Can the mechanical tension, metabolic stress, and muscle damage model explain all of the ways in which hypertrophy could occur?

Chris Beardsley
Sep 18, 2018 · 5 min read

Recently, I shared a study showing that the size of the central motor command in a strength training exercise with a light load was increased by the presence of fatigue.

In the light of recent work, this finding was not entirely surprising.

Several studies (both experimental and involving computer models) have shown that motor unit recruitment increases with increasing fatigue, during submaximal force production, through progressive reductions in motor unit recruitment threshold.

However, the study was very surprising to many people who believed that metabolic stress was the key mechanism by which motor unit recruitment increased during light load strength training to failure, because the methods used by the research group in this study were designed to prevent the subjects from accumulating metabolites while they developed fatigue.

Let’s take a closer look at this study.


What did the researchers do?

The research group who performed this study were primarily interested in understanding whether the perception of effort was associated with the magnitude of the central motor command during a strength training exercise, across different loads and states of fatigue.

The subjects did single-arm biceps curls with a light weight (20% of 1RM), and also with a heavier weight (35% of 1RM), with 1-second lifting and lowering phase durations. They did these lifts while their arm was unfatigued, and again after it had been fatigued with a previous bout of exercise. While the subjects did these lifts, the researchers recorded the amplitudes of their movement-related cortical potentials (MRCPs) using electroencephalogram activity, which is a measurement of the size of the central motor command.

The unique feature of this study was the way in which fatigue, or the reduction in the capacity to exert voluntary force, was produced.

During many types of strength training, fatigue is observed in conjunction with increases in motor unit recruitment and alongside the accumulation of metabolites, such as lactate. However, not all types of fatiguing contractions lead to metabolite accumulation. Indeed, it is possible to produce a reduction in voluntary force-producing capacity with a series of eccentric contractions, and this occurs without any change in lactate levels.

In this study, the researchers programmed an exercise bout of repeated eccentric contractions with 20 seconds of rest between repetitions, and they confirmed that blood lactate levels were not affected by the fatiguing exercise by taking blood samples from the right earlobe.

The researchers wanted to avoid the accumulation of metabolites because the primary goal of the study was to assess the link between the size of the central motor command and the perception of effort, and it has been suggested that metabolite accumulation might stimulate sensory feedback through group III and IV muscle afferents, and thereby cause an increased perception of effort.

Indirectly, this experimental process benefits our study of hypertrophy, because it allows a study of how neural drive to the muscle is affected by fatigue, when metabolic stress is absent.


What does this mean?

To integrate this study into the hypertrophy literature, we first have to decide whether or not the increase in central motor command, measured by MRCP during a series of exercises that are identical except in relation to the weight on the bar and the state of fatigue, is reflective of an increase in motor unit recruitment. Since this measurement is an indicator of the activity of the premotor and motor areas of the brain insofar as they relate to voluntary muscle contractions, this is not totally unreasonable.

Assuming that we accept this, then we next need to decide whether we think that this increase in motor unit recruitment would lead to a hypertrophic stimulus, despite the light load being lifted.

If we think that both of these inferences are reasonable, then we have to accept that the traditional three-part model of hypertrophy mechanisms (mechanical loading, metabolic stress, and muscle damage) cannot explain all of the ways in which muscle growth might be stimulated.

(Note that in the traditional model, mechanical loading is assumed to occur through high muscle forces, incurred when lifting heavy weights or producing large efforts against slow-moving or static objects, rather than because of the high muscle fiber forces caused by the force-velocity relationship).

In the traditional, three-part model, hypertrophy is believed to occur after heavy strength training primarily because of mechanical loading, and after light load strength training to failure primarily because of metabolic stress, which is thought to stimulate muscle growth through: (1) increased motor unit recruitment, (2) systemic hormone release, (3) muscle cytokine release, (4) reactive oxygen species release, and (5) muscle cell swelling.

Yet, this study suggests that we can increase motor unit recruitment during light load strength training without incurring any metabolic stress.

Therefore, the three-part model seems to require another part, to describe the role of fatigue on motor unit recruitment, when the type of fatigue does not involve the accumulation of metabolites. Perhaps the three-part model should be a four-part model including non-metabolic stress-related fatigue?


What is the alternative?

The alternative to the traditional three-part model of hypertrophy is a single-factor model involving mechanical loading on individual muscle fibers (rather than on whole muscles).

In this alternative model, fibers increase in volume after they experience a sufficiently high level of mechanical loading, which is equal and opposite to the force produced by the fiber itself in a muscular contraction (according to Newton’s Third Law).

The amount of force that a fiber can exert during a muscular contraction is determined mainly by its contraction velocity (because of the force-velocity relationship), but also by its length while it contracts (because of the length-tension relationship). Just as when a vehicle tows a trailer, the external load being moved has no impact on the force that a muscle fiber (or any engine) can exert, except insofar as it alters either of these two internal factors.

Importantly, any type of local, muscular fatigue (whether associated with metabolic stress or not) can also cause the contraction velocity of the working muscle fibers in a muscle to slow down, while also causing high-threshold motor units to be recruited. This increases the force produced (and therefore the mechanical loading experienced) by the muscle fibers of newly-recruited motor units, even while the force being produced by the fatigued, previously-recruited motor units is reduced.


What does this mean?

Metabolic stress probably cannot explain every way in which motor unit recruitment increases during fatiguing, submaximal strength training efforts with light loads. Therefore, the traditional, three-part model of how hypertrophy works is likely incomplete.

An alternative (and simpler) model proposes that single muscle fibers are stimulated to increase in volume when they experience a sufficient level of mechanical loading, which is determined by the force-velocity (and length-tension) relationships of the working muscle fibers. The force-velocity relationship can be manipulated to increase the force produced by each fiber by either the weight on the bar, or by the state of fatigue of the muscle, regardless of whether this fatigue occurs alongside metabolite accumulation.

Chris Beardsley

Written by

This is how strength training works