Strength training, which causes increased strength and muscle size, involves producing force through repeated muscular contractions.
When muscles contract repeatedly, they are often damaged.
Some researchers have suggested that the damage that results from strength training contributes to muscle growth, because the types of strength training that produce more hypertrophy often leave us with more muscle damage. Also, when muscles are damaged after strength training, this triggers a large increase in the rate of muscle protein synthesis, an increase in satellite cell activation, and structural adaptations that may be helpful for future increases in muscle size.
But is this the best interpretation of the facts?
Bodybuilders have traditionally linked muscle soreness and hypertrophy, and often believe that muscles must be damaged before they can grow.
Indeed, it is commonly claimed that muscles grow precisely because they are damaged, on the assumption that the growth process involves building broken muscle tissue back up again after a hard workout.
However, muscle growth, and the process of muscle repair after damage, are quite separate processes, although they both require an increase in muscle protein synthesis rates.
Muscle growth involves an increase in the protein content of a muscle fiber. Since muscle fibers are long, thin cylinders, this process can involve either an increase in the diameter of the fiber, or an increase in its length. Increases in fiber diameter involve an increase in the number of myofibrils in parallel. The myofibrils contain strings of actin and myosin myofilaments that bind together to produce force. Increases in fiber length involve an extension in the length of each of the myofibrils, because of an increase in the number of sarcomeres in series. Sarcomeres are the individual contractile units that link together in a long chain to form the myofibrils.
We can increase the number of myofibrils in parallel, or the length of each of the myofibrils, without first damaging them. Damaging one myofibril has no effect on our ability to build another one, and damaging the sarcomeres at any point along the length of a myofibril has no effect on our ability to add sarcomeres to its end, where they are usually created.
Muscle damage occurs when the internal structures of a muscle fiber, or its outer wrapping layers, are damaged. The myofibrils and the cytoskeleton that supports them are most easily damaged, and we can observe this as shifts in the distribution of the Z disk, which is a key landmark in the sarcomere. When the outer wrapping layers of the muscle fiber are made more permeable (perhaps by being damaged), this causes some of the contents of the muscle fiber to leak out into the spaces between muscle fibers, and subsequently into the bloodstream. This is observed as an elevation in creatine kinase levels.
Importantly, muscle fibers can be damaged to varying degrees.
Low levels of damage involve only disruptions to sarcomeres, while greater levels of damage involve damage to the outer wrapping layers. When the muscle fiber can be repaired by retaining the existing structures, removing the broken parts, and replacing them with new proteins (called repair). However, when the fiber is too badly damaged to be repaired, such as when it is torn completely in half, it can become necrotic. When this happens, the fiber is broken down inside its cell membrane, and a completely new, replacement fiber is grown inside it (called regeneration).
In summary, muscle fiber growth involves an increase in muscle fiber volume, either by the addition of new myofibrils, or by an increase in the length of the existing myofibrils. Muscle fiber repair involves the removal of damaged areas of a muscle fiber, and their replacement. Muscle fiber regeneration involves the complete removal of the old muscle fiber, and the creation of a new muscle fiber inside the existing muscle cell membrane.
Surprisingly, the cause of muscle damage is somewhat contentious.
It is commonly believed that muscle damage is caused by exposure to high levels of mechanical loading while muscles are lengthening, which causes individual sarcomeres in the chains of myofibrils to “pop” and elongate past their elastic limit.
However, this model cannot explain why (1) concentric training causes small amounts of muscle damage, nor can it explain why (2) strength training with very light loads and blood flow restriction can cause meaningful amounts of muscle damage. These types of training involve little force production while the muscle is lengthening, and should not therefore cause any damage.
An alternative proposal is that muscle damage is the result of the build-up of intracellular calcium and inflammatory neutrophils in response to fatiguing muscular contractions, which degrade the inside of the muscle fiber.
Any sustained muscular contraction that involves fatigue can increase the levels of calcium ions, which disrupts the muscle fiber membrane through protease activation. Indeed, research has shown that blocking the influx of extracellular calcium into the muscle fiber from stretch-activated ion channels during eccentric contractions reduces the amount of damage experienced by the cell membrane and the cytoskeleton. This shows that calcium ions are responsible for part of the damage that we might otherwise attribute to mechanical loading while lengthening.
Similarly, various types of exercise (not only eccentric contractions) can stimulate the release of inflammatory neutrophils. These act to degrade damaged tissues and may actually be the primary cause of the disruptions to cell membranes following eccentric contractions.
Overall, it seems likely that both direct mechanical loading and the effects of sustained contractions interact to cause damage. Muscular contractions produce mechanical loading, which damages fibers directly, but repeated contractions under fatiguing conditions release intracellular calcium and inflammatory neutrophils, which degrade the inside of the fiber. The weakened fiber is then more easily damaged by the mechanical loading produced by muscular contractions. Indeed, fatigue reduces the ability of fibers to absorb energy while lengthening, and this increases the likelihood that they will be damaged, since the amount of energy that a muscle must absorb relative to its capacity is linked to the damage it experiences.
Even though the processes by which muscle fibers increase in size and are repaired or regenerated are completely separate, early researchers proposed a hypothesis that exercise-induced muscle damage contributed to hypertrophy, on the basis of three, connected observations.
Firstly, they noted that there was an increase in muscle protein turnover after damaging exercise, since both muscle protein synthesis and breakdown rates are increased. Secondly, they observed that this occurred in conjunction with increased muscular inflammation and elevated intramuscular calcium ions. Thirdly, they noted that eccentric training, which produces more muscle damage than other types of muscular contraction, appeared to cause greater hypertrophy than either isometric or concentric training.
Decades later, these observations are still the foundation of the hypothesis, although one or two other findings have been added.
Later researchers identified that exercise-induced muscle damage affects gene expression, which probably triggers adaptations inside the muscle fibers that are beneficial for withstanding the effects of future, damaging contractions. Some commentators have taken this finding as further evidence that muscle damage contributes to hypertrophy, since such structural changes might feasibly support a later increase in muscle fiber volume. However, it is entirely speculative whether such alterations in gene expression, and the subsequent adaptations, are related to muscle fiber growth, or whether they are simply helpful for reducing the risk of future muscle damage.
More importantly, it has recently been proposed that exercise-induced muscle damage could enhance muscle growth after strength training because of a greater level of satellite cell activation and subsequent differentiation, and consequently through a larger increase in the number of nuclei inside each muscle fiber. Given the clear role of satellite cells in the repair and regeneration of damaged muscle fibers, this is a key issue.
In summary, some researchers have suggested that exercise-induced muscle damage can contribute to hypertrophy because muscle protein turnover is increased after damaging workouts (perhaps mediated by inflammatory or calcium ion-related signaling), because eccentric training, which causes more muscle damage than other contraction types, may stimulate more muscle growth than other types of training, and because satellite cell activity is often elevated when muscles are damaged, and increases in the number of nuclei inside each muscle fiber are likely necessary for long-term hypertrophy.
Some research groups believe that muscle damage does not contribute to muscle growth, and point to research showing that exercise-induced muscle damage can cause muscle loss, rather than muscle gain. In their model, muscle damage is an unnecessary side-effect of strength training, rather than a contributory factor. Consequently, the key observations about muscle-damaging exercise are explained in different ways.
The greater increase in muscle protein turnover that occurs after damaging workouts (mediated by either inflammatory or calcium ion-related signaling) is explained by the need to remove the damaged areas of muscle fibers (increased muscle protein breakdown), and to replace them with new ones (increased muscle protein synthesis). This process of replacement need not involve the growth of new myofibrils, nor need it involve the extension of myofibrils by adding new sarcomeres.
This interpretation is supported by research showing that in the early phases of long-term strength training programs, there is an increase in the level of muscle protein synthesis that is unrelated to muscle growth, which appears to be entirely directed towards the repair of muscle damage. Thus, overall muscle protein synthesis rates are very high, but this does not translate to increased hypertrophy.
The (possibly) greater muscle growth that occurs after eccentric contractions compared to other muscle actions can be explained by the greater mechanical tension that the muscle fibers exert and therefore experience in contractions at either the same relative load (percentage of maximum strength) or at the same level of muscle activation.
The greater mechanical tension experienced by muscle fibers during eccentric contractions results from force being produced by both active (actin-myosin crossbridges) and passive elements (mainly titin, but also collagen). During concentric contractions, force is produced solely by the active elements. The additional contributions from the passive elements therefore allow greater forces to be produced during eccentric contractions, even though muscle activation is similar.
This interpretation is supported by research showing that the superior effects of eccentric training are closely associated with the greater mechanical tension that is produced.
The increased satellite cell activity that occurs when muscles are damaged can be explained as being a simple response to exercise, or solely directed towards muscle fiber repair, rather than a process that increases the number of nuclei in each muscle fiber.
The former interpretation is supported by research showing that satellite cell activation occurs similarly after aerobic exercise and after strength training in both rodents and humans, and the latter interpretation is supported by research showing that the increase in satellite cell activation that occurs at the start of strength training programs (when muscle damage is most severe) does not convert into increased nuclei inside the muscle fibers.
Most of the discussions about whether muscle damage can contribute to hypertrophy center on analyses of the theoretical mechanisms, rather than on direct evidence.
Current research groups working on the problem have stated that it is very difficult to design appropriate studies that assess the impact of muscle damage as the primary factor, without also altering other training variables that might be expected to influence the amount of muscle growth.
However, some insightful studies have been performed.
Frequently, comparisons are made between programs of eccentric or concentric contractions, since eccentric contractions produce much more muscle damage. Even so, the difference in the amount of muscle growth that results from training with each contraction type is probably quite small, may involve muscle growth in different regions of the muscle, and even when the eccentric contractions produce demonstrably more muscle damage, this does not trigger more hypertrophy.
One unique study assessed the effects of two different work-matched eccentric training programs. In one group, there was a 3-week build-up phase before an 8-week training block. In the 3-week build-up phase, the level of force and the volume started extremely low (5 minutes per workout). This group experienced little sign of any muscle damage. In the other group, there was no build-up phase, and the subjects simply started with a suitable level of force and volume for increasing muscular strength and size. This group experienced signs of muscle damage. Ultimately, both groups improved strength and size to a similar extent, suggesting that there was little benefit of incurring the higher level of muscle damage.
Overall, these studies suggest that there is likely no obvious beneficial effect for hypertrophy of incurring muscle damage during strength training, and any case must be made based upon the mechanisms through which it is proposed to exert its effects.
The repair process after muscle damage follows a fairly similar course, regardless of the way in which the muscle tissue is injured.
Whether the damage was caused by the muscle being forcibly elongated under fatiguing conditions, as occurs during exercise or passive stretching, or whether the muscle was subjected to a blunt impact or a laceration, as frequently occurs in many popular contact sports, the process of muscle repair follows a similar pattern.
When muscles are damaged during exercise, or during passive stretching, this involves mechanical tension being applied to the fibers. This mechanical tension is detected by mechanoreceptors, and it triggers the signaling cascades that lead to muscular hypertrophy. This is why both active and passive mechanical loading of muscle fibers causes muscle growth. In contrast, when muscles are damaged by compression or laceration, there is no mechanical tension. However, in each case, the muscle fibers are damaged, and they must repair themselves.
We can therefore use compression models to study the hypertrophic effects of muscle damage. If muscle damage can trigger hypertrophy because the repair process leads to an increase in the size of the muscle fiber, then compression injury should lead to muscle growth. On the other hand, if it is mechanical tension that is solely responsible for hypertrophy, and muscle damage is a side effect, then compression injury should not produce any beneficial effects on muscle size.
Such research shows that muscle damage caused by compression does not lead to hypertrophy, but actually causes some muscle fibers to be lost, and overall muscle mass is reduced. Therefore, it is likely that it is the mechanical tension that leads to muscle growth after muscle-damaging exercise, and not the repair process subsequent to muscle damage.
Muscle damage has been proposed to contribute to hypertrophy, although the processes by which fibers increase in volume, and the processes by which they are repaired, are quite different. The idea that muscle damage can contribute to muscle growth is based on observations that damaging exercise causes large increases in muscle protein turnover and satellite cell activation, as well as unique structural adaptations, and on the possibly greater hypertrophy that occurs after eccentric training, compared to after concentric training.
However, the large increase in muscle protein synthesis that results from damaging exercise does not appear to contribute to hypertrophy, and the satellite cell activation that occurs does not seem to lead to the addition of new nuclei inside muscle fibers. The potentially greater hypertrophy that occurs after eccentric training can be explained simply by the greater mechanical loading that is involved, because of the contribution of the passive elements of the muscle fibers to force production. When muscle damage is avoided during long-term strength training, this seems to have no negative effects on the muscle gains that result, and when muscle damage is produced by means other than through exercise, this does not cause hypertrophy.
Overall, it seems likely that muscle damage is not a contributory factor to hypertrophy, and is merely a side effect that occurs when muscles are exposed to repeated muscular contractions.
