Aches are frequent during the practice of physical activities and sports. They occur after intense and / or unusual eccentric muscle exercise, within 12 to 48 hours. The exact term used in the literature is that of Delayed Onset Muscle Soreness (DOMS) or delayed onset muscle pain.
Pains occur 12 to 48 hours after physical activity including unusual or intense eccentric exercise and will persist for two to five days. They will most often occur during the resumption of a sporting activity, or during an increase or modification of the type of training. These pains will diminish with the repetition of the training and sometimes as soon as the second session.
The realization of an unusual eccentric effort is thus the main triggering factor even in a sporting subject.
We do not find any notion of sudden pain during the effort that would lead to a traumatic lesion of the elongation or breakdown type.
Pains can affect all muscle groups but are more frequently marked in large muscle groups such as quadriceps and surgical triceps, but sometimes also in the ischiojambiers. They are more rare in the upper limbs except in the case of intense and specific work like bodybuilding. The palpation of the muscle is diffuse, sometimes with a more precise pain at the myotendinous junction or in the pinnate part of the muscle, which can lead to confusion with a traumatic muscular lesion. There is also a deficit of muscular strength, and in some cases a decrease in joint amplitudes.
More rarely, an ome of low abundance can be seen.
The muscle is swollen and painful at rest as well as passive stretching, or during isometric or dynamic tests. In the latter, the pain is much more pronounced during an eccentric exercise (active stretching) rather than concentric.
Biologically, there is a delayed increase in plasma levels of muscle enzymes such as creatine kinase and an increase in collagen components in the urine.
Imaging (ultrasound or MRI) complementary examinations are unnecessary in everyday practice due to the lability of this condition. They are of interest only in the search for differential diagnoses such as, for example, a traumatic lesion.
In terms of research, MRI showed that the duration of intramuscular changes was significantly longer than the time of clinical manifestations with an increase in signal up to j3 or j6 and an increase in volume up to three weeks.
Physiopathology of DOMS:
All forms of exercise, when performed intensively, can cause muscle pain.
But only eccentric work, especially if it is unusual, results in delayed onset muscle pain and stiffness.
Characteristics of eccentric muscular work:
Eccentric muscular exercise has different biomechanical and metabolic characteristics than static or concentric work.During an eccentric type of work, the stressed muscle resists an external force greater than the force developed by the engaged motor units.
This is explained in particular by the fact that there is a force gain associated with the stretch resistance of the elastic components which are parallel (epimysium, perimysium and endomysium) and in series (tendons, aponeuroses). This includes the resistance of intra- and intersarcomeric structural proteins and that of actomyosin bridges, probably in combination with the cascade reattachment of the latter once broken. When all the motor units are recruited, the maximum developed force is thus greater than that obtained during a maximum work carried out in an isometric mode or in a concentric mode under equivalent conditions, that is to say at the same angular velocity . Under submaximal force conditions, the production of a given force level requires a lower activation level in the eccentric than in the concentric. Added to the so – called mechanical breakage of certain actomyosin bridges caused by the stretching force and therefore without the need for ATP, this results in a lower energy cost.
Working in an eccentric mode has therefore very interesting biomechanical and bioenergetic advantages, but it must be stressed that, practiced in an intense or unusual way, it can lead to structural and functional alterations of the muscles under stress. These may persist for several days to several weeks. Indeed, the resorption of the muscle microlésions generated by the exercise generally requires the development of an inflammatory process necessary for their resorption. This is typically accompanied by transient alterations in neuromuscular function and a diffuse and delayed pain sensation described by Miles and Clarkson as “Delayed Onset Muscle Soreness” (DOMS) and commonly referred to as ” “.
The DOMS begin 12 to 48 hours after an eccentric exercise and disappear gradually in three to five days. However, according to Howell et al. the DOMS would not be correlated either with the magnitude or with the timing of the muscle microlésions. For Newham et al., The initial lesions would nevertheless be the prodromes of more extensive muscle lesions associated with the inflammatory mechanism. While this seems to be a partial explanation of WHO, the exact underlying mechanisms are complex and remain at the center of much scientific work.
Microlésions of the muscular and connective tissues:
This theory was the first mentioned to explain the DOMS. Since then, numerous works have demonstrated the the presence of prolonged but reversible microsions of a small number of myocytes following intense eccentric work. The active stretches of eccentric work result in minimal and localized lesions of the cytoskeleton, resulting in disorganization of some sarcomera, with possible lesions of the sarcolemma, transverse tubules and sarcoplasmic reticulum. Although the hypothesis of associated lesions of neuromuscular spindles has recently been called into question by the work of Gregory et al.
The eccentric work provokes a mechanical stress which has been suggested by Asmussen since 1956 and which would be the major cause of the observed signs. For Lieber and Friden, the degree of stretching would be the main mechanical factor responsible for the appearance of microlésions. On the other hand, the data obtained in animals and in humans suggest preferential damage of type II muscle fibers. These fibers are characterized by narrower Z ribbons and a less developed extracellular matrix than those of type I. It would also appear that their increased fatigability may result in a prolonged contraction of certain sarcomers, thus creating an intersarcomber and inter-fiber heterogeneity in the resistance to stretching. More recently, Brockett et al. have proposed that the degree of stretching of type I and II fibers in a given eccentric force be examined in relation to that of the muscle to which they belong. According to this hypothesis, a large difference between their respective optimal lengths should lead to an increased degree of stretching of some muscle fibers in the eccentric, thus promoting the appearance of microlésions.
Although they are observed following eccentric exercise, microlésions can not be directly responsible for DOMS since they occur during exertion while pain occurs only within 12 to 48 hours.
Following the so-called “initial” lesion phase, Armstrong et al. have differentiated three phases, called “autogenic”, “phagocytic” and “regeneration”, specific to the inflammatory process:
* the “autogenic” stage takes place during the first three hours after exercise and corresponds to the onset of self –degradation of the injured membrane structures;
In the “phagocytic” stage, the lesion is invaded by numerous monocytes which are transformed into phagocytes. There is an increase in the internal temperature of the muscle which reflects catabolism and anabolism reactions.
The release by injured tissues of chemical mediators causes a plasma extravasation which increases the internal pressure of the muscle. The sensation of diffuse pain can be explained by these chemical, thermal and mechanical changes;
* finally, the “regeneration” stage, which begins four to six days after the initial lesion and which could last from one to several weeks depending on the severity of the damage.
Muscle pain is partly attributed to the sensitization of nociceptive afferents belonging to the type III and IV (small diameter) afferent group. These are derived from free nerve endings, located in the whole of the muscular and connective tissues, in particular at the myotendinous junction.
These afferences are referred to as polymodal, as they may vary depending on several physicochemical parameters related to muscular damage and / or metabolic fatigue.
When muscle inflammation occurs, increased pressure, internal muscle temperature, and synthesis of bradykinin and prostaglandins increase the spontaneous discharge of receptors belonging to the Type III and IV afferent group.Clarkson and Newham, however, described a peak in tired limb circumference increase on the fifth day post – exercise, nearly three days after the DOMS peak. This time lag suggests that the muscular edema is only a factor of the DOMS markup and not a cause of their initial trigger.
Once stimulated, the free nerve endings located in the injured tissues release neuropeptides (in particular substance P), which leads to an amplification of the inflammatory response and to a “self-maintenance” of the activation of these same nerve endings. According to Grigg, some of these nociceptive terminations which were until then silent would thus be sensitized.
This results in an increase in the overall nociceptive response thus contributing to the phenomenon of hyperalgesia. In the case of nociceptors, those of type III would induce rather acute and localized pain, whereas those of type IV would lead to a dull and diffuse pain. As a result, it is legitimate to assume that Type IV nerve fibers are the main cause of pain.
Recent work also highlights the involvement of large diameter mechanoreceptors (from neuromuscular spindles) which may partly explain the lack of correlation of DOMS with the magnitude of muscle microlésions.
Activating the “pool” of motoneurons:
When fatigue results from isometric work done voluntarily or by electrostimulation, the activation of the resulting small diameter afferents would seem to induce a partial inhibition of the “pool” of motoneurons α innervating the muscle under stress. Some authors have hypothesized that type III and IV afferents are the cause of presynaptic inhibition of fusoria afferences, as well as an inhibition of spinal interneurons involved in the oligosynaptic pathways of these same afferents. Although recently questioned by Löscher et al., This reflex regulation the delayed activation changes due to the presence of muscle microlésions.
However, the literature on the influence of afferents III and IV on central and reflex activation remains contradictory in cases of inflammation and / or pain.
The hypothesis of protection of muscle fatigued by an inhibition of the central and / or reflex activation of the “pool” of motor neurons rests on numerous works carried out in man and in the animal. When the stimulus comes down to muscle pain, it seems to be accompanied by a decrease in the maximum voluntary activation and changes in intermuscular coordination during dynamic exercises. Other studies report reduced activity of the synergistic muscles and increased coactivation of the antagonist muscles. Other authors refer to the inverse hypothesis of a “vicious circle” in which type III and IV afferents would activate the γ – motor neurons thus increasing the fusorial sensitivity, which would increase the activity of motor neurons α and thus to accelerate the development of fatigue. Several studies confirm this hypothesis in animals by reporting an increase in the frequency of fusimotor discharge following intra – arterial injection of pro – inflammatory substances. However, the literature remains controversial as to the validity of this hypothesis in man.
To these mechanisms must be added the modulation at the supraspinal level of these afferences. For example, the influence of type III and IV afferent sensitization on the excitability level of Renshaw cells (recurrent motoneuron inhibition) varies depending on the state of the muscle (active or resting). Also illustrating this complexity, Martin et al.have recently demonstrated in humans that the sensitization of small diameter afferents of agonist or antagonist muscles tended to inhibit motor neurons of the extensor muscles and to facilitate those of the flexors. In case of muscle pain, Qerama et al. for example, a reduction in the frequency of discharges of the motor units. Data from the use of TMS also reveal a lower excitability of the motor cortex. In this sense, it should be emphasized that peripheral and central adjustments seem to depend on the stage of muscular regeneration, the presence or absence of pain, and the chosen test task. Recent studies aim to study the possibility of contralateral effects of unilateral fatigue.
Consequently, all of this work highlights the importance but also the complexity of eccentric work phase on the production of force and modulations of central and peripheral origins of the activation of the muscles involved.
Other etiologies have often been mentioned:
Lactic acidosis can partly explain the pain that occurs at the end of an intense effort but in no case can it contribute to those that appear delayed several hours later. Indeed, the elimination of the lactic acid requires only twenty minutes in active recovery and around two hours in passive recovery.
Moreover, the production of lactic acid for the same level of effort is clearly higher in isometric and concentric than in eccentric, whereas the DOMS appear after eccentric work. In this sense, the decrease in strength shown after intense isometric or concentric exercise normally normalizes within two hours of sporting activity. On the other hand, when it is an eccentric exercise, structural and functional alterations are maximal on the second day after exercise and may last up to one to two weeks.
Following the observation of increased levels of basic muscle activation after eccentric work, muscle spasm was suspected to be the cause of vascular ischemia resulting in the accumulation of potentially active substances, activate nociceptive afferences. Activation of these afferents would reflexively amplify the state of spasm and thus prolong ischemia according to the “vicious circle” theory. Electromyographic data do not tend to confirm this hypothesis at this time.
Functional Consequences of Muscle Micro-Damage:
This type of lesion is specific to many forms of locomotion (marathon, 10 km run, rebound exercises) because of the repetition of the impacts on the ground followed by the eccentric work phases that they involve. A recent review of the literature highlights the biphasic character of functional recovery, with large immediate reductions in neuromuscular performance, followed by partial or total recovery within two to three hours of exercise, before further declines persist several days.
Passive stiffness at stretching is characterized by an immediate decrease which contrasts with its delayed increase.
The delayed phase of recovery is also characterized by a reduction of the joint amplitude with alteration of the direction of the force and of the position. Our last work (in progress) confirms the deterioration of the direction of the position as well as an alteration of the direction of movement on the second day of the exercise.
When it is desired to quantify the neuromuscular fatigue caused by different modes of contraction, maximal and submaximal isometric force tests are generally performed. It is thus known that, for equal work, the drops of force induced by eccentric work are higher than those generated by concentric or isometric work.
The maximum isometric performance analysis underlines the importance of the maximum falls in force and activation, on average 40%, and confirms the biphasic evolution of their recovery. Partial inhibition of the activation is found during the phase of production of maximum force and an increase in the level of activation during a work of maintenance of submaximal isometric force, which is in favor of a compensation of muscle fatigue by the central nervous system.
In tests specific to locomotion, there is a decrease in maximum performance associated with a decrease in tolerance to ground impacts. This is certainly explained by the weakening of the contractile system but also by changes in activation, both central and reflex. Several studies have demonstrated an adjustment of the central control even before the impact. In this sense, the recent data recorded during exhausting bounce exercises and the various stages of the recovery phase emphasize the progressive and specific adaptation of the muscular activation strategies in each of the preparation, braking and thrust phases on the ground. An increased preactivation was observed during submaximal rebounds (compensation of contractile fatigue) but decreased during maximal rebounds (attenuation of the stiffness of the musculotendinous system and hence peak impact on the ground). When the level of performance imposed is submaximal, the braking phase which follows the impact is inhibited while the preactivation is increased. This could reflect an attempt to protect the tired muscle during its active stretching. This “cushioning” results in a loss of elastic energy and the need for increased work during the pushing phase. The increased activation in the last phase reflects an attempt to compensate by the central control for the weakening of the contractile device.
All these observations underline the existence of distinct adjustments of the activation of motor neurons to the constraints of the imposed task and throughout the slow structural regeneration. The possibility of adjustments in the medium – term reflex pathways of activation of motoneurons reinforces the hypothesis of intervention of type III and IV afferents.
The observation of the decreases in performance (races, jumps) typically associated with crushing (less tolerance) on impact led to the search for the potential influence of this type of fatigue on the spinal reflex sensitivity and the contribution of this last to the stiffness of the musculotendinous system. The sensitivity of the monosynaptic component of the myotomic reflex to this type of fatigue was evaluated for some limb extensor muscles in the post –impact braking phase (active stretching), but also for passive dorsiflexions induced by a specific ergometer. The latency and amplitude of electromyographic (EMG) and reflex mechanical responses were recorded for a period of four to seven days.
The influence of eccentric work on the myotomic reflex may be affected by the presence of intrafusal fiber damage.This test was supplemented by the Hoffman (H) reflex test. To limit the influence of a slowing of the muscular conduction of the action potentials with the fatigue, the reflex responses H were normalized with respect to the M wave (H / M). These studies reveal a strong immediate reduction followed by a slow recovery over several days of the reflex H / M response and the reflex MEG and mechanical responses to passive stretching. With regard to the immediate effects of an exercise, it is necessary to add to the immediate (direct and indirect) influences of the damages previously described, those of metabolic order. It is rare indeed that muscular work includes only eccentric actions.Most activities of everyday life or sports include a succession of eccentric and concentric actions. The concentric mode being less economical than the eccentric, the increase in the intensity of the effort often results in muscular acidosis.Recent work suggests that the development of intense eccentric efforts by a muscle in a state of acidosis may aggravate its lack of impact tolerance and result in longer structural and functional recovery. In addition to sensitizing type III and IV afferents, acidosis may also limit the contribution of neuromuscular spindles to spinal reflex control.
With regard to the delayed phase of recovery, the slow recovery of EMG and reflex mechanical responses seems to be related to the evolution of various muscle microlasure resorption indexes. The recovery of the passive stretch reflex is, for example, correlated with the plasma creatine kinase decrease and evolves in parallel with the reduction of muscle swelling [ED]. These data confirm the existence of an inhibition of the activation of the injured muscles, probably via the activation of free type III and IV nerve endings sensitized by the thermal, chemical and mechanical variations occurring within the muscles under stress.
In summary, intense and / or unusual eccentric work phases can lead to decreased proprioceptive qualities, decreased joint amplitudes, decreased muscle strength and maximum activation in static maximum condition as dynamic.
These deficits usually persist two to ten days longer than mere painful manifestations (DOMS). This represents a significant risk for the joints since the weakening of the “active ligaments” constituted by the muscles is systematically and very clearly underestimated when the pain disappears (especially on the third day) and can therefore contribute to the occurrence of injuries.
DOMS should be distinguished from pain that occurs during an acute traumatic accident during exercise.
Muscular intolerance to exercise can have various etiologies.
Faced with a picture of weakness and / or myalgia, it is necessary to eliminate the etiologies “non-mechanical”. The first step consists in asserting the muscular origin and then evoking pathological myalgias such as myopathies of origin viral, inflammatory or infectious, or a deficiency of glycolytic or mitochondrial enzymes. It will also be necessary to eliminate a syndrome of lodge, a rhabdomyolysis whose mechanisms of occurrence can be close to the pains of origin vascular or neurological.
Treatment of DOMS:
Many treatments have been proposed without being validated:
* cryotherapy, stretching, anti-inflammatories, ultrasound (and other physiotherapy techniques), homeopathy, massages, compression and hyperbaric oxygen therapy;
* TENS (analgesic transcutaneous electric stimulations) or NSAIDs have shown no efficacy in this area;
* other treatments are possibly effective such as early massages performed less than two hours after exercise or intake of L. Carnitine. Estrogen therapy in oral contraception appears to have a protective effect, but these data need to be confirmed.
Prevention of DOMS:
Since microlensions or muscle lesions in the DOMS are caused by unusual eccentric exercise or performed at high intensity, repetition of the exercise would be the best known prevention of DOMS through a real attenuation of muscle damage.
Adjustment following a first exercise results in very marked attenuations of the symptomatology during the repetition of the exercise. There is thus less decrease in strength, pain, swelling and stiffness after a second exercise of the same type. It is the effect of repetition or repeated. This process of adaptation is also called a protective effect. Assumptions of structural and nervous origin have been put forward.
At the structural level, Rathbone et al. have recently shown that satellite cell proliferation was responsible for half the recovery of maximum strength in mice. The activation of the satellite cells will in fact cause the synthesis of proteins of the cytoskeleton which results in the addition of sarcomers in series. At the functional level, this gives rise to a better force of resistance to a given stretch, that is to say a shift in the force -to- length relationship. This seems to reflect a mechanism of muscle protection through the addition of sarcomeres within the injured muscle myofibrils. Some authors have also suggested that the connective tissue muscle content may increase.
The hypothesis of nerve adaptation was advanced by studies that repeated an eccentric exercise within two or three days after a first eccentric exercise. The second exercise had a protective effect, induced very rapidly, whereas the recovery was incomplete. The authors then suggested that a nervous adaptation could explain such a rapid adaptation.
Independently of the mechanisms involved, these adaptations are extremely interesting since the symptomatology is not aggravated when a second eccentric exercise is repeated after a first exercise involving DOMS.
In less trained subjects, however, it is advisable to observe the recovery week following the first eccentric exercise in order to obtain a total recovery of the activation and the force. This no longer seems necessary for the following demands and, less and less, for trained subjects.
If the DOMS are unpleasant, they are therefore not of any gravity since they merely reflect the existence of a parallel inflammation of a structural remodeling which will contribute to increase the muscular strength. In addition, the sensation of DOMS generally leads to an overprotection of the injured muscle which then favors the regeneration of the latter.
They will diminish during exercise (many unusual mechanical and thermal stimuli at rest becoming normal to exercise) and disappear before the return of structural and functional integrity. In view of the major role of “active ligaments” played by skeletal muscles, the attenuation of DOMS, while various neuromuscular disturbances continue, favors the occurrence of wounds. The high frequency of rupture of the antero-external cruciate ligament on the third day of skiing is probably one of the illustrations.
Intense and / or unusual eccentric muscular work may lead to muscle microlésions, followed by a slow recovery of the integrity of the injured tissues. These muscle microsions are generally accompanied by a characteristic sensation of diffuse pain and discomfort, called “DOMS” (Delayed Onset Muscle Soreness). These microlésions occur within a few hours, but the regeneration involves an inflammatory phase of about four days and it is only after one to two weeks that the muscle has regained not only its structural integrity but also its functional abilities. If the DOMS lead to an overprotection of the injured muscle, they have the major disadvantage of disappearing before the return to structural and functional integrity. It is therefore necessary to warn the athlete during this period “postcurves” in the course of which one frequently tends to overestimate its abilities.