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Journal of Sports Sciences Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/rjsp20

Delayed onset muscle soreness: Mechanisms and management a

M.J. Cleak & R.G. Eston

b c

a

Wolverhampton School of Physiotherapy , Education Centre , New Cross Hospital, Wolverhampton, WV10 OQP, UK b

Department of Movement Science and Physical Education , University of Liverpool , Liverpool, L69 3BX, UK c

Physical Education Unit , Chinese University of Hong Kong , Shatin, New Territories, Hong Kong Published online: 14 Nov 2007.

To cite this article: M.J. Cleak & R.G. Eston (1992) Delayed onset muscle soreness: Mechanisms and management, Journal of Sports Sciences, 10:4, 325-341, DOI: 10.1080/02640419208729932 To link to this article: http://dx.doi.org/10.1080/02640419208729932

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Journal of Sports Sciences, 1992, 10, 325-341

Delayed onset muscle soreness: Mechanisms and management

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M.J. CLEAK 1 and R.G. ESTON 2 1 Wolverhampton School of Physiotherapy, Education Centre, New Cross Hospital, Wolverhampton WV10 OQP, UK and 2Department of Movement Science and Physical Education, University of Liverpool, Liverpool L69 3BX, UK and Physical Education Unit, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong

Accepted 14 June 1991

Abstract This review describes the phenomenon of delayed onset muscle soreness (DOMS), concentrating upon the types of muscle contraction most likely to produce DOMS and the theories underlying the physiological mechanisms of DOMS. Ways of attempting to reduce the effects of DOMS are also summarized, including the application of physical and pharmacological therapies to reduce the effects of DOMS and training for reduction or prevention of DOMS. Keywords: Creatine kinase, connective tissue, eccentric exercise, spasm, training. Introduction

Soreness occurs as a result of extreme physical activity and may be immediate or delayed. The immediate discomfort may be due to the biochemical end-products of metabolism affecting free nerve endings (Asmussen, 1956; Friden, 1984a) or temporary hypoxia due to muscle ischaemia (Francis, 1983). This pain is short-lived and disappears when the activity stops. In contrast, delayed onset muscle soreness (DOMS) is the sensation of discomfort and stiffness in the muscles, often after taking part in unaccustomed physical activity, that normally increases in intensity in the first 24 h after exercise, peaks from 24 to 72 h, then subsides so that by 5-7 days post-exercise it is gone (Talag, 1973; Armstrong, 1984; Byrnes and Clarkson, 1986; Jones et al., 1986; Newham, 1988).

Type of exercise associated with DOMS Eccentric contractions are characterized by elongation of the muscle at the same time as the contraction. Delayed onset muscle soreness is associated with the performance of unfamiliar and high force muscle work, particularly eccentric contractions (Schwane et al., 1983b; Byrnes et al., 1985a; Newham et al., 1986; Newham, 1988), although it can also be produced to a lesser extent by isometric work (Clarkson et al, 1986a, 1987; Triffletti et al, 1988). Even concentric work has been found to produce soreness when high forces are involved (Asmussen, 1956; Abraham, 1977), although the exercise protocol in these studies combined both concentric and eccentric muscle contraction. Clarkson et al. (1986b) compared 0264-0414/92 © 1992 E. & F.N. Spon

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isometric, eccentric and concentric work, and found that eccentric work resulted in a greater degree of DOMS than isometric work. There was no significant increase in soreness with concentric work, despite the fact that the intensity of the eccentric work done was less than the concentric work. Talag (1973) found soreness after all three types of exercise, with peak soreness at 24 h for isometric and at 48 h for concentric and eccentric work, although only the eccentric data reached a statistically significant level.

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Force and velocity characteristics of eccentric muscle work

Exercise employing eccentric or concentric actions induces distinct physiological responses. In order to produce the same tensions, the muscles utilize a much smaller volume of oxygen in eccentric work and the accompanying circulatory and respiratory responses are correspondingly smaller (Knuttgen et al., 1971; Davies and Barnes, 1972). Furthermore, there is no evidence of a training effect on these physiological parameters as is the case with concentric work. At comparable velocities, eccentric contractions result in far greater external force development at a lower metabolic cost than similar concentric contractions (Rodgers and Berger, 1974; Knuttgen, 1986; Newham, 1988), and the highest force that can be developed is in a fast eccentric contraction (Ästrand and Rodahl, 1986). Also, at equivalent submaximal force developments, far fewer motor units need to be recruited for eccentric as compared to concentric contractions (Friden, 1984a; Knuttgen, 1986), although EMG studies show that there is the same degree of motor unit recruitment in maximal eccentric and concentric efforts (Rodgers and Berger, 1974; Ästrand and Rodahl, 1986). Stauber (1989) reported that, during eccentric contraction, the cross-bridges which form after the binding of myosin and actin has taken place must be forcibly separated. This requires more force than for normal concentric cross-bridge cycling and thus greater tension is developed per active motor unit during submaximal and maximal eccentric contraction. DOMS and its relationship to exercise intensity, duration and velocity As a general rule, the soreness produced is closely related to the magnitude of torque produced during eccentric exercise. Because higher torques are normally generated by maximal or high-intensity, high-velocity eccentric activity, these are the situations in which maximal soreness and damage seem to occur. The duration of the exercise is also a factor. Tiidus and Ianuzzo (1983) attempted to quantify the effects of intensity and duration of exercise in DOMS and muscle damage using serum enzyme markers. They defined the intensity of exercise as the percentage of 10 repetition maximum (10RM) of the dead-weight resistance lifted, and defined duration of exercise as the number of contractions performed. They found that DOMS and enzyme levels were significantly elevated by increased intensity and increased duration of exercise, with intensity having the more pronounced effect. Peak soreness occurred at 24-48 h post-exercise, with serum enzymes peaking at 8-24 h postexercise. In Tiidus and Ianuzzo's study, the exercise was a mixture of concentric and eccentric quadriceps exercise. Previous work has shown that there is a significant training effect, which can reduce DOMS and markers of muscle damage, and which can last for several weeks following an initial bout of exercise (Jones and Newham, 1985b; Byrnes and Clarkson, 1986; Clarkson and Tremblay, 1988). McCully and Faulkner (1986) also found that injury to muscle fibres (measured by histological appearance) was directly related to the duration of exercise and the force developed, during electrically stimulated eccentric work in mice. Extending the duration of contraction beyond 5 min did not result in additional injury. Peak

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force development decreased to 50% of the initial value during the first 5 min of exercise, suggesting that loss of peak force due to fatigue may prevent further injury to the muscle fibres. These investigators also observed an increased incidence of muscle damage with increases in velocity of contractions. However, caution is required in applying the results of animal studies to humans. Clarkson et al. (1987) used a contraction speed of 9 degrees per second (0.16 rad s~1) in a study of eccentric hamstring work. Although soreness peaked 48 h later, no subject rated soreness at higher than 4 on a scale of 1-10. In a later study, Vrabel and Clarkson (1989) observed that when peak torques generated during exercise were similar, the contraction speed (2.09 and 1.05 rad s ~*) did not influence muscle damage. This was assessed using the following criteria: DOMS, serum enzymes, isometric strength and range of motion. A length-dependent component has also been found to be a factor in the development of pain and fatigue after eccentric exercise. Newham et al. (1987) demonstrated that, for maximum effect, the eccentric contractions needed to be performed over a joint range that involved near maximal lengthening of the active muscle. Tenderness was greatest when the subjects' arms were exercised with the shoulder fully extended. Exercise protocols which produce DOMS The intensity, velocity and duration of eccentric contraction needed to produce significant DOMS and other markers of post-exercise muscle damage vary from study to study. Some use a dead-weight resistance method, whereby the subject lowers a weight tray, using, for example, eccentric hamstrings work or eccentric biceps curls (Clarkson et al., 1986b, 1987; Clarkson and Tremblay, 1988), where the initial contraction is set at one repetition maximum (1RM) for concentric activity. It may be argued, therefore, that subsequent eccentric contractions are not maximal. Furthermore, as weights have to be removed from the tray as the subject fatigues and graduations are not infinite, considerable inter-subject variability must be introduced in terms of intensity of contractions. This problem can be overcome if maximal contractions can be performed throughout by each subject, e.g. by using an isokinetic exercise machine (Friden et al., 1983a), or a system for dynamic isotonic exercise such as that designed by Jones and Newham (1985a). Other designs use stepping down offa bench to produce eccentric muscle activity (Asmussen, 1956; Newham and Jones, 1985; Buroker and Schwane, 1987), sometimes including a percentage of body mass to increase exercise intensity (Bacharach et al, 1987), or downhill running (Byrnes et al., 1985b; Dick and Cavanagh, 1987) or lowering of body mass by going down from tiptoe (Bobbert et al., 1986). Downhill running is usually performed for 45 min (Schwane et al., 1987; Donnelly et al., 1988a), although the incline of the slope is not always defined. Box and bench-stepping designs show greater variability (Asmussen, 1956; Davies and White, 1981; Newham et al., 1983a; Bacharach et al., 1987; Hasson et al., 1989b) in terms of rate of stepping and duration. Designs involving eccentric work of a more circumscribed and less 'functional' nature also show considerable variations in design detail. Komi and Viitasalo (1977) described their subjects as performing 40 maximum eccentric contractions of the quadriceps. Friden et al. (1986) elicited DOMS by using a dead-weight pulley system for eccentric work of the ankle dorsi-flexors. Their subjects performed 400 contractions at 15% of maximum voluntary contraction (MVC). Many workers in the field have investigated DOMS using the forearm flexor muscles. As with lower limb studies, the opposite limb can be used as a control if required, but an advantage in using the upper limb is that it is not needed for subject mobility during the measurement period, where inter-subject variability in walking or running

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activity could introduce undesirable variation. Clarkson et al. (1986b) and Clarkson and Tremblay (1988) used a weight tray for biceps curls, with their subjects undergoing 60 and 70 MVECs respectively, weight lowered being based on 1RM concentric ability. Howell et al. (1985) used a similar protocol but required their subjects to do 'as many contractions as possible', which varied from 20 to 65 in total. Abraham (1977) also used dumbell curls for biceps to produce DOMS, but both concentric and eccentric work was performed on the experimental arm with the subjects completing as many repititions as possible. Talag (1973) chose 30% MVC from 45° elbow flexion to straight, until the subjects fatigued. The exercise protocol described by Jones et al. (1987) attempted to overcome the problems inherent in dead-weight resistance methods by using a set-up in which each contraction was a maximal one. The damaging exercise consisted of 1 MVEC every 15 s for a total of 20 min (80 MVECs) with rest periods at 5- or 10-min intervals. The velocity of contraction was not specified. It can be seen that the numerous variations in exercise protocol and the lack of detail given in many studies relating to intensity, number of repetitions, range through which the limb is moved, rest periods and velocity of eccentric contraction, make comparisons between studies and their replication very difficult. Also, many of the DOMS studies have used 10 or less subjects, mostly of college age, which precludes extrapolation to a wider population. Theories of delayed muscle soreness Introduction: The pain stimulus The pain associated with DOMS has been studied by various groups of investigators since 1902, and a number of hypotheses to explain the condition have resulted. Pain is thought to be related to stimulation of the small diameter group III myelinated and group IV unmyelinated nerve endings which subserve specific and also polymodal receptors found in muscle tissue, especially in the musculotendinous junctions and fascial sheaths (Kumazawa and Mizumura, 1977; Casey, 1982). Various noxious stimuli, including chemical, thermal and mechanical agents, may produce pain. The particular agents involved in DOMS have not been specifically identified (Armstrong, 1984), although many potential culprits have been suggested. Chemical agents include the protein enzyme products of muscle breakdown such as creatine kinase (Newham et al., 1983a, 1986), and metabolic waste-products such as lactic acid (Asmussen, 1956). Elevated temperature changes in muscle following eccentric exercise have been measured by Davies and Barnes (1972), but such changes do not follow the pain time-course. Elevated pressure and mechanical distortion of the tissue which accompanies oedema could also activate nocioceptors in the muscle and elicit the sensation of DOMS (Brendstrup, 1962; Friden et al, 1986; Hagerman et al., 1984). Whether the initiating stimulus is chemical, thermal or mechanical is not certain, but the various theories of causation of DOMS implicate one or a combination of these agents. Lactic acid theory Lactic acid accumulation in the muscles is commonly thought to be the cause of delayed soreness by the lay public. The assumption was examined by Asmussen (1956). His results showed that it was unlikely that excessive production of metabolic substances was the cause of DOMS, as the higher degree of metabolism occurring in concentric or positive work did not cause delayed soreness, only acute muscle pain and fatigue. Later research has confirmed his ideas. Eccentric contractions require lower energy expenditure (Dick and Cavanagh,

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1987) and lower oxygen consumption, and they produce less lactate than exercise with concentric contractions at the same power output (Davies and White, 1981; Schwane et al., 1983a). Davies and Barnes (1972) found only a negligible increase in lactate following downhill running. In a later study, Schwane et al. (1983b) directly tested the lactic acid theory by comparing lactic acid production and VO2 in subjects running at the same speed for 45 min, on a treadmill that was level or inclined downhill. They found that downhill running required significantly lower VO2 and produced less lactic acid than level running, but resulted in greater DOMS. Although lactic acid may cause the acute pain associated with fatigue after intense exercise, there is no evidence available to explain satisfactorily how lactic acid produced during exercise can cause the delayed pain which appears 24-48 h later. Spasm theory This theory, originally described by de Vries (1961a), proposed that exercise could cause ischaemia in the active muscle, which in turn would result in the production of a pain substance. If too much of this substance accumulated, pain endings would be stimulated. The resulting pain would, in turn, produce more reflex spasms that would prolong the ischaemia and initiate a 'vicious cycle' (de Vries, 1966). These suggestions were made following experiments in which de Vries observed that subjects with DOMS had higher electrical activity of the muscle as recorded by surface electromyography (de Vries, 1961a, 1966). Other workers have found increased EMG activity in muscles following eccentric exercise, but the magnitude of activity was not related to the perception of soreness (McGlynn et al., 1979). McGlynn and co-workers used a bipolar surface electrode technique, which de Vries (1966) maintained was not sensitive enough to record the electrical activity in sore muscles, and that surface unipolar electrodes should be used. This may explain why Abraham (1977), Torgan (1985) and Talag (1973) did not make these same observations, although they all argue that bipolar electrodes utilize differential amplification to limit outside interference and thus signal contamination. Abraham (1977) also stated that the comparison of bipolar and unipolar techniques under similar conditions showed the bipolar system to be three times more sensitive to change. Newham et al. (1983c) used unipolar electrodes and did not observe increased EMG in sore muscles. Also, de Vries' results may not relate to the classical exercise-induced DOMS, because his subjects had a wide variety of 'accidentally-induced muscle pain' rather than experimentally induced DOMS. Connective tissue damage theory The connective tissues of skeletal muscles form sheaths around various bundles of muscles and include the endomysium, perimysium and epimysium. The endomysium is perhaps the most important in relation to this theory of damage, since it forms a sheath around each myofibril and may interconnect adjacent myoflbrils (Stauber, 1989). Hough (1902) found that DOMS was closely associated with mechanical tensions in the muscles. He suggested that some sort of rupture within the muscle itself was the cause of the phenomenon, and pointed especially to the connective tissue as the site for these ruptures. Asmussen (1956), and later Komi and Buskirk (1972) and Abraham (1977), postulated that DOMS was due to overstretching of the muscle's elastic components including the tendons, and the connective tissue. Asmussen (1956) found that the tension per active unit was higher in negative than in positive work, leading to a higher chance of mechanical strain with this type of exercise. He found that soreness and pain, assessed by interview and palpation by a

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physiotherapist, were increased far more after negative work, and were most localized to the tendinous attachments. He reasoned that muscle fibres are highly elastic, whereas connective tissue is rather stiff, pointing to the latter as the site of injury. He suggested that the soreness was due to the mechanical stimulus of swelling caused by the damage to the connective tissue. Unfortunately, the precise method of pain and soreness assessment by the physiotherapist was not described, and no evaluation was peformed to indicate whether the changes were statistically significant. Soreness was also found to be localized to the musculotendinous junctions by Komi and Buskirk (1972), although their appraisal was subjective and indirect. More recently, Newham et al. (1983c) and Edwards et al. (1981) found that the soreness after eccentric exercise occurred in the area of the musculotendinous attachment, and they too concluded that delayed soreness was most likely due to mechanical damage, predominantly to the connective tissue. Abraham (1977) reported a significant positive correlation between urinary excretion of hydroxyproline (OHP) and subjective reports of muscle soreness following eccentric work. Hydroxyproline was selected as a marker since it is a breakdown product of connective tissue and is an indicator of collagen metabolism. In this study, OHP excretion was maximal at 48 h post-exercise in those subjects who reported the greatest soreness. Abraham theorized that as collagen is known to decrease in tensile strength with rise in temperature and fall in pH, then it was logical to assume that severe exercise might cause a reduction in the physical strength of the collagen, allowing it to become damaged. He also indicated that the OHP changes could reflect collagen synthesis as well as collagen degradation. However, in the relevant section of this study, where step-testing was used to produce soreness and measure OHP levels, only five of the seven subjects developed soreness. Eccentric or concentric types of contraction were isolated to each leg to induce soreness. Soreness was reported in both the positively and negatively working legs. There was also a large variation in work times between individual subjects. Due to these methodological problems, it is difficult to relate OHP excretion specifically to DOMS in the context of eccentric exercise. Other studies have not corroborated Abraham's findings. Gissal and Hall (1983) did find a greater increase in OHP excretion following high-intensity bench-stepping exercise compared to low-intensity exercise of equivalent workload, but the difference was not significant. Horswill et al. (1988) also found that exercise which produced DOMS did not produce significant increases in OHP. However, a limitation to this study was that OHP was followed for only 48 h postexercise. The method of measuring soreness was not stated in this study and it was not made clear whether significant soreness was produced. The exercise protocol consisted of a circuit composed of nine different exercises involving upper and lower limb and trunk activity. The extent of eccentric activity was not made clear, it was not localized and it was not comparable between subjects. Further research would seem to be necessary in order to clarify some of these issues.

Muscle damage theory Hough (1902) reported that delayed pain was closely associated with mechanical tensions in the muscles, which led him to suggest that soreness had its origin in 'some sort of rupture within the muscle itself. Recent evidence indicates that skeletal muscle damage may be the primary mechanism contributing to muscle soreness (Armstrong et al., 1983; Newham et al., 1983b; Friden et al., 1981, 1983a, 1988; Friden, 1984b; Jones et al., 1986). There is considerable evidence that eccentric contractions cause significantly more damage than

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other types of contraction (Friden et al, 1981; Newham et al, 1983b; Armstrong et al, 1983). Friden et al. (1981) were the first to demonstrate ultrastructural changes within skeletal muscle fibres following an exercise protocol of repeated stair descents which caused severe DOMS. Post-exercise samples showed myofibrillar disturbances consisting of Z-band disruption and streaming. Armstrong et al. (1983) utilized an animal model and found similar changes in histological appearance except that damage was predominantly in type I fibres, as opposed to type II fibre damage found in human subjects (Friden et al., 1983b; Newham et al., 1983b). Eccentric work caused far greater damage than similar concentric work. Unfortunately, animals cannot report their level of soreness, making it difficult to suggest a connection between soreness and muscle damage from the animal model. Although damage has been observed in activities that result in DOMS, studies show that soreness is greatest before peak degenerative changes are noted (Friden et al., 1981,1983a; Newham et al., 1983b; Jones et al., 1986). It should also be noted that damage is seen immediately after exercise, a number of hours before any discomfort is felt (Newham, 1988). Furthermore, as Newham (1988) pointed out, damage of this nature is commonly seen in patients with myopathic diseases such as polymyositis and muscular dystrophy. Similar features, although of a less severe nature, have also been reported in the symptom-free muscle of healthy young people (Meltzer et al., 1976). In addition to morphological evidence of ultrastructural damage to muscle tissue, various blood enzymes have also been used as evidence of muscle damage (Komi and Viitasalo, 1977; Schumate et al., 1979; Melamed et ah, 1982; Schwane et al., 1983b; Newham and Jones, 1985; Newham et al, 1983a, 1986; Clarkson et al, 1986a,b; Evans et al, 1986; Horswill et al, 1988; Triffletti et al, 1988). The presence in the blood of enzymes that are normally localized in muscle fibres is taken as evidence of disruption, or increased permeability of the muscle cell membranes (Armstrong et al, 1983; Newham et al, 1983a). Creatine kinase (CK) is considered the best indicator of muscle damage, since this enzyme is found almost exclusively in muscle, both skeletal and cardiac (Clarkson et al, 1987). However, it is unlikely that such markers of muscle damage actually result in pain production, as the majority of authors have found a mismatch between the time-courses of the damage and the pain, with delayed peak enzyme efflux occurring 4-7 days post-exercise, and DOMS peaking earlier at 24-72 h post-exercise (Komi and Viitasalo, 1977; Clarkson et al, 1986b; Newham and Jones, 1985; Newham et al, 1983a, 1986). Other substances normally contained within muscle fibres also appear in the blood in the period following exercise (e.g. myoglobin). Appearance of this substance in the urine is one of the primary clinical signs of rhabdomyolysis (dissolution of muscle). Exertional rhabdomyolysis has been found to occur when subjects are exposed to severe and prolonged exercise. It is commonly diagnosed in military recruits in the early stages of basic training (Smith, 1968; Melamed et al, 1982). However, Abraham (1977) demonstrated that as myoglobinuria was present in 92% of his subjects after concentric contractions that did not produce DOMS, it was not a useful marker of the sort of delayed soreness produced by eccentric activity. These studies, therefore, imply that the muscle damage is not a direct cause of the DOMS. Other factors must intervene. Inflammation as a cause of DOMS There is some evidence to suggest that delayed onset muscle damage involves inflammation. Brendstrup (1962) proposed that tissue damage triggers an inflammatory process. He found

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that the oedema was maximum in rabbit muscle 48 h after negative muscle work. Mononuclear cell infiltration has been implicated in this type of muscular damage in both animal (Armstrong et al., 1983) and human studies (Jones et al., 1986). However, the timecourse of the inflammatory cell infiltration in the study by Jones et al. was much slower than the incidence of pain and occurred when the pain was either decreasing or had disappeared. In contrast, Franklin and Franklin (1988) reported significant elevations in white blood cell count 12 h post-exercise. Hagerman et al. (1984) demonstrated ultrastructural changes of inflammatory response associated with necrotic changes occurring in the muscles of 10 male runners throughout the week of post-marathon recovery, with both pain and inflammatory changes peaking 1-3 days after the event. As the inflammatory process began immediately after the marathon, when pain was not a feature, they suggested that this may have served as a 'liminal stimulus' to surrounding free nerve endings, and that when the inflammatory process reaches a certain level, the nerve endings for pain then respond. Thus, it was reasoned that DOMS is caused by inflammation. However, these investigators did not explain how pain was measured or how the magnitude and time-course of the inflammatory response was measured. In addition, no statistical analysis was performed to demonstrate any significant relationship between the two factors, making it difficult to draw firm conclusions from this experiment. Schwane et al. (1983b) found that increases in neutrophil and total white blood cell counts, which usually accompany inflammation, did not occur in association with soreness following downhill running. Bobbert et al. (1986) also found no difference between pre- and postexercise means of white blood cell count. They found soreness was related to the increase in leg volume following eccentric calf muscle work that was not intravascular in origin. They therefore proposed that the soreness was caused by oedema, which did not reflect classical muscle inflammation. Although no statistical evidence was presented, they hypothesized that the oedema was caused by Z-band disruption leading to the formation of protein-bound ions, which would exert an osmotic pressure. This sequence of events was also suggested by Friden (1984a). Changes in arm volume, similar to the ones noted in the study by Bobbert et al. (1986), were also observed by Talag (1973) in the upper arm after exercise-inducing DOMS in the biceps, although he found no significant correlation between limb volume and soreness. Hill and Richardson (1989) found significant increases in upper arm circumference as measured with a tape. The increases peaked at day 4 following soreness-producing exercise. However, it is not clear from their study whether the exercise was purely eccentric or a mixture of concentric and eccentric exercises. Application of a topical analgesic/antiinflammatory cream did not affect the circumference measures significantly, although the investigators did find a significant improvement in soreness perception, on a scale of 0-10, above a placebo cream, on days 3, 4 and 5 post-exercise. Other methods of measuring intramuscular pressure in painful muscles have also produced conflicting results. Friden et al. (1986) used a slit-catheter technique to measure tissue fluid pressure in the anterior tibial compartment of the leg and found peak pressure occurring at the same time as peak soreness, 2 days after performing eccentric exercise. Using a similar technique, Newham and Jones (1985) found no significant difference in intramuscular pressure between control and exercised biceps. Newham (1988) suggested that the conflicting results may be due to the greater compliance and distensibility of the elbow flexor compartment. Friden et al. (1988) found that muscle fibre swelling was directly associated with delayed muscle soreness after eccentric exercise.

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Reducing or preventing DOMS Methods of alleviating DOMS

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Although the pathophysiological processes underlying DOMS are not completely understood, many researchers have investigated various treatments in an attempt to reduce the soreness. These treatments have focused on reducing the inflammation, or oedema, consequent to tissue damage, and/or breaking up the cycle which is thought to provoke tonic muscle spasm or pain. Stretching

de Vries's (1961a,b, 1966) examination of the ability of static stretch to reduce soreness led to the proposal of his spasm theory. In one study, de Vries (1961a) reported stretching exercises to have helped to relieve the pain in seven of nine subjects, de Vries's method was to have the subject lock the limb, using body weight, in such a position that the muscle in question was held at its maximum length for 1-3 min, but no details were given of the timing, frequency and duration of the treatment. In addition, there was no controlled trial to produce DOMS: 'accidentally induced muscle pain' was the criterion, and the subjects included in the study had varying degrees of soreness in a variety of muscle groups, making comparisons difficult. It was stated that resting EMG and soreness were reduced after stretching, but there are no details of how soreness was measured or whether the effects were significant. In a further study (de Vries, 1966), static stretching for 2 min reduced resting EMG activity and soreness 48 h post-exercise. Soreness was experimentally induced by eccentric dumbell curls for the elbow flexors. The stretching protocol consisted of two sets of static stretches, each ensuring that the biceps were fully stretched, and each lasting for 2 min, with a 1-min rest in between. Soreness and EMG were measured at 48 h pre- and post-stretching and both parameters were found to be significantly reduced. A three-point scale was used to measure soreness. The length of time for which soreness was reduced was not assessed. In a related study (de Vries, 1961b), 17 subjects performed an exercise bout consisting of bilateral wrist hyperextensions. Stretch was applied to the non-dominant arm for 1 min immediately after exercise and at various time intervals (2,6,20 and 22 h) post-exercise. Significantly less distress was noted in the treatment arm at 24 and 48 h. It should be noted, however, that the exercise design entailed the performance of both eccentric and concentric contractions of the forearm extensors, and so fatigue may have limited maximum eccentric activity and subsequent localized soreness.

The effectiveness of stretch EMG biofeedback was examined by McGlynn et al. (1979). Following eccentric exercise at 80% MVC to fatigue, their subjects received 15-min sessions of either biofeedback, static stretch or neither, over a time-course of 6, 25, 30, 49 and 54 h. The stretch protocol was as used by de Vries (1966). Although there was no increase in EMG immediately after exercise, there was a significant increase at 24 h. Both biofeedback and stretch significantly decreased EMG activity but had no effect on perceived pain as measured on a 30-point scale. This finding contradicts the work of de Vries, which demonstrated significant decreases in perceived pain as a result of static stretching. McGlynn et al. offered no explanation for this apparent discrepancy in results, other than the differences in experimental design. Torgan (1985) also measured the effect of static stretching upon soreness induced by eccentric hamstring activity. There was no change in EMG activity, but a marked (although not statistically significant) decrease in pain, which was temporary in

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nature and returned the following day. Buroker and Schwane (1989) found that post-exercise static stretching did not alleviate DOMS, either on a temporary or longer-term basis, in subjects who performed an eccentric hamstrings step-test protocol for 30 min. The stretching protocol differed from the studies of de Vries (1961a,b, 1966), Torgan (1985) and McGlynn et al. (1979). Each session consisted of 10 repetitions of 30 s stretch, performed immediately post-exercise and at 2-h intervals for the first 24 h post-exercise and at 4-h intervals throughout the remaining 48-h post-exercise period. Although the total amount of stretching was much greater than previous authors had used, it is possible that each 30-s stretch was not long enough to overcome the monosynaptic stretch reflex. Cold application Following acute soft tissue injury, the application of cold is known to decrease inflammation and pain as well as decrease muscle spasm via suppression of the monosynaptic stretch reflex. Ice massage causes the greatest reduction in intramuscular temperature when compared to other cryotherapy techniques (Kowal, 1983). This reasoning led Yackzan et al. (1984) to investigate the effects of cold application on soreness. In addition, they suggested that if muscle spasm occurred, the resultant muscle shortening would create a decreased range of motion (ROM). Consequently, they measured ROM and perceived soreness in 30 subjects who completed an eccentric arm exercise. The subjects received ice massage for 15 min either immediately after the exercise or at 24 or 48 h post-exercise. Although the investigators found a decrease in ROM that was proportional to an increase in muscle soreness, cold application did not relieve soreness or improve ROM in any of the three groups. Braun and Clarkson (1989) examined the effect of ice bath immersion of the arm for 25 min prior to 70maximum voluntary eccentric contractions in seven female subjects, who also wore a cold pack during the exercise. The contralateral arm served as a control and performed the exercise without the treatment. The cold treatment did not reduce the damage response to eccentric exercise as measured by isometric strength, CK levels, relaxed elbow angle and flexed elbow angle, which were assessed pre-exercise, immediately post-exercise and for 6 days following exercise. All measures showed significant changes which had still not returned to baseline day 6 post-exercise. Ultrasound Ultrasound was found to be effective in reducing DOMS in one study (Hasson et al., 1989b). The experimental group of six subjects was compared to 'sham' treatment and control groups of the same size, after 10 min of bench-stepping involving eccentric exercise only for the left leg. Ultrasound treatment, given 24 h later, was applied to the proximal area of the vastus lateralis and the distal vastus medialis, which were found to be areas that were sore. The dosage was 20 min pulsed at a ratio of 1:4, an intensity of 0.8 W cm" 2 and a frequency of 1.0 MHz. Significant reductions in soreness were found among the members of the experimental group after 48 h compared to the 'sham' and control groups. Transcutaneous electrical nerve stimulation Low-frequency transcutaneous electrical nerve stimulation (TENS) of pulse width 300 /is was applied to the upper arm in eight female subjects who experienced DOMS of the elbow flexors (Denegar et al., 1989). It reduced the perception of pain and increased the range of

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elbow extension significantly. Treatment using TENS of low frequency and a pulse width of 300 /is was also applied at four sites associated with the relief of upper arm pain. The range of movement improved significantly immediately after treatment, as well as at 20 and 40 min post-treatment. As there was no control group, the passage of time could also have been responsible for the results. Pharmacological agents

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Various pharmacological agents have been administered in order to alleviate DOMS. One of the main functions of vitamin C is the synthesis of collagen, an important component of connective tissue. Donnelly (1988) hypothesized that vitamin C supplementation might increase collagen synthesis in normal muscle, and so increase its resistance to damage. After administration of 500 mg of vitamin C twice daily for 34 days, no difference in soreness response was observed between treatment and placebo groups. Various non-steroidal antiinflammatory agents have also been used to alleviate DOMS without success (Janssen et dl., 1983; Kuipers et al., 1985; Donnelly et al., 1988a,b). A steroidal anti-inflammatory agent, prednisolone, was found to reduce CK efflux significantly after treadmill running in dogs, but again it was impossible to measure its effect on DOMS (Wagner and Critz, 1968). Headley et al. (1985) examined the effects of prednisolone in human subjects in a double-blind crossover design and found no significant difference in either pain scores or CK levels between the experimental and placebo groups. In contrast, Francis and Hoobler (1987) observed that aspirin, also an anti-inflammatory agent, significantly reduced DOMS 48 h after eccentric exercise when compared to a control group. Topical analgesic anti-inflammatory creams (10% triethanolamine salicylate) have also been found to reduce DOMS (Politino et al., 1985; Hill and Richardson, 1989). Both of these studies incorporated a double-blind design with large numbers of subjects and included placebo groups. A significant reduction in DOMS was found by Hill and Richardson (1989) on days 3,4 and 5 following exercise that produced soreness, the values on a 0-10 soreness scale being 'approximately 3.4 in the analgesic group and 4.4 in the placebo group'. It is questionable, however, whether subjects can truly distinguish between such scores. The study by Politino et al. (1985) used a very large sample (39 in the active group and 44 in the placebo group), but their results are highly questionable due to the massive variation in types of exercise used to produce DOMS. These ranged from marathon dancing to weightlifting, and for unspecified durations or intensities. From the information given by the authors, the methodology would be impossible to replicate. The subjects rated their pain relief as 'poor', 'fair' or 'good', none of which were defined by the authors. Exercise

Exercise is often considered to reduce the effects of DOMS. Donnelly et al. (1988a) investigated the effect of a light bout of eccentric exercise 1 day after heavy eccentric exercise consisting of 70 maximum eccentric contractions of the forearm flexor and extensor muscles of the non-dominant arm. The experimental group of nine subjects performed 25 submaximal contractions with the same arm. Although there was no difference in DOMS between the two groups 19 days after exercise, there was a significant reduction in CK enzyme efflux on days 2-6 for the experimental group. A study by Hasson et al. (1989a) found that a high-velocity concentric isokinetic exercise

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(6 x 20 MVC of the knee flexors and extensors at 5.23 rad s" 1 , with 3 min recovery between each set) performed 24 h after DOMS-producing stepping exercise, significantly reduced DOMS and facilitated the return of strength after 48 h in five subjects when compared with a control group. Nevertheless, the results showed that the soreness and strength loss were still significantly above baseline levels at 48 h.

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Massage Massage has also been used in an attempt to reduce DOMS. However, Wenos et al. (1990) did not find any significant difference in soreness or in strength loss, post-exercise, in the quadriceps muscles of the treatment leg when compared with the control leg in a group of nine subjects. Unfortunately, it is difficult to drav/ any distinct conclusions from the body of literature concerned with the alleviation of DOMS, due to the wide range of methods and the variety of subjective scales utilized to classify the degree of pain or soreness. Furthermore, unless a control group is used, it is not necessarily possible to distinguish how much of the treatment effect is physiologically induced or how much is of psychological origin. Training to reduce or prevent DOMS Hough (1902) observed that DOMS did not occur when a trained muscle was exercised. Other workers have since described the effect of training, not just in alleviating the soreness response, but also in reducing morphological changes, performance changes and CK activity in the blood (Komi and Buskirk, 1972; Schwane and Armstrong, 1983; Friden et al, 1983b; Jones and Newham, 1985b; Byrnes et al., 1985b; Byrnes and Clarkson, 1986; Knuttgen, 1986; Clarkson et al., 1987; Clarkson and Tremblay, 1988; Schwane et al, 1987; Miller et al., 1988; Newham et al., 1987, 1988). It seems that DOMS resulting from eccentric exercise is reduced by training that specifically involves eccentric contractions (Newham et al., 1983c). Sforzo and Lamb (1985) found that concentric training did not reduce DOMS in subsequent eccentric exercise. In animals, the muscle damage that occurs during downhill running is prevented by downhill and level training, both of which incorporate eccentric muscle contractions, but not by uphill training (Schwane and Armstrong, 1983). The protective effect of a prior bout of exercise, that in itself may produce only minimal soreness, has been found to last for prolonged periods. Byrnes et al. (1985b) observed that the muscle soreness response to downhill running was reduced by up to 6 weeks following an initial bout of downhill running. The same effect was observed by Kuipers et al. (1985). Jones and Newham (1985b) suggested that the training effect may last up to 10 weeks after the initial bout. Some studies have used a number of weeks of training to produce an effect. Friden et al. (1983b) used 8 weeks of training on a cycle ergometer and Komi and Buskirk (1972) used 7 weeks of eccentric forearm flexor work. However, a number of recent investigations have shown that the prophylactic effect of training may be due to the performance of a single initial exercise bout (Armstrong et al., 1983; Byrnes et al., 1985b; Clarkson et al., 1987). Clarkson and Tremblay (1988) found that as few as 24 maximum voluntary eccentric contractions produced a training effect and resulted in no CK response, less soreness and smaller strength decrements when 70 MVECs were performed 2 weeks later. Even 12 training contractions have been found to produce similar training effects (Ebbeling and Clarkson, 1989). Clarkson et al. (1987) indicated that this protective effect is specific to the muscle which is exercised at the first bout. This may mean that the 'repeated bout effect' occurs at the level of the muscle

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exercised, and is not a central effect. Pierrynowski et al. (1987) found that as little as two 12-min bouts of downhill running at a gradient of 10% were sufficient to protect against the occurrence of DOMS in a subsequent downhill run 3 days later, which had produced DOMS in the control group. Interestingly, they found the training was insufficient to prevent a 2- to 3-day loss of muscular strength, suggesting that strength loss and DOMS may have different physiological causes. In relation to muscle soreness, 'prevention is better than cure' would seem to be the best approach, and prior exercise utilizing the 'repeated bout effect' seems to offer considerable protection against further damage to muscle and the related soreness. Other treatments employed show varying results but, on the whole, few seem to reduce DOMS effectively. Statistically significant results cannot necessarily be translated into clinically significant results. Conclusion

A wide variety of protocols involving intense eccentric exercise has been found to produce DOMS in the upper and lower limb muscle groups. Greater soreness tends to be produced primarily by greater intensity of exercise, with exercise duration also a factor. Due to considerable individual variation in response to eccentric exercise, protocols ensuring maximal contractions throughout (such as that used by Jones et al., 1987) may help control for some error variables. The weight of evidence is against the 'spasm' and 'lactic acid' theories being causal in delayed soreness, and there is little evidence that either muscle or connective tissue damage, found to occur after intense eccentric exercise, has a direct causal link either. Secondary factors probably intervene. Some studies do suggest that inflammation subsequent to damage may be more closely associated with DOMS, and this aspect may benefit from further study. Although some success has been reported by a few authors using stretch, ultrasound, TENS or topical anti-inflammatory creams to alleviate DOMS, the majority of studies indicate that no effective way has yet been found to reduce the soreness once it has occurred. Prevention seems to be better than cure, and a number of studies show that training using submaximal eccentric exercise protocols may prevent DOMS in subsequent maximal bouts using the same muscle groups. The training effect may last for up to several weeks. While strength loss and muscle shortening are found to be consequent upon sorenessinducing eccentric exercise, it is unlikely that either physical correlate is causally linked to DOMS. Further study is necessary to clarify the exact nature and direct causes of delayed onset muscle soreness. References

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Delayed onset muscle soreness: mechanisms and management.

This review describes the phenomenon of delayed onset muscle soreness (DOMS), concentrating upon the types of muscle contraction most likely to produc...
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