calcium ions such that calcium ions are no longer released into muscle fibers despite the presence of an action potential at the triadic junction of the cell membrane, and [4] a reduction in sarcolemmal excitability such that action potentials are not propagated along the cell membrane despite a signal from the central nervous system reaching the neuromuscular junction, which is probably initially caused by ionic changes and later by the actions of reactive oxygen species stimulating the production of phospholipases.

The two most important mechanisms during strength training sets are the impairment of crossbridge function and excitation-contraction coupling failure. These two mechanisms alter their proportional contributions over the course of a fatiguing bout of exercise, and also differ between the fibers controlled by low-threshold and high-threshold motor units. Additionally, there are also differences in the metabolic efficiencies of slow twitch and fast twitch muscle fibers at different velocities, which affects our understanding of how fatigue differs between the muscle fibers controlled by low-threshold and high-threshold motor units when looking at different parts of a set where bar speed reduces over time.

Once we appreciate these points, the rationale underpinning the stimulating reps model of hypertrophy during strength training with maximal effort on each rep makes becomes clear.

#A. How does fatigue alter over the course of a set?

For many years, it has been known that the nature of peripheral fatigue differs over the course of a maximal effort muscular contraction.

Specifically, peripheral fatigue develops in three phases. The first two phases involve predominantly metabolite accumulation, while the third phase mainly involves excitation-contraction coupling failure.

Firstly, there is a small reduction in muscle fiber force (without any change in muscle fiber contraction velocity). This phase is dominated by metabolite accumulation, which has the *potential* to affect both muscle fiber force (by phosphate production) and muscle fiber contraction velocity (by acidosis). However, during this phase, phosphocreatine is being broken down to provide energy, and the reaction that breaks down phosphocreatine removes the hydrogen ions as quickly as they are produced. Therefore, the resulting acidosis is unable to cause a change in fiber shortening velocity.

Secondly, there is a long period in which muscle fiber contraction velocity reduces steadily, while muscle fiber force does not change. This phase is also dominated by metabolite accumulation. In this phase, acidosis impedes muscle fiber shortening velocity without being stopped by the breakdown of phosphocreatine, because that process has ceased. However, an accumulation of ADP and the phosphorylation of myosin regulatory light chains decrease muscle fiber shortening velocity while simultaneously increasing muscle fiber force (thereby compensating for the negative effects of phosphate ions on muscle fiber force).

Thirdly, there is a phase in which muscle fiber force reduces dramatically, while muscle fiber contraction velocity continues reducing steadily. This phase is likely produced by excitation-contraction coupling failure, which has a large effect on muscle fiber force, but seems to have a fairly minor effect on muscle fiber contraction velocity.

The different effect of excitation-contraction coupling failure on muscle fiber force and contraction velocity can be observed by comparing the fatiguing effects of eccentric and concentric contractions.

Eccentric contractions produce minimal metabolite accumulation: most of the fatigue they cause involves excitation-contraction coupling failure. Workouts involving solely eccentric contractions produce large reductions in muscle force but minimal reductions in muscle fiber shortening velocity. Concentric contractions produce a great deal of metabolite accumulation, but minimal excitation-contraction coupling failure (as can be deduced by observing the rapid recovery of force that occurs post-workout). Workouts involving solely concentric contractions produce large reductions in muscle fiber shortening velocity, and much smaller reductions in muscle force.

#B. How does fatigue differ between muscle fibers of low-threshold and high-threshold motor units?

During normal strength training, the muscle fibers of low-threshold motor units perform both eccentric and concentric contractions (since they are active in both phases of the lift), while the muscle fibers of high-threshold motor units only experience concentric contractions, since they are only active in the harder, lifting phase.

Consequently, we can expect that the muscle fibers of low-threshold motor units will experience excitation-contraction coupling failure due to their exposure to eccentric contractions, while the muscle fibers of high-threshold motor units will not (since the effort levels in the eccentric phase are very low, even during strength training with maximal effort in the lifting phase).

Additionally, research has shown that the much more oxidative muscle fibers of low-threshold motor units tend to experience excitation-contraction coupling failure as their primary form of peripheral fatigue, while the more glycolytic muscle fibers of high-threshold motor units tend to experience an impairment of actin-myosin crossbridges.

#C. How does metabolic efficiency differ between slow twitch and fast twitch muscle fibers?

We tend to learn in textbooks that slow twitch muscle fibers are much less susceptible to fatigue than fast twitch muscle fibers, because they have more mitochondria and are therefore more oxidative. However, most fatigue tests that study the differences between slow twitch and fast twitch muscle fibers are done in isometric contractions, and do not vary contraction velocity.

Yet, research has shown that fast twitch fibers are more metabolically efficient at fast contraction velocities, while slow twitch fibers are much less efficient. Therefore, if extrapolate from studies of fatigue during isometric contractions to high-velocity movements, we will overestimate the fatigue effect on fast twitch muscle fibers, while simultaneously underestimating the fatigue effect on slow twitch muscle fibers. Indeed, the likelihood is that the muscle fibers of high-threshold motor units will fatigue much less than we might predict in the early reps of a strength training set performed with maximal effort on each rep (when bar speed is high), while the muscle fibers of low-threshold motor units will experience more fatigue than we might predict.

What can we say about fatigue during maximal effort strength training?

During maximal effort strength training with a moderate load (such as in most velocity-based training studies), effort is high on every rep and therefore motor unit recruitment is nearly maximal on every rep. However, the velocity is high at the start of the set, and this means that the mechanical tension experienced by the muscle fibers of the high-threshold motor units must be comparatively small (which is why when velocity-based training is done with very small losses in bar speed, there is minimal muscle growth).

So how does mechanical tension achieve sufficiently high levels towards the end of a set of this type of strength training, without peripheral fatigue reducing the force produced by the muscle fibers controlled by high-threshold motor units?

In the first few reps of the set, bar speed is very fast but quickly starts to fall. This occurs primarily because of an impairment of crossbridge function in the muscle fibers of the high-threshold motor units (which causes a reduction in muscle fiber shortening velocity, but no change in muscle fiber force) as a result of metabolite accumulation, but also because of excitation-contraction coupling failure experienced by the muscle fibers of the low-threshold motor units (which causes a reduction in muscle fiber force). During this phase, bar speed is falling while the muscle fiber contraction velocity of the muscle fibers of high-threshold motor units is falling (which is why velocity-based training studies show close relationships between metabolite accumulation and bar speed) and force production of the muscle fibers of low-threshold motor units is falling (although this fatiguing effect will not contribute materially to changes in performance because bar speed is too fast for those fibers to contribute much to force production anyway).

In the final (stimulating) reps of the set, bar speed reduces to the point at which muscle fiber contraction velocity is slow enough for the muscle fibers of high-threshold motor units to experience high levels of mechanical tension. This point has been reached partly because of a reduction in the muscle fiber shortening velocity of those muscle fibers (which occurs without affecting their ability to produce force), and partly due to the excitation-contraction coupling failure that is experienced by the muscle fibers of low-threshold motor units (which reduces their ability to produce force). This creates a state in the final few reps of the set that is very similar to the one produced by bodybuilding training, in which the muscle fibers of the high-threshold motor units produce a high level of mechanical tension at slow speeds, due to a reduced level of force being produced by the muscle fibers of low-threshold motor units.

N.B. Slow twitch excitation-contraction coupling failure

The muscle fibers controlled by low-threshold motor units experience excitation-contraction coupling failure in the early part of a strength training set in which reps are done with maximal effort for several reasons. Firstly, that is the form of peripheral fatigue that these muscle fibers are predisposed to experience anyway. Secondly, the low-threshold motor units are active in both the eccentric and concentric phases, and not just in the concentric phase in which maximal effort is being used (eccentrics trigger excitation-contraction coupling failure extensively by the opening of stretch-activated ion channels). Thirdly, all low-threshold motor units control slow twitch muscle fibers, which are less metabolically efficient at fast speeds than at slow speeds. Therefore, these muscle fibers will fatigue more quickly when working in the early reps of the set.

The effect of excitation-contraction coupling failure of the muscle fibers of low-threshold motor units will be hugely underestimated in models using data drawn from isometric contractions, partly because there is no eccentric phase in that type of exercise, and partly because muscle fiber contraction velocity in the concentric phase is too slow.

What is the takeaway?

The stimulating reps model involves hypertrophy resulting from mechanical tension being experienced by the muscle fibers of high-threshold motor units, due to the force-velocity relationship. In this model, stimulating reps are the ones at the end of a set, when effort levels are high and bar speed is slow.

The applicability of the model to athletic training (in which lifters perform each rep of a set with maximal effort) has been been criticized on the basis that peripheral fatigue at the beginning of the set might reduce the force exerted by the muscle fibers of high-threshold motor units at the end of the set, and hence reduce the mechanical tension that they experience, and this in turn would prevent hypertrophy from being stimulated.

Nevertheless, fatigue during dynamic strength training does not reduce force and velocity to the same extent, nor does it affect the muscle fibers controlled by the high-threshold and low-threshold motor units similarly. The fatiguing processes that occur actually primarily impair the velocity of the muscle fibers controlled by high-threshold motor units in the early part of the set, while reducing the force of the muscle fibers controlled by low-threshold motor units, with the result that the muscle fibers controlled by high-threshold motor units do experience high levels of tension towards the end of a set of training with maximal efforts on each rep.

If you enjoyed this article, you will like my second book (see on Amazon).