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Is there a role for physiotherapy in ameliorating the DOMS response to exercise induced muscle injury?

Topic for Summary and Critique - by Greg Wootton

Statement of the Topic
Introduction
Mechanical Injury
Metabolic Damage
Clinical Features
Treatment of DOMS
Clinical Implications
Conclusion
References
Short Answer Review Questions

Statement of the Topic

Introduction

Before it can be determined if there is a role for physiotherapy in the relief of delayed onset muscle soreness (DOMS) an appreciation of the mechanical and metabolic processes that produce the clinical signs of DOMS must be developed. There is variance in the literature with respect to the exact mechanism of the exercise induced muscle injury (EIMI) that leads to the symptoms of DOMS.

Mechanical Injury

It is agreed (Kuipers 1994, Clarkson and Newham 1995) that eccentric muscle work produces greater muscle damage than isometric and concentric exercise. Strenuous unaccustomed exercise damages the cellular structure of the muscle causing disruption of the extra-cellular matrix and impairing muscle function. Kuipers (1994) suggests eccentric exercise in particular causes structural damage as, for a given tensile load, there are fewer motor units recruited within the muscle, increasing the tensile load per motor unit. This tension on the cross bridges of the muscle fibre causes mechanical disruption of the myofibrils leading to Z band irregularities (or streaming) and subsequent Z band material distribution through the sarcomere. This disruption of the sarcomere and loss of membrane integrity leads to an increase of cytoskeletal and myofibrillar proteins that may be demonstrated histologically (MacIntyre et al 1995). Mair et al (1995) demonstrated a transient rise in the serum concentrations of muscle proteins such as creatine kinase (CK), myogloblin and myosin heavy chain fragments (MHC), indicators of muscle damage, that peaked around day two ro three post exercise, and were still significantly elevated four days post exercise.

Warren et al (1993) found that the degree of muscle damage was closely related to the peak force developed by the eccentric muscle action. Other researchers however suggest the degree of damage is more related to the change of length or magnitude of strain within the muscle with more damage at longer muscle lengths. A relationship between the velocity of lengthening and muscle damage with higher lengthening speeds increasing damage has also been documented (Lieber et al 1993).

Metabolic Damage

Metabolic stress or disturbances in cellular metabolism are likely to occur post unaccustomed or exhaustive exercise. Many causes have been suggested for this ongoing tissue degradation post activity including insufficient ATP generation, ischaemia, hypoxia, alterations of ion concentrations, and accumulation of waste products (Pyne 1994).

Inflammation

Histological analysis of muscle post EIMI demonstrates an inflammatory response within the muscle. This inflammatory response alters the fluid and cellular balance within the muscle. The injury site is invaded with neutrophils initially, then leukocytes and macrophages later. Lowe et al (1995) showed an increase in protein degradation 48 hours post exercise and correlated this with the increase in macrophages at the injury site. The presence of macrophages gives rise to cytokines that may further perpetuate the damage by potentiating cytotoxic mechanisms to enhance free radical production and release proteolytic enzymes.

With the alterations of osmotic pressures and fluid balance due to the inflammatory response there is an increase in fluid volume of the muscle or muscle swelling (Clarkson et al 1992). Initially the swelling is intra-muscular (24-48 hours) and then becomes subcutaneous later (after 72 hours), increasing over the first two days and then plateauing from day 3 to day 5, before diminishing after day 7 (Chleboun et al 1998). The relevance of this in consideration of the symptoms of DOMS is unclear as treatment aimed at decreasing the effects of swelling have been reported to have little or no beneficial effects.

The release of inflammatory mediators such as bradykinin, serotonin and histamine throughout this inflammatory response may account for a portion of the pain of DOMS through the sensitization of the pain afferents.

Calcium Homeostasis

Damage to the sarcoplasmic reticulum or muscle membrane can increase the intracellular calcium and trigger calcium degradative pathways. Animal studies post EIMI have shown increased intramuscular calcium (Warren 1995). Armstrong et al (1991) suggested that this increase in calcium reduced the ability of the muscle to relax, accumulated in the mitochondria of the cell inhibiting ATP generation, and activated proteolytic enzymes that perpetuate tissue degradation. Calcium accumulation in the mitochondria and subsequent lower ATP generation may alter the ability of the membrane pumps to maintain the ion homeostasis of the muscle causing cellular swelling. The ATP generation may also in part be responsible for depletion of muscle glycogen levels which can remain diminished for up to 10 days post eccentric exercise, indicating metabolic exhaustion and continued tissue degradation (Asp et al 1995).

The increase in calcium is also suggested to have a role in the disruption of the cytoskeleton and Z bands by cleaving the cytoskeletal proteins that attach the actin to the Z disc, weakening the bonds and making the Z band vulnerable to further damage (Lieber et al 1996).

Oxidative Damage

Another rationale presented for ongoing cell injury in the days following initial injury is the generation of reactive oxygen species (ROS). Free radicals are normally produced as a consequence of cell metabolism but due to the increased oxygen utilisation of exercise the bodies normal scavenging defence systems may be overwhelmed. Eccentric exercise increases the demand for oxygen and may lead to the formation of free radicals via electron leak from the mitochondria, reperfusion of ischaemic tissue, activation of the NADPH oxidase system and xanthine oxidase system activation resulting in oxidative damage to cellular components (Pyne 1995).

Clinical Features

DOMS is characterised by a delayed onset of muscle soreness after unaccustomed muscle activity. Unaccustomed activity includes the sedentary individual commencing physical activity, athletes returning to training after a break, or a change in training involving a change in routine or increased workload. Typically the pain develops and peaks between 24 and 72 hours post exercise.

The muscle displays an increase in resistance to passive movement (stiffness) immediately post exercise for up to four days (Howell et al 1993, Chleboun et al 1998) and reduced range of movement. Chleboun et al (1998) also demonstrated an increase in muscle volume (swelling) post exercise peaking at around day four.

Immediately post exercise there is a loss of muscle strength of up to 60% with a prolonged inability of the muscle to generate force for more than 10 days (Clarkson et al 1992).

The difficulties in explaining the alterations in muscle function are demonstrated in that the loss of muscle strength is immediate post exercise where the demonstrated effects of swelling and pain are delayed.

Several rationales for the loss of muscle strength have been proposed by researchers. Alterations in the transport of glycogen and the significant reduction in muscle glycogen stores for up to 10 days post exercise is suggested by Asp et al (1995) to decrease ATP levels and lead to muscle fatigue and degradation. Brown et al (1996) found a delay in the time from stimulation to contraction in an electronically stimulated muscle three days post eccentric exercise. Long lasting low frequency fatigue with a decreased ability of the muscle to generate muscle force could explain decreased muscle strength. A more basic explanation could be that the damage and loss of collagen cross bridges reduces the ability of the muscle to generate tensile force (Saxton and Donnelly 1996).

Pain inhibition as a possible cause of reduced muscle strength has been questioned as strength loss is immediate post exercise and pain is only perceived after several hours.

Treatment of DOMS

Many treatment modalities have been used in attempting to allieviate the symptoms of DOMS, predominantly with minimal beneficial effects. Modalities described include cryotherapy, ultrasound, massage, TENS, oral analgesics, compression, exercise and non-steroidal anti-inflammatory drugs. There is some controversy in the literature in regard to the benefits of these various modalities and the preferred treatment regime.

Pneumatic compression has been demonstrated to be somewhat beneficial in the reduction of muscle swelling and stiffness following EIMI. Although this compression temporarily decreased muscle circumference measures it had no effect on the muscle strength or pain perceived (Chleboun et al 1995).

A significant reduction of the pain perceived during DOMS was reported after the use of naproxen-sodium DS- an analgesic and anti-inflammatory drug (MacIntyre et al 1995). These benefits were supported by Dudley et al (1997) who found naproxen-sodium significantly reduced the muscle soreness and increased muscle strength following EIMI. Naproxen-sodium acts to inhibit the production and release of prostaglandin E- an inflammatory mediator. Prostaglandin E perpetuates protein degradation, sensitises the local free nerve endings, and increases exudate and oedema of the inflammatory response. Thus inhibition of prostaglandin E by naproxen-sodium may limit inflammation and reduce the pain perceived following exercise. Dudley et al (1997) suggested the return of muscle strength was more likely due to the analgesic effects of the medication.

Hasson et al (1989) examined the effects of active resisted exercise of the affected muscle groups 24 hours following EIMI and found a decrease in symptoms. Tiidus (1997) supported the findings of a reduction in DOMS after light exercise of the affected muscles. Tiidus (1997) hypothesised that the alteration of muscle blood flow during exercise enhances nutrient and oxygen supply and aids in removal of waste and byproducts such as lactate and hydrogen ions. The muscle contraction may also act as a muscle pump to alter fluid flow.

The use of massage has been observed with varying results. Athletic massage two hours following EIMI reduced the perception of DOMS and CK levels (Smith et al 1991). Tiidus and Shoemaker (1995) reported subjective changes after massage treatment of DOMS but found no conclusive objective evidence to justify its use in the allieviation of symptoms.

Cryotherapy is used therapeutically to reduce secondary cell hypoxia during the inflammatory process following insult or injury (Knight 1995). Theoretically it would thus be beneficial in the reduction of cell damage of EIMI but the various studies have shown no positive effects.

Clinical Implications

With an appreciation of the limited success of treating DOMS the most beneficial management is to exercise in such a manner as to prevent the muscle damage from occurring. Kuipers (1988) reported that one bout of eccentric exercise protects against the soreness and enzyme release of a second bout of eccentric exercise. Mair et al (1995) supported this and demonstrated that after a second session of eccentric exercise, four days after the initial session, there was significantly less strength loss, less soreness reported and no increase in CK and MHC levels. After a third session at day 13 subjects reported no soreness, no strength loss and increase in CK and MHC levels.

Kuipers (1988) proposed that this training adaptation is due to alterations of the central neural motor recruitment pattern within the affected muscle and an increase in the collagen/CT content of the fibres. Alternative theories have suggested that the reduction in soreness and loss of function with bouts of eccentric exercise after the initial bout is a result of the healing and repair process increasing the tensile strength of the previously weak, and subsequently damaged muscle fibres (Armstrong et al 1991).

Stauber (1989) recommends that the commencement of a training program with the specific muscle to be exercised in a shortened position under mild loads is the best method of reduction of DOMS. As training progresses the muscle adapts to the eccentric loading conditions and ROM and muscle length is increased, along with the load placed on the muscle, until the muscle is working eccentrically through full ROM. This program in itself, regular eccentric exercise against resistance, is the single best preventative measure in the management of DOMS.

Conclusion

DOMS is a result of strenuous unaccustomed eccentric muscle work. This eccentric tensioning of the muscle causes mechanical disruption of the myofibril and releases cytoskeletal and myofibrilla proteins. There is still some debate as to whether the magnitude of strain or peak force developed in the muscle action is the determinant of the degree of muscle damage. Following this primary mechanical injury damage there is continued secondary metabolic damage. The clinical features of muscle soreness, increased stiffness, and loss of muscle strength are self limiting and recovery is achieved over several days. Currently there are no proven treatment modalities effective in the reduction of DOMS. The best treatment is prevention or minimisation with a suitably designed training program.

References

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Chleboun G, Howell J, Conatser R, and Giesey J (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 P, Nosaka K, and Braun B (1992): Muscle function after exercise induced muscle damage and rapid adaptation. Medicine and Science in Sports and Exercise 24:512-520.
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Knight K (1995): Cryotherapy in Sports Injury Management. Champaign, Human Kinetics.
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Stauber W (1989): Eccentric action of muscles: physiology, injury, and adaptation. Exercise and Sports Science Reviews 17:157-185.
Warren G, Hayes D, Lowe D and Armstrong R (1993): Mechanical factors in the initiation of eccentric contraction-induced injury in the rat soleus muscle. Journal of Physiology 464:457-475.