Does leverage determine muscle force (and does that matter)?

Recently, I was sent a post that attempted to criticize using the principle of neuromechanical matching to inform strength training exercise selection on the basis that leverage determines muscle activation and not muscle force. In this article, I will explain why muscle activation is actually far more important than muscle force in the context of exercise selection for muscular hypertrophy.

How does the brain determine which muscles to switch on during an exercise?

How does the brain determine how much each muscle is activated during any given strength training exercise? The answer is by reference to the principle of neuromechanical matching. This principle states that a muscle is activated in proportion to its leverage for a joint action during any given movement, as measured by its internal moment arm length. If a muscle has poor leverage, it will display a low level of activation, while if it has good leverage, it will display a high level of activation.

Importantly, this principle is evolutionarily viable since it makes us more efficient. If instead we sent central motor command preferentially to those muscles that have poor leverage (as some fitness influencers suggest) then we would be much weaker and less efficient at those movements than we actually are. It bears repeating that this principle has been studied directly several times in skeletal (inspiratory) muscles. What is more, we can see it happening indirectly in a great many muscle groups simply by comparing muscle internal moment arm length curves with muscle activation levels at different joint angles. Overall, it works pretty well.

Does the internal moment arm length (leverage) of a muscle determine muscle force?

So does the internal moment arm length of a muscle determine muscle force? No, of course it does not. Both the active and passive length-tension relationships necessarily affect the size of all of the activated muscle fiber forces and can easily alter the shape of the muscle force-to-joint angle curve relative to the leverage-to-joint angle curve.

Does this invalidate the principle of neuromechanical matching? No, of course not. The principle of neuromechanical matching is intended to describe how the brain allocates muscle activation between muscles in any movement or exercise. It does not predict or even try to predict what the whole muscle force output will be. (In fact, we know from previous studies that the brain does not take any passive mechanical tension contributions into account during the allocation of muscle activation between muscles). So there is no challenge to how the principle of neuromechanical matching is stated to work.

So does that mean that instead of using the principle of neuromechanical matching to identify the best joint angle to train a muscle (and therefore identify the most suitable exercise), we should instead identify the joint angle (and therefore muscle length) at which muscle force is highest in accordance with the active and/or passive length-tension relationships? Well, let’s take a look.

How does the active length-tension relationship influence hypertrophy?

Muscle fiber active force production varies according to the active length-tension relationship. When muscle fibers are working in the middle of the plateau region, they produce more active mechanical tension. When they work at shorter lengths or longer lengths relative to this plateau region, they produce less active mechanical tension. At face value, this implies that we should aim to work muscle fibers always on the plateau region of the active length-tension relationship (which is what many fitness influencers are currently arguing). But is this correct?

In fact, it is not correct because the hypertrophy stimulus that a muscle fiber experiences during a strength training set is not purely determined by the magnitude of force it produces but also by the duration of time for which it experiences that force (the force-time integral). So we cannot just look at the magnitude of force that muscle fibers are producing according to their position on the active length-tension relationship. We also must look at how long they can produce that force for before fatiguing.

To generate active mechanical tension, we form actin-myosin crossbridges, which requires the use of ATP. When we work closer to the plateau of the active length-tension relationship, we form more crossbridges per second and therefore we burn ATP at a faster rate than when we work further from the plateau. Burning ATP at a faster rate means that metabolite-related fatigue (which is the primary fatigue mechanism during strength training) occurs more rapidly. Therefore, if you perform muscular contractions at a given level of muscle activation while on the plateau (such that muscle force is indeed higher), you will not be able to hold that muscle contraction for as long as a similar contraction at the same level of muscle activation but working further from the plateau. In other words, while your level of force is higher, the duration of force application is shorter. Therefore, the hypertrophy stimulus that you end up with is identical. The hypertrophy stimulus for the muscle fiber is really just the total number of actin-myosin crossbridges that have formed in the training session.

So for example, if we identify that the gluteus maximus has a plateau of active mechanical tension at 45 degrees of hip flexion, then training the muscle with peak contractions at 0, 45 or 90 degrees of hip flexion will produce identical hypertrophy so long as the level of muscle activation that the muscle achieves is the same (and hence the number of muscle fibers that are activated is also the same). While peak active mechanical tension levels of the working muscle fibers differ between those joint angles (and therefore muscle fiber lengths), the dosage of mechanical tension stimulus does not differ because the time to fatigue is shorter when working on the plateau region (due to more rapid ATP usage) than when working at either longer or shorter muscle lengths.

In contrast, if we identify that the gluteus maximus has maximum leverage at 0 degrees of hip flexion (and hence achieves its maximum levels of muscle activation at this joint angle), then training the muscle with peak contractions at 0, 45 or 90 degrees of hip flexion will produce different hypertrophy. Hypertrophy is greatly affected by the number of activated muscle fibers because muscle growth occurs on a fiber-by-fiber basis (we say that it is an intrinsic process mediated by internal mechanoreceptors). If a muscle fiber is not activated, it will not experience any mechanical tension and therefore will not grow. So if training at 0 degrees of hip flexion allows 90% of the muscle fibers to be activated but training at 45 degrees of hip flexion allows 85% of the muscle fibers to be activated, training with peak contractions at 0 degrees will always be superior to any other angle (and will also lead to a larger maximum possible muscle size in the future).

So we can see that the joint angle at which maximum active mechanical tension is generated is NOT important, while the joint angle at which the level of muscle activation is highest is very important for hypertrophy.

How does the passive length-tension relationship influence hypertrophy?

Muscle fiber active force production also varies according to the passive length-tension relationship. When muscle fibers are working further down the descending limb, they generate more passive mechanical tension. When they work at shorter lengths, they produce less passive mechanical tension. At face value, this implies that we should always try to work muscle fibers as far down the passive length-tension relationship as possible (which is what many fitness influencers are currently arguing). Does this really make sense?

For a full write-up on how stretch-mediated hypertrophy occurs as a result of passive mechanical tension, please see my previous article. Here, I just want to note that the adaptation caused by passive mechanical tension is not the same as the adaptation caused by active mechanical tension. Active mechanical tension causes muscle fibers to add myofibrils, while passive mechanical tension causes them to add sarcomeres in series. So we cannot really combine the two length-tension curves and argue that the total sum of the mechanical tensions is a valid construct. They cause totally different adaptations to happen. In other words, even if you can show a combined length-tension relationship that has a higher level of total tension at long muscle lengths, the higher passive mechanical tension is not going to compensate for a lack of activation in those extended joint angles. Passive mechanical tension cannot stimulate myofibrillar addition. To achieve maximum hypertrophy you are still going to have to train the muscle at the joint angle where it experiences maximum activation, and that means you are going to need the principle of neuromechanical matching.

What are the conclusions?

Maximum hypertrophy of any given muscle will happen when the largest number of its muscle fibers are exposed to a sufficiently high magnitude of mechanical tension. In contrast, hypertrophy will be suboptimal if a much smaller number of muscle fibers are exposed to slightly higher levels of mechanical tension, especially if this is mediated by means of working in the middle of the plateau of the active length-tension relationship. So, we should focus on [1 identifying training methods that maximize motor unit recruitment levels, and on [2] identifying exercises that maximize the level of muscle activation in specific muscles.