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    Delayed Onset Muscle Soreness

    Background / New Knowledge:
    Delayed Onset Muscle Soreness (DOMS) is pain or discomfort in muscles that have undergone unaccustomed exercise. Eccentric exercise produces greater soreness, fatigue and damage than isometric and concentric contractions (Clarkson and Newham 1995). It is a temporary condition characterised by time course of pain following activity. The soreness usually develops within 24 hours of exercise and is characterised by a dull ache with tenderness and stiffness. Soreness subsides within 5 to 7 days regardless of further activity (Stauber 1996).

    Various authors have proposed different mechanisms of injury following eccentric exercise, however very little is known about the mechanisms involved in the production of DOMS or the accompanying responses such as prolonged loss of ROM and strength, increased muscle enzymes in the blood, swelling and structural damage (Clarkson and Newham 1995). It is thought that firstly a mechanical injury followed by a biochemical injury is responsible for the changes in the muscle following eccentric exercise (MacIntyre et al 1995).

    Mechanical injury:
    Histological and ultrastructural changes range from mild damage where single sarcomeres throughout the muscle show evidence of Z line streaming or bulging with extension into the A band and myofibrillar disruption. More severe damage results in cytoskeletal and myofibrillar damage, oedema, invading mononuclear cells, muscle fibre atrophy and necrosis. Regeneration occurs from 10 days for mild damage up to three weeks for severe damage (Clarkson and Newham 1995). Increased tension per individual cross-bridge causes mechanical disruption of the ultrastructural elements within muscle fibres such as the Z line (Z line streaming) and contractile filaments. Changes in the Z-line are attributed to loss of alpha-actin and vimentin (MacIntyre et al 1995).

    Stauber et al (1996) suggests that a complex set of reactions including disruption of muscle fibre and connective tissue (CT) is responsible for DOMS. CT damage involves endomysial separations which is assumed to occur during exercise. The injury may result from cytoskeletal damage to the intermediate filaments (desmin, Vimentin and synemin) or proteolytic enzymes may be released from the initial injury causing further degradation of the cytoskeleton (MacIntyre et al 1995).

    Progressive structural damage (Metabolic Injury?):
    Mechanisms proposed for the progressive nature of structural damage include accumulation of intracellular calcium following the mechanical insult. This triggers calcium mediated processes. It appears that fast twitch fibres are most affected as they fatigue early and enter a high state of stiffness due to an inability to regenerate ATP. Subsequent stretch mechanically disrupts the fibres causing cytoskeletal and myofibrillar damage (Clarkson and Newham 1995).

    Sarcolemma damage leads to disruption of muscle cell calcium homeostasis resulting in increased intracellular calcium concentration. This results in further muscle contractile protein and membrane degeneration which is likely to be caused by calcium induced activation of muscle protease and phospholipidase enzymes. Markers of muscle damage and membrane disruption such as CK are evident in the blood at this time. These factors are proposed to cause prolonged reductions in muscular strength (Tiidus 1997).

    Following skeletal muscle damage several intramuscular proteins leak into the blood including creatine kinase (CK), myoglobin, lactate dehydrogenase, aspartate aminotransferase, myosin heavy chain fragments. These are elevated following eccentric exercise. There is a delay in the appearance of these proteins in the blood from24-72 hours. It is suggested that the release and slow removal from extracellular spaces provide colloid osmotic pressure to produce oedema (Clarkson and Newham 1995).

    Biochemical Injury:
    To date the role of inflammation during exercise induced muscle injury has not been clearly defined. The role of neutrophil infiltration in exercise-induced muscle injury is not known although several studies have reported that macrophages were the predominant inflammatory cell present in exercise induced muscle injury. Different subpopulations of macrophages have been associated with distinct stages of recovery following muscle injury (Smith 1991).
    Smith (1991) suggests the sequence of events with DOMS begins with connective and contractile tissue injury. A significant elevation in circulating neutrophils follows at approximately 3 hours and migration to the site of injury. Monocytes then emigrate at 6-12 hours with large numbers present at 24 hours peaking at 48 hours. The macrophages synthesise PGE2 which sensitises type III and IV pain afferents. Bradykinin, histamine, serotonin and achetylcholine also sensitise pain afferents (Smith 1991).

    The Cause of Muscle Soreness:
    The exact cause is unknown however inflammation and swelling are considered prime factors (Smith 1991). Fluid accumulates in the muscle for five days after exercise then moves into the subcutaneous area as demonstrated in MRI studies. Swelling within the muscle compartment could produce pain and increase intramuscular pressure in low compliance compartments. It may also result in sensitisation of pain receptors to other noxious stimuli (Clarkson and Newham 1995).

    Slow release of cellular infiltrates from damaged cells may explain the delayed sensation of soreness associated with an acute inflammatory response (Clarkson and Newham 1995). The reason soreness is present on movement or palpation but not at rest is that the former increases intramuscular pressure and stimulate sensitised pain receptors (Smith 1991).

    Loss of muscle function:
    This has been observed up to one hour following exercise. It may take up to two weeks for  maximal recovery of isometric strength. It has been demonstrated that little or no relationship exists between the development of soreness and the loss of muscle strength. Therefore reduced performance occurs due to muscle tissue damage independant of pain induced inhibition of muscle (Clarkson and Newham 1995). It is not clear whether the initial loss in muscle strength is due to muscle injury, fatigue or both. It is proposed that immediate strength reduction is due to overstretched sarcomeres with reduced overlap between actin and myosin. Some sarcomeres may maintain their length and others are overstretched beyond overlap. This relates to findings of greater strength deficits at long compared to short muscle lengths (MacIntyre et al 1995).

    Two declines in muscle strength have been reported following eccentric exercise. The greatest decline in eccentric torque immediately follows exercise then partially recovers (2-4 hrs) and declines again 20-24 hours post exercise. It is suggected that a secondary biochemical injury results in free radical production by injured tissue from the phagocytic activity at the site of the original damage. Neutrophils and macrophages release oxygen radicals and proteases with the potential to cause further damage (MacIntyre et al 1995; Stauber et al 1996).

    The Cause of Stiffness:
    Stiffness following eccentric activity is suggested to be the result of swelling and spontaneous shortening due to the abnormal accumulation of calcium inside the muscle cell as a result of loss of sarcolemma integrity or dysfunction of the sarcoplasmic reticulum (Clarkson and Newham 1995). The immediate increase in stiffness is thought to be the result of altered calcium homeostasis. Stiffness is then influenced by swelling which peaks on day 4. Stiffness declines by day 7-11 in accordance with reduction in swelling (Chleboun et al 1998).

    Clinical Implications:
    1) The Preventative Effect of Training:
    It is believed that training prevents or reduces muscle damage and consequent soreness. DOMS only occurs following the first or second bouts of a new exercise program. Studies assessing CK activity (which indirectly assesses muscle damage) following a training program report reduced serum CK in response to a given exercise. Suggestions for this phenomenon initially centred around damage to a pool of fragile or stress susceptible muscle fibres resulting in a large serum CK response. The dynamic process of degeneration-regeneration that follows results in fewer stress susceptible muscle fibres on repetition of the exercise. More recent evidence has suggested that training does not eliminate a stress susceptible fibre population but provides a sufficient stimulus to increase the resistance of muscle fibres to injury (Armstrong 1990, Byrnes et al 1986).
    Friden et al (1983) demonstrated that the negative effects of eccentric exercise could be reduced by eccentric training. 15 subjects cycled 2-3 times per week for 4-8 weeks on a bicycle ergometer modified for use in eccentric work. Each time they cycled until severe fatigue at progressively increased work intensities. All subjects suffered from pronounced soreness of the knee extensors after the first 3-4 stints but following this symptoms gradually decreased and all subjects were free from complaints following 2-3 weeks of training. Additionally, following the eight weeks of training a single episode of maximal eccentric work caused a negligible decrease in maximal dynamic strength and a dramatic improvement in maximal eccentric work capacity was noted. Following the eight week training period, type 2B fibers were preferentially recruited. This coordination effect was proposed to lead to fewer units being recruited (Friden et al 1983). The protective effect of endurance training may convert type 2B to type 2A fibres thereby preventing type 2B fibre fatigue with eccentric exercise (Friden and Lieber 1992).

    Stauber (1991) recommends prevention of DOMS by emphasising types of exercises producing less damage early in any training or rehabilitation program. He suggests a program using specific muscles in shortened positions under mild loads then gradually increasing ROM with each training session until the muscle is active throughout the entire range. The best prevention is regular exercise and repetition of an activity containing eccentric muscle activity to protect the muscle from repeated injury.

    2) Effects of Compression:
    The relationship between  swelling and stiffness was highlighted in a study by Chleboun et al (1995) in which external pneumatic compression was applied daily for five days to the arm following exercise induced muscle injury. A reduction in arm circumference and stiffness on days two and three post exercise was demonstrated, although strength loss was not affected (Chleboun et al 1995).

    3) Effects of Cryotherapy:
    Very few studies have investigated the effects of cryotherapy on muscle soreness and strength following eccentric exercise. Of those that have addressed this issue the results suggest there are limited benefits. However, the methodology of these experiments is questionable in light of the characteristics of muscle oedema highlighted by Chleboun et al (1998).

    Paddon-Jones and Quigley (1997) found no significant difference between the immersed and control arms in recovery of elbow flexor strength and reducing the severity of DOMS following eccentric exercise. They suggest there is no therapeutic benefits of cryotherapy immediately following damaging eccentric exercise. However, the sample size of eight was very small to make these conclusions. The protocol of cryotherapy employed consisted of 5x20 minute immersions in ice water which commenced immediately following exercise with 60 minute rest periods between applications. The time of application may be inappropriate in light of recent evidence that swelling increase to peak on day 4! (Chlebourn et al 1998). It is possible that a greater number of cold applications would be required to significantly influence recovery. The method of measurement of arm volume was not specific to the compartments affected by the eccentric exercise. The protocol involved immersion, collection and weighing of water overflow. Possibly an ultrasonic method similar to that employed in the Chlebourn  et al (1998) study would have been more specific.

    4) Effects of Massage:
    There is limited research substantiating the routine use of sports massage in speeding recovery from vigorous exercise. Most studies concluding massage as ineffective have administered it either immediately after exercise or 24-48 hours following exercise (Smith et al 1994).

    Smith et al (1994) investigated the effects of athletic massage on DOMS, creatine kinase (CK) and neutrophil count in fourteen untrained subjects following eccentric isokinetic contractions of the biceps. Two hours following the exercise bout a thirty minute sports massage or a placebo was performed. The massage involved effleurage and petrissage. The choice of the two hour post exercise administration of massage was based on the principles of restorative massage used by the Soviet sports therapists at the time, which was reported to enhance relaxation and restoration of the athletes body. It is proposed that masssage between 1-3 hours post exercise interferes with the initiation of the acute inflammatory response. The critical event during this time is the accumulation of neutrophils followed by a decline in their circulation as they marginate to the vessel walls and subsequently emigrate to the traumatised tissue. The subsequent accumulation of macrophages depends on the initial accumulation of neutrophils. This process has been reported following eccentric exercise. It is hypothesised that massage disrupts margination and subsequent emigration of neutrophils into the area of injury causing prolonged elevation of circulating neutrophils thereby reducing the intensity of inflammation and reducing pain and discomfort associated with DOMS. Results indicated significantly reduced levels of DOMS and CK, prolonged elevation of neutrophils and diminished diurnal reduction in cortisol in the massaged group. The rationale behind massage causing these effects is based on the premis that massage increases blood flow through the vascular beds preventing margination of neutrophils. The vigorous nature of the massage would additionally shear marginated cells from vessel walls and hinder emigration of cells from the circulation into tissue spaces. The lower CK levels in the massaged group may be  due to CK efflux as a result of mobilisation of neutrophils at the site of injury. During the eight hour post exercise period the massaged group showed less reduction in cortisol levels possibly due to the body interpreting the vigorous massage as stress thereby increasing the release of cortisol into the circulation. Glucocorticoids have profound anti-inflammatory properties. They inhibit neutrophil adherence to vessel walls interfering with emigration.

    Application of a second sensation such as massage to a sore muscle could increase discharge from other low threshold sensory fibres thereby temporarily blocking the sensation of soreness. It is suggested that light exercise also temporarily diminishes muscle soreness by this mechanism. If oedema, swelling and inflammation are significant factors in the sensation of muscle soreness then massage may reduce their presence and affect soreness (Tiidus 1997).

    Studies investigating the effect of massage on skeletal blood flow have produced conflicting results. The differences may be accounted for by the different sizes of muscles studied and the type of massage employed. Smaller muscles report increased blood flow although a larger muscle mass may reduce the ability of topical pressures to induce emptying of deeper capillaries (Tiidus and Shoemaker 1995). Tiidus and Shoemaker (1995) found a small but significant tendency for massage to reduce DOMS after 48 hours post exercise and propose that massage induces an analgesic effect on muscle sensory receptors and induces physiological relaxation.

    5) Effects of Light Exercise:
    Light muscle contractions have been found to improve blood flow in muscle even more effectively than manual massage as shown on Dopper ultrasound. If enhanced muscle blood flow improves healing then light muscle contractions should be more effective than massage (Tiidus 1997).

    Performing light exercise with exercise damaged muscles is reported to temporarily reduce soreness (Tiidus 1997). Continuing light exercise immediately following intense activity enhances muscle blood flow and thereby improves oxygen and nutrient delivery. This will aid recovery from muscle fatigue by enhancing the efflux of lactate and hydrogen ions from muscle. Elevation of hydrogen ions is caused by decreased muscle potassium, increased phosphocreatine breakdown and increased muscle carbon dioxide levels. The hydrogen interferes with the ability of muscle contractile proteins to generate force by reducing the total number of cross bridges formed or the force generated per cross bridge. Therefore simple warm-down exercises would enhance short term recovery (Tiidus 1997).
    Tiidus and Shoemaker (1995) report significantly elevated arterial and venous blood velocity above resting levels in the quadriceps muscle following light quadriceps muscle contractions.

    Hasson et al (1989) found a therapeutic regimen of high speed voluntary muscle contractions following eccentric exercise was effective in decreasing muscle soreness and facilitating return of normal muscular performance. Maximal voluntary contraction, peak torque and total work of the quads showed a significant reduction in percent decrease from baseline. Soreness perception index was significantly less at 48 hours post muscle soreness. The regimen consisted of 20 voluntary maximal knee extension and flexion contractions at 300 degrees per second with 3 minutes recovery repeated for 6 sets. This was initiated 24 hours post exercise. The authors suggest that concentric muscle contractions especially at submaximal levels do not produce tissue damage and therefore do not elicit an inflammatory response. Additionally, the "muscle pump action" reduces oedema and intramuscular pressure.

    6) Effects of Ultrasound:
    Hasson et al (1990) found soreness perception following pulsed ultrasound was significantly less at 48 hours post exercise compared to a placebo and control. Muscle performance also significantly improved in the ultrasound group however values remained significantly lower than baseline values. 18 subjects were tested with the ultrasound group receiving 0.8 w/cm2 pulsed ultrasound (1:4 ratio). This treatment intensity has been shown to elicit anti-inflammatory effects and fluid streaming in the tissue. Streaming may alter vascular permeability and lessen the pressure gradient across the myosium. The dose was administered 24 hours post exercise however the authors suggest that immediate delivery of ultrasound to control the initial inflammation and reduce muscle oedema and intracompartmental pressures may improve results.

    7) Iontophoresis:
    Hasson et al (1992) investigated the effects of dexamethasone iontophoresis on DOMS. Iontophoresis consisted of direct current for 20 minutes at varying intensities. DOMS was significantly slowed from 24 to 48 hours compared to the placebo and control groups. There was no significant difference in muscle function indicating that soreness perception and muscle function are not directly related. Iontophoresis has become a method of drug administration for therapists as it permits constant drug delivery over a specific amount of time and provides a highly localised drug concentration and low systemic dose of the drug. The anti-inflammatory action of dexamethasone occurs when the corticosteroid combines to cellular membrane sites and inhibits prostaglandin formation and secretion.

    Summary:
    The exact cause of the pain in DOMS is not known although clinicians acknowledge damage to skeletal muscle via exercise as responsible for the perception of pain. As the condition is self limiting, medical attention is seldom required (MacIntyre et al 1995).
    Clinical examination reveals restricted range of motion, localised muscle tenderness and weakness. There is no pain at rest but discomfort with any movement developing muscle tension (MacIntyre et al 1995).

    Prevention should be emphasised through regular exercise, endurance training and repetition of eccentric activity. The intrinsic process of adaptation with eccentric exercise training reduces muscle damage and soreness. Stauber (1996) suggests emphasis should be placed on exercise producing less damage early in a training regimen. Initially muscles may be used in shortened positions with mild loads, gradually progressing the load and increasing the range of movement until the muscle is active throughout the entire range.

    One of the most effective means of reducing DOMS is via active-resisted exercise of the affected muscle groups. Submaximal exercise enhances short term recovery by increasing blood flow.

    To enhance recovery a variety of treatments may be utilised. Intermittent pneumatic compression has been shown to reduce swelling and stiffness especially on days 2-3 post exercise. Cryotherapy requires further investigation to substantiate its use following EIMI. Research needs to be conducted investigating the effect of ice in isolation and for a longer time frame into the period of peak swelling on day 4. Massage may be effective if performed 2 hours following exercise to increase blood flow and disrupt the inflammatory reaction. Additionally there is an analgesic effect on sensory receptors and physiological relaxation is induced. Ultrasound within 24 hours improves muscle performance and reduces DOMS. The parameters demonstrated to be most effective are 0.8 W/cm2 with a 1:4 ratio on pulsed producing anti-inflammatory effects and fluid streaming. Finally, iontophoresis is a useful adjunct to treatment.

    References:
    Armstrong RB (1990): Initial events in exercise-induced muscular injury. Medicine and Science in Sports and Exercise 22:429-435.
    Byrnes WC, Priscilla FR and Clarkson PM (1986): Delayed onset muscle soreness and training. Clinics in Sports Medicine  5:605-614.

    Chleboun GS, Howell JN, Conaster RR and Giesey JJ (1998): Relationship between muscle swelling and stiffness after eccentric exercise. Medicine and Science in Sports and Exercise  30:529-535.

    Chleboun GS, Howell JN, Heather LB, Ballard TN, Graham JL, Hallman HL, Perkins LE, Schauss JH and Conatser RR (1995): Intermittent pneumatic compression effect on eccentric exercise-induced swelling, stiffness and strength loss. Archives of Physical Medicine and Rehabilitation 76:744-749.

    Clarkson PM and Newham DJ (1995): Associations between muscle soreness, damage, and fatigue. In Gandevia SC, Enoka RM, McComas AJ Stuart DG and Thomas CK (Eds): Fatigue: Neural and muscular mechanisms.New York:Plenum Press pp457-469.

    Friden J and Lieber RL (1992): Structural and mechanical basis of exercise-induced muscle injury.Medicine and Science in Sports and Exercise  24:521-530.

    Friden J, Seger J, Sjostrom M, and Ekblom B (1983): Adaptive response in human skeletal muscle subjected to prolonged eccentric training. International Journal of Sports Medicine 4:177-183.

    Hasson S, Barnes W, Hunter M and Williams J (1989): Therapeutic effect of high speed voluntary muscle contractions on muscle soreness and muscle performance. Journal of Orthopaedic and Sports Physical Therapy 10:499-504.

    Hasson SM, Wible CL, Barnes WS, and Williams JH (1992): Dexamethasone iontophoresis: Effect on delayed muscle soreness and muscle function. Canadian Journal of Sport Sciences 17:8-13

    Hasson S, Munorf R, Barnes W Williams J and Fujii M (1990): Effect of pulsed ultrasound versus placebo on muscle soreness perception and muscular performance. Scandinavian Journal of Rehabilitation Medicine 22:199-205.

    MacIntyre DL, Reid WD and McKenzie DC (1995): Delayed muscle soreness. Sports Medicine 20:24-40.

    Paddon-Jones DJ and Quigley BM (1997): Effect of cryotherapy on muscle soreness and strength following eccentric exercise. International Journal of Sports Medicine 18:588-593.

    Smith LL (1991): Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Medicine and Science in Sports and Exercise  23:542-551.

    Smith LL, Keating MN, Holbert D, Spratt DJ, McCammon MR, Smith SS and Israel RG (1994): The effects of athletic massage on delayed onset muscle soreness, creatine kinase, and neutrophil count:A preliminary report. Journal of Sports Physical Therapy 19:93-99.

    Stauber WT (1996): Delayed-onset muscle soreness and muscle pain. In Zachazewski J, Magee D and Quillen W (Eds): Athletic Injuries and Rehabilitation. Sydney: WB Saunders Company, pp. 92-97.

    Tiidus PM (1997): Manual massage and recovery of muscle function following exercise:A literature review. Journal of Sports Physical Therapy  25:107-112.

    Tiidus PM and Shoemaker JK (1995): Effleurage massage, muscle blood flow and long-term post-exercise strength recovery. International Journal of Sports Medicine 16:478-483.

    Response to Statements of the Speaker for the Negative:
    The principle issues presented for the negative included:
    a) lack of an inflammatory response to EIMD reflected the inappropriateness of physiotherapy intervention, and
    b) the injury is irreversible and therefore prevention is the only intervention indicated.
    The role of inflammation in EIMD has been an area of conflict however it is now generally accepted that it plays a part in the overall sequence of events. The cardinal signs of inflammation such as swelling, warmth and pain are present even in the absence of bleeding. Therefore, the physiotherapeutic modalities/techniques described above aimed at reducing the effects of the inflammatory response can reduce the pain perception and enhance muscle performance.

    It is true that the tissue disruption following EIMD cannot be reversed however the production of prostaglandins can be affected. If production is decreased prior to a large fluid accumulation by retarding the inflammatory response and reducing fluid compartmental pressure, DOMS should be reduced.

    Physiotherapy does have a role in ameliorating the DOMS response to EIMD. The physiotherapists role ranges from preventative to alleviation of symptoms. Knowledge of exercise prescription and time course of injury allows physiotherapists to effectively educate, treat and prescribe appropriate exercises specific to clients needs.

  2. #2
    Elite Lulu66's Avatar
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    Re: Delayed Onset Muscle Soreness

    Bump for a great read.
    US Goverment Policy: If It Ain't Broken, Fix It Till It Is.

  3. #3
    Senior Moderator NbleSavage's Avatar
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    Re: Delayed Onset Muscle Soreness

    Nice post, Stacked!

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    Elite 63Vette's Avatar
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    Re: Delayed Onset Muscle Soreness

    There is one thing I must disagree with in this article....

    "DOMS only occurs following the first or second bouts of a new exercise program."

    I have DOMS two days after leg day damn near every time. It has been that way for years. In fact, I now pin my quads on leg day before I work out and it seems to actually keep the DOMS to a more tolerable level.

    Great find, and I very much appreciate the post!

    Respect,
    Vette

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