Pathophysiology of Acute

Exercise-Induced Muscular

Injury: Clinical ImplicationsPhillip Page, MS, ATC, PT, LAT

Abstract: Acute muscular injury is themost common injury affecting athletesand those participating in exercise.Nearly everyone has experienced sore-ness after unaccustomed or intense exer-cise. Clinically, acute strains and de-layed-onset muscle soreness are verysimilar. The purpose of this paper is toreview the predisposing factors, mecha-nisms of injury, structural changes, andbiochemical changes associated withthese injuries. Laboratory and clinicalfindings are discussed to help athletictrainers differentiate between the twoconditions and to provide a backgroundknowledge for evaluation, prevention,and treatment of exercise-induced mus-cular injury.

Tnhe musculotendinous unit is theforce-generating component offunctional movement. However, it

is one of the least understood links inhuman movement and one of the mostfrequently injured tissues during exer-cise. Athletic trainers evaluate and treatmusculoskeletal injuries daily. This pa-per provides a review of contemporaryliterature on the pathophysiology ofacute strains and delayed-onset musclesoreness. Predisposing factors and mech-anisms of injury are presented to aid thereader in the prevention of muscular in-jury, while structural and biochemicalchanges are reviewed for the purpose ofevaluation and treatment. By understand-ing the pathophysiology of exercise-induced muscle injury, we may be better

able to prevent, evaluate, and treat theseinjuries.

Muscle Injury ClassificationMusculoskeletal injuries are very

common in both athletes and nonath-letes. Although both acute and chronicinjuries are seen, we will limit this re-view to acute muscular injuries. Acuteinjuries result from: 1) direct trauma,causing a contusion at the point of con-tact, or 2) indirect trauma, causing a dis-ruption in the myofibers without contact.Indirect injuries may be passive or ac-tive. Passive injuries result from a tensileoverstretch of the muscle without con-traction, whereas active injuries usuallyresult from eccentric overload of themuscles.28 32'46 These active injuries canbe classified as acute strains or exercise-induced muscle soreness (see Figure).

Because most exercise-induced mus-cular injuries result from active contrac-tion of muscles, our discussion will focuson injuries resulting from eccentric over-load: acute strains and exercise-inducedsoreness. Exercise-induced muscularsoreness or delayed-onset muscle sore-ness (DOMS) may be considered symp-toms of injury. DOMS, however, limitsperformance resulting from decreasedmotion, decreased force production, and

ACUTE INJUlRIES

Direct Indirect

Contusion Active Passive

Eccentric Overload Tensile Overstretch

Acute Strain IDOMS

Types of acute muscular injury.

pain 14,15,2648,51,58; therefore, it is rele-vant to our discussion of acute exercise-induced muscular injury.

Both acute strains and DOMS usuallyoccur as a result of eccentric overloadand structural alteration26'54 and result inan inflammatory reaction.56 Althougheach presents similar clinical symptomsand functional limitations, they shouldbe differentiated to determine propertreatment. For example, acute strainsmay require rest, whereas DOMS mayrespond better to stretching and activity.

Clinically, acute muscle strain injuriescan be distinguished from DOMS basedon the history of the injury. A strain re-sults from a specific episode, is painful,and is easily recognized by the patient asan injury.28 DOMS, however, usually be-gins 12 to 48 hours postexercise, with nospecific event causing the injury2'11'63other than repeated eccentric musclecontraction. In both injuries, palpation,passive stretching, and active movement

28,56ioanwill cause pain. Classification andclinical findings of acute exercise-induced muscular injury are summarizedin Table 1.

Acute StrainAcute muscular strains result from

macrotrauma with immediate and directsigns and symptoms.'7'30 Most experi-mental studies, however, focus on acutemuscular strain resulting from passivestretch in animal models. Taylor et a16'noted that both clinical and experimentalstrains result from large tensile forcesthat cause damage to the musculotendi-nous structure. In a review by Garret,28many laboratory studies were identifiedthat were consistent with clinical find-ings of muscular injury.

Predisposing FactorsGarret28 suggested three types of mus-

cle that are at possible risk for injury:Two-joint Muscles. Motion at one

joint can place two-joint muscles in aposition of increased passive tension.The increased passive tension may leadto an overstretch injury.

Muscles Contracting Eccentrically.Functional activities in exercise requireboth concentric and eccentric contrac-tions. Muscular strains are considered toresult most often from eccentric contrac-

Journal of Athletic Training 29

Phillip Page is a staff physical therapist/athletic trainer at HealthSouth Sportsmedi-cine & Rehabilitation in Metairie, LA 70006.

Table 1.-Clinical Manifestations of Exercise-Induced Muscular InjuryEvaluation Acute Strain DOMS

History One specific episode Unaccustomed/intense exerciseStructures Musculotendinous Muscle and connective tissue

involved junctionMuscle Eccentric Eccentric

contractionsPain Immediate, localized Delayed, diffuse, dull achePalpation Point tenderness, ± defect Point tenderness, no defectSwelling - +Stretching Painful PainfulWeakness Yes YesActive movement Painful Painful

tions28'32'57'66 because higher specifictensions produced in eccentric exerciselead to myofiber overload injury.2586'Eccentric contractions are common inthe deceleration phase of activity.

Muscles With a Higher Percentageof Type II Fibers. These fast-twitchmuscles create greater speed of contrac-tion which may predispose a muscle toinjury. Because most of the muscle ac-

tion involved with running and sprintingis eccentric, muscle strains most oftenoccur in sprinters or "speed athletes."

Arnheim4 noted that the muscles withthe highest incidence of strains in sportsare the hamstrings, gastrocnemius, quad-riceps, hip flexors, hip adductors, erectorspinae, deltoid, and rotator cuff. In addi-tion, he stated that a fault in the recipro-cal coordination of the agonist and an-

tagonist muscles may cause muscularstrain. Knapic et a143 reported that flexi-bility imbalances between agonists andantagonists may predispose athletes toinjury. Interestingly, however, the flexi-ble sides were most likely to be injured.

Previously injured muscle may also bemore vulnerable to reinjury.30 Jonhagenet al4l reported that sprinters with recenthamstring injuries had tighter andweaker hamstrings than uninjured sprint-ers, although it was not known if thisfinding was a cause or a result of injury.Inadequate rehabilitation may not restorefull strength, flexibility, and enduranceto the involved tissues before return toactivity. Subsequently, muscle weak-ness, tightness, and fatigue may predis-

24,28pose muscle to injury.Stretching and warmup before exer-

cise have been advocated to preventmuscular injury6,60,64 on the assumption

that cold or tight muscles23 might predis-pose one to muscular strain. Few exper-imental studies exist supporting theseclaims. However, inadequate warm-upexercises have been shown to be associ-ated with muscle strains.37 Increased tis-sue temperatures of 1C53 and 40C60 al-lowed greater elongation of the musclebefore failure. Similarly, Noonan et al50reported that warm muscles (40°C) were

less stiff than cold (25°C) muscles andrequired greater length to fail, offeringexperimental data to support warm-up as

an aid in injury prevention and enhancedperformance.

Mechanism of InjuryAcute muscular strains usually result

from a specific event of macro-

trauma.'7'30 A strain may involve themuscle itself or adjacent tissue, such as

fascia or tendon.4 The severity of the in-jury is in direct relation to the forcesplaced upon the muscle.45 Mechanically,an acute strain may be caused by an ab-normal muscular contraction,4 a re-

sponse to high specific tensions,2 or forc-ible stretching of a muscle while it isactive.28 Each of these mechanisms is re-

lated to eccentric contraction, in whichsufficient tensile forces develop to cause

irreversible changes in the structure ofthe musculotendinous unit.6i

Prevention of Acute StrainsPrevention of acute muscular strains

should begin with adequate preseason

screening of flexibility and strengthbalances in major joints such as theknee, shoulder, and ankle. Evaluationof previous muscle injuries should beperformed to assess flexibility,

strength, endurance, and propriocep-tion. Preseason and in-season condi-tioning of muscle groups is also vitalfor prevention. Adequate agonist/antagonist ratios for strength and flex-ibility should be attained for majormuscle groups, including quadriceps/hamstrings, shoulder internal rotators/external rotators, ankle dorsiflexors/plantarflexors, and abdominals/paraspinals. Muscles must bestrengthened in the mode in which theyare used functionally; ie, eccentricmuscles should be strengthened eccen-

trically.Warmup and stretching before activity

are thought to prevent muscular strains.Smith55 offers an excellent review of theliterature supporting the efficacy of thispractice. Active warmup such as joggingor biking should be performed beforespecific muscle stretching with emphasison muscles at risk for strain, includingtwo-joint muscles and those with highpercentages of fast-twitch fibers (ham-strings, gastrocnemius, quadriceps, bi-ceps), and muscles with high incidenceof strain (hip flexors, hip adductors, erec-

tor spinae, rotator cufl). Muscles whichcontract eccentrically or decelerate infunctional high-speed activities, such as

the posterior rotator cuff in throwing ath-letes or the hamstrings in sprintersshould be stretched for 15 to 20 sec-

onds6'8'62 and repeated four times.62Static stretching in combination withpassive heating may be more effectivethan passive heating alone.38

Structural ChangesThe most vulnerable site for an indi-

rect strain injury is just distal to the mus-culotendinous junction or the tendon-bone junction5'28-31i61; therefore,knowledge of musculoskeletal surfaceanatomy and palpation skill is important.Pain, swelling, deformity, and point ten-derness may be localized over the mus-

culotendinous junction immediately afterinjury. Tendons themselves are very re-

silient to injury and are rarely injuredacutely. Tendons will pull away from a

bone, a bone will break, or a muscle willtear before tendons are injured.4 How-ever, in contrast to the musculotendinousjunction, tendons are more susceptible tomicrotrauma.30

30 Volume 30 * Number 1 * 1995

A muscle strain may be partial or

complete, depending on the amount anddegree of fiber disruption within themuscle.28 Strains can be classified bythree degrees: first degree, a minute sep-

aration of muscle fibers; second degree,partial tearing of some fibers; and thirddegree, a complete rupture or tendinousavulsion. While full-thickness tears dooccur, partial or incomplete tears or

strains are more common30 and are clin-ically characterized by focal pain andswelling.28 A palpable defect such as a

bulge or gap in the muscle may be foundin a complete or partial tear. Disruptionsin the fibers cause biochemical changesboth from direct injury to the fibers andfrom the inflammatory reaction.

Biochemical ChangesSerum creatine kinase (CK) and lac-

tate dehydrogenase (LDH) enzyme lev-els are used to indirectly assess muscledamage following eccentric exer-

cise. 1,2,12,14-16,26,47,48,54,58 In addition tothe release of these biochemical markers,all acute strains undergo similar inflam-matory reactions. Acute inflammation isthe fundamental reaction designed to

protect, localize, and remove injuriousagents from the body in preparation forhealing and repair.4 Chemical mediatorsare present in acute muscular strain, as

with any inflammation. These include:histamine, serotonin, bradykinin, andprostaglandin.4 These chemicals increasethe capillary membrane permeability,change blood vessel diameter, and stim-ulate pain receptors. Edema results froman accumulation of proteins and transu-date in the interstitial space. This accu-

mulation is a result of increased capillarymembrane permeability secondary to thechemical mediators. Therefore, the char-acteristic swelling, heat, redness, andpain of inflammation are due to bio-chemical changes4 caused by the chem-ical mediators. Nikolaou et a149 noted an

inflammatory reaction and edema at 1 to

2 days after a stretch-induced muscularinjury. The acute phase of inflammationlasts up to 3 to 4 days after the initialinjury4 unless the tissue continues to be

traumatized, as is commonly seen when

injured athletes return to activity too

soon or are progressed too rapidly. Pro-liferation of fibroblasts, increased colla-gen production, and degradation of ma-

ture collagen have an overall weakeningeffect on the tissue; therefore, efforts to

stretch the tissue perpetuate the irritationand progressive limitation,42 leading tochronic muscle strains.As the inflammatory phase subsides,

repair begins and lasts for 2 to 3 weeks.The repair phase is characterized by cap-

illary growth and fibroblast activity to

form immature collagen. This immaturecollagen is easily injured if overstressed;however, proper growth and alignmentcan be stimulated with appropriate ten-

sile loading in the line of normal stress-es.42 The final stage of healing is matu-

ration and remodeling of collagen,occurring from 2 to 3 weeks after onset

until there is pain-free functional use ofthe muscle.42 If the healing fibers are not

properly stressed, the fibers adhere to

surrounding tissue and form a restrictingscar which is resilient to remodeling.

Treatment of Acute StrainsThe key to retuming any injured ath-

lete to competition safely is to provide an

optimal environment for healing and toprogress the patient according to: 1) theseverity of the injury, 2) the natural heal-ing process of the body, and 3) the re-

sponse of the tissue to new demands.Treatment goals for any soft-tissue in-jury must take the natural healing pro-

cess into consideration. The overall goalis to assist the body with its natural heal-ing process. The body must go througheach stage with any soft tissue injury;therefore, the athletic trainer must not re-

turn the athlete to activity too soon. Twoto three weeks of restricted activity maybe a minimum to allow for collagen for-mation and prevent reinjury in all soft-tissue injuries.

Inflammatory Phase. Effective man-

agement of muscular strains begins at thetime of injury. Care for acute injuriesmust be initiated as quickly as possiblewith rest, ice, compression, and elevation(RICE) for at least 48 hours. Cold slowsthe inflammatory process and decreasespain and muscle spasm; compression andelevation reduce edema. An ice bagwrapped with an elastic wrap, elevation,and crutches may be used. Rest protectsthe injured tissue; however, immobiliza-tion may be detrimental to healing and

the uninjured tissue. As the inflammationsubsides, pain-free, passive range of mo-

tion (ROM) and gentle joint mobilizationshould be initiated to maintain soft-tissueand joint integrity. Gentle, pain-free,submaximal isometric muscle sets may

be used at multiple angles to maintainstrength and keep the developing scar

tissue mobile. Aggressive stretching andstrengthening is contraindicated. Any in-crease in pain, swelling, warmth, or red-ness indicates a proliferation of the in-flammatory phase which should betreated only with RICE. Modalities forpain and edema such as electrical stim-ulation and pulsed ultrasound should beused during both the inflammatory andrepair phases.

Repair Phase. The inflammatory andrepair phases overlap during the firstweek after injury. As the inflammationsubsides, the athlete may attempt too

much activity too soon. This prolongsthe inflammatory phase and leads to

chronic muscle strain. However, as col-lagen is laid down, it must be appropri-ately stressed in the normal lines of ten-sion. This is a critical "turning point" inthe treatment of muscle injuries and maybe the most important stage for thetrainer or therapist in any rehabilitation.Signs of inflammation (pain, swelling,redness, warmth) are used to determinewhether the tissues are being over-

stressed with activity. The rehabilitationprogram must be constantly evaluated.Frequency, intensity, and duration of ex-

ercises are altered to allow for healingand to prevent inflammation for the next

1 to 2 weeks. Cold in the form of cryo-

stretch or cryokinetics (see Ref. 44) maybe beneficial initially to allow for pain-free exercise to aid in the formation ofthe scar tissue. Heat in the form of warmwhirlpools, moist heat, or ultrasound isused to promote capillary growth and in-crease ROM. Contrast baths may bemost beneficial during this period. Gen-tle, pain-free stretching and pain-freesubmaximal isometrics can be incorpo-rated into contract-relax techniques to

help align collagen fibers. These exer-

cises are progressed to active ROM for

the agonist. Active or resistive motion of

the antagonist or contralateral extremitymay also be incorporated. Finally, a car-

diovascular conditioning program should

be incorporated for any athlete not capa-

ble of full athletic participation.

Journal of Athletic Training 31

Maturation and Remodeling Phase.As collagen matures, it requires tensionin the line of normal stresses to remodelproperly. Clinically, this stage presentsat about 2 to 3 weeks after injury and ischaracterized by: 1) the absence of in-flammation, 2) full, pain-free ROM, and3) pain after tissue resistance, which isfelt with passive ROM.42 The athlete isprogressed as tolerated with limited par-

ticipation in his/her sport. Rehabilitationincludes more vigorous stretching,closed- and open-chain strengthening,cardiovascular training, and sport-spe-cific activities. It is vital to rememberthat muscles must be stressed and over-

loaded in the manner in which they are

used functionally, following the princi-ple of specificity. Type of contraction(eccentric vs concentric), metabolism(aerobic vs anaerobic), and functionalpattern (diagonal vs cardinal plane)should be specific to the activity inwhich they are used. Eccentric exerciseis functional in most athletic activities,develops greater tension than concentricexercise, and may be more comfortablein the early stages of rehabilitation.7 Ec-centric contraction may be performedagainst manual, isotonic, isokinetic, or

elastic resistance. Massage, aquatic ther-apy, and plyometrics are beneficial toany soft-tissue treatment. Proprioceptiveand endurance training are used in theadvanced stages of rehabilitation. Mo-dalities before and after activity may bebeneficial as well. An elastic or neoprene

wrap with a felt pad directly over theinjury site provides warmth and com-

pression. After the athlete has regainedfull, pain-free active ROM and over 90%strength bilaterally, full participation isallowed. Maintenance programs shouldbe independent and individualized toavoid any dysfunctional adaptation or

compensation.

Delayed-Onset MuscleSorenessDOMS is commonly seen in patients

performing new exercises or in athletesinvolved in weight-lifting or other ec-

centric activities. DOMS results frommuscle damage2'11'15'26'58 followingeccentric exercise. The onset of DOMSis characterized as a dull, aching pain usu-

ally beginning 12 to 48 hours after exer-

cise.2''63 Clarkson et al5 found thatsoreness peaks 2 to 3 days followingeccentric exercise and subsides linearlywithin 10 days. In addition to pain,other symptoms include decreased mo-

tion and decreased force produc-tion2,14,15,26,48,51,58,65 Newham and asso

ciates,47 however, reported a decreasedforce production with electrical stimula-tion of these muscles, indicating that thesoreness itself does not inhibit force pro-

duction.Muscles adapt to a single bout of ec-

centric exercise. This is evidenced byless damage to the muscle after the sameexercise months later.15 The muscle isrepaired without any residual dysfunc-tion or scarring and the muscle is oftenable to resist even greater forces.12'16'61

Predisposing FactorsArmstrong1 suggested two possible

causative factors during the initial eventsof DOMS2'58: high tensions and meta-bolic changes.High Tensions. High tensions pro-

duced during eccentric exercise are more

apt to produce myofiber injury than iso-metric or concentric contractions.

Metabolic Changes. Increased tem-perature, decreased aerobic capacity, anddecreased pH of the muscle may have a

role in causing DOMS.

Mechanism of InjuryExercise that results in the develop-

ment of soreness is associated with therapid destruction of muscle tissue.11'26The soreness usually results from muscledamage following repetitive eccentricexercise or after the first or secondsession of a new training pro-

2,11,1522,58gram. DOMS is also associ-ated with muscle spasm, as evidenced byincreased EMG activity. 52DOMSresults primarily from structural muscledamage and microtrauma and may be re-

lated to the resultant biochemicalchanges of the inflammatory process.

Prevention of DOMSFew studies exist on the prevention of

DOMS. Because it is known that eccen-

tric contractions cause muscle damage,DOMS may be prevented with warmup

and stretching before and after eccentricor novel exercise. Ideally, DOMS is pre-

vented by avoiding eccentric or unaccus-

tomed exercise. Clinically, this is notpossible. Athletes in competition, weightlifters, and patients undergoing early re-

habilitation commonly perform eccentricexercise. This eccentric training devel-ops strength to resist further damage.15Therefore, specific eccentric training isneccesary for any sport activity to helpprevent further damage or injury. Eccen-tric training sessions should be limited totwo per week to allow adequate rest andrecovery between sessions. Patientsshould be educated about the importanceand need for eccentric exercises, as wellas about the possiblity of DOMS.

Effective prevention of DOMS may

begin in the acute stages of treatment be-fore symptoms begin. Prophylactic ibu-profen administered before or immedi-ately after heavy eccentric exercise maydecrease the pain associated withDOMS.34 Yackzan et a165 found thatsubjects who received ice massage im-mediately after eccentric exercise hadmore ROM 24 hours later than thosewho did not receive it. Further researchis needed on the prevention of DOMS,including the roles of warmup, stretch-ing, and immediate treatment after in-tense eccentric exercise.

Structural ChangesStructural damage to subcellular com-

ponents following eccentric exercise hasbeen found by microscopic evalua-tion. 3,11,26,40 High specific tensionsseen in eccentric contractions could me-

chanically disrupt the connective tissue,myofilaments, sarcomere, sarcolemma,or sarcoplasmic reticulum.1'2'9'10 Fridenet al25'26 found alteration of Z-bands intype II fibers both immediately and 3days after eccentric exercise.Damage to the extracellular matrix

(ECM, the interface between the myofi-ber and fascia) following eccentric exer-

cise has been evaluated by Stauber andassociates.58'59 Myofiber and ECM dam-age result directly from eccentric con-

tractions.27 Stauber et a159 reported thateccentric muscle action is related to me-chanical shearing at the ECM. Thesestructural changes then cause biochemi-cal changes within the injured tissue.

Biochemical ChangesDamage to the sarcolemma and ECM

creates an altered chemical environment

32 Volume 30 * Number 1 * 1995

Table 2.-Treatment of DOMS

Authors Treatment Efficacy

Ciccone et al'3 Trolamine salicylate phonophoresis EffectiveDenegar et al'8 TENS EffectiveDeVries20'21 Static stretching EffectiveHasson et al33 High speed, voluntary muscle contraction EffectiveHasson et al34 Ibuprofen EffectiveHaynes & Perrin3 Topical counterirritant EffectiveHill & Richardson39 Topical trolamine salicylate cream EffectivePrentice52 Static or PNF stretching + cold or heat EffectiveMcGlynn et al46 Stretching and biofeedback Reduced EMG, but not painPrentice52 Heat Not effective aloneYaczan et al65 Ice massage Not effective alone

Continuous ultrasound Increases painDenegar et al'9 Microcurrent Not effective, + analgesic effectHasson et a135 Dexamethasone lontophoresis Questionable

within the muscle. The release of pro-

teins and ions into the plasma as a resultof inflammation is similar to that foundin acute strains.1'2'59 Increases in theselevels indicate damage to the sarco-

lemma. Elevations of CK, LDH, proteinmetabolites, and myoglobin have beenfound in plasma up to 48 hours followingeccentric exercise.2 3'14'54'58'63 These biochemical events occur within the musclecells themselves and begin approxi-mately 24 hours postexercise,15 beforephagocytic cells enter the injury site.1Time-specific clinical events (such as

peak soreness at 2 to 3 days) may corre-

spond to the time of increased enzyme

levels (such as CK increase at 2 days).While Tiidus63 reported such a correla-tion between soreness and enzyme lev-els, Clarkson et al15 cautioned againstclaiming a cause-and-effect relationshipbased on limited research.

The structural disruption leads to thenormal inflammatory response: an in-crease in chemical mediators such as his-tamine, bradykinin, prostaglandin, andserotonin,4 causing pain and swelling.The products of the inflammatory re-

sponse sensitize free nerve endings inmuscle,11'56 thus increasing soreness.

Stauber et a159 concluded that the DOMSafter repeated eccentric muscle action isnot because of actual myofiber damage,but more likely results from inflamma-tion.

Treatment of DOMSBecause DOMS results from micro-

trauma, structural damage in DOMS is

not as severe as in acute strains resultingfrom macrotrauma. The symptoms ofDOMS resolve relatively quickly with-out any residual dysfunction; therefore,DOMS can be treated symptomatically.In any exercise-induced muscular injury,RICE is the ideal immediate treatment todecrease inflammation and pain. How-ever, because DOMS begins at 24 to 48hours after exercise and peaks at 2 to 3days after exercise, treatment may notbegin immediately after injury.

The goal of treatment of DOMS is toreduce the pain, swelling, inflammation,and muscle spasm. These goals are sim-ilar to those in the acute stage of any

soft-tissue injury. Several authors havestudied the efficacy of these treatments(Table 2). Static or proprioceptive neu-

romuscular facilitation (PNF) stretch-ing, 0,21,52 high-speed muscularconcentrics,33 nonsteroidal anti-inflam-matory drugs (NSAIDs),34 and topicalcounterirritants3639 have been shown tobe effective in reducing pain associatedwith DOMS. Phonophoresis'3 and trans-cutaneous electrical nerve stimulation(TENS)18 may be effective, but the ben-efits of iontophoresis35 and biofeed-back46 remain questionable.

Most studies report significant im-provement in DOMS with combinationsof exercise and modalities. DOMS can

be treated symptomatically by reducingthe pain, soreness, swelling, and musclespasm. NSAIDs and topical counterirri-tants may decrease soreness. Static or

PNF stretching in combination withcryotherapy (spray-and-stretch or ice

massage) also help to decrease the symp-toms of DOMS. In addition, high-speed,rapid concentric muscular contractionsmay provide relief. Further research isneeded on the use of massage, pulsedultrasound, and electrical stimulation (in-cluding TENS, iontophoresis, and micro-current) in the treatment of DOMS.

ConclusionBoth acute strains and DOMS present

similar clinical signs; however, they can

be differentiated by history of the injury.While many studies exist on the struc-tural changes and biochemical changesof exercise-induced muscular injury,many questions remain unanswered. Theexact changes in human muscle after an

acute strain have not been determined. Acause-and-effect relationship for DOMShas not been firmly established. We havereviewed the literature on these acute in-juries and provided clinical findings toaid in the care of musculoskeletal inju-ries. Further research is needed on thecauses of these injuries, as well as on

effective preventive and treatment tech-niques to return athletes and patientsback to preinjury levels.

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34 Volume 30 * Number 1 * 1995