Muscle growth is predominantly caused by activated, single muscle fibers increasing in size after they have experienced mechanical loading during strength training.
The main determinant of this mechanical loading is the force-velocity relationship. However, the length-tension relationship can also have an effect, and it explains why full ranges of motion and eccentric training produce the results that they do.
Also, if we look carefully, the length-tension relationship can help explain how regional muscle growth could occur even when we achieve full motor unit recruitment during the strength training workouts of a program.
How is hypertrophy caused by strength training?
In humans, hypertrophy (an increase in the size of a whole muscle) is almost entirely the result of single muscle fibers increasing in volume. This usually occurs due to an increase in muscle fiber diameter, but also happens because of increases in muscle fiber length.
While increases in fiber number (hyperplasia) have been reported in rodent models of muscle growth, the same results have not been duplicated in humans after strength training. Moreover, bodybuilders seem to have approximately the same number of muscle fibers in a muscle as untrained individuals, despite having much larger muscles overall.
Single muscle fibers are stimulated to increase in size once they have detected mechanical loading or deformation with receptors located either inside the muscle fiber or at the cell membranes, which are called mechanoreceptors. This mechanical loading must be equal and opposite to the force that each muscle fiber itself produces. Importantly, the mechanical loading that is experienced by the whole muscle cannot trigger hypertrophy because the muscle has no means of detecting it. The mechanical loading experienced by the whole muscle is closely related to the external force, which we can record by reference to the load lifted.
The force produced by any given muscle fiber during a muscular contraction (and therefore the degree of mechanical loading that it experiences) is largely determined by (1) whether the muscle fiber is activated, and (2) the speed at which the muscle fiber shortens, due to the force-velocity relationship.
Activated fibers that shorten slowly produce high forces and experience high levels of mechanical loading. It is important to realize that the force produced by any given muscle fiber is *completely unrelated* to the force produced by the whole muscle, because motor unit recruitment levels can change, which alters the number of muscle fibers that contribute to a contraction. And the more muscle fibers that are active, the more force can be produced.
While these factors are the most important determinants of mechanical loading experienced by a muscle fiber during a muscular contraction, the length-tension relationship also plays a role.
What is the length-tension relationship?
The length-tension relationship is the observation that single muscle fibers do not produce the same amount of isometric force when they are activated at different static lengths.
In fact, muscle fibers produce low forces at short lengths (the ascending limb of the length-tension relationship), produce progressively greater forces up to a point at moderate lengths (the plateau of the length-tension relationship), and finally produce sharply increased forces when very long lengths are tested (the descending limb of the length-tension relationship).
The force that muscle fibers produce at any given muscle fiber length during muscular contractions arises due to both active and passive mechanisms (which produce active and passive force).
- Active force — the active mechanism involves energy metabolism and the movement of myofilaments against one another during the actin-myosin crossbridge cycle.
- Passive force — the passive mechanism involves structures inside the muscle fiber that elongate elastically when they are pulled apart. Lengthening these structures produces tensile forces without any chemical reactions, which is why the force is called “passive” instead of active.
- The passive length-tension relationship is very simple because it is just the behavior of an elastic material. Passive force is very low throughout most of the working range of motion of the sarcomeres inside the muscle fiber, but it increases dramatically once each sarcomere approaches the end of its working range, and the passive structures inside the muscle fiber begin to be stretched. The passive structures that elongate elastically comprise titin (inside the muscle cell) and collagen (surrounding the muscle cell). Researchers have found that both of these structures can contribute to passive tension during muscle fiber elongation. However, titin is probably the greater contributor to passive force throughout normal ranges of motion.
- The active length-tension relationship is more complex. Active force is very low when the sarcomere is very short, because there is little overlap between the actin and myosin myofilaments. This means that they cannot bind together to produce force. As the muscle fiber (and therefore each sarcomere within it) is tested at longer lengths, the available sites for myosin to bind to actin are increased, and the amount of force increases. Once all of the available sites are overlapping, active force reaches a plateau. Theoretically, the overlap can also reduce once the sarcomeres are stretched too far, but this point corresponds with the sharp increase in passive force, so is not usually observed.
As regards the mechanical loading that single muscle fibers experience during strength training, the most important takeaway is that single muscle fiber force production (and therefore mechanical loading) is greater during strength training when the passive elements are able to contribute to tensile force in the contraction.
But greater mechanical loading due to tension provided by passive elements does not just cause greater hypertrophy. It also alters the type of hypertrophy that occurs.
How does the length-tension relationship affect muscle fiber hypertrophy?
When muscle fibers produce force and the passive structures are able to contribute to force production (and therefore increase mechanical loading on individual muscle fibers), this has two effects.
- Overall greater hypertrophy — the overall amount of force that can be exerted by the muscle fiber is greater, which causes greater mechanical loading, and therefore more muscle growth. Indeed, research seems to show that the mechanical loading produced by active and passive force production (stretching) is additive for hypertrophy.
- Preferential increase in fiber length — when muscle fibers experience high levels of loading on their passive elements (either by contracting at long muscle lengths instead of at short muscle lengths, or by contracting eccentrically rather than), they respond by increasing preferentially in length rather than diameter. This is genuine muscle growth, and leads to an overall increase in mass. Recent research has shown that this most likely happens because titin, which is probably most responsible for producing the passive force, is also involved in detecting the mechanical tension that causes muscle fibers to increase in length.
So how does this apply to normal strength training?
How does the length-tension relationship affect the amount of mechanical loading and hypertrophy in practice?
We can observe the effects of higher levels of passive force production during strength training at large ranges of motion (or longer muscle lengths) and also during eccentric contractions. Interestingly, these two types of training are biologically far more similar than most people realize.
#1. Larger ranges of motion
When a muscle fiber contracts at a long muscle length, its passive structures (including titin but also collagen) are already elongated when it is activated. This allows these structures to contribute to force production, leading to enhanced mechanical loading.
This greater load on the passive structures is most likely why conventional strength training involving long ranges of motion and isometric strength training at joint angles corresponding to long muscle lengths often cause greater hypertrophy than strength training programs involving partial ranges of motion or at short muscle lengths. It is also why strength training involving long ranges of motion and isometric strength training at joint angles corresponding to long muscle lengths often causes greater increases in muscle fascicle length than other types of training.
#2. Eccentric contractions
When a muscle fiber contracts initially at a short length, and is then lengthened by an eccentric contraction, titin (a key passive element) contributes to force production despite the short length.
This happens because of a change in the function of the titin molecule when the muscle fiber is activated, such that its elastic segment cannot elongate, and its stiff segment must lengthen instead. When the fiber is lengthened without being activated, its stiff segment does not increase in length during fiber elongation until the elastic segment had already lengthened, which happens at much longer fiber lengths.
The effect of the muscle fiber being activated before being lengthened is to allow titin to contribute to force production at far shorter fiber lengths (this is the reason why we are able to exert approximately 30% more force during eccentric contractions than in similar concentric contractions). As a result, eccentric training tends to cause slightly more muscle growth than equivalent concentric training, and proportionally much greater increases in muscle fascicle lengths.
How are isometric strength training at long muscle lengths and eccentric training similar (and how are they different)?
As explained above, eccentric contractions involve very similar biological conditions to isometric strength training at long muscle lengths (and dynamic strength training through large ranges of motion), because they both involve passive force being produced by titin. Isometric strength training at long muscle lengths does this by moving titin to a long length before activating the muscle fiber, while eccentric training compels the stiff segment of titin to contribute to force production even at shorter lengths.
Eccentric training has the additional effect that the titin molecule can be stretched to much greater lengths, allowing a far larger signaling effect, and potentially much larger adaptations. Indeed, eccentric training certainly causes larger increases in muscle fascicle length than large range of motion conventional strength training.
Additionally, eccentric contractions may allow titin to be elongated to a degree that causes longitudinal hypertrophy in muscles that might not be able to experience this type of mechanical loading during strength training with long ranges of motion. Although it is not well-known, not all muscles contain muscle fibers with sarcomeres that work on the descending limb of the length-tension relationship during contractions at long muscle lengths. In fact, some muscles contain fibers that work on the plateau region for the majority of the time. This makes it difficult for them to experience meaningful loading on the passive structures, and to trigger longitudinal hypertrophy.
How can the length-tension relationship help explain regional hypertrophy?
Since mechanical loading determines muscle fiber growth (and not simply whether the muscle fiber is activated due to its motor unit being recruited), and since both muscles and muscle regions can display differing sarcomere lengths, it is possible for strength training to cause differing amounts of muscle growth in different regions of a muscle or in the individual muscles of a group. This can happen because mechanical loading can differ (due to the length-tension relationship) even when muscle activation does not differ.
For example, while the signal from the central nervous system to the quadriceps is very similar across the four muscles during knee extension movements, the mechanical loading in high degrees of knee flexion is likely to be slightly greater in the muscle fibers of the vastus medialis than in those of the vastus lateralis, due to the longer sarcomere lengths that are reached. This could lead to preferentially larger gains in vastus medialis muscle size when using exercises with larger knee flexion ranges of motion.
Similarly, sarcomere lengths are known to vary between regions of the tibialis anterior muscle in humans. This may help explain region-specific muscle growth after strength training, because of greater levels of mechanical loading experienced in one region than in another. Importantly, this can occur even though all of the muscle fibers are activated in training, as shown by studies that have used electrical stimulation to produce muscular contractions. Such studies show that it is most likely the differences in mechanical loading produced by the variations in sarcomeres between regions of the muscle that are responsible for region-specific hypertrophy.
What is the takeaway?
The main determinant of the mechanical loading experienced by active muscle fibers in a muscular contraction is the force-velocity relationship. However, the length-tension relationship also plays a role. The key feature of the length-tension relationship is the extra force that can be exerted during muscular contractions when the passive elements are able to contribute, which occurs when the muscle is elongated to long lengths during normal strength training, and also during eccentric training.
This extra force seems to be provided largely by titin, which contributes high levels of passive tension both when the muscle is elongated to long lengths (as in strength training with full ranges of motion) and also when the muscle is lengthened after being activated (as in eccentric contractions). During both types of training, titin senses the mechanical loading that it is exposed to, and triggers longitudinal fiber hypertrophy to occur. The behavior of titin during strength training can explain the (slightly inconsistent) effects of strength training with full ranges of motion and eccentric training in various muscles, as well as the phenomenon of regional hypertrophy.