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

Proposition for Debate - by Martin Berg

Contents

• Statement of the Topic
• Introduction
• Background Knowledge
• Physiotherapy Treatments
• Prevention
• Conclusion
• Short Answer Review Questions
• References

Statement of the Topic

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

Introduction

Delayed onset muscle soreness (DOMS), usually occuring 24-72 hours post eccentric exercise, is a controverisal topic. To date all the mechanisms are not totally understood. Several theories have been proposed during the years. This paper will present a brief overview regarding potiential sources and mechanism, and more focus on the existing evidence regarding physiotherapy treatment for DOMS.

Background Knowledge

Muscle soreness ­ Muscle damage

Muscle damage due to eccentric muscle action is one potential source and damage have been found at sacromeres and Z-lines after exercise (Stauber 1996). Clarkson and Sayers (1999) concludes damage to the sarcolemma, T-tubuli, myofibrils and cytosceletons as well as streaming of the Z-lines. The damage could be increased by a disturbed calcium homeostasis and also by inflammatory response (Clarkson and Sayers 1999). Disturbed calcium homeostasis occurs when the sarcoplasmic retinaculum is damaged, which leads to decreased uptake of calcium and therefore increased intracellular calcium levels (Clarkson and Sayers 1999, McArdle et al 1996).

The reports of increased myoglobin and creatine kinase in the blood are signs of muscle injury and have been also been reported after exercise. Creatine kinase could be responsible for muscle soreness, however the peak concentration of creatine kinase was found to occur as the soreness was resolving (Alter 1996).

Performance deficit

Directly after an eccentric exercise bout a reduction in capacity to produce force, this can be present for up to five days post-exercise. Pain and soreness are partially responsible for the performance reduction, the rest is likely to be cause by muscle damage (Stauber 1996).

Location of soreness

The musculotendinous junction is most commonly reported as the point where DOMS are experianced as most intense (Stauber 1996).

Residual swelling

Swelling is a common finding with DOMS (Chleboun et al 1998, Stauber 1996). This swelling can explain some of the stiffness that also is associated with DOMS (Chleboun et al 1998). Chleboun et al (1998) studied the relationship between swelling and stiffness and found that swelling gradually increased during the first four days, whereas stiffness occured immediately. It was suggested that the initial stiffness could be due to the disturbance of calcium homeostasis that is associated with DOMS and that swelling could contribute to the stiffness in the later stages.

Inflammation

In regards or inflammation different views have been reported. Stauber (1996) suggests that it is not a true inflammatory response that occurs and supports this with findings that not all inflammatory mediators have been found present and also tha ineffectiveness of anti-inflammatory medication. On the other hand Clarkson and Sayers (1999) describes a normal inflammatory response.

Pain

Pain or tenderness is one of the main factors associated with DOMS. The inflammation process is accompanied by release of substances such as bradykinin, histamines and prostaglandins, which all can sensitise and activate the nociceptors. This occurs both from a chemical and mechanical point of view (Stauber 1996).

Current Knowledge of Creatine

It is now known that creatine plays a vital role in the ATP-PC system (the immediate energy system) and that 95% of the creatine in our body is stored in the skeletal muscles, the majority of the rest being found in the heart, brain and testes (Balsom et al 1994). Two thirds of this store is in the form of phosphocreatine, the rest simply as creatine (Fillmore et al 1999).

The average daily requirement of creatine is 2g/day dependent upon body size and activity levels. It is acquired from meat and other animal products (50% of our daily requirement) and from endogenous synthesis in the kidneys, liver and pancreas. (Fillmore et al 1999). Vegetarians and others who don�t ingest meat or animal products are capable of synthesizing sufficient quantities endogenously. However, it is noted in the literature that their resting levels of creatine are generally lower then non-vegetarians. (Engelhardt et al 1998).

Physiotherapy Treatments

In this section the physiotherapy treatment modalities are presented. With each modality is evidence both in support and contrary to the proposition.

Massage

Supporting evidence

Ernst (1998) hypothesised that massage, due to pressure on the local muscle tissue, increases the lymph flow and local blood flow and therefore could be a potential alleviator of DOMS. The explanation for this would be that the increased circulation would reduce ischemia and decrease swelling, which are potiential pain generators. However, in his review he found some scientific evidence supporting this view. Most of the articles revieled faulty research designs and small sample groups and this could be the explanation for the lack of support. Despite this the author see a trend pointing towards massage as a potiential treatment for DOMS.

Evidence to the Contrary

Tiidus (1997) concluded in his review that although some research suggests trends towards positive effect of massage in treating and reducing DOMS, most research have not been able to show good results. In fact light exercise seems to provide equal if not better result.

Transcutaneous electrical nerve stimulation (TENS)

Supporting evidence

TENS has been found to have a positive effect on delayed onset muscle soreness (Denegar et al 1989). Denegar and coworkers (1989) used low frequency TENS, at maximal tolerance for 30 minutes, 48 hours after an eccentric exercise bout. The results showed decreased perception of pain and increased elbow extension.

Evidence to the Contrary

These findings is opposed by the findings of Craig et al (1997). This research group used a larger sample size and both a controll and a placebo group. In addition they tested both low frequency TENS and high frequency TENS. When evaluating range of movement, resting angle and perceived tenderness during three executive days they found no significant changes between groups.

Hyperbaric oxygen therapy

Evidence to the Contrary

The potential for hyperbaric oxygen therapy have been put forward lately. The proposed effects of hyperbaric oxygen therapy are an increase in oxygen content of the arterial blood and a vasoconstriction. An increase in PaO2 would give an increase in diffusion gradient of O2, which would increase healing potentials for the damaged tissue. Vasoconstriction would lead to a reduction of the inflammatory response. However, the literature have note been able to prove any effect on induced muscle damage (Harrison et al 2001, Mekjavic et al 2000). Harrison et al (2001) found that all the parametres used in the experiment (cross sectional area, T2 relaxation time, isometric strength, serum creatine kinase and rating of percived soreness) were significantly affected by the eccentric exercise task, but there was no difference between the different groups.

Ultrasound

Evidence to the Contrary

Plaskett et al (1999) performed ultrasound treatment on ten subjects after they had been exposed 9 sets of 12 knee-extension exercise at 60% of 1 RM. Ultrasound treatment where conducted with pulsed 1.0 W/cm_ for 8 minutes daily for 4 days, to the quadriceps muscle of a randomly selected leg. Placebo treatment was conducted on the opposite quadriceps muscle. The results showed no differance in between limbs regarding knee-extension peak torque or DOMS.

Craig et al (1999) conducted a well designed study on the effects of pulsed ultrasound on delayed onset muscle soreness. The subjects were randomised into four groups, controll, placebo, low-dosage pulsed ultrasound (0.8 W/cm_, 7 minutes) and high-dosage pulsed ultrasoound (0.8 W/cm_, 14 minutes). The subjects received treatement after the exercise regim and the two following days. The authors found no significant differences regarding range of movement, mechanical pain threshold or subjective perception of pain that would indicate an effect of the ultrasound treatment.

Acupuncture

Evidence to the Contrary

Barlas et al (1999) studied the effects of acupuncture on DOMS. Four groups including control, placebo, and two different treatment groups. One were acupuncture was given in specific acupuncure points and the other were acupuncture was given in tender points. The authors measured range of movement, resting angle and subjectively perceived tenderness. From the results it was concluded that acupuncture have no effect on the signs and symptoms of DOMS.

Cryotherapy

Evidence to the Contrary

Cryotherapy is widely used as a treatment of traumatic soft tissue injuries. Paddon-Jones and Quigley (1997) proposed that if cryotherapy have an effect for these injuries, a similar effect on exersice induced muscle injury and delayed onset muscle soreness could be possible. However in their study the found no evidence to support this theory. They used a repeated protocol of 5 sessions of 20 minutes ice-water immersions, which would be regarded as a normal approach following acute soft-tissue injuries. Using the contralalteral arm as controll they found no differences in arm volume, muscle pressure soreness or strength assessment.

Prevention

MacArdle, Katch and Katch (1996) reports that a significant prophylactic effect can be achived by the use of a single bout of exercise prior to commencing more heavy training.

Conclusion

In conclusion the studies review and reported are of varying standard. Most of them include quite small sample sizes, which makes statistical analysing very difficult. Further more, a number of the articles are using the contralateral limb or muscle as controll, which could be seen as questionable since some of these treatments quite possible could have an effect not only localy but systemic or at least contralaterally. Controll groups are essential to enable a fair comparison and to produce solid scientific research. More studies following the standard set by Craig et al (1999) are warranted. These factors taken into consideration, it seems that most physiotherapy treatment evaluated to date have little influence in reveiling the symptoms associated with EIMD and DOMS. More thorough research may well change this current trend.

Short Answer Review Questions

1. What are the general characteristics associated with DOMS?
2. What muscle action will generally induce DOMS, especially when it is unacustomed?
3. What parametres are present in the blood and indicates a muscle injury and are they present in DOMS?
4. Explain the relationship between swelling and stiffness during DOMS.
5. What would the main considerations be if one were to conduct further research in the area of physiotherapy treatment for DOMS?

References

Alter MJ (1996)

Muscular Soreness: Etiology and consquences. Science of Flexibility. Champaign: Human Kinetics,

Chleboun GS, Howell JN, Conatser RR and Giesey JJ (1998)

Relationship between muscle swelling and stiffness after eccentric exercise. Medicine and Science in Sports and Exercise 30:529-535.

Clarkson PM and Sayers SP (1999)

Etiology of exercise-induced muscle damage. Canadian Journal of Applied Physiology 24: 234-248.

Denegar CR, Perrin DH, Rogol AD and Rutt R (1989)

Influence of transcutaneus electrical nerve stimulation on pain, range of motion, and serum cortisol concentration in females experiancing delayed onset muscle soreness. Journal of Sports and Physical Therapy 11:100-103.

Harrison BC, Robinson D, Davidson BJ, Foley B, Seda E and Byrnes WC (2001)

Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Medicine and Science in Sports and Exercise 33: 36-42.

McArdle W, Katch F and Katch V (1996)

Exercise Physiology. (4th ed.) Baltimore: Williams & Wilkins.

Mekjavic IB, Exner JA, Tesch PA and Eiken O (2000)

Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness. Medicine and Science in Sports and Exercise 32: 558-563.

Stauber WT (1996)

Delayed-onset muscle soreness and muscular pain.

Zachazewski J, Magee D and Quillen W (Eds)

Athletic injuries and rehabilitation. Philadelphia: WB: Saunders Company,

Exercise Physiology Educational Resources 2001