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Delayed Onset Muscle Soreness (DOMS) is a common phenomenon experienced by individuals who perform unaccustomed exercise that typicdly involves an eccentriccomponent. The soreness will begin to occur at approximately 8 - 24 hours post-exercise and will peak at approximately 48 hours post exercise. The soreness is most often experienced upon movement (Le. muscle action) or upon palpation of the muscle. At rest there is usually no perception of soreness (Smith 1992). Perception of soreness is generally reduced at 72 hours with residud soreness remaining beyond that time frame.The symptoms usually appear a couple of hours to a day, peak between 1 and 3 days, and may subside within 5 to 7 days, after the exercise( Clarkson & Hubal,2002).This constellation of symptoms is often called " Delayed Onset Muscle Soreness(DOMS)". DOMS may be experienced by athletes who have not trained for a period of 6-8 weeks, by which time the protective adaptation of a training effect within the muscle has been lost, or who modify their training regime to incorporate new and therefore unaccustomed components to exercise (Ronnelly, Clarkson et al. 1992). Individuais who are beginning a training schedule are aiso at ris k for developing DOMS. Doms is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity.DOMS is also common when athletes are first introduced to certain types of intensive activities regardless the time and season of the year.DOMS may be expenenced after performing either aerobic or anaerobic exercise, but generally requires an eccentric component.
Soreness develops 24 to 48 hours after exercise "is usually approximately 24 hours after the exercise bout and may linger for an additional 24 to 48 hoursand peaks at 48-72 hours after exercise. It is suggested that a sequence of events starting with exercise causes muscle damage and than muscle protien break down, resulting in cell inflammation and increased local muscle temperature. As a result, pain receptors are activated, causing the sensation of Delayed onset muscle soreness (DOMS). Exercise-induced muscle damage (EIMD) has been hypothesized to be initiated by disruption of the force generating and / or transmitting structures and loss of sarcolemma integrity followed by a calcium overload phase resulting in an influx of extra cellular calcium ( Caa2+) that activates several intrinsic degradative pathways. The specific event that serves to initiate exercise induced muscle fibre injury is not known.It is generally recognized that this type of injury is associated with eccentric contractions. However, there are 2 possible initial events as responsible for the subsequent damage: Damage to the Excitation- contraction coupling system and disruption at the level of sarcomeres.Other changes seen after eccentric exercise include a fall in active tension, shift in optimum length for active tension and rise in passive tension were found, on a abalance, to favour sarcomere disruption as the starting point for the damage.
In the initial event, sarcomeres in myofibrils are disrupted and damage to the excitation-contraction (E-C) coupling system takes place.In a review, warren et al( 2001), summarised their position by declaring that 75% or more of the decline in tension after eccentric exercise was attributable to a failure of the E-C coupling process.The remaining damage seen during the first few days after the exercise was attributed by the authors to physical disruption of the tension-bearing elements within the muscle.
Negative implications of DOMS include minimal to severe soreness, The inability to continue safe and effective training or performance, biomechanical alterations predisposing individuals to injury, decrease in strength and power, interruption of activities of daily living ( ADL'S) and a decreased motivation and willingness to continue training due to negative experiences of the soreness( Weber servedio et al.1994).
In 1902, Hough published the first report on muscle soreness. He found out that soreness experienced in the finger flexor muscles, 8-10 hours after performing rhythmical exercise, was most likely due to "some sort of rupture within the muscle". In the early 1980's with the advent of more sophisticated techniques, morphological alterations were observed and were interpreted to indicate Myofibrillar disruption( Friden et al.,1981; Friden et al., 1983; Newham et al.,1983;).These findings stimulated a renewal interest in DOMS and during the past two decades, a considerable amount of information has been obtained on this topic and the prevailing hypothesis is that the myofibril structure becomes ruptured.However the mechanism underlying DOMS still remains unclear( Warrenetal.,1999; Clarkson & Hubal., 2002;Lieber & Friden.,2002;), but how ever from the previous reviews it was found that mainly the eccentric contractions leading to the symptoms of DOMS. Experiments have shown that for the same work load eccentric exercises uses fewer fibers and requires less energy.Hence a greater amount of force per unit muscle fibre is applied thus increasing the likelihood of muscle fiber damage.Also during eccentric exercise the body recruits more type II fibers which are more prone to muscle fiber damage due to their wider Z lines.In addition during eccentric action the muscle lengthens under tension thus stretching the connective tissue components associated with tendons/muscle fibers, causing their damage and thus eccentric exercises causes more pain.
PROPOSED TIMELINE OF DOMS
The initial mechanical damage ( the autogenic phase) is characterized by loss of membrane integrity( Clarkson, 1997;Pyne,1994).The autogenic phase begins with the mechanical damage and can last up to several hours post exercise( Ji, 1999). Membrane integrity is commonly measured by the efflux of cytosolic enzymes, primarily CK in to the blood stream( Clarkson, 1997;Clarkson & Hubal,2002; Pyne,1994). So both creatine kinase ( CK) and lactate dehydrogenase ( LDH) elevates from 6 to 48 hours and peaks up to 96 hours and in some conditions, remains elevated for more than seven days.
One of the most valid and reliable methods for assessing muscular damage is to check for increases in blood serum levels of creatine kinase (CK), the primary enzyme regulating anaerobic metabolism, because a high percentage of the body's CK is present in skeletal muscle tissue. Assessing CK levels has been commonplace for more than 3 decades in studies investigating muscular damage.Creatine kinase is located in the sarcolemma and mitochondrial intermembrane space of healthy muscle cells and is responsible for catalyzing the movement of phosphate from phosphocreatine to adenosine diphosphate, forming adenosine triphosphate (ATP) and creatine. Creatine kinase is present in the body as 3 isozymes: the skeletal muscle, cardiac muscle, and brain tissue types. In some clinical situations, it may be relevant to check for one of the 3 types of isozymes. If cardiac pathology is suspected, increases in the cardiac muscle type can be expected. In cases of head injury, increases in the brain tissue type can be expected. However, strenuous exercise that damages skeletal muscle cell structure results in an increase in total CK, with a mixture of all 3 isozymes.Therefore, when analyzing CK, one may mistakenly conclude that physical exercise caused damage to heart or brain tissue. However, most research shows the increase in the cardiac and brain CK isozymes to be a negligible amount of the total exercise-induced increase in CK. Also, most studies indicate that the CK elevation is from skeletal muscle, not cardiac muscle. Nosaka and Clarkson pointed out that the exact mechanism by which CK enters the general blood circulation is unknown; however, it is thought that when acute damage occurs to the muscle cell structure, CK leaks into the interstitial fluid and is picked up by the lymphatic system. The CK then travels through the lymphatic system and is eventually emptied back into the general blood circulation, which results in an increase in serum levels of CK. Thus, increases in blood levels of CK are one indicator of muscular trauma.Strenuous exercise that damages skeletal muscle cell structure at the level of sarcolemma and z disks92 results in an increase in total CK93,94
DOMS may leave individuals in a condition of mild to moderate soreness depending on the intensity of their activityand their level of fitness. This may discourage the general population from continuing to participate in such activities.DOMS may also decrease the effectiveness of performance for those individuals who participate at high levels of competition. Regardless of the population, it is necessary to determine whether or not there is a method that may be able to reduce DOMS. Although DOMS has been demonstrated by researchers to cause negative impacts on performance, (Davies & White.,1981; Smith.,1992;Saxton & Clarkson etal.,1995;Machytyre & Reid etal., 1996; Paddon-Jones & Quigly.,1997;).To date there has been inconclusive research in the area of effective treatment interventions or DOMS prevention.In order to minimize negative experiences associated with DOMS and potential detrimental effects on performance, it is necessary to identify a successful treatment intervention.If an efficacious treatment can be developed and there will be minimal risk of causing further injury or pain,than the negative efects of DOMS may be substantially reduced.
In India, Recently increasing numbers are participating in athletic activities and are taking a more active approach to achieve in health and wellness. This increase in activity exposes individuals to DOMS and the associated negative effects. More commonly most of the individuals and athletes experience the muscle soreness after unaccustomed exercises and due to lack of training, this highly demands some intervention, but researches that can be detrimental to the field are outlined in India. Also, the exact role of a physiotherapist in alleviating the DOMS and therapeutic interventions were not found to be successful in our country.