Muscle Soreness and

Delayed-Onset Muscle
Soreness
Paul B. Lewis, MD, MSa,*, Deana Ruby, APN, ACNP-BCb,
Charles A. Bush-Joseph, MDb

KEYWORDS
• Muscle soreness • DOMS • Delayed-onset • Muscle ache
• Stiffness

The novice and elite athlete is familiar with the postexercise muscle discomfort known
as delayed-onset muscle soreness (DOMS) after unfamiliar exercises. While common
in occurrence, most patients will self-treat the condition unless symptoms are
progressive in nature. The sports medicine clinician needs to maintain this diagnosis
among their active differential diagnoses. Associated symptomology of muscle
soreness can be quite debilitating and the presentation of this phenomenon is as
diverse as the population that experiences it.
Immediate or delayed-onset muscle soreness with a nonuniform intramuscular
distribution may portray itself as a nonmuscular injury with an unrecalled or vague
traumatic event. The prudent clinician is to base their advisory guidance, medical
management and/or surgical treatments on sound medical and/or surgical principles.
The purpose of this communication is to describe the clinical presentation, cellular
mechanisms, preventative measures, and management options related to muscle
soreness and DOMS for the sports medicine clinician.

CLINICAL PRESENTATION

Muscle soreness is classified as a type I muscle strain1 and refers to the immediate
soreness perceived by the athlete while or immediately after participating in exer-
cises. Muscle soreness presents with muscle stiffness, aching pain, and/or muscular
tenderness. These symptoms are experienced for only hours and are relatively
transient compared to those of DOMS. The symptomatology of DOMS shares similar

The authors have nothing to disclose.

a
Department of Diagnostic Radiology & Nuclear Medicine, Rush University Medical Center, 1653
West Congress Parkway, Chicago, IL 60612, USA
b
Department of Orthopedic Surgery, Rush University Medical Center, Third Floor, 1611 West
Harrison Street, Chicago, IL 60612, USA
* Corresponding author.
E-mail address: paul_lewis@rsh.net

Clin Sports Med 31 (2012) 255–262

doi:10.1016/j.csm.2011.09.009 sportsmed.theclinics.com
0278-5919/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
256 Lewis et al

quality and intensity to that of immediate exercise-induced muscle soreness but

symptom onset is at about 24 hours after the athlete has completed their exercise.2,3
In the ensuing days, the related symptoms peak within 72 hours and slowly resolve in
5 to 7 days.2,3 While the presentation of these conditions differs temporally, there is
a shared subtly that may lead one to the clinical question of more concerning pain
generators (eg, stress fracture, ligamentous sprain, or tendon tear).
Muscle soreness may begin as a concerted area sensitive to passive manipulation
and active movement.4,5 This early perception may later be perceived as broad
muscle soreness with focal points of tenderness referred from the active process
within the musculotendinous junction.6 This latter presentation is more ambiguous,
and accordingly more concerning. The clinical responsibility is to discern DOMS from
a non-muscular injury with an unrecalled or vague traumatic event (eg, ligamentous
rupture, chondral defect, stress fracture). To do so, it requires an understanding of the
characteristics of DOMS and competing diagnoses.
Clinically, focal exercise-induced soreness can be separated from a nonmuscular
etiology with reproducible active and passive, weight-bearing and non–weight-
bearing range of motion. Moreover, the clinician can use specific tests to the possible
surrounding nonmuscular etiologies. Expanding the diagnostic thought process to
include recent changes in workout intensity, exercise duration, and the individual’s
baseline exercise tolerance will further direct one toward or away from an etiology.
Finally, consideration of new activities the patient may have performed is warranted,
particularly in patients who were already well conditioned.
Independent of the patient’s previous condition, there is an associated muscle
weakness after an episode of acute or delayed muscular soreness.5,7–11 This decline
in muscular performance is intuitively related to the associated cell damage and
subsequent inflammatory response.12–14 The identified cellular damage related to
unaccustomed exercise is loss of membrane integrity15,16 and excitation-contraction
coupling.12,14 Restoration of muscle strength from the causative exercise may take up
to 2 weeks to occur.4 The delay in recovery has been attributed to the inflammatory
cell infiltration and accumulation.61,63 Clinically, the strength deficit and its duration
deserve to be included when advising patients whom are considering beginning or
increasing their exercise program.
Concurrently, as focus turns to “return to play” during or after the resolution of
muscle soreness, the clinician is to remain grounded with injury risk factors that
include but are not limited to subtle deficiencies in joint stabilization and cushioning,17
gross coordination,17,18 and, as above, strength.12–14
CELLULAR MECHANISMS

Paralleling the diverse population and clinical presentation of muscle soreness,

there are 6 competing theories for the mechanism of DOMS: lactic acid accumu-
lation,19,20 muscle spasm,21,22 microtrauma,23–25 connective tissue damage,25
inflammation,5,9,26 and electrolytes and enzyme efflux.19,27,28 While these 6
theories were presented independently from one another, the current consensus
is that a single theory alone is insufficient to explain the process; instead, they
work in concert.19,20,29 –31
The mechanism of muscle soreness, immediate and delayed onset, begins at the
time of exercise with strain on the muscle’s functional unit—the sarcomere. Subse-
quent to breakdown of the functional unit, there is an intracellular accumulation of
calcium, causing further degradation of the sarcomere. This intracellular damage
increases the demands on surrounding connective tissue. Following this is an
inflammatory response with recruitment of inflammatory cells and cytokines that
 Muscle Soreness and Delayed-Onset Muscle Soreness 257

potentiate the nerve endings and perception of pain. Passive manipulation and active
movement alter intramuscular pressures and stimulate mechanoreceptor nerve
endings, contributing to the perception of soreness.19,20,29 –31
Explanation of disproportionate (nonuniform) exercise-induced soreness begins
with the intramuscular architecture.32–34 Each imposed stress on muscles (eg,
concentric versus eccentric actions) recruits different branches of a structural,
intramuscular organization. Demands on selected parts within muscle develop
selective pathways for electrical activity, hypertrophy, and generation of forces.35– 41
The gross manifestation of this intramuscular architecture is the orientation and shape
of muscle. Had such intramuscular architecture not existed, the gastrocnemius would
be a homogeneous, uniform cylinder of muscle tissue between the tendons. The
demanded contractions during unaccustomed exercises may overload underdevel-
oped muscle fibers and lead to cellular damage.42– 44 Subsequent inflammation
remains specific to those posits of underdeveloped myocytes within that architec-
ture.5,9,26 Ultimately, this translates into focal points of tenderness overlying typical
locations of long bone stress fractures or superficial to a ligament’s site of insertion.

PREVENTIVE MEASURES

Effective prevention of muscle soreness is difficult; it is a physiologic response to activity.

The most effective prophylaxis of muscle soreness would be abstaining from prolonged,
intense unfamiliar physical exercises. Identifying such activities before participating often
carries a commensurate degree of difficulty. When such tasks are identified or anticipated
however, there are inherent modalities—physical preparation, demand reduction and
nutritional resources— can minimize anticipated muscle soreness.
Prevention of muscle soreness through stretching is supported by the rationale of
viscoelastic and stress-relaxation behaviors of muscle.20 The benefit of stretching,
however, is marginal.45,46 The 2011 Cochrane Database review by Herbert and
colleagues46 found the reduction of DOMS is maximized with stretching before and
after activity.
Use of assistive devices may alleviate the demand on muscle fibers and decrease
subsequent soreness.47 When desired to maintain muscle demand and recruitment,
the athlete is to be advised regarding nutritional supplements.
Carbohydrate and protein supplement drinks are seen to be most beneficial when
consumed after, not prior to, muscle-damaging exercise activity.48,49 In a sophisti-
cated, double-blind study by Matsumoto and colleagues,50 protein supplement
surpassed the placebo drink in reducing muscle soreness and fatigue after prolonged
physical exercise.
The use of supplements, assistive devices, and stretching is to be done cautiously
and with a confirmation of understanding from the athlete on instructions. Additional
preventative measures are also included next because of the crossover between
prevention and symptom management.

SYMPTOM MANAGEMENT

Completing the physiological mechanism of muscle soreness is the only effective

treatment. Each clinician is to approach the most compatible options for the athlete with
a sound understanding of existing basic science that supports or refutes the selected
modalities. The primary responsibility of the clinician is to prevent the athlete from
injuring himself or herself with the chosen management(s).
The outcomes from clinical research on massage are too variable28,51–55 to
confidently support its gainful benefit; its use should be directed empirically by athlete
258 Lewis et al

perception. As suggested by Cheung and colleagues,20 the variability of outcomes

from massage are likely related to the variations in timing and methods of the studied
tissue massage. Additionally, it is unclear if massage increases local blood flow to
affected muscle.56 –58
Recommendations of cryotherapy, vibration treatment, and nutriceutics (eg, pome-
granate juice) carry the same degree of neutrality. Sample sizes, scheduling, and
treatment administration have limited the value of studies of such methods.59 –70
The rationale and outcomes of pharmaceutical intervention with nonsteroidal
anti-inflammatory drugs (NSAIDs) are supported consistently and thus are recom-
mended when provided with a reasonable guidance on the dangers71 of their use.
Clinically, NSAIDs decrease perceived muscle soreness associated with DOMS72–77
but fail to impact the length or degree of muscle weakness.72–77
Further research is needed but supported in the use of mechanical lower extremity
compression as it has been shown to reduce swelling and decrease perceived muscle
soreness.78 The same study by Kraemer and colleagues78 showed continuous
compression also allowed the maintenance of elbow range of motion and promotion
of strength reconditioning.
The most effective, and highly recommended, modality to treat muscle soreness is
continued exercise.19,20,79 The basic principle supporting exercise is the increase in
local blood flow and endorphin release it produces and its subsequent analgesic
effects.20,25,80 While effective, the athlete is more likely to cause muscular injury while
exercising81 and benefits diminish at the cessation of activity.
Surgical intervention82 is not recommended as a prophylactic or treatment
modality.

SUMMARY

Immediate and delayed-onset muscle soreness differ mainly in chronology of pre-

sentation. Both conditions share the same quality of pain, eliciting and relieving
activities and a varying degree of functional deficits. There is no single mechanism for
muscle soreness; instead, it is a culmination of 6 different mechanisms. The
developing pathway of DOMS begins with microtrauma to muscles and then
surrounding connective tissues. Microtrauma is then followed by an inflammatory
process and subsequent shifts of fluid and electrolytes. Throughout the progression
of these events, muscle spasms may be present, exacerbating the overall condition.
There are a multitude of modalities to manage the associated symptoms of
immediate soreness and DOMS. Outcomes of each modality seem to be as diverse
as the modalities themselves. The judicious use of NSAIDs and continued exercise
are suggested to be the most reliable methods and recommended. This review article
and each study cited, however, represent just one part of the clinician’s decision-
making process.83 Careful affirmation of temporary deficits from muscle soreness is
not to be taken lightly, nor is the advisement and medical management of muscle
soreness prescribed by the clinician.

REFERENCES

1. Safran MR, Seaber AV, Garrett WE Jr. Warm-up and muscular injury prevention. An
update. Sports Med 1989;8:239.
2. Byrnes WC, Clarkson PM. Delayed onset muscle soreness and training. Clin Sports
Med 1986;5:605.
3. Ebbeling CB, Clarkson PM. Exercise-induced muscle damage and adaptation. Sports
Med 1989;7:207.
 Muscle Soreness and Delayed-Onset Muscle Soreness 259

4. Lieber RL, Friden J. Morphologic and mechanical basis of delayed-onset muscle

soreness. J Am Acad Orthop Surg 2002;10:67.
5. MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle soreness. The inflammatory
response to muscle injury and its clinical implications. Sports Med 1995;20:24.
6. Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Delayed onset muscle soreness at
tendon-bone junction and muscle tissue is associated with facilitated referred pain.
Exp Brain Res 2006;174:351.
7. Faulkner JA, Brooks SV, Opiteck JA. Injury to skeletal muscle fibers during contrac-
tions: conditions of occurrence and prevention. Phys Ther 1993;73:911.
8. MacIntyre DL, Reid WD, Lyster DM, et al. Presence of WBC, decreased strength, and
delayed soreness in muscle after eccentric exercise. J Appl Physiol 1996;80:1006.
9. Paulsen G, Crameri R, Benestad HB, et al. Time course of leukocyte accumulation in
human muscle after eccentric exercise. Med Sci Sports Exerc 2010;42:75.
10. Raastad T, Hallen J. Recovery of skeletal muscle contractility after high- and moder-
ate-intensity strength exercise. Eur J Appl Physiol 2000;82:206.
11. Raastad T, Risoy BA, Benestad HB, et al. Temporal relation between leukocyte
accumulation in muscles and halted recovery 10-20 h after strength exercise. J Appl
Physiol 2003;95:2503.
12. Ingalls CP, Warren GL, Williams JH, et al. E-C coupling failure in mouse EDL muscle
after in vivo eccentric contractions. J Appl Physiol 1998;85:58.
13. Louis E, Raue U, Yang Y, et al. Time course of proteolytic, cytokine, and myostatin
gene expression after acute exercise in human skeletal muscle. J Appl Physiol
2007;103:1744.
14. Warren GL, Ingalls CP, Shah SJ, et al. Uncoupling of in vivo torque production
from EMG in mouse muscles injured by eccentric contractions. J Physiol 1999;
515(Pt 2):609.
15. Brancaccio P, Maffulli N, Buonauro R, et al. Serum enzyme monitoring in sports
medicine. Clin Sports Med 2008;27:1.
16. Byrnes WC, Clarkson PM, White JS, et al. Delayed onset muscle soreness following
repeated bouts of downhill running. J Appl Physiol 1985;59:710.
17. Smith LL. Causes of delayed onset muscle soreness and the impact on athletic
performance: a review. J Appl Sport Sci Res 1992;6:135.
18. Edgerton VR, Wolf SL, Levendowski DJ, et al. Theoretical basis for patterning EMG
amplitudes to assess muscle dysfunction. Med Sci Sports Exerc 1996;28:744.
19. Armstrong RB. Mechanisms of exercise-induced delayed onset muscular soreness: a
brief review. Med Sci Sports Exerc 1984;16:529.
20. Cheung K, Hume P, Maxwell L. Delayed onset muscle soreness: treatment strategies
and performance factors. Sports Med 2003;33:145.
21. De Vries HA. Neuromuscular tension and its relief. J Assoc Phys Ment Rehabil
1962;16:86.
22. De Vries HA. Quantitative electromyographic investigation of the spasm theory of
muscle pain. Am J Phys Med 1966;45:119.
23. Bobbert MF, Hollander AP, Huijing PA. Factors in delayed onset muscular soreness of
man. Med Sci Sports Exerc 1986;18:75.
24. Friden J, Seger J, Ekblom B. Sublethal muscle fibre injuries after high-tension
anaerobic exercise. Eur J Appl Physiol Occup Physiol 1988;57:360.
25. Hough T. Ergographic studies in muscular fatigue and soreness. J Boston Soc Med
Sci 1900;5(3):81–92.
26. MacIntyre DL, Reid WD, Lyster DM, et al. Different effects of strenuous eccentric
exercise on the accumulation of neutrophils in muscle in women and men. Eur J Appl
Physiol 2000;81:47.
260 Lewis et al

27. Gulick DT, Kimura IF. Delayed onset muscle soreness: what is it and how do we treat
it? J Sport Rehab 1996;5:234.
28. Gulick DT, Kimura IF, Sitler M, et al. Various treatment techniques on signs and
symptoms of delayed onset muscle soreness. J Athl Train 1996;31:145.
29. Armstrong RB. Initial events in exercise-induced muscular injury. Med Sci Sports
Exerc 1990;22:429.
30. Smith LL. Acute inflammation: the underlying mechanism in delayed onset muscle
soreness? Med Sci Sports Exerc 1991;23:542.
31. Weerakkody NS, Whitehead NP, Canny BJ, et al. Large-fiber mechanoreceptors
contribute to muscle soreness after eccentric exercise. J Pain 2001;2:209.
32. Lieber RL, Friden J. Clinical significance of skeletal muscle architecture. Clin Orthop
Relat Res 2001;(383):140 –51.
33. Lieber RL, Friden J. Functional and clinical significance of skeletal muscle architec-
ture. Muscle Nerve 2000;23:1647.
34. Noonan TJ, Garrett WE Jr. Injuries at the myotendinous junction. Clin Sports Med
1992;11:783.
35. Brown JM, Solomon C, Paton M. Further evidence of functional differentiation within
biceps brachii. Electromyogr Clin Neurophysiol 1993;33:301.
36. Foley JM, Jayaraman RC, Prior BM, et al. MR measurements of muscle damage and
adaptation after eccentric exercise. J Appl Physiol 1999;87:2311.
37. Levy AS, Kelly BT, Lintner SA, et al. Function of the long head of the biceps at the
shoulder: electromyographic analysis. J Shoulder Elbow Surg 2001;10:250.
38. Meyer RA, Prior BM. Functional magnetic resonance imaging of muscle. Exerc Sport
Sci Rev 2000;28:89.
39. Sakurai G, Ozaki J, Tomita Y, et al. Electromyographic analysis of shoulder joint
function of the biceps brachii muscle during isometric contraction. Clin Orthop Relat
Res 1998;(354):123–31.
40. Sarti MA, Monfort M, Fuster MA, et al. Muscle activity in upper and lower rectus
abdominus during abdominal exercises. Arch Phys Med Rehabil 1996;77:1293.
41. Ward SR, Hentzen ER, Smallwood LH, et al. Rotator cuff muscle architecture:
implications for glenohumeral stability. Clin Orthop Relat Res 2006;448:157.
42. Friden J, Lieber RL. Eccentric exercise-induced injuries to contractile and cytoskeletal
muscle fibre components. Acta Physiol Scand 2001;171:321.
43. Lieber RL, Shah S, Friden J. Cytoskeletal disruption after eccentric contraction-
induced muscle injury [review]. Clin Orthop Relat Res 2002;(403 Suppl):S90 –9.
44. Patel TJ, Das R, Friden J, et al. Sarcomere strain and heterogeneity correlate with
injury to frog skeletal muscle fiber bundles. J Appl Physiol 2004;97:1803.
45. Herbert RD, de Noronha M. Stretching to prevent or reduce muscle soreness after
exercise. Cochrane Database Syst Rev 2007;7:CD004577.
46. Herbert RD, de Noronha M, Kamper SJ. Stretching to prevent or reduce muscle
soreness after exercise. Cochrane Database Syst Rev 2011;7:CD004577.
47. Howatson G, Hough P, Pattison J, et al. Trekking poles reduce exercise-induced
muscle injury during mountain walking. Med Sci Sports Exerc 2011;43(1):140 –5.
48. Cockburn E, Stevenson E, Hayes PR, et al. Effect of milk-based carbohydrate-protein
supplement timing on the attenuation of exercise-induced muscle damage. Appl
Physiol Nutr Metab 2010;35(3):270 –7.
49. McBrier NM, Vairo GL, Bagshaw D, et al. Cocoa-based protein and carbohydrate
drink decreases perceived soreness after exhaustive aerobic exercise: a pragmatic
preliminary analysis. J Strength Cond Res 2010;24(8):2203–10.
 Muscle Soreness and Delayed-Onset Muscle Soreness 261

50. Matsumoto K, Koba T, Hamada K, et al. Branched-chain amino acid supplementation

attenuates muscle soreness, muscle damage and inflammation during an intensive
training program. J Sports Med Phys Fitness 2009;49:424.
51. Frey Law LA, Evans S, Knudtson J, et al. Massage reduces pain perception and
hyperalgesia in experimental muscle pain: a randomized, controlled trial. J Pain
2008;9:714.
52. Hart JM, Swanik CB, Tierney RT. Effects of sport massage on limb girth and
discomfort associated with eccentric exercise. J Athl Train 2005;40:181.
53. Isabell WK, Durrant E, Myrer W, et al. The effects of ice massage, ice massage with
exercise, and exercise on the prevention and treatment of delayed onset muscle
soreness. J Athl Train 1992;27:208.
54. Weber MD, Servedio FJ, Woodall WR. The effects of three modalities on delayed
onset muscle soreness. J Orthop Sports Phys Ther 1994;20:236.
55. Zainuddin Z, Newton M, Sacco P, et al. Effects of massage on delayed-onset muscle
soreness, swelling, and recovery of muscle function. J Athl Train 2005;40:174.
56. Cafarelli E, Flint F. The role of massage in preparation for and recovery from exercise.
An overview. Sports Med 1992;14:1.
57. Hovind H, Nielsen SL. Effect of massage on blood flow in skeletal muscle. Scand J
Rehabil Med 1974;6:74.
58. Tiidus PM. Manual massage and recovery of muscle function following exercise: a
literature review. J Orthop Sports Phys Ther 1997;25:107.
59. Ayles S, Graven-Nielsen T, Gibson W. Vibration-induced afferent activity augments
delayed onset muscle allodynia. J Pain 2011;12(8):884 –91.
60. Bakhtiary AH, Safavi-Farokhi Z, Aminian-Far A. Influence of vibration on delayed onset
of muscle soreness following eccentric exercise. Br J Sports Med 2007;41:145.
61. Connolly DA, McHugh MP, Padilla-Zakour OI, et al. Efficacy of a tart cherry juice blend
in preventing the symptoms of muscle damage. Br J Sports Med 2006;40:679.
62. Denegar CR, Perrin DH. Effect of transcutaneous electrical nerve stimulation, cold,
and a combination treatment on pain, decreased range of motion, and strength loss
associated with delayed onset muscle soreness. J Athl Train 1992;27:200.
63. Lau WY, Nosaka K. Effect of vibration treatment on symptoms associated with
eccentric exercise-induced muscle damage. Am J Phys Med Rehabil 2011;90(8):
648 –57.
64. Raub W. From the National Institutes of Health. JAMA 1990;264:1086.
65. Rhea MR, Bunker D, Marin PJ, et al. Effect of iTonic whole-body vibration on
delayed-onset muscle soreness among untrained individuals. J Strength Cond Res
2009;23:1677.
66. Rowsell GJ, Coutts AJ, Reaburn P, et al. Effect of post-match cold-water immersion
on subsequent match running performance in junior soccer players during tourna-
ment play. J Sports Sci 2011;29(1):1– 6.
67. Rowsell GJ, Coutts AJ, Reaburn P, et al. Effects of cold-water immersion on physical
performance between successive matches in high-performance junior male soccer
players. J Sports Sci 2009;27:565.
68. Trombold JR, Barnes JN, Critchley L, et al. Ellagitannin consumption improves
strength recovery 2-3 d after eccentric exercise. Med Sci Sports Exerc 2010;42(3):
493– 8.
69. Trombold JR, Reinfeld AS, Casler JR, et al. The effect of pomegranate juice supple-
mentation on strength and soreness after eccentric exercise. J Strength Cond Res
2011;25(7):1782– 8.
70. Weerakkody NS, Percival P, Hickey MW, et al. Effects of local pressure and vibration
on muscle pain from eccentric exercise and hypertonic saline. Pain 2003;105:425.
262 Lewis et al

71. Adams SS, Bough RG, Cliffe EE, et al. Some aspects of the pharmacology, metab-
olism, and toxicology of ibuprofen. I. Pharmacology and metabolism. Rheumatol Phys
Med 1970;10:Suppl 10:9 –26.
72. Cannavino CR, Abrams J, Palinkas LA, et al. Efficacy of transdermal ketoprofen for
delayed onset muscle soreness. Clin J Sport Med 2003;13:200.
73. Donnelly AE, McCormick K, Maughan RJ, et al. Effects of a non-steroidal anti-
inflammatory drug on delayed onset muscle soreness and indices of damage. Br J
Sports Med 1988;22:35– 8.
74. Dudley GA, Czerkawski J, Meinrod A, et al. Efficacy of naproxen sodium for exercise-
induced dysfunction muscle injury and soreness. Clin J Sport Med 1997;7(1):3–10.
75. Francis KT, Hoobler T. Effects of aspirin on delayed muscle soreness. J Sports Med
Phys Fitness 1987;27:333.
76. Hasson SM, Daniels JC, Divine JG, et al. Effect of ibuprofen use on muscle soreness,
damage, and performance: a preliminary investigation. Med Sci Sports Exerc 1993;
25:9.
77. Lecomte JM, Lacroix VJ, Montgomery DL. A randomized controlled trial of the effect
of naproxen on delayed onset muscle soreness and muscle strength. Clin J Sport
Med 1998;8:82.
78. Kraemer WJ, Bush JA, Wickham RB, et al. Influence of compression therapy on
symptoms following soft tissue injury from maximal eccentric exercise. J Orthop
Sports Phys Ther 2001;31:282.
79. Smith LL. Cause of delayed onset muscle soreness and the impact on athletic
performance: a review. J Appl Sport Sci Res 1992;6:135.
80. Carlsson CA, Pellettieri L. A clinical view of pain physiology. Acta Chir Scand
1982;148:305.
81. Mair SD, Seaber AV, Glisson RR, et al. The role of fatigue in susceptibility to acute
muscle strain injury. Am J Sports Med 1996;24:137.
82. Micklewright D. The effect of soft tissue release on delayed onset muscle soreness: a
pilot study. Phys Ther Sport 2009;10:19.
83. Steves R. Appraising clinical studies: a commentary on the Zainuddin et al and Hart et
al studies. J Athl Train 2005;40:186.