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Curtin University of Technology
School of Physiotherapy

There is a role for physiotherapy in ameliorating the DOMS response to EIMD!

Proposition for Debate - by Martin Meyer

Contents

Statement of the Topic

Does Physiotherapy ameliorate the DOMS effect in EIMD?

Introduction

Delayed onset muscle soreness (DOMS) is a common ailment experience by anyone who has undergone unaccustomed exercise, and suffered from exercise induced muscle damage (EIMD) (MacIntyre et al 1995). It is agreed that eccentric muscle contractions produce a greater soreness response than concentric and isometric, and that it begins usually 48 to 72 hours post activity (Gulik and Kimura 1996, Cleak and Eston 1992). Pain is not the only factor associated with this condition. There is also an associated loss of strength, loss of motion and swelling of the involved musculature (Cleak and Eston, 1992,MacIntyre et al 1995).

The aim of this paper is to identify whether physiotherapy intervention can in-fact help alleviate the signs and symptoms of DOMS. Before one can do this reviewing the possible causes of DOMS is important.

Background Knowledge

There are various theories being proposed as the cause of the effects of DOMS, and none have been effectively been proven. As such, DOMS has very much remained an enigma.

Cleak and Eston (1992) describe several theories in their review. These include the lactic acid theory, the spasm theory and the connective tissue damage theory.

More recently, it has been shown with histological examination of an eccentrically exercised muscle, that there is damage to the micro-structure of the muscle fibers, sarcolemma, myofibrils and cytoskeleton (Clarkson and Sayers 1999). It is proposed that mechanical damage induces changes in calcium homeostasis and an inflammatory response, all of which result in what is known as DOMS.

Mechanical Factors

During eccentric muscle contractions there are fewer motor units, thus fewer muscle fibers, activated. This may lead to an increase in tension taken through the cross bridges of the muscle fiber resulting in disruption of the Z band causing Z streaming (Clarkson and Sayers 1999).

It has been demonstrated that there is a rise in creatine kinase (CK), myosin heavy chain fragments and myoglobin levels, all of which are indicators of muscle damage (Franklin et al 1991, Mair et al 1995).

It has been proposed that it isn't high tension alone that causes muscle damage (Warren et al 1993) but rather the strain during active lengthening (Frienden and Lieber 1993). Therefore tension at a longer muscle length will result in more damage than at shorter lengths.

Calcium Homeostasis

Damage to the muscle fibers after eccentric activity sees damage to the sarcoplasmic retinaculum which, in turn, will lead to an increase in the intracellular calcium levels (Clarkson and Sayers 1999). The elevation of calcium levels may alter the intracellular ion homeostasis and thus cause cellular swelling. The raised levels may also propogate tissue damage due to an inability for the muscle to relax which leads to proteolytic enzymes accumulation (Armstrong 1991).

Inflammation

Muscle fiber damage seen post eccentric muscle activity is thought to cause an inflammatory response (Clarkson and Stayers 1999, Cleak and Eston 1992). Neutrophils are thought to be the first to infiltrate the area followed by leukocytes and macrophages. This slow infiltration of inflammatory mediators and changes in osmotic pressures is what is thought to produce the muscle swelling seen 24 to 48 hours post exercise (Clarkson et al 1992).

It is interesting to note that the use of anti-inflammatory medications has shown to have very little effect on the time course of DOMS (Almekinders 1999). It could be assumed then that the process occuring here is not strictly an inflammatory one.

Effects of Damage

The intracellular changes that occur after a bout of eccentric exercise are believed to manifest themselves into the clinical features that we see in the subject with DOMS. As mentioned earlier, these include pain, muscle stiffness and loss of muscle strength. Once again there are different opinions as to the reasons why these eventuate.

Pain

Several reasons have been proposed for the cause of pain in DOMS. Smith (1991) believes it is the swelling and the intracellular oedema that causes compression on the pain sensitive nerve endings. This may lead to sensitisation of these nerves and thus pain. He supports this theory by rationalising that this is why pain is only felt only on movement and palpation but not at rest. As the muscle is placed under mechanical stress pressure increases within, and compression of nerve endings occurs.

Clarkson and Newham (1995) however believe it is the mediators released in the inflammation process, such as bradykinin, serotonin and histamine that sensitise the pain nerve endings and thus pain results.

Muscle Stiffness

It is proposed that muscle stiffness occurs as a result of swelling and oedema within the muscle (Clarkson and Stayers 1999). Chleboum et al (1998) however, noticed that peak swelling occurs after four days, whereas stiffness peaks much quicker and remains similar over the next few days. It was concluded therefore, that swelling and stiffness were not directly related.

Another suggestion is that it is the dysfunction of the sarcoplasmic retinaculum and accumulation of intracellular calcium that leads to the increased stiffness (Clarkson and Newham 1995).

Muscle Strength

Strength losses of up to 60% are evident directly after exercise, and these can last up to ten days (Clarkson and Stayers 1999). It was hypothesised initially that this is due to pain inhibition, but the strength losses are seen well before pain perception. It is believed that over-stretching of the sarcomeres and a reduction in actin and myosin overlap is the main cause for this strength loss (Clarkson and Newham 1995).

Westerbald et al (1993) suggested that it is fatigue due to a reduction in calcium production from the damaged sarcoplasmic reticulm, that may lead to an inability to generate force.

Does physiotherapy treatment work?

In reviewing this question several types of physiotherapy treatments were researched. These include electrotherapeutic modalities including ultrasound (US) and electrical stimulation (ES), massage and accupressure, repeat bout exercise and cryotherapy. Other non-physiotherapy treatments will also be mentioned, including hyperbaric and anti-inflammatory medications.

Ultrasound

The effect of US on DOMS has been shown to be variable. Hasson et al (1990) demonstrated that the use of pulsed US once at a ratio of 1:4, intensity of 0.8Wcm and a frequency of 1.0Mhz seemed to significantly reduce the soreness 48 hours post eccentric quadriceps activity, compared to a placebo and a control group. There was also improvement in muscle function, yet it was still less compared to the pre-exercise values. Unfortunately though subject groups were very small (n=6) which may make statistical analysis inconclusive. Furthermore, the muscles tested were unable to be rested and were exercised in normal walking. It would therefore be difficult to assume that it was just the US that was affecting DOMS.

More recently, other authors have found conflicting results. Plaskett et al (1999) found that there was no difference in pain levels or muscle performance between the experimental group receiving pulsed US at 1.0 Wcm and a placebo group. In this study however there was no control group and a small subject groups, which may limit the conclusions.

Craig et al (1999) used a double blinded, placebo controlled randomized design to study the effects of two different US dosages. Forty-eight subjects were divided into four groups; control, placebo, low dose pulsed US or high dose pulsed US. The researchers induced DOMS in the elbow flexors and noted pain scores, elbow range of movement and tenderness on palpation over three days. Muscle strength was not measured. Conclusions revealed that the use of US over three continuous days made no significant difference in the management of DOMS. They did note though that low dose pulsed US was slightly more beneficial than high dose US. The methodology of this study warrants the results more valid, even though muscle strength over the period was not measured.

Electrical Stimulation

Again, the opinions as to the effectiveness of ES in the management of DOMS, is varied. One study has shown transcutaneous electrical nerve stimulation to significantly improve joint range of motion and pain perception using low frequency and, long pulse width (Denegar et al 1989). More recent research using interferential current supports these findings (Schmitz et al 1997). Limitations to these studies however include the lack if a control group and the fact that the authors, in both cases didn't report whether or not the benefits of treatment continued over a longer time period. Both measured the effect over approximately one hour but no longer. Neither studies measured what the effect of ES was on muscle strength.

Allen et al (1999) used a more controlled study design to evaluate the effectiveness of micro current ES on DOMS in elbow flexors. They found that there was no difference in pain scores and range of movement between the treatment and the placebo groups. Like other studies though, they failed to use a control group and did not measure muscle strength. Without a control group it is not possible to distinguish between physiological and psychological effects. They did however measure the variables over a 72 hour time course which was a limitation in other studies.

Massage and accupressure

Results of research investigating the effectiveness of massage on DOMS has been slightly more positive than the other forms of management, although still there is not complete agreement in the literature.

Ernst (1998) reviewed data bases attempting to answer this very question. He found that out of seven studies addressing this question, five demonstrated significant reductions in pain scores, muscle function and CK levels. Unfortunately each study had serious methodological flaws, most commonly a small sample size, which renders the results questionable. Two of these also investigated massage in conjunction with other interventions, which makes it difficult to imply a specific massage effect. Ernst (1998) therefore concludes that massage appears to have potentially a positive effect on management of DOMS. To be proven though, a trial with a large enough sample size and massage as the only intervention must be performed.

In one well designed study, accupressure was specifically investigated (Charles-Liscombe 1998). The full article unfortunately was not witnessed by this author, only the abstract. It was concluded that accupressure applied directly, 24 and 48 hours post exercise, can significantly improve range of movement, reduce pain scores and improve muscle function compared to controls. Unfortunately the investigator used small sample groups which limits statistical power, and used the quadriceps muscle, which, as mentioned earlier, cannot be rested, so exercise effects may confound the results.

Repeat Bout Exercise

Repeat exercise has thought to reduce the effects of DOMS. Smith (1994) investigated whether repeated eccentric muscle activity would be of any benefit. They concluded that there was no change in time-course and characteristics of DOMS after eccentric exercise was repeated 48 hours after the initial bout.

In differing results, Hasson et al (1989) found that performing high velocity isokinetic concentric exercise, at 300 deg/sec, 24 hours after a bout of eccentric exercise, reduced the perceived pain and improved muscle function compared to controls. A problem arises though as they used the quadriceps muscle, which, as discussed in other sections, may present to be a confounder in the results. Furthermore a very small sample number was used (n=5).

Cryotherapy

Cryotherapy is usually effective in reducing soft tissue injuries. In DOMS though the application of ice to alleviate signs and symptoms is questionable. Braun and Clarkson (1989) found that ice bath emmersion prior to eccentric exercise, combined with the use of an ice pack during the exercise, made no difference on pain scores, muscle strength, muscle length or CK levels post exercise. Research that has used cryotherapy post eccentric exercise has found similar results (Paddon-Jones and Quigley 1997). Once again though, sample sizes were small, so statistical power is an issue.

Preventative training

It is suggested that the best method to reduce the effects of DOMS, is by pre-training the involved muscles. It may be most appropriate to use submaximal eccentric exercise protocols, before moving into maximal muscle activity (Cleak and Eston 1992, Friden et al 1983). Some authors recommend that performing a few maximal voluntary eccentric contractions may be sufficient to get a training response and thus prevent DOMS from occurring (Clarkson and Tremblay 1988).

Other

Further studies have been performed to determine whether hyperbaric oxygen therapy, and anti-inflammatory medications were effective in reducing the signs and symptoms of DOMS (Mekjavic et al 2000, Almekinders 1999). Both have been shown to be in-effective in managing DOMS, although the use of ibuprofen has had mixed results.

Conclusion

The exact cause of DOMS is not yet known, but the manifestation of the signs and symptoms, and the debilitating effects of it are very well known. DOMS is characterised by pain, loss of muscle length and loss muscle strength after a bout of unaccustomed eccentric exercise. These become evident usually about 48 hours post activity and the effects can last up to ten days.

Many treatments have been investigated including massage, electrical stimulation, ultrasound, massage, accupressure, cryotherapy, repeat bout exercise, preventative training, anti-inflammatory medications and even hyperbaric oxygen therapy. Unfortunately none have been shown to undoubtedly benefit DOMS. The common problems underlying the majority of these studies are poor study designs and not large enough sample sizes to allow significant conclusions to be drawn. Certainly more investigation is needed into the pathophysiology and treatment of DOMS, and until then, prevention is better than cure.

References

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Short Answer Review Questions

  1. What is DOMS?
  2. What type of muscle contraction predominantly leads to DOMS? What is
  3. proposed to be the mechanical effects of this contraction?
  4. What are the other proposed theories behind EIMD and DOMS?
  5. What are the proposed theories behind the signs and symptoms of EIMD?
  6. In your opinion, does it appear that the physiotherapy modalities reviewed
  7. are effective in controlling DOMS?
  8. If further research is to be conducted into the effect of physiotherapy on
  9. DOMS, what are the crucial components of the study that must be considered?

Exercise Physiology Educational Resources 2000