Do eccentric and concentric training produce different types of muscle growth?

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During normal strength training, we lift and lower weights repeatedly. Sometimes, as in the squat exercise, we begin with the lowering phase, and then perform the lifting phase to return to the start. Other times, as in the biceps curl exercise, we begin with the lifting phase, and then perform the lowering phase to return to the beginning.

When we lift the weight, the muscle fibers inside the muscle shorten. This is called a concentric muscle action. When we lower the weight, the muscle fibers lengthen. This is called an eccentric muscle action.

Occasionally, athletes use strength training methods that involve only either the lifting phase (as in some ballistic exercises) or only the lowering phase (as in the Nordic curl). These are called “concentric-only” and “eccentric-only” strength training, respectively. Among bodybuilders, concentric-only strength training is rare, but the use of eccentric-only strength training in the form of “negatives” is commonplace.

Research that has compared the effects of concentric-only and eccentric-only strength training has found that they produce different effects on muscle growth, in respect of increases in fiber length versus fiber diameter, in respect of different regions of the muscle, and in respect of slow twitch and fast twitch muscle fiber area.

So what causes these different effects?

What happens when muscle fibers shorten?

When muscle fibers shorten, they produce force because of the actions of active elements inside them. Active elements are those structures that exert force by using energy to move in response to the electrical signal that is sent from the central nervous system.

Each muscle fiber contains long, thin chains of structures called sarcomeres, which are made up of many strands (myofilaments) of molecules. For active force production, the key myofilaments inside each sarcomere are those made of actin and myosin molecules. When the electrical signal from the central nervous system arrives at the muscle fiber, it causes calcium ions to be released into the area around these actin and myosin myofilaments.

Regulatory proteins located on the actin strand respond to the presence of these calcium ions. When there are few calcium ions present, as is the case when the muscle is inactive, these proteins prevent myosin from binding to actin. The release of calcium ions into the area around the strands of actin and myosin molecules alters the positions of these regulatory proteins, and allows myosin to bind to actin. This binding process, which involves the formation of crossbridges, causes actin to slide past myosin in each sarcomere along the length of the muscle fiber, and this movement deforms the whole fiber, and subsequently the whole muscle.

Importantly, the actin and myosin myofilaments do not themselves change length when crossbridges are formed. Rather, the amount of overlap between the actin and myosin myofilaments within each sarcomere increases. Since muscle fibers do not change volume when they deform by decreasing in length, this increasing overlap at various points along the length of the fiber causes it to bulge outwards at the center of each sarcomere. This outward deformation in the transverse plane of the muscle fiber can be detected by mechanoreceptors, and thereby stimulate muscle growth.

The process by which myosin binds to actin to produce crossbridges is driven by chemical energy provided in the form of adenosine triphosphate (ATP). During strength training, as this ATP is used, it is replenished by the oxidative, glycolytic, and creatine-phosphate energy systems. When moderate or high reps are used, the glycolytic system is heavily used, and this leads to the formation of metabolic byproducts such as lactate, hydrogen ions, phosphate, and adenosine diphosphate (ADP), which has been termed metabolic stress, and whichi is closely linked to the fatiguing process that causes increased motor unit recruitment and a reduction in muscle shortening velocity.

What happens when muscle fibers lengthen?

When muscle fibers lengthen, they produce force because of the actions of both active and passive elements inside them. Passive elements are elastic structures that exert force by resisting being deformed, rather than by using energy to move.

Since muscle fibers use both active and passive elements to produce force while they are lengthening (but they can only use active elements to produce force while they are shortening), they can necessarily exert higher forces in lowering (eccentric) movements, than in lifting (concentric) movements.

Single muscle fibers can produce approximately 50% more force while they are lengthening, than when they are shortening, and we are usually 25–30% stronger when lowering a weight, than when lifting a weight in the same exercise. Single muscle fibers are probably stronger when lengthening than whole muscles because they are tested during electrical stimulation, rather than in voluntary movements, in which the central nervous system probably limits how much force we exert, as a safety mechanism.

There are three elements of muscle fibers that are deformed during lengthening: (1) the extracellular matrix, or collagen layer (endomysium) that covers over the cell membrane, (2) the internal structure (cytoskeleton) of the muscle fiber, and (3) the giant molecule titin, which plays a particularly important role when the muscle fiber is active.

Titin is therefore very important for an understanding of eccentric contractions, and of eccentric-only strength training.

Titin molecules contain two elements in series with each other: (1) elastic tandemimmunoglobulin (Ig) domains, and (2) a stiff PEVK segment. These two elements are separated by a very small N2A segment. When muscle fibers are elongated without being activated, the Ig domains of titin molecules are lengthened, and since they are quite elastic, this provides only a small amount of resistance to stretch. When muscle fibers are elongated while they are activated, the N2A segment binds to actin (thin) myofilaments, and this limits how much of the change in titin length can be accomplished by the lengthening of the elastic Ig domains. Consequently, changes in titin length must be achieved by elongating the stiffer PEVK segment, which provides much more resistance to stretch.

As muscle fibers produce force actively while lengthening, the actin and myosin myofilaments experience progressively less and less overlap, and do not bulge outwards in the middle of each sarcomere as much as they do during fiber shortening. In fact, since fibers do not change volume when they deform, they must actually reduce in diameter as they increase in length. Yet, the longitudinal (rather than outward) deformation of the muscle fiber is likely still detected by mechanoreceptors, and thereby stimulates muscle growth.

When muscle fibers produce force actively while lengthening, they require metabolic activity to produce the ATP that powers the binding of myosin to actin to produce crossbridges, just as they do when producing force while shortening. However, the amount of ATP required to produce force while lengthening is much less than the amount required to produce force while muscle fibers are shortening. In fact, eccentric muscle actions are more than twice as energy efficient as concentric muscle actions. Thus, the fatiguing processes that leads to muscular failure when muscle fibers are lengthening do not involve a high level of metabolite accumulation, and the fatiguing process does not produce a reduction in movement velocity, but instead seems to increase the proportional load on the passive elements, as the contribution of the active elements reduces.

How do concentric-only and eccentric-only contractions differ from each other?

When muscle fibers shorten in concentric-only strength training, they produce force through the actions of the active elements, and this leads to the muscle fiber being deformed by reducing its length and by bulging outwards in the middle of each sarcomere.

This process requires a high level of energy metabolism, through a fairly inefficient process, causing a large amount of metabolite accumulation as the fiber fatigues. Moreover, as the fiber fatigues, this leads to a reduction in muscle shortening velocity, and this increases mechanical loading on the fibers of newly recruited motor units, because of the force they exert in accordance with the force-velocity relationship.

When muscle fibers lengthen during eccentric-only strength training, they produce force through the actions of both active and passive elements, and this leads to higher forces being developed, and means that the muscle fiber is deformed by increasing its length and by decreasing its diameter.

This process requires a much lower level of energy metabolism, through an efficient process, and causes minimal metabolite accumulation as the fiber fatigues. As the fiber fatigues, this increases the load on the passive elements, relative to the active elements.

How do the long-term effects of concentric-only and eccentric-only training differ from each other?

Overall, it seems likely that eccentric-only and concentric-only strength training produce largely similar increases in muscle volume, although early researchers tended to find indications that eccentric-only training caused greater increases in muscle size.

It is possible that eccentric-only training might produce slightly greater overall gains in size, although this effect would most likely be related to the greater overall forces involved, rather than any specific characteristic of the contraction type.

More importantly, recent research has shown that eccentric-only strength training causes greater gains in muscle fiber length, while concentric-only strength training leads to greater increases in muscle fiber diameter, even while overall increases in muscle volume are similar. These effects may be connected to differences in regional muscle growth between the two types of training, because eccentric-only strength training causes greater increases in muscle size in the distal region, while concentric-only strength training causes greater increases in the middle region of the muscle.

So what causes the similar overall muscle growth, but differences in the direction that fibers grow, and differences in regional hypertrophy?

Can the effects of concentric-only and eccentric-only strength training be explained by mechanical tension, metabolic stress, and muscle damage?

Traditionally, researchers have attempted to predict the resulting muscle growth that occurs after concentric-only and eccentric-only strength training by reference to a model involving mechanical tension, metabolic stress, and muscle damage, although some researchers regard muscle damage as a positive factor that enhances muscle growth, while others regard it as a negative factor that limits muscle growth.

Early researchers suggested that while eccentric-only strength training involves higher muscle fiber forces (and therefore higher levels of mechanical tension), concentric-only strength training involves more metabolic stress, because of the greater accumulation of metabolites that occurs. They suggested that these competing factors might explain the similar growth that occurs after the two types of training.

Metabolic stress has been proposed to cause muscle growth primarily through increased motor unit recruitment, and secondarily through the release of systemic hormones, muscle cytokines, reactive oxygen species, and cellular swelling. However, recent evidence suggests that the perception of effort, and not the accumulation of metabolites, is responsible for the increase in motor unit recruitment during strength training. This perception of effort can increase due to fatigue that occurs through any mechanism, whether linked to the accumulation of metabolites or not.

Later researchers proposed that while eccentric-only strength training involves higher muscle fiber forces (and therefore higher levels of mechanical tension), it also causes greater muscle damage, which might reduce its effectiveness, and cause it to produce similar muscle growth as concentric-only strength training. Indeed, muscle damage can indeed lead to muscle loss when it is particularly severe.

Consequently, the model of hypertrophy that involves mechanical loading, metabolic stress, and muscle damage produces untestable hypotheses in relation to the differences in hypertrophy that might arise after eccentric-only and concentric-only strength training. Any outcome can be explained, either by a preferentially greater role of metabolic stress, or by a preferentially greater role of muscle damage. In addition, the model cannot explain why muscle fibers grow in different directions and produce differing regional muscle growth after each type of training.

What is actually happening?

It is commonly assumed that the mechanical loading stimulus that causes hypertrophy is a scalar quantity (having only magnitude) rather than a vector (having both a magnitude and a direction).

However, different types of mechanical loading (which lead to deformations of the fiber in different directions and which cause different anabolic signals), seem to produce different muscle fiber adaptations, possibly because the deformations are detected by different mechanoreceptors.

When deformations occur that involve temporary increases in length and reductions in diameter (as during eccentric-only strength training), this stimulates the fiber to grow in volume by increasing in length. This effect might be mediated by titin sensing the stretch that is imposed upon it, when the fiber is deformed longitudinally.

When deformations occur involving temporary increases in diameter (by bulging outwards in the middle of each sarcomere) and reductions in length (as during concentric-only strength training), this stimulates the fiber to grow in volume by increasing in diameter.

What about fiber type-specific hypertrophy?

Some researchers have suggested that eccentric training might produce preferentially greater growth of the muscle fibers of high-threshold motor units, which control mainly type II muscle fibers. This might then be observed as a preferentially greater increase in average type II than type I muscle fiber diameter, in comparison with normal strength training.

Indeed, some studies have reported this tendency.

However, it is important to note that strength training routinely causes greater increases in type II muscle fiber diameter compared to in type I muscle fiber diameter anyway, because type II muscle fibers are more responsive to the anabolic stimulus provided by strength training. This is likely because type II muscle fibers are less oxidative. It is difficult for highly oxidative, type I muscle fibers to increase in diameter without becoming dysfunctional.

Therefore, any apparent preferential increase in type II fiber area resulting from eccentric training could be a result of greater overall hypertrophy resulting from a higher level of mechanical loading.

Additionally, it is important to appreciate that the size principle is still applicable during eccentric contractions, and also that greater forces can be exerted with less motor unit recruitment while muscles are lengthening, because this involves force production by both active and passive elements of the muscle fibers. Consequently, when producing the same amount of force at the same speed, all the motor units that are recruited in eccentric contractions are also recruited in concentric contractions, but the concentric contractions recruit additional motor units as well. However, when efforts are maximal, all motor units are recruited in both contraction types.

Therefore, it is unlikely that differences in motor unit recruitment can explain any preferential increase in type II fiber area after eccentric training. In fact, it is more likely that eccentric-only strength training would lead to greater type I muscle fiber growth for this reason, because of reduced levels of motor unit recruitment (and therefore reduced type II muscle fiber activation) during most muscular contractions.

Therefore, some researchers have suggested that since type II muscle fibers are more easily damaged after eccentric training, this greater damage could be a mechanism by which greater growth of these fibers then occurs. Indeed, greater satellite cell activation has been observed in type II fibers than in type I fibers after eccentric training, which might be taken as support for this idea. Even so, satellite cell activation can be directed towards muscle damage repair only, and need not imply that fiber growth has occurred.

In fact, it is more likely that a difference in titin-based sensing of mechanical loading is responsible for any preferential hypertrophy in type II muscle fibers after eccentric training, because titin molecules can vary in size between muscle fibers.

Overall, type I muscle fibers seem to contain longer, larger titin molecules and therefore display less titin-related passive stiffness, while type II muscle fibers tend to display shorter, smaller titin molecules that give them greater titin-related passive stiffness. The greater contribution of the stiffer type II muscle fibers to force production could allow them to experience greater mechanical loading during eccentric contractions, and thereby grow to a greater extent. This would then explain why fast eccentric contractions seem to display a greater tendency towards fiber type-specific hypertrophy than slow eccentric contractions, because they involve a greater contribution to force production from the passive elements of muscle fibers.

What is the takeaway?

Strength training using only the lifting phase, when muscle fibers are shortening (concentric-only training) and strength training using only the lowering phase, when fibers are lengthening (eccentric-only strength training) lead to similar increases in muscle fiber volume, but different effects on fiber length and diameter.

Eccentric-only strength training causes greater gains in fiber length, as well as greater increases in the size in the distal region of the muscle. Concentric-only strength training causes greater increases in fiber diameter, as well as greater increases in the middle region of the muscle. It seems likely that these specific adaptations arise in response to the deformations of the fibers in different directions that occur during each type of training, and which lead to different anabolic signals after the workout.

Additionally, eccentric-only training might permit preferential increases in fast twitch muscle fiber size, because an element of the mechanical loading during eccentric contractions is produced by the passive element titin, and fast twitch fibers tend to display greater titin-based stiffness than slow twitch muscle fibers.

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