eMedicine Specialties > Physical Medicine and Rehabilitation > Muscle Pain Syndromes

Postexercise Muscle Soreness

Author: Divakara Kedlaya, MBBS, Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine
Coauthor(s): Timothy Kuang, MD, Pain Management Fellow, Department of Physical Medicine and Rehabilitation, Loma Linda University Medical Center
Contributor Information and Disclosures

Updated: Jun 6, 2008

Introduction

Background

Hough gave the first detailed description of delayed-onset muscle soreness (DOMS) in 1902. DOMS is a widely recognized entity and is experienced by nearly everyone during his/her lifetime. It 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. Although DOMS is experienced widely, there are still controversies regarding its origin, etiology, and treatment.

Related eMedicine topics:
Contusions
Exercise Physiology
Myofascial Pain in Athletes
Overuse Injury

Related Medscape topic:
Resource Center Exercise and Sports Medicine

Pathophysiology

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.

Etiology and pathophysiology

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.1 The intensity seems to be more important in the determination than is the duration.

Five hypotheses are used to explain the pathophysiology of DOMS.

  • 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.
    • The rhythmic and tetanic contractions that cause the greatest acute fatigue and discomfort in the muscles during exercise results 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.
    • 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.2
  • 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 19423 and a later series of experiments by Cobb and colleagues4 demonstrated elevated electromyographic activity in sore muscles.5 Altered nerve control and vasoconstriction lead to decreased blood flow and ischemia, which in turn initiate a pain-spasm-pain cycle.6 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

Frequency

United States

The incidence of DOMS is difficult to calculate, because most people with DOMS do not seek medical attention, instead accepting DOMS as a temporary discomfort. Every healthy adult most likely has experienced DOMS on countless occasions. DOMS occurs regardless of the person's general fitness level.

Mortality/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.
  • 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.

Race

No race predilection is associated with DOMS.

Sex

  • 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.7
  • MacIntyre and coauthors found that the patterns of DOMS and torque differed between males and females after eccentric exercise.8
  • In a study by Dannecker and colleagues, no sex differences were detected, except that higher affective ratios were reported by men than by women.9

Age

DOMS generally is not reported in children. Adults of all ages can experience DOMS.

Clinical

History

  • A history of heavy, unaccustomed exercise, particularly involving eccentric muscle contractions (eg, downhill exercise) is reported.
  • The patient complains of pain, soreness, swelling, and a stiff or tender muscle spasm.
  • The muscles are sensitive, especially upon palpation or movement.
  • Decreased range of motion and reduced strength is noted (especially 24-48 hours postexercise).
  • The patient has a sense of reduced mobility or flexibility.
  • DOMS begins 8-24 hours after exercise and peaks 24-72 hours postexercise; it then subsides over the next 5-7 days
  • Acute onset muscle soreness begins during exercise and continues for approximately 4-6 hours after exercise.

Physical

  • 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.
  • Muscle tenderness is present.
  • Decreased muscle strength and flexibility also are noted.

Causes

  • Heavy, unaccustomed exercises contribute to the development of DOMS.
  • 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.

More on Postexercise Muscle Soreness

Overview: Postexercise Muscle Soreness
Differential Diagnoses & Workup: Postexercise Muscle Soreness
Treatment & Medication: Postexercise Muscle Soreness
Follow-up: Postexercise Muscle Soreness
References
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Further Reading

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Keywords

postexercise muscle soreness, delayed-onset muscle soreness, DOMS, post-exercise muscle soreness, muscle overuse, rhabdomyolysis, metabolic waste product accumulation, spastic contracture, myofibrillar alterations, cytoskeletal alterations

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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
Divakara Kedlaya, MBBS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, and Colorado Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

 
 
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