EFFICACY OF THREE PHYSIOTHERAPY INTERVENTIONS IN INFLUENCING CLINICAL AND BIOCHEMICAL CHANGES OF DELAYED ONSET MUSCLE SORENESS(DOMS) IN RECREATIONAL ATHLETES

Synopsis Submitted to SAVEETHA UNIVERSITY For the award of the degree of DOCTOR OF PHILOSOPHY in PHYSIOTHERAPY by S. SUDHAKAR Research Supervisor Dr. G. Arun Maiya, Ph.D

DEPARTMENT OF PHYSIOTHERAPY SAVEETHA UNIVERSITY CHENNAI-602105 October 2010

CONTENTS S.No 1. CHAPTERS CHAPTER 1 INTRODUCTION 1.1 Introduction 1.2 Problem Statement 1.3 Recent trends in the scientific study of the importance of Physiotherapy Modalities in ameliorating the delayed onset muscle soreness (DOMS) of recreational athletes. 1.4 Need for the study 1.5 Significance of the proposed study in the context of current status 1.6 Operational Definitions 2. CHAPTER 2: OBJECTIVES, PLAN AND SCOPE 2.1 2.2 2.3 3. Aim of the study Objectives of the study Relevance and Scope of the study 6 6 7 7 7 7 8 8 10 10 11 11 13 13 Page No 4 4 5 6

CHAPTER 3: MATERIALS AND METHODS 3.1 3.2 3.3 3.4 Study Procedure Induction Of Delayed Onset Muscle Soreness Treatment Protocols Post test Measurements

4.

CHAPTER 4: STATISTICAL ANALYSIS AND RESULTS 4.1 Creatine kinase (CK)

4.2 Lactate dehydrogenase (LDH) 4.3 Maximum isometric voluntary contraction (MIVC) 4.4 Repeated measures ANOVA results for dependent variables CK, LDH and MIVC 4.5 Pain score 5. 6. 7. 8. CHAPTER 5: DISCUSSION CHAPTER 6: CONCLUSION CHAPTER 7: REFERENCES List of Publications

15 18 19 19 20 21 22 23

INTRODUCTION 1.1 INTRODUCTION Delayed Onset Muscle Soreness (DOMS) is a common phenomenon experienced by individuals who perform unaccustomed exercise that typically involves an eccentric component. The soreness begins to occur at approximately 8 - 24 hours post-exercise and peaks at approximately 48 hours post exercise. Perception of soreness is generally reduced at 72 hours with residual soreness remaining beyond that time frame. After the exercise, 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, (Clarkson and Hubal, 2002).This constellation of symptoms is often called Delayed Onset Muscle Soreness (DOMS). DOMS PHYSIOLOGICAL CAUSES: By mid 80s the thought of lactic acid build up in the muscles as a cause for DOMS was put to rest. Likewise from the 80's and early 90's the main theories that seem to be still active are DOMS is due to muscle cell damage (ruptured cells spilling contents), where the repair process makes nerve endings sensitive to the pain signal, or it is due to an

inflammatory response ( Tidball 1995). The latter suggests that the 48 hour period when DOMS hits is the peak time for cell death (Armstrong 1984).From the reviews it is assumed that the pain is actually the building up of the new muscle fiber material where other fibers are getting pushed out of the way as new tissue comes in. PATHOPHYSIOLOGY OF DELAYED ONSET MUSCLE SORENESS (DOMS): Five hypotheses are used to explain the pathophysiology of DOMS. 1. Structural damage from high tension. 2. Metabolic waste product accumulation. 3. Increased temperature. 4. Spastic contracture. 5. Myofibrillar remodeling. WHY DOMS NEED TO BE TREATED: DOMS can temporarily reduce muscle performance. The diminished performance results from reduced voluntary effort due to the sensation of soreness and from the muscle's lowered capacity to produce force. DOMS hurts and the consequent effects are decreased range of motion, increased size from swelling, and
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less power to work in the affected muscles. 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 (ADLS) and a decreased motivation and willingness to continue training due to negative experiences of the soreness( Weber servedio et al.1994). In order to minimize negative experiences associated with DOMS and potential detrimental effects on performance, it is necessary to identify a successful treatment intervention. HOW DOMS CAN BE TREATED: DOMS can be treated either by advising complete rest from the participation, by medical management and various physiotherapy approaches to reduce the soreness symptoms. VARIOUS PHYSIOTHERAPY APPROACHES: Physiotherapy Interventions play a major role both in prevention and treatment for the negative effects associated with DOMS. Many treatments have been investigated which include massage, electrical stimulation, ultrasound, acupuncture (Barlas, 2000), cryotherapy, repeat bout exercise, stretching (Johansson 1999), Low intensity Laser therapy (Craig 1999), Iontophoresis (Hasson 1992), Transcutaneous electrical nerve stimulation (TENS) (Craig 1996), preventative training, and even hyperbaric oxygen therapy (Mekjavic, 2000). 1.2 PROBLEM STATEMENT: Strength, range of motion, and a feeling of competence are important factors in performing sports and exercise. Unaccustomed eccentric exercise causes adverse effects on these factors (Bourgeois, MacDougall, 1999).Eccentric exercise, therefore may cause significant reduction in performance during training and competition and/or increase the risk of further injury. If athletes perform eccentric exercise with several muscles during training, it is possible that the exercise efficiency on the subsequent day might be impaired. To date, a sound and consistent treatment for DOMS has not been established. Although multiple practices exist for the treatment of DOMS, few have scientific support. Suggested treatments for DOMS are numerous and include pharmaceuticals, herbal remedies, stretching, massage, nutritional supplements, and many more. As DOMS has been shown to alter biomechanics of movement (Ebbeling and Clarkson 1989) and predispose participants to injury, it is important to determine an effective treatment intervention that will reduce the negative impacts of
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DOMS. The present research is done on recreational athletes as they usually begin a new exercise programme, increase their exercise intensity and commonly change their sports activity.
1.3 RECENT TRENDS IN THE SCIENTIFIC STUDY OF THE IMPORTANCE OF PHYSIOTHERAPY MODALITIES IN AMELIORATING THE DELAYED ONSET MUSCLE SORENESS (DOMS) OF RECREATIONAL ATHLETES: In the past, gentle stretching was one of the recommended ways to reduce exercise related muscle soreness, but a study by Australian researchers published in 2007 found that stretching is not effective in avoiding muscle soreness. Recently study was done on better attenuation effects of compression in DOMS, compression (and compression suits) have been studied over the past 8 years. In another recent study Rhea, Bunker (2009), investigated DOMS pain reduction with Vibration, Perceived pain was measured at 12, 24, 48, and 72 hours post workout. Many studies have been done to find out the significance effects of modalities on DOMS, but none of the studies so far have been shown much significant results in the markers of DOMS and in relieving the symptoms of muscle soreness. 1.4 NEED FOR THE STUDY: The extensive reviews of the literature reveal that, there is paucity of studies on role of various Physiotherapy modalities in ameliorating the DOMS. Coaches, athletes, and medical practitioners are well aware of the symptoms of muscle damage after eccentric exercise because it clearly affects subsequent exercise or performance (i.e., strength, power, range of motion and probably exercise economy). Muscle weakness requires a longer recovery and might have more impact on performance than soreness sensation. Therefore the present study is needed to help for the athletes to be safe from the above problems arising out of muscle damage. 1.5 SIGNIFICANCE OF THE PROPOSED STUDY IN THE CONTEXT OF CURRENT STATUS: INTERNATIONAL STATUS: Developed countries with their modern Know how are progressing rapidly in exploring the possibilities of various physiotherapy modalities to supplement the medical management thereby to facilitate early recovery.

NATIONAL STATUS: The wealth of knowledge that has been provided by our researchers regarding the use of various physiotherapy modalities for DOMS has to be collaborated with detailed well organized study. Such a scientific study will facilitate Indian researchers and clinicians to use these modalities to treat DOMS effectively. 1.6. OPERATIONAL DEFINITIONS: Delayed onset muscle soreness (DOMS) Muscle soreness experienced by individuals Who perform unaccustomed exercise that involves an eccentric component

Eccentric action Lengthening of a muscle under tension (Hall, 1991)

RECREATIONAL ATHLETE: Recreational athlete" means an individual participating in fitness training and conditioning, sports or other athletic competition, practices or events requiring physical strength, agility, flexibility, range of motion, speed or stamina and who is not affiliated with an amateur, educational or professional athletic organization or any association that sponsors athletic programs or events in the State. 2. OBJECTIVES PLAN AND SCOPE OF THE STUDY 2.1 AIM OF THE STUDY: To investigate the effects of three physiotherapy interventions in delayed onset muscle soreness and its influence on biochemical markers in recreational athletes. 2.2 OBJECTIVES OF THE STUDY: 1. To investigate creatine kinase (CK) and Lactate dehydrogenase (LDH) enzymatic activity taken at repeated time measures in 3 different physiotherapy interventions and compared with a control group. 2. To evaluate the effect of 3 physiotherapy modalities on Maximum isometric voluntary contraction (MIVC) in experimentally induced delayed onset muscle soreness in recreational athletes 3. To determine the effect of physiotherapy on pain parameters using VAS scale. 4. To compare the effectiveness of physiotherapy modalities on biochemical parameters(CK & LDH), maximum isometric voluntary contraction and pain scale taken at different
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times after experimentally inducing delayed onset muscle soreness in recreational athletes. 2.3 RELEVANCE AND SCOPE OF THE STUDY: Delayed onset muscle soreness (DOMS) is a familiar experience for the elite as well as the novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS (Cheung, Hume, Maxwell Sports Med. 2003). DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. Several theories have been proposed to explain the underlying cause of delayed onset muscle soreness, however none is universally accepted. There are also many anecdotal claims that the effects of DOMS can be reduced with various treatment modalities. Again no method has any conclusive, empirical support for the prevention of delayed onset muscle soreness. In India, recently increasing numbers are participating in athletic activities and are taking a more active approach to achieve health and wellness. This increase in activity exposes individuals to DOMS and the associated negative effects. Even though the benefits of regular exercise are well known, many of us don't do it. One reason may be that pain or discomfort sometimes goes along with fitness activities. Starting or continuing an exercise program may be easier if you understand what muscle soreness is and what to do about it. Interventions such as physiotherapy play a major role both in prevention and treatment for the negative effects associated with DOMS. Most of the individuals and athletes experience muscle soreness after unaccustomed exercises due to lack of training, this highly demands some intervention, and not much research have been done in India to meet those demands. Also, the exact role of a physiotherapist in alleviating the DOMS and therapeutic interventions is also not successful in India. 3. MATERIALS AND METHODOLOGY SUBJECTS: 160 normal collegiate recreational athlete subjects in the age group 18-25 years who were not under any training protocols and with no history of upper arm injury were recruited after approval from the Institutional Ethics committee. The number of subjects was determined by a power analysis with 90% power and a 1-tailed level of significance of P <.0.5 based on data from the pilot study. During the experimental period, subjects were

requested not to take any medication, change their diet, or perform any strenuous exercise. All subjects were informed about the meaning of the study. SAMPLING: Quota sampling technique was used and all the subjects were randomized equally in to four groups, each group having forty subjects. STUDY PERIOD: The study was conducted for a total period of two years and eight months. STUDY CENTER: The whole study was conducted in Saveetha University. PILOT STUDY: A pilot study was performed prior to data collection for the present study. The goal of the pilot study was to: (1) to collect data that will provide an opportunity to gain some practical experience in carrying out the proposed protocol, (2) ensure that instructions to subjects are clear and concise, and make modifications where necessary, (3) determine whether or not the soreness inducing exercise session would elicit the expected level of perceived soreness, (4) collect and analyze preliminary data. After the approval of ethical clearance from university, the pilot study was conducted. The main objective of the pilot study was to know the percentage of 1 RM to be selected for inducing delayed onset muscle soreness (DOMS) and to know their recovery from DOMS. In the pilot study, 9 college athletes were selected, and they were divided in to 3 groups, each group having 3 participants.70 % of 1 RM for group A, and 80 % of 1 RM for group B, and 90 % of 1 RM for group C have been taken to induce DOMS experimentally. Subjects were then given a VAS scale with specific instructions on how to record information regarding their level of soreness. From the results it was found that group B (80% of 1 RM) recovered faster when compared to group C. Group A did not developed the symptoms of DOMS. Group C took much time for pain recovery. Pain by VAS scale is the outcome measure taken at 24 hours and after 96 hours.
GROUP A (70% of 1RM) Mean 24 Hours 96 Hours 3 0.6 SD 1 1.15 GROUP B (80% of 1RM) Mean 7 4.3 SD 1 0.57 GROUP C (90 % of 1 RM) Mean 8.3 7.3 SD 0.57 0.57

From the results of the pilot study it was found that 80 % of 1 RM was enough to induce DOMS experimentally when compared to 70% and 90% of 1 RM. STUDY DESIGN: The research design consisted of Pre test- Post test true experimental study design with two factors (Groups and time) with repeated measures on time.
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3.1 STUDY PROCEDURE

PROCEDURE

160 collegiate athletes Participated in the study

Study divided in to 4 phases

PHASE-I BASELINE MEASUREMENT

PHASE-2 DOMS INDUCTION

Serum CK, LDH, MIVC and Pain measurement were taken at the baseline before inducing DOMS.

All participants were induced DOMS by an eccentric loading protocol with barbell after calculating 1 RM.

PHASE-3 TREATMENT After inducing DOMS, Participants were allocated randomly in to four groups. Each group consisting of 40 participants.

PHASE -4 POST TESTMEASUREMENT

Serum CK, LDH,MIVC and Pain measurement were taken at 24, 48, 72 and 96 hours before the treatment intervention

Group I Cryotherapy

Group II Ultrasound

Group III Exercises

Group IV Control

Treatment was applied at 24, 48, 72 and 96 hours.

3.2 INDUCTION OF DELAYED ONSET MUSCLE SORENESS: All the subjects were induced delayed onset muscle soreness (DOMS) by an eccentric loading protocol with a barbell (Tiidus and Ianuzzo, 1983) Eccentric Loading Protocol: 1 RM Calculation: The subject was asked to lift a fixed weight in his hand from a fully extended to a fully flexed position in standing position. The amount of weight was determined by subject's perception. Initially 1 Repetitive maximum (RM) was calculated by using the formula [Number of repetitions + 1] X Weight used. 30 80 % of 1 RM was calculated and used for inducing DOMS. Concentric contractions were followed by eccentric contractions for 7 seconds. Assistance was given for concentric contractions and no assistance given for eccentric contractions and all the subjects were verbally encouraged. The subjects were instructed to perform 4 sets, 1 set consisting of 10
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repetitions, with a rest period of 3-5 minutes between each set. After inducing DOMS the subjects were divided into one of four treatment groups. 3.3 TREATMENT PROTOCOLS Treatments were administered at 24, 48, 72, and 96 hours post exercise. The following protocols outline the treatment that subjects received in their respective groups. Group I: Cryotherapy-Ice massage was given by a method of direct application with ice bag technique for duration of ten to fifteen minutes after 24, 48, 72 and 96 hours. Group II: Phonophoresis- Participants in group II received Phonophoresis ( Phyaction 190i ultrasound), Intensity of 0.8 watts/cm2 for a duration of 8 minutes given after 24, 48, 72 and 96 hours. Group III: Participants in group III were instructed to do an exercise protocol. The individuals in the exercise group performed mild full ROM elbow flexion and extension exercises, with only the gravitational pull on the hand and arm providing resistance. The repetitions were performed continuously during a 20-second period and then rested for 40 seconds. This exercise /rest interval was continued for a total treatment time of 15 minutes. Group IV: Control-No therapy was administered. Rest advised for them.

3.4 POST TEST MEASUREMENTS DEPENDENT VARIABLES: Maximum isometric voluntary contraction (MIVC) of elbow flexors by modified hand held dynamometer, Plasma Creatine kinase (CK) and Lactate dehydrogenase (LDH) activity were measured from blood samples taken from Cubital veins. Pain assessment was made from VAS scale. All measurements were taken at the baseline, 24, 48, 72 and 96 hours after inducing delayed onset muscle soreness (DOMS). DATA COLLECTION: SERUM CK AND LDH LEVELS: The analysis is done in Erba Chem 5 plus v2 instrument, Blood samples of 2 ml were collected from all the subjects using a disposable syringe and the serum separated. Than 50 micro liters of serum added to1 ml of CK reagent, and incubated at 37 degree Celsius for 100 seconds in an incubator. Similarly 50 micro liters of serum added to 1 ml of LDH reagent, and incubated at 37 degree Celsius for 1 minute in an incubator.

11

Test has been done by using the kits from Agappe diagnosis following the standard protocol and readings displayed in the instrument were noted. This procedure was done at baseline, 24, 48, 72 and 96 hours and the values were noted.

MAXIMUM ISOMETRIC VOLUNTARY CONTRACTION (MIVC): INSTRUMENT: The dynamometer is a modified Wika pressure gauge (van der Ploeg, 1984) the pressure range is 0-300 Newton (N). The meter is equipped with a maximum indicating pointer with a resetting knob and a curved applicator. MEASUREMENT TECHNIQUE AND TEST PROCEDURE: At least one practice trial was given to the participants to familiarize them with the feel of pushing against the dynamometer. The participants then performed the action actively until they performed it correctly. Participants were asked to build their force gradually to a maximum voluntary effort over a self-determined 2-second period. They then maintain maximum effort for 5 additional seconds during which dynamometer was held stationary against the limb segment. A rest period lasting 1 or 2 minutes was provided before a second (repeat) measure of an action was taken. Peak force values were recorded for each trial from the digital readout on the dynamometer. The test was repeated three times and an average measure was taken. SUBJECT POSITION- Shoulder at neutral, elbow flexed at 900, Forearm supinated. Dynamometer placement- elbow just proximal to styloid process. Stabilization of subjectSuperior aspect of shoulder or arm. PAIN MEASUREMENT: The VAS consists of a 10-cm line with the two endpoints labeled with verbal descriptors. The patient is required to place a mark on the 10 cm line at a point that corresponds to the level of pain intensity he or she presently feels (Turk and Melzack 1992). VAS consists of a 10 cm line with descriptors at each end. At the left end there was the number zero with the descriptor "no soreness at all", and at the right end there was the number ten with the descriptor "soreness as bad as it could be". Each subject placed an x dong a 10 cm line to describe the amount of muscle soreness he/she was presently experiencing. Data was collected at baseline and at 96 hours. The Outcome measurements Creatine Kinase (CK), Lactate Dehydrogenase (LDH), Pain measurement, and Maximum Isometric voluntary contraction (MIVC) were taken at the baseline before inducing DOMS, and taken at 24, 48, 72 and 96 hours after inducing delayed onset muscle soreness (DOMS).
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4. STATISTICAL ANALYSIS AND RESULTS 4.1 CREATINE KINASE (Normal level =60-180 I Units/Liter) To find out the difference between the groups in each measure ONE WAY ANOVA is done. CREATINE KINASE VALUES IN CONTROL AND IN 3 EXPERIMENTAL GROUPS TAKEN AT DIFFERENT TIMES POST EXERCISE
Groups Baseline Mean Cryotherapy Phonoporesis Exercise Control Anova f value p value 86.38 81.50 94.70 86.80 2.19 SD 23.33 18.67 28.93 21.05 24 hours Mean 276.55 252.10 327.78 313.08 6.14 SD 66.21 71.58 122.16 80.07 48 hours Mean 606.50 589.95 558.70 661.00 2.32 SD 156.18 146.07 242.53 147.65 72 hours Mean 921.48 905.98 544.00 1003.05 19.44 SD 222.80 305.10 368.53 254.28 96 hours Mean 1134.18 1043.70 479.60 1244.65 27.49 SD 342.42 430.79 448.04 414.39

.091 NS

.001***

.077NS

.000***

.000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) RESULTS: From the above table values, it is noted that at baseline and at 48 hours, there is no significant difference seen in creatine kinase elevation between the four groups (p >0.05), But significant difference were observed at 24 hours, and after 72 hours and 96 hours (p<0.001) PAIRED t TEST ANALYSIS: To find out the changes between baseline-24 hours, 24-48 hours, 48-72 hours, 72-96 hours for all the four groups paired t test was used.
CREATINE KINASE VALUES ANALYSIS WITHIN THE GROUPS AT DIFFERENT TIMES

CK measures Mean Baseline-24 hrs 24-48 hrs 48-72 hrs 72-96 hrs 190.17 329.95 314.97 212.69

Cryotherapy SD 67.20 146.65 157.74 241.00 t value 17.89 14.22 12.62 5.58 p value .000*** .000*** .000*** .000*** Mean 170.6 337.85 316.02 137.72

Phonoporesis SD 71.6 121.20 250.905 259.74 t value 15.06 17.62 7.96 3.35 p value .000*** .000*** .000*** .002**

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CK measures Mean Baseline24 hrs 24-48 hrs 48-72 hrs 72-96 hrs 233.0 SD 113.48

Exercise t value 12.98 p value .000*** Mean 226.27 SD 79.48

Control t value 18.00 p value .000***

230.92 14.70 64.39

175.24 225.67 175.54

8.33 0.411 2.320

.000*** .683 .026

NS NS

347.92 342.04 241.60

119.03 185.64 293.98

18.48 11.65 5.19

.000*** .000*** .000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) RESULTS: In the above table it is observed that changes between baseline-24 hours, 24-48 hours, 48-72 hours, 72-96 hours for group 1 (Cryotherapy), group 2 (phonophoresis) and group 4 (control) were showing significant difference statistically (p<0.001), where as in group 3 (exercise) alone, the CK measures between baseline-24 hours and 24-48 hours were having significant difference (p<0.001) but measures between 48-72 hours and 72-96 hours were not showing significant difference statistically (p>0.05) ONE WAY ANOVA RESULTS: To find out the significant difference of changes of Creatine kinase measure from baseline- 24 hours, 24-48 hours, 48-72 hours, 72-96 hours (within the period) between the groups, One-way ANOVA test was used.

CK measures

Cryotherapy Mean SD

Phonoporesis Mean SD

Exercise Mean SD

Control Mean SD

f value

p value

0-24 hrs 24-48 hrs 48-72 hrs 72-96 hrs

190.17 329.95 314.97 212.69

67.20 146.65 157.74 241.00

170.6 337.85 316.02 137.72

71.6 121.20 250.90 259.74

233.0 230.92 14.70 64.39

113.48 175.24 225.67 175.54

226.27 347.92 342.04 241.60

79.48 119.03 185.64 293.98

4.88 5.82 26.68 12.54

.003** .001*** .000*** .000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.005) RESULTS: From the above table it is found that changes of creatine kinase measure from baseline- 24 hours, 24-48 hours, 48-72 hours, 72-96 hours (within the period) between the groups, were having statistical significant difference (p<0.001).

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CREATINE KINASE MEANS VALUES OF THE CONTROL AND 3 EXPERIMENTAL GROUPS TAKEN AT DIFFERENT TIME MEASURES

4.2 LACTATE DEHYDROGENASE (Normal level = 220-400 I Units/Liter) I.PAIRED t TEST ANALYSIS: To find out the changes between baseline-24 hours, 24-48 hours, 48-72 hours, 72-96 hours for all the four groups paired t test was used. LACTATE DEHYDROGENASE VALUES ANALYSIS WITHIN THE GROUPS IN DIFFERENT TIMES POST EXERCISE
Exercise LDH measures Baseline-24 hrs 24-48 hrs 48-72 hrs 72-96 hrs Mean 177.77 97.89 85.0 87.19 SD 85.15 90.79 120.55 77.26 t value 13.20 6.81 4.45 7.13 p value .000*** .000*** .000*** .000*** Mean 210.67 189.77 122.14 4.85 SD 85.14 87.12 94.92 171.91 Control t value 15.64 13.77 8.13 0.17 p value .000*** .000*** .000*** .859 NS

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LDH measures Mean

Cryotherapy SD t value p value Mean

Phonoporesis SD t value p value

Baseline-24 hrs 24-48 hrs 48-72 hrs 72-96 hrs

174.25 200.79 84.72 14.32

53.04 100.96 79.03 121.28

20.77 12.57 6.77 0.74

.000*** .000*** .000*** .460NS

171.62 191.799 87.12 25.19

74.15 78.88 130.03 137.48

14.63 15.37 4.23 1.15

.000*** .000*** .000*** .253NS

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) RESULTS: In the above table it is observed that changes between baseline-24 hours, 24-48 hours, 48-72 hours for all the four groups the LDH measures were showing significant difference (p<0.001), but the changes between 72-96 hours also were showing significant difference statistically only in group 3 (exercises), but in other 3 groups between 72-96 it was not having significant difference (p>0.05). II. ONE WAY ANOVA: To find out the difference between the groups in each measure one way ANOVA is done. LACTATE DEHYDROGENASE VALUES IN CONTROL AND IN 3 EXPERIMENTAL GROUPS TAKEN AT DIFFERENT TIMES POST EXERCISE
Groups Baseline Mean Cryotherapy Phonoporesis Exercise Control ANOVA f value p value 256.35 288.5 275.2 288.6 6.67 SD 35.77 28.53 46.88 35.85 24 hours Mean 430.6 460.12 452.97 499.35 4.77 SD 56.56 75.99 102.82 89.05 48 hours Mean 631.4 651.92 550.87 689.12 9.31 SD 122.35 94.22 143.96 118.39 72 hours Mean 716.12 739.05 465.87 811.27 50.38 SD 126.09 131.17 141.39 136.77 96 hours Mean 730.45 713.85 378.67 806.42 38.82 SD 171.23 207.03 119.97 249.70

.000***

.003**

.000***

.000***

.000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) RESULTS: The above table shows that at baseline, 24hours, 48 hours,72 hours and at 96 hours the LDH values between the four groups were statistically having significant difference (p<0.001).
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III.ONE WAY ANOVA: To find out the significant difference of changes of lactate dehydrogenase measure from baseline- 24 hours, 24-48 hours, 48-72 hours, 72-96 hours (within the period) between the groups, One-way Anova test was used.
Cryotherapy LDH measures Mean SD Mean SD Mean SD Mean SD Phonoporesis Exercise Control f value p value

Baseline24 hrs 24-48 hrs 48-72 hrs 72-96 hrs

174.25

53.04

171.62

74.15

177.77

85.15

210.67

85.14

2.33

.076Ns

200.79 84.72 14.32

100.96 79.03 121.28

191.799 87.12 25.19

78.88 130.03 137.48

97.89 85.0 87.19

90.79 120.55 77.26

189.77 122.14 4.85

87.12 94.92 171.91

11.59 29.68 4.48

.000*** .000*** .005**

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) RESULTS: One way ANOVA results shows that the LDH changes between the four groups were found to have significant difference statistically at 24-48 hours, 48-72 hours and at 7296 hours. LACTATE DEHYDROGENASE MEAN VALUES OF THE CONTROL AND 3 EXPERIMENTAL GROUPS TAKEN AT DIFFERENT TIME MEASURES

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4.3.

Maximum Isometric Voluntary Contraction(MIVC):

MIVC MEAN VALUES OF THE CONTROL AND 3 EXPERIMENTAL GROUPS TAKEN AT DIFFERENT TIME MEASURES

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4.4 REPEATED MEASURES ANOVA RESULTS:

To find out the overall changes within the group Repeated ANOVA was adopted.
REPEATED MEASURES ANOVA FOR DEPENDENT VARIABLES CK, LDH AND MIVC BY GROUP AND TIME Groups Creatine Kinase IU/L (CK) Lactate dehydrogenase IU/L (LDH) Repeated measures ANOVA f value 1947.39 2333.43 840.49 1599.87 Maximum Isometric Voluntary contraction (MIVC) lbs P value Repeated P value measures ANOVA f value 0.000*** 1531.01 0.000*** 0.000*** 1790.19 0.000*** 2226.80 0.000*** 2600.80 0.000*** 0.000*** 0.000***

Cryotherapy Phonophoresis Exercise Control

Repeated measures ANOVA f value 844.63 512.93 136.23 759.53

P value

0.000*** 0.000*** 0.000*** 0.000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.005) RESULTS: Repeated measures ANOVA results shows that the CK, LDH and MIVC measures overall changes within the groups for all the four groups were found to have difference statistically significant (p<0.001) 4.5 Pain Score: To find out the difference between the groups in each measure one way ANOVA is done. PAIN VAS SCORES FOR FOUR GROUPS TAKEN AT PRE AND POST TREATMENT LEVELS
Groups Mean Cryotherapy Phonoporesis Exercise Control Anova f value p value 5.08 5.12 5.07 5.13 0.110 . 954NS 24 hours SD 0.512 0.51 0.52 0.62 Mean 2.90 1.145 1.94 2.915 183.4 .000*** 96 hours SD 0.49 0.258 0.33 0.459

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The above table shows that pain scores at 24 hours between the groups were not found to have significant difference (p>0.05) but at 96 hours the pain scores were showing statistically significant difference (p<0.001). To find out the significant difference of changes of Pain measure from 24-96 hours (within the period) between the groups, One-way ANOVA test was used.

Cryotherapy

Phonoporesis

Exercise

Control f value p value

Pain measures

Mean

SD

Mean

SD

Mean

SD

Mean

SD

24-96 hours.

2.18

0.41

3.98

0.55

3.13

0.38

2.21

0.50

133.19

.000***

Note: *p<0.05, **p<0.01, ***p<0.001, NS- Not significant (p>0.05) The differences of change in pain measure from 24-96 hours between the groups were found to be statistically significant in between the four groups (p<0.001)

5. DISCUSSION: The onset of muscle pain in all the four groups occurred within the first 24 hours following the eccentric exercise protocol, which is consistent with other studies, investigated the onset of DOMS resulting from exercise-induced muscle damage. (Nosaka, 1995) In the present study, three different Physiotherapy modalities were compared to facilitate the recovery of DOMS. In the present study, we found that electrotherapy modalities Cryotherapy and Phonophoresis do not have direct influence on reducing the biochemical markers like Creatine kinase (CK) and Lactate Dehydrogenase (LDH). However the modalities are useful in reducing the pain. When we compared the maximum isometric voluntary contraction (MIVC), Ultrasound is found to be better in improving the muscle
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contraction at 72 hours as compared to cryotherapy. The probable reason may be pain gate mechanism and anti-inflammatory action of Ultrasound is better than cryotherapy. In the present study, we compared exercises and electro modalities; exercise is effective in all the four parameters-CK, LDH, MIVC and pain. The probable reason may be breakup of adhesions from the injured, sore muscles takes place during exercise. Increased blood flow or temperature in the muscle helps to decrease the accumulation of noxious waste products. Endorphin release by neurons in the central nervous system increases during exercise. Increased afferent input is noted from large, low-threshold sensory units in the muscles (muscle group-Ia, Ib, and II fibers [gate control theory]). The training effect appears to be highly specific, not only for the particular muscles involved in the exercise, but also for the type of contractions performed. For example, Schwane and Armstrong (1983) found that in rats, the muscle damage that occurs during downhill running is prevented by downhill or level training but not by uphill training. The eccentric protocol causes more DOMS and rise in the plasma CK and LDH activity. Subjective enzymatic values (CK & LDH) remained elevated for at least 4 days after exercise induced muscle damage in group1 (cryotherapy), group 2 (phonophoresis) and in group 4 (control), but in group 3 (exercises), the values remained elevated for 2 days only, than the values start to decrease at 72 hours and the values were reaching near to the baseline values in day 4. Maximum Isometric voluntary contraction (MIVC) scores were found to be decreasing until 48 hours in all the groups, But however in group 3 (Exercises), the scores started to increase after 48 hours and in group 2 (Phonophoresis) the scores started to increase after 72 hours. In group 1 (Cryotherapy) and Group 4 (Control) the MIVC scores were not much improving even till 96 hours. Therefore we strongly recommend that exercises can be advised for the early recovery of DOMS in recreational athletes to facilitate their early participation.

6. CONCLUSION: In conclusion, the eccentric protocol causes more muscle soreness and rise in the plasma CK and LDH activity. Subjective enzymatic values remained elevated for at least 4 days after exercise induced muscle damage in group1 ( cryotherapy), group 2 ( phonophoresis ) and in group 4 ( control), but in group 3 ( exercises), the values remained elevated for 2 days only, than the values reached near to the baseline values in day 4. But in the variables MIVC and VAS scores, both phonophoresis (group 2) and exercises (group 3) were found to be effective when compared to cryotherapy (group 1) and control groups.
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7. REFERENCES: Armstrong, R. B. (1984). Mechanisms of exercise-induced delayed onset muscular soreness: a brief review- Medicine and Science in Sports and Exercise 16(6): 529-538. Arnheim DD. Modern Principles of Athletic Training. 7th ed. St Louis, MO: Times Mirror/Mosby; 1989:198-231. Barlas P, Robinson J, Allen J, et al. Lack of effect of acupuncture upon signs and symptoms of delayed onset muscle soreness [In Process Citation]. Clin Physiol. Nov 2000; 20(6):44956. Cannavino CR, Abrams J, Palinkas LA, et al. Efficacy of transdermal ketoprofen for delayed onset muscle soreness. Clin J Sport Med. Jul 2003; 13(4):200-8. Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. Am J Phys Med Rehabil. 2002 Nov; 81(11):S52-S69. Cobb CR, deVries HA, Urban RT, et al. Electrical activity in muscle pain. Am J Phys Med. Apr 1975; 54(2):80-87. Connolly DA, Lauzon C, Agnew J, et al. The effects of vitamin C supplementation on symptoms of delayed onset muscle soreness. J Sports Med Phys Fitness. Sep 2006; 46(3):462-7. Craig JA, Barron J, Walsh DM, et al. Lack of effect of combined low intensity laser therapy/phototherapy (CLILT) on delayed onset muscle soreness in humans. Lasers Surg Med. 1999; 24(3):223-30. Davis WJ, Wood DT, Andrews RG, et al. Elimination of delayed-onset muscle soreness by pre-resistance cardio acceleration before each set. J Strength Cond Res. Jan 2008; 22(1):21225. Friden, j, sjostrom, m. & ekblom, b. (1981). A Morphological study of delayed muscle soreness. Experientia 37, 506507. Friden, j., seger, j., sjostrom, m. & ekblom, b. (1983). Adaptive response in human skeletal muscle subjected to prolonged eccentric training. International Journal of Sports Medicine 4, 177183.
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Hedayatpour N, Falla D, Arendt-Nielsen L, et al. Sensory and electromyography mapping during delayed-onset muscle soreness. Med Sci Sports Exerc. Feb 2008; 40(2):326-334. Hough.T. (1902). Ergographic studies in muscular soreness. American Journal of Physiology 7, 7692. Johansson PH, Lindstrom L, Sundelin G, et al. The effects of preexercise stretching on muscular soreness, tenderness and force loss following heavy eccentric exercise. Scand J Med Sci Sports. Aug 1999; 9(4):219-25. McAnulty S, McAnulty L, Nieman D, et al. Effect of NSAID on muscle injury and oxidative stress. Int J Sports Med. Nov 2007; 28(11):909-15. Mekjavic IB, Exner JA, Tesch PA, et al. Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness. Med Sci Sports Exerc. Mar 2000; 32(3):558-63. Smith LL. Acute inflammation: the underlying mechanism in delayed onset muscle soreness? Med Sci Sports Exerc. 1991; 23:542-551. Tidball, 3. G. (1995). Inflammatory ce11 response to acute muscle injury. Medicine and Science in Sports and Exercise 27: 1022-1032. Warren GL, Ingalls CP, Lowe DA, Armstrong RB. Excitation-contraction uncoupling: major role in contraction-induced muscle injury. Exercise and Sport Sciences Reviews. 2001; 29:8287. Weber, M. D., F, J. Servedio, et al. (1994). The effects of three modalities on delayed onset muscle soreness. The Journal of Orthopaedic and Sports Physical Therapy 20(5): 236-242. LIST OF PUBLICATIONS: 1. Role of Physiotherapy in Ameliorating the Delayed Onset Muscle Soreness (DOMS) and Influence on Biochemical Markers of Recreational Athletes. The Journal of Indian Physiotherapists April 2010 Volume 4, Issue 1: 20-28.

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