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Postexercise Muscle Soreness

  • Author: Divakara Kedlaya, MBBS; Chief Editor: Consuelo T Lorenzo, MD  more...
 
Updated: Jan 25, 2016
 

Overview

Postexercise muscle soreness, also known as delayed-onset muscle soreness (DOMS), is defined as the sensation of discomfort or pain in the skeletal muscles following physical activity, usually eccentric, to which an individual is not accustomed.

The incidence of DOMS is difficult to calculate, because most people who experience it do not seek medical attention, instead accepting DOMS as a temporary discomfort. Every healthy adult most likely has developed DOMS on countless occasions, with the condition occurring regardless of the person's general fitness level. However, although it is experienced widely, there are still controversies regarding the origin, etiology, and treatment of DOMS.

Eccentric muscle contractions

Exercise involving eccentric muscle contractions results in greater disruption or injury to the muscle tissues than does concentric exercise. Thus, any form of exercise with eccentric muscle contractions causes more DOMS than does exercise with concentric muscle contractions. Ample evidence from histologic studies, electron microscopic examination, and serum enzymes of muscular origin supports this notion.

To produce a given muscle force, fewer motor units are activated in an eccentric contraction than in a concentric contraction. In eccentric contractions, the force is distributed over a smaller cross-sectional area of muscle. The increased tension per unit of area could cause mechanical disruption of structural elements in the muscle fibers themselves or in the connective tissue that is in series with the contractile elements; however, it has not been proven that injury to muscle cells or to connective tissue is the causative factor in DOMS.

Muscle pain mechanism

The sensation of pain in skeletal muscle is transmitted by myelinated group III (A-delta fiber) and unmyelinated group IV (C-fiber) afferent fibers. Group III and IV sensory neurons terminate in free nerve endings. The free nerve endings are distributed primarily in the muscle connective tissue between fibers (especially in the regions of arterioles and capillaries) and at the musculotendinous junctions. The larger myelinated group III fibers are believed to transmit sharp, localized pain. The group IV fibers carry dull, diffuse pain.

The sensation of DOMS is carried primarily by group IV afferent fibers. The free nerve endings of group IV afferent fibers in muscles are polymodal and respond to a variety of stimuli, including chemical, mechanical, and thermal. Chemical substances that elicit action potentials in muscle group IV fibers in order of effectiveness are bradykinin, 5-hydroxytryptamine (serotonin), histamine, and potassium.

Morbidity

Only temporary morbidity (pain, soreness, reduced muscle performance) is associated with DOMS. Diminished performance results from reduced voluntary effort due to the sensation of soreness and from the muscle's lowered inherent capacity to produce force.[1]

No evidence exists to support the idea that DOMS is associated with long-term damage or reduced muscle function. Animal studies indicate that injured muscles regenerate during the period following exercise and that the process essentially is completed within 2 weeks.

Sex- and age-related demographics

Stupka and colleagues showed that muscle damage following unaccustomed eccentric exercise is similar in males and females; however, the inflammatory response is attenuated in women.[2]

MacIntyre and coauthors found that the patterns of DOMS and torque differed between males and females after eccentric exercise.[3] In a study by Dannecker and colleagues, no sex differences were detected, except that higher affective ratios were reported by men than by women.[4] DOMS generally is not reported in children. Adults of all ages can experience DOMS.

Diagnostic findings

With regard to lab studies, the serum creatinine kinase level usually is elevated in DOMS, but it is nonspecific. The diagnostic efficacy of imaging studies in DOMS has also been investigated. In a study by Dierking and colleagues, diagnostic ultrasonography, when used in the diagnosis of DOMS, was not sensitive enough to detect changes in a cross-sectional muscle area.[5]

Magnetic resonance imaging (MRI) can detect muscle edema in DOMS but is not indicated clinically for the diagnosis. In a prospective evaluation of DOMS, abnormalities found in MRI persisted up to 3 weeks longer than did symptoms.

Patient education

The patient needs to be educated concerning a specific progressive exercise training program before engaging in a heavy, unaccustomed exercise, particularly one that involves eccentric muscle contractions. For patient education information, see Muscle Strain.

Consultations

Consultation with the patient's athletic trainer and coach may be indicated.[6, 7]

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Etiology

DOMS results from overuse of the muscle. Any activity in which the muscle produces higher forces than usual or in which it produces forces over a longer time period than usual can cause DOMS. According to Tiidus and Ianuzzo, the degree of muscle soreness is related to the intensity of the muscle contractions and to the duration of the exercise.[8] The intensity seems to be more important in the determination than is the duration.

The following 5 hypotheses are used to explain the etiology of DOMS:

  • Structural damage from high tension
  • Metabolic waste product accumulation
  • Increased temperature
  • Spastic contracture
  • Myofibrillar remodeling

Structural damage from high tension

This hypothesis originally was proposed by Hough and is the most scientifically accepted theory. The delayed pain is related directly to the development of peak forces and to the rate of force development in rhythmic contractions. DOMS is not related to the state of fatigue of the muscle. (See Table 1, below.)

The rhythmic and tetanic contractions that cause the greatest acute fatigue and discomfort in the muscles during exercise result in the least delayed pain following the exertion. The structural damage is evident in muscles that are not trained for the particular exercise.

Metabolic waste product accumulation

One of the most popular concepts in the lay exercise community is that delayed soreness is a result of lactic acid accumulation in the muscles. The degeneration and regeneration of muscle fibers observed after 2-3 hours of ischemia are similar temporally and quantitatively to the forces resulting from exercise-induced injury. (See Table 1, below.)

An apparent relationship exists between exercise intensity and the extent of soreness. Much evidence against the metabolic hypothesis also may be noted. The most convincing evidence is that the muscle contractions that cause the greatest degree of soreness require relatively low energy expenditure. Exercise involving eccentric contractions requires lower oxygen consumption and produces less lactate than does exercise with concentric contractions at the same power output. Energy use per unit area of active muscle appears to be less in eccentric exercise than in equivalent concentric exercise.

Schwane and colleagues tested the metabolic hypothesis. Their results indicated that downhill running requires significantly lower oxygen uptake (VO2) and produces less lactic acid than does level running but that it nonetheless results in greater DOMS.[9]

Increased temperature

Type III and IV nerve endings are sensitive to temperatures of 38-48°C. Elevated temperature could conceivably damage the structural element in the muscle, resulting in necrosis of muscle fibers and breakdown of connective tissues. Eccentric muscle exercise may generate higher local temperatures than do concentric contractions. Rhabdomyolysis (extreme of DOMS) is more prevalent in untrained subjects during exercise in the heat.

Spastic contracture

Studies by Travell and co-investigators in 1942[10] and a later series of experiments by Cobb and colleagues[11] demonstrated elevated electromyographic activity in sore muscles.[12] Altered nerve control and vasoconstriction lead to decreased blood flow and ischemia, which, in turn, initiate a pain-spasm-pain cycle.[13] The magnitude of pain depends on the number of motor units involved. Other investigators have been unable to detect increased electrical activity in sore muscles.

Myofibrillar remodeling

The literature suggests that myofibrillar and cytoskeletal alterations are the hallmarks of DOMS and that they reflect adaptive remodeling of the myofibrils. There are 4 main types of changes:

  • Amorphous, widened Z-disks
  • Amorphous sarcomeres
  • Double Z-disks
  • Supernumerary sarcomeres

Table 1. Comparative Features of Exercise-Related Pain (Open Table in a new window)

  Pain During or Immediately Following Exercise Delayed Onset Muscle Soreness (DOMS) Muscle Cramps Associated with Exercise
Etiology Probable buildup of metabolic by-products (include lactic acid, pyruvic acid) Unaccustomed eccentric exercise Hyperexcitability of lower motor neuron, possibly related to loss of fluid and electrolytes and low magnesium level
Onset During exercise 12-48 hours postexercise During or after exercise
Duration/recovery Diminishes upon termination of exercise and return of normal blood flow Recovery within 7-10 days Lasts usually between a few seconds and several minutes
Type of nerve ending Type IV free nerve ending Primarily type IV free nerve ending;



type III is also involved



Most likely type III free nerve ending
Type of muscle contraction associated Sustained or rhythmic concentric and isometric contractions Unaccustomed eccentric muscle



exercise



Severe, involuntary, electrically active contraction
Treatment Terminate exercise Exercise the “sore muscle”; no other proven effective treatment Gentle stretch of the affected muscle;



contraction of antagonistic muscle



Prevention No proven effective preventive measure No proven effective preventive measure Stretching the affected muscles may be effective, but evidence is insufficient;



quinine is effective, but side effects are too serious for routine use[14]



 

Comparison of postoperative myalgia to postexercise muscle soreness

Postoperative myalgia due to succinylcholine can occur in about 50% of the cases. It usually starts the first postoperative day and lasts 2-3 days, but occasionally it persists for as long as a week. Symptoms are commonly described as the pain one might suffer after an unaccustomed degree of physical exercise as in delayed-onset muscle soreness (DOMS), and it is usually located in the neck, shoulder, and upper abdominal muscles.[15, 16]

The mechanism of succinylcholine-induced postoperative myalgia is still not understood fully. Several mechanisms have been proposed to explain this phenomenon. Postoperative myalgia is often described as being similar to myalgia after unaccustomed exercise. Fasciculations involve vigorous contraction by muscle bundles with no possibility of shortening and without synchronous activity in adjacent bundles. This might produce muscle fiber rupture or damage, thus causing pain. Postoperative myalgia has been attributed to muscle fiber damage produced by the shearing forces associated with the fasciculations at the onset of phase one block.

Postoperative myalgia due to succinylcholine may be prevented with using nondepolarizing muscle relaxants, lidocaine, nonsteroidal anti-inflammatory drugs, gabapentin, or pregabalin. However, the most effective way to prevent succinylcholine-induced myalgia is to avoid the use of succinylcholine itself.[15, 17, 18]

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Histologic Findings

Immediately after exercise, free erythrocytes and mitochondria may be observed in the extracellular spaces.

Increase in the numbers of circulating neutrophils and interleukin-1 occurs within 24 hours after exercise. A prolonged increase in ultrastructural damage and muscle protein degradation occurs, as well as a depletion of muscle glycogen stores.

Friden and colleagues observed Z-line streaming within eccentrically exercised muscle fibers that occasionally led to total disruption of the Z-band area; this resulted in disorganization of surrounding myofilaments.[19]

From 1-3 days postexercise, the period of time when DOMS is most intense, phagocytes are present in the muscle fibers, and injury to the muscle usually is more apparent.

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History and Physical Examination

History A history of heavy, unaccustomed exercise, particularly involving eccentric muscle contractions (eg, downhill exercise), is reported in DOMS. The patient complains of pain, soreness, swelling, and a stiff or tender muscle spasm.

DOMS begins 8-24 hours after exercise and peaks 24-72 hours postexercise; it then subsides over the next 5-7 days. The muscles are sensitive, especially upon palpation or movement, and a decreased range of motion and reduced strength are noted (especially 24-48 hours postexercise), with the patient having a sense of decreased mobility or flexibility.

Acute onset muscle soreness begins during exercise and continues for approximately 4-6 hours after exercise.

Physical examination

Muscle tenderness is present. Decreased muscle strength and flexibility also are noted. The tenderness often is described as localized in the distal portion of the muscle, in the region of the musculotendinous junction.

According to one study, tenderness in this region could be due to the fact that muscle pain receptors are most concentrated in the region of the tendon and connective tissue in the muscle. The fibers' angles to the long axis of the muscle are greatest in the region of the musculotendinous junction, increasing the susceptibility of the fibers to mechanical trauma.

In severe DOMS, the pain is generalized throughout most of the muscle belly. Swelling of the muscle belly can occur.

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Physical Therapy and Exercises

Although it provides only temporary relief, active exercise of the sore muscle probably is the best way to reduce DOMS. Muscular soreness diminishes acutely with exercise. With the cessation of exercise, however, the soreness returns, and this cycle continues until the muscle becomes conditioned sufficiently through training. Why exercise decreases DOMS is not clear, although several possibilities exist, including the following:

  • Breakup of adhesions from the injured, sore muscles takes place during exercise
  • Increased blood flow or temperature in the muscle helps to decrease the accumulation of noxious waste products
  • Endorphin release by neurons in the central nervous system increases during exercise.
  • Increased afferent input is noted from large, low-threshold sensory units in the muscles (muscle group-Ia, Ib, and II fibers [gate control theory])
  • Subjects direct attention to the activity and away from the pain

In a randomized controlled trial comparing the effect of active exercise versus massage on DOMS, active exercise using elastic resistance provides similar acute relief of muscle soreness as compared with massage. For both types of treatment, the greatest effect on perceived soreness occurred immediately after treatment.[20]

The training effect appears to be highly specific, not only for the particular muscles involved in the exercise, but also for the type of contractions performed. For example, Schwane and Armstrong found that in rats, the muscle damage that occurs during downhill running is prevented by downhill or level training but not by uphill training.[9]

A study by Cha and Kim reported that the hold-relax technique with agonist contraction may help to relieve DOMS. Patients were treated with this therapy at the hamstring muscle, with hamstring muscle activity and fatigue being found to significantly increase and decrease, respectively.[21]

A Cochrane review of evidence from randomized studies suggests that muscle stretching, whether conducted before, after, or before and after exercise, does not produce clinically important reductions in delayed-onset muscle soreness in healthy adults.[22] . A systematic review and meta-analysis of physiotherapeutic interventions for treating signs and symptoms of exercise-induced muscle damage showed that massage was slightly effective to reduce DOMS, but there is no evidence to support the use of cryotherapy, stretching, and low-intensity exercise for DOMS.[23]

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Other Treatment Modalities

A study by Barlas and colleagues indicated that acupuncture generally is not effective in the treatment of DOMS.[24] A randomized, controlled trial by Fleckenstein et al also found no benefit from acupuncture on DOMS. The study, which involved 60 patients, reported no significant improvement in DOMS within 72 hours from either needle or laser acupuncture in comparison with sham needle acupuncture, sham laser acupuncture, and no treatment at all.[25] However, an unblinded study by Lin and Yang suggested that acupuncture is effective against DOMS.[26]

Mekjavic and co-investigators concluded that hyperbaric oxygen therapy does not affect recovery from DOMS.[27]

Zhang and colleagues noted that a double layer of Farabloc, an electromagnetic shield, wrapped around the thigh has been shown to reduce DOMS.[28]

In a study by Craig and coauthors, combined low-intensity laser therapy was not shown to be effective against DOMS.[29] However, a study by Douris and colleagues that used 8J/cm2 of phototherapy did show a beneficial effect.[30]

In one small (6 subjects in each group), randomized, double-blind, placebo-controlled study by Hasson and coauthors, individuals treated with pulsed ultrasonographic therapy (PUS) showed significantly reduced soreness.[31] However, in a larger (12 patients in each group) randomized, double-blind, placebo-controlled study by Craig and co-investigators, no significant benefit from PUS was demonstrated.[32] In a study by Ciccone and coauthors, there was some suggestion that ultrasonography may enhance DOMS and that phonophoresis with salicylate may have therapeutic benefits.[33]

Tourville and colleagues showed that sensory-level, high-volt, pulsed electrical current was not effective in reducing the measured variables associated with DOMS.[34]

Transcutaneous electrical nerve stimulation (TENS), in an uncontrolled study by Denegar and Perrin, showed some benefit in relieving the soreness associated with DOMS.[35] However, in a randomized, placebo-controlled study by Craig and colleagues, the use of TENS did not show any significant benefit.[36, 37]

In a small study by Hasson and coauthors, dexamethasone iontophoresis immediately after exercise was shown to decrease muscle soreness perception in DOMS.[38]

Studies have shown that whole body vibration (WBV) is effective in reducing the severity of DOMS and in preventing DOMS after eccentric exercise.[39, 40]

Ice-water immersion and ice massage are frequently used, particularly among high-level athletes, to minimize the symptoms of DOMS. A randomized, controlled study by Sellwood and colleagues challenged the use of ice-water immersion as a recovery strategy for athletes.[41] In this investigation, ice-water immersion did not effectively minimize or prevent symptoms of muscle damage after eccentric exercise in young, relatively untrained individuals. A Cochrane review of cold immersion therapy for DOMS concluded that there was some evidence for cold-water immersion therapy to reduce DOMS after exercise compared with passive interventions involving rest or no intervention.[42]

Given that trained athletes are relatively well protected against DOMS, ice-water immersion is likely to offer them even less benefit for the minimal soreness they may experience after eccentric exercise.

Another study by Isabell and coauthors, showed that the use of ice massage or ice massage with exercise did not significantly reduce the symptoms of DOMS.[43]

Continuous low-level heat-wrap therapy has been studied in a small randomized study for the prevention and early-phase treatment of symptoms and deficits in self-reported physical function related to low back DOMS.[44] It has shown to be effective in the prevention and early-phase treatment of low back DOMS.

Another study compared the effect of 3 different heat modalities—ThermaCare heat wraps, hydrocollator heat wraps, and a chemical moist-heat wrap in the treatment of DOMS—and showed that chemical moist heat helps the most in reducing the soreness in DOMS.[45]

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Pharmacologic Therapy

In many controlled studies, general analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) have not been consistently effective against DOMS.[46]

In a randomized, placebo-controlled study, Cannavino and colleagues showed that transdermal 10% ketoprofen cream was effective in alleviating self-reported DOMS in isolated quadriceps muscles of patients following repetitive muscle contraction, particularly after 48 hours.[47] This relief was apparently secondary to the effects of the medication, because no other medications or pain relief measures were used in the study. In an another study, the topical menthol-based analgesic decreased perceived discomfort to a greater extent and permitted greater tetanic forces to be produced compared with ice application in subjects with DOMS.[48]

In a randomized, placebo-controlled study, Connolly and co-investigators showed that tart cherry juice can decrease some of the symptoms of exercise-induced muscle damage.[49] Most notably, strength loss averaged over the 4 days after eccentric exercise was 22% with the placebo but only 4% with the cherry juice.

Oral ascorbic acid (vitamin C) and other antioxidants also have been investigated as possible medications for DOMS, with mixed results. A study by Connolly and coauthors suggested that a vitamin-C supplementation protocol of 1000mg taken 3 times a day for 8 days is ineffective in protecting against selected markers for DOMS.[50]

The homeopathic medicine Arnica 30x was studied in a randomized, double-blind, placebo-controlled study and was found to be ineffective in treating DOMS.[51]

Bajaj and colleagues showed that the prophylactic intake of tolperisone hydrochloride provides no relief of postexercise muscle soreness but that it does result in a reduction in isometric force.[52]

In a randomized, placebo-controlled study, Pumpa and collegues showed that Panax notoginseng did not have an effect on performance, muscular pain, or assessed blood markers in well-trained males after an intense bout of eccentric exercise that induced DOMS.[53]

Branched-chain amino acid (BCAA) supplementation was studied in a cross-over double-blind design and shown to be effective in reducing squat-exercise-induced DOMS.[54] . Another study has shown that the additional supplement of taurine with BCAA would be a useful way to attenuate DOMS and muscle damages induced by high-intensity exercise.[55]

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Deterrence

Armstrong states in his review that there are no preventive measures for DOMS except previous specific training of the involved muscle.[56] A randomized controlled study by Olsen et al has demonstrated that proper warm-up before resistance exercise may prevent muscle soreness at the central but not distal muscle regions, but it does not prevent loss of muscle force.[57]

Johansson and colleagues discovered that preexercise static stretching has no preventive effect on the muscular soreness, tenderness, and force loss that follows heavy, eccentric exercise.[58]

NSAIDs are not effective in preventing DOMS. However, Thompson and coauthors noted that oral contraceptive use attenuates soreness following exhaustive stepping activity in women, although no association can be drawn between estrogen ingestion and exercise-induced muscle damage.[59]

Boyle and co-investigators showed that yoga training and a single session of yoga appear to attenuate peak muscle soreness in women following a bout of eccentric exercise.[60] These findings have significant implications for coaches, athletes, and the exercising public, who may want to implement yoga training as a preseason regimen or as a supplemental activity to lessen the symptoms associated with muscle soreness.

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Contributor Information and Disclosures
Author

Divakara Kedlaya, MBBS Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine; Medical Director, Physical Medicine and Rehabilitation and Pain Management, St Mary Corwin Medical Center

Divakara Kedlaya, MBBS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Colorado Medical Society, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD Medical Director, Senior Products, Central North Region, Humana, Inc

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Acknowledgements

Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Timothy Kuang, MD Pain Management Fellow, Department of Physical Medicine and Rehabilitation, Loma Linda University Medical Center

Timothy Kuang, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Association

Disclosure: Nothing to disclose.

Curtis W Slipman, MD Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center

Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Table 1. Comparative Features of Exercise-Related Pain
  Pain During or Immediately Following Exercise Delayed Onset Muscle Soreness (DOMS) Muscle Cramps Associated with Exercise
Etiology Probable buildup of metabolic by-products (include lactic acid, pyruvic acid) Unaccustomed eccentric exercise Hyperexcitability of lower motor neuron, possibly related to loss of fluid and electrolytes and low magnesium level
Onset During exercise 12-48 hours postexercise During or after exercise
Duration/recovery Diminishes upon termination of exercise and return of normal blood flow Recovery within 7-10 days Lasts usually between a few seconds and several minutes
Type of nerve ending Type IV free nerve ending Primarily type IV free nerve ending;



type III is also involved



Most likely type III free nerve ending
Type of muscle contraction associated Sustained or rhythmic concentric and isometric contractions Unaccustomed eccentric muscle



exercise



Severe, involuntary, electrically active contraction
Treatment Terminate exercise Exercise the “sore muscle”; no other proven effective treatment Gentle stretch of the affected muscle;



contraction of antagonistic muscle



Prevention No proven effective preventive measure No proven effective preventive measure Stretching the affected muscles may be effective, but evidence is insufficient;



quinine is effective, but side effects are too serious for routine use[14]



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