Journal of Electromyography and Kinesiology 21 (2011) 356–362

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Journal of Electromyography and Kinesiology

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Evaluation of exercise-induced muscle damage by surface electromyography

Yue Zhou a, Yang Li b, Ruiyuan Wang a,⇑a Beijing Sport University, Graduate School, Beijing 100084, Chinab Chinese Winter Sport Federation, Beijing 100044, China

a r t i c l e i n f o a b s t r a c t

Article history:Received 27 December 2009Received in revised form 27 August 2010Accepted 27 September 2010

Keywords:ElectromyographyExercise-induced muscle damageEvaluateSerum CK

1050-6411/$ - see front matter � 2010 Elsevier Ltd. Adoi:10.1016/j.jelekin.2010.09.009

⇑ Corresponding author. Tel./fax: +86 10 62989978E-mail address: wangry@vip.sina.com (R. Wang).

Objective: To investigate the feasibility of a non-invasive and instant method to evaluate the degree ofexercise-induced muscle damage.Methods: Thirteen male college athletes (23.4 ± 1.0 year, 180.03 ± 3.51 cm, 75.93 ± 6.70 kg) took part inthe trial. Measures included serum creatine kinase (CK) after eccentric and endurance exercise, and sur-face electromyography (sEMG) during knee extension and flexion on a Biodex unit. Relation analysis wasemployed between sEMG and serum CK after the eccentric and endurance exercise.Results: There were positive correlations between serum CK at 24 and 48 h after eccentric exercise andthe AREA of sEMG for the slow isokinetic contraction before eccentric exercise (r = 0.69, P < 0.01 and0.64, P < 0.05, respectively). The zero crossing rate (ZCR) immediately after exercise was negatively cor-related with serum CK at 48 h after exercise for the slow and fast tests (r = �0.63 and �0.59, P < 0.05,respectively). Mean power frequency (MPF) and ZCR of sEMG at 6 h post endurance exercise were posi-tively correlated with serum CK at 24 h (r = 0.73 and 0.69, P < 0.05, respectively) for the fast isokinetictest.Conclusions: Exercise-induced muscle damage as evaluated by serum CK was associated with the AREA ofsEMG after eccentric exercise. The ZCR of sEMG was a good predictor of muscle damage after enduranceexercise.

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1. Introduction

Exercise-induced muscle damage (EIMD) is particularly preva-lent in intense strength training and endurance exercise. Typicalsymptoms are delayed onset muscle soreness and the decrease ofmuscle strength. EIMD usually increases during the 24 h after exer-cise, peaks between 24 and 72 h, and then gradually declines (Arm-strong, 1990). As it affects normal training and competition, it isvery important to have timely and effective evaluation methodsof skeletal muscle injury.

Mechanical stress of eccentric muscle action initiated the EIMDby changed the organization of the sarcolemma and sarcomerestructure. Disturbances in Ca2+ homeostasis with elevated intracel-lular [Ca2+]i activate the nonlysosomal cysteine protease, calpain.Calpain triggers the response of skeletal muscle protein breakdownand inflammatory changes (Zhang et al., 2008).

Despite the minor muscle damage after the endurance exercise,the changes in cytokines and other inflammatory mediators werequite higher than that following eccentric exercise (Suzuki et al.,1999; Hirose et al., 2004). Free radicals produced by incomplete

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reduction of oxygen in the respiratory chain can cause extensivedamage to cells, including their membranes (Petersen et al., 2001).

When muscle cells are injured, some proteins and enzymes leakout of the cells and enter the bloodstream. Skeletal troponin I(sTnI), creatine kinase (CK), myoglobin (Mb), and myosin heavychain (MHC) fragments can be used as plasma markers of skeletalmuscle damage after exercise (Sorichter et al., 1997). CK is themost important indicator that reflects an athlete’s muscle damage.It is related to the training intensity and sports characteristics(Clarkson et al., 1986). Sorichter et al. (1995) considered that CKis a more sensitive indicator in assessing muscle fiber damage thanmagnetic resonance imaging (MRI).

Measurement of CK is invasive, requiring blood obtained byintravenous methods or by a large quantity of finger blood. Regularmonitoring of CK can be very painful for athletes. In addition, themaximum level of serum CK often occurs 24–72 h after a high-intensity exercise bout (Armstrong et al., 1991; Ebbeling and Clark-son, 1989). This delays evaluation of the athlete’s muscle damage.Hence, it is necessary to explore a method that is non-invasive,straightforward and instantly reflects the status of muscle.

Morgan and Allen (1999) thought the changes in organization ofthe sarcomere structure and changes in excitation–contraction cou-pling appear to be the main contributors to the early reduction intension. Surface electromyography (sEMG) has become a common

Y. Zhou et al. / Journal of Electromyography and Kinesiology 21 (2011) 356–362 357

method used in athlete technical analysis (Nuber et al., 1986),muscle fiber type identification (Gerdle et al., 2000) and musclefatigue research (Taylor and Gandevia, 2008). Additionally, somescholars (e.g., McHugh et al., 2000) suggest that sEMG can indicatemuscle damage by selective recruitment of difference motor units.

Therefore, we hypothesized that sEMG, as a non-invasive andinstant method, would be associated with the exercise-inducedmuscle damage indicated by serum CK.

2. Methods

2.1. Participants

Thirteen male college athletes (23.40 ± 1.06 year; 75.93 ± 6.70kg; 180.03 ± 3.51 cm) volunteered to participate in this study afterthey were informed in detail of the nature of the experiment andpossible risks.

Written informed consent was given by each participant, and alocal ethics committee for the protection of research participantsgave approval concerning the project before its initiation. At theonset of the study, all participants completed health question-naires to screen for any potential health risk and attended the lab-oratory for a familiarization session.

The participants include sprinters, long jumpers, and middledistance runners. All are in good condition, and in preparationtraining period. During the test, athletes will not participate inintensive training courses any more.

2.2. Test procedure

The model of EIMD was built by both eccentric exercise andendurance exercise. Serum CK and surface EMG before and afterthese exercises were measured to assess the extent and character-istics of the muscle damage.

In the first testing period, seven participants performed theeccentric exercise and six performed the endurance exercise. Onemonth later in the second testing period, participants completedthe other exercise, so that each participant performed the twoexercises. VO2max was measured 2 days before the enduranceexercise.

Before each exercise, participants carried out a standardizedwarm-up. This consisted of 10 min (min) of jogging, five submaxi-mal and five maximal continuous jumps and standardizedstretches of the quadriceps muscles. Verbal encouragement was gi-ven to the participants during all exercise bouts.

The same experimental procedure (sEMG and serum CK mea-sures) was conducted before exercise, immediately after exercise(0 h), and 24-, 48-, and 72-h post exercise. Venous blood of 3 mlwas collected before every sEMG test.

2.2.1. Eccentric exerciseThe eccentric exercise consisted of three rounds of vertical jump

with 30 jumps in each round. Participants were expected to blastoff as high as possible. There was a 1-min rest between rounds.This was a submaximal eccentric exercise which would result insevere EIMD.

2.2.2. Endurance exerciseVO2max was measured by a graded load test on a cycle ergom-

eter (818E, Monark, Varberg, Sweden). Expired air was collectedand measured with Max II (Physio-Dyne Instrument Corporation,Quogue, NY). Two days later, the endurance exercise was con-ducted at 60% VO2max on the cycle ergometer for 60 min. Thiswas submaximal endurance exercise which was beyond the usualhabit of the 45 min running of the subjects.

It took about 15–20 min to measurement VO2max, which wouldnot affect the endurance exercise performance two days later.

2.3. sEMG test

Surface EMG (sEMG) of the vastus lateralis was measured bymaximal voluntary isokinetic contraction (MVC), which was per-formed on a Biodex isokinetic dynamometer (Biodex Corporation,Shirley, NY, United States). The concentric contraction includedfive bouts of slow (60�/s) and 15 bouts of fast (240�/s) left kneemaximal extension and flexion. The low and high angular velocitiesin isokinetic measurements are often used. It is generally thoughtthat a low angular velocity relates to maximal voluntary contrac-tion and a high angular velocity relates to muscle coordinationwhich is important in functional activities (Meeteren et al., 2002).

The participants were in a seated position with restrainingstraps across the chest and over the pelvis, in accordance withthe Biodex instructions. The axis of the dynamometer was alignedwith the axis of the knee joint. Range of movement (ROM) was10�–90� anatomical knee joint angle (0� at the full extension). Be-fore the measurements, there was a warming-up period duringwhich the submaximal movement was done three times. The restperiod between the two angular velocities maximal effort was2 min.

Two surface electrodes were fixed to the left leg over the vastuslateralis, with 20 mm interelectrode distance, and with the refer-ence electrode being fixed adjacently. Hair was removed with a ra-zor, and skin was cleaned with alcohol. Signals were recorded witha MegaWin ME3000 device (MEGA Electronics, Ltd., Kuopio, Fin-land), sampling rate of 1000 Hz, and analyzed by MegaWin 2.07EMG analysis software.

Integrated EMG was divided by the integration time and consid-ered as average EMG (AREA), which reflects the discharge magni-tude of the active muscle. The number of times that theamplitude of the signal crossed the zero value of the signal (zerocrossing rate, ZCR) and the mean power frequency (MPF) reflectsthe characteristics of frequency of EMG, on the basis of fast Fouriertransformation.

In the present study, we chose slow (60�/s) and fast (240�/s)knee extension movements as the standard tests. The purposewas to determine the distinguishing characteristics between fastand slow motor unit recruitment in muscle contraction. It iscommonly thought that more motor units can be recruited inthe slow movement, and thus produce greater force (Barnes,1980).

2.4. Serum CK measurement

Blood samples were obtained from the antecubital vein. Coagu-lated blood was separated immediately by centrifugation at 1200gfor 10 min at �4 �C. The serum samples were frozen and stored at�40 �C for later analysis of CK. The serum CK activity was deter-mined by enzyme dynamic method with kits purchased from Bio-sino Biotechnology Company Ltd. A Rayto RT-1904C semi-autochemistry analyzer was used for measurement.

2.5. Statistical analysis

All data are expressed as mean ± SD (tables) or ±SE (figures).The data recorded during the exercise and recovery were statisti-cally tested using a one-factor (time) ANOVA. When significantmain effects were found, the Tukey test was used for post hoc anal-ysis. Significance was accepted when P < 0.05. All statistical analy-ses were undertaken using SPSS 13.0 (SPSS, Inc., Chicago, IL).

Correlational analyses and linear regression were employed toassess whether there were relationships between muscle electrical

Fig. 1. (A) Serum CK concentration before and after high-intensity eccentric exercise. (B) sEMG index, AREA for the slow (sAREA) and fast contractions (fAREA) of kneeextensor before and after high-intensity eccentric exercise. (C) sEMG index, MPF for the slow (sMPF) and fast contractions (fMPF) of knee extensor before and after high-intensity eccentric exercise. (D) sEMG index, ZCR for the slow (sZCR) and fast contractions (fZCR) of knee extensor before and after high-intensity eccentric exercise.

358 Y. Zhou et al. / Journal of Electromyography and Kinesiology 21 (2011) 356–362

activity and changes in exercise-induced muscle damage indicatedby serum CK.

3. Results

3.1. Changes in serum CK and sEMG after eccentric exercise

After high-intensity eccentric exercise, the serum CK concentra-tion increased over time (Fig. 1A). There was a progressive increasefrom 24 to 48 h after exercise (P < 0.05). The CK level was still equiv-alent to seven times higher than baseline at 72 h after exercise.

As shown in Fig. 1B, the AREA of the slow isokinetic extensordecreased in the 6 h after high-intensity eccentric exercise(P < 0.05). After a slight increase, there was a sharp decline at72 h post exercise (P < 0.05). MPF and ZCR showed similar patterns(Fig. 1C and D, respectively).

The fast isokinetic extensor AREA, MPF and ZCR showed trendssimilar to the slow speed, but with slightly lower values.

3.2. Changes in serum CK and sEMG after endurance exercise

After the endurance exercise, serum CK increased to a maxi-mum at 24 h post exercise (P < 0.05), then decreased gradually(Fig. 2A).

As shown in Fig. 2B–D, after endurance exercise the AREA and MPFchanged slightly after exercise for the slow isokinetic movement. Theminimum value of ZCR appeared at 6 h after exercise; this value wassignificantly different from the other time-points (P < 0.05).

The fast isokinetic extensor AREA, MPF and ZCR of sEMGshowed similar patterns to the slow speed movement after endur-ance exercise, but the values were lower.

3.3. Correlation and regression between the CK and sEMG indicators

3.3.1. Eccentric exerciseAs shown in Table 1, there were positive correlations between

the serum CK at 24 and 48 h after eccentric exercise and theEMG AREA for slow isokinetic contraction before eccentric exercise(r = 0.69, P < 0.01 and 0.64, P < 0.05, respectively). ZCR immediatelyafter exercise was negatively correlated with serum CK at 48 hafter exercise for the slow and fast tests (r = �0.63 and �0.59,P < 0.05, respectively).

In order to estimate muscle damage after eccentric exercise,regression analysis was used to establish the serum CK forecastingequation through the EMG indicators pre or post exercise, asshown in Fig. 3.

3.3.2. Endurance exercisesFor the slow contraction, there were no significant correlations

between indicators of EMG and serum CK pre and post enduranceexercise (Table 2). In contrast, for the fast contraction the MPF andZCR of sEMG at 6 h post exercise were positively correlated withserum CK at 24 h post exercise (r = 0.73 and 0.69, P < 0.05,respectively).

To estimate muscle damage after endurance exercise, regres-sion analysis was used to establish the serum CK forecasting equa-tion through the EMG indicators after exercise, as shown in Fig. 4.

4. Discussion

The purpose of this study was to determine whether sEMG canmeasure muscle ultrastructural damage as a non-invasive and in-stant alternative method to serum CK.

Fig. 2. (A) Serum CK concentration before and after endurance exercise. (B) sEMG index, AREA for the slow (sAREA) and fast contractions (fAREA) of knee extensor before andafter endurance exercise. (C) sEMG index, MPF for the slow (sMPF) and fast contractions (fMPF) of the knee extensor before and after endurance exercise. (D) sEMG index, ZCRfor the slow (sZCR) and fast contractions (fZCR) of knee extensor before and after endurance exercise.

Y. Zhou et al. / Journal of Electromyography and Kinesiology 21 (2011) 356–362 359

Muscle fatigue can be identified by a decrease in the frequencycomponents of the EMG signal, typically represented by a fall inthe center frequency (Doud and Walsh, 1995). Fatigue is the de-cline of muscular fiber function and weakening of contractionpower, but muscle damage emphasizes the disruption of fibersstructure. Muscle fiber damage will cause muscle fatigue.

There are two neural mechanisms responsible for controllingmuscular contractions: rate coding and recruitment. Rate codingrepresents the changes in firing frequency of the active motorunits, whereas recruitment indicates the total number and typeof motor unit activated (Stein, 1974). When the skeletal musclewas damaged, the EMG will produce corresponding changes.

4.1. Changes in EMG after high-intensity eccentric exercise

The EMG signal area such as iEMG can reflect the total potentialof activating motor units during muscle contraction. Many studieshave reported EMG changes during muscle contraction. For exam-ple, Tesch et al. (1990) found that iEMG during concentric contrac-tion was higher than in eccentric contraction. Those studiesfocused on the EMG changes during exercise-induced muscle fati-gue. Recently some researches have investigated changes in EMG

Table 1Correlation analysis between EMG indicators and CK after eccentric exercise.

Pre 0 h 6 h

AREA MPF ZCR AREA MPF ZCR AREA

60�/s CK24h 0.69** �0.44 �0.52 0.32 �0.37 �0.51 0.31CK48h 0.64* �0.50 �0.57* 0.51 �0.55 �0.63* 0.41

240�/s CK24h 0.50 �0.33 �0.44 0.03 �0.12 �0.35 0.27CK48h 0.64* �0.36 �0.49 0.37 �0.37 �0.59* 0.29

* P < 0.05.** P < 0.01.

after exercise. For example, Semmler et al. (2007) reported thateccentric exercise altered motor unit activation.

The results of this study showed that the trends in AREAchanges were similar in both the fast and slow speed contractions.There were, however, differences in the amplitude of the EMG in-crease during exercise to fatigue. After eccentric exercise, the mus-cle activity decreased during tests. A possible reason is that somemuscle fibers were inhibited by ultrastructure damage after eccen-tric contraction, and this impaired the neuromuscular function.

The loss of cytoskeleton (e.g., desmin and dystrophin), whichwas part of the muscle cell damage, was early and specific featuresof eccentric damage that contributed to the sarcomeric disorgani-zation (Lieber et al., 1996). The cytoskeleton damage and mem-brane disruption were mediated primarily by increased Ca2+

influx into muscle cells and subsequent activation of calpain, leadto muscle weakness and damage (Zhang et al., 2008).

Because isokinetic contractions are maximal contractions bynature at different contractile velocities, it would seem probablethat all available motor units were recruited and each of theseunits had achieved its maximum firing frequency (Barnes, 1980).Exercise-induced ultrastructure damage reduced the quantity ofavailable motor units.

24 h 48 h

MPF ZCR AREA MPF ZCR AREA MPF ZCR

�0.59* �0.59* 0.75** �0.43 �0.37 0.80** �0.71** �0.67*

�0.33 �0.37 0.63* �0.49 �0.29 0.59* �0.57* �0.54

�0.36 �0.41 0.20 �0.14 �0.11 0.04 �0.04 �0.390.03 �0.08 0.21 �0.02 �0.08 0.02 0.34 �0.04

Fig. 3. The relationships between serum CK at 48 h after eccentric exercise and theAREA of sEMG for the slow isokinetic contraction before eccentric exercise (solidline), and the ZCR of sEMG immediately after exercise for the slow contraction(dash-dot line).

Fig. 4. The relationships between serum CK at 24 h after endurance exercise andthe ZCR (solid line) and MPF (long dash line) of sEMG for the fast isokineticcontraction at 6 h post endurance exercise.

360 Y. Zhou et al. / Journal of Electromyography and Kinesiology 21 (2011) 356–362

For the EMG frequency domain indicators MPF and ZCR, wefound that the frequency decreased slightly during the isokineticcontraction test immediately after eccentric exercise. Althoughthe frequency recovered after 6 h, this result was a trend only.The left shift of the frequency spectrum is generally explained asa motor neuron discharge in sync or less fast motor units inhibitedor removed from the contraction. Wretling et al. (1997) reportedthat the absolute plateau level of MPF for the vastus lateralis mus-cle showed a significant negative correlation with the area percent-age of type I fibers (r = �0.71). Kupa et al. (1995) confirmed thatmuscles with a greater percentage of fast fibers exhibited greaterinitial values of medium frequency (MF) as well as a greater reduc-tion over the course of the contraction.

From the results above, it appears that eccentric exercise re-cruits more fast twitch fibers and may result in greater fast motorunit injury.

4.2. sEMG changes after endurance exercise

As time domain indicators of EMG, AREA showed no substantialchange in either the fast or slow speed isokinetic tests after endur-ance exercise. This was in contrast with the decline after eccentricexercise. These results for the AREA of sEMG might be related tothe extent of the muscle damage and the recruitment features ofdifferent fiber types. As indicated by the smaller increase in serumCK, the endurance exercise resulted in less muscle damage thanthe eccentric exercise.

Linssen et al. (1991) studied patients with congenital myopathyand found that the patients with 95–100% type I fibers showed less

Table 2Correlation analysis between EMG indicator and CK after endurance exercise.

Pre 0 h 6 h

AREA MPF ZCR AREA MPF ZCR AREA

60�/s CK24h �0.29 0.25 0.28 �0.32 0.10 0.22 0.03CK48h �0.41 0.36 0.28 �0.47 0.20 0.23 �0.19

240�/s CK24h �0.47 0.27 0.43 �0.48 0.20 0.31 �0.49CK48h �0.49 0.35 0.45 �0.51 0.23 0.28 �0.49

* P < 0.05.** P < 0.01.

fatigability than those with predominantly type II fibers. This resultwas evident in a nearly absent decrease in muscle membraneexcitability and only a slight increase in the sEMG amplitude,and was compared with patients having 80% type I fibers andhealthy controls.

As frequency indices, MPF and ZCR showed similar trends forthe slow and fast tests after endurance exercise. They bothdecreased slightly after exercise, and reached the lowest level at6 h post exercise for ZCR (P < 0.05) and 24 h post exercise forMPF, then gradually recovered. The decline was more marked thanafter eccentric exercise.

The relationship between the ZCR and motor unit action poten-tials is linear for low- and constant-level contractions (Avela et al.,1999). There is a good correlation between the time course of theZCR and the median frequency, and thus the ZCR of the EMG canbe used as a simple method to measure surface EMG spectralchanges, under a variety of conditions (Inbar et al., 1986).

It has been suggested (Potvin, 1997) that the MPF decreaseassociated with fatigue may be due to a temporal elongation ofthe motor unit action-potential waveform, increased lactate levelsand/or impairment of the ionic pump and a subsequent decrease inmuscle fiber conduction velocities. In the current study, the ob-served declines in frequency appear to be due to the latter, andassociated with the mechanism of muscle damage induced byexercise. It is also clear that contracting skeletal muscles generatefree radicals (Davies et al., 1982; Alessio et al., 1988), and impor-tantly, intense and prolonged exercise can result in oxidative dam-age to both proteins and lipids in the contracting myocytes(Powers and Jackson, 2008). Alternative explanations include theeffects of ionic changes on the action potential, failure of SR Ca2+

24 h 48 h

MPF ZCR AREA MPF ZCR AREA MPF ZCR

0.01 �0.12 �0.37 0.00 0.25 �0.45 0.30 0.270.09 �0.02 �0.32 �0.03 0.26 �0.55 0.21 0.15

0.73** 0.69* �0.57 0.62* 0.58 �0.64* 0.22 0.190.47 0.51 �0.47 0.37 0.58 �0.74** 0.27 0.14

Y. Zhou et al. / Journal of Electromyography and Kinesiology 21 (2011) 356–362 361

release by various mechanisms, and the effects of reactive oxygenspecies (Allen et al., 2008).

4.3. The correlation analysis between serum CK and EMG

The correlation analysis indicated that the peak CK had amoderate correlation with AREA of slow isokinetic tests beforeexercise(r = 0.69–0.64, P < 0.05). Interestingly, this suggests thatthe higher the activity of the muscle was, the more serious thedamage would be after eccentric exercise. The peak CK had a mod-erate negative correlation with ZCR of slow isokinetic immediatelyafter exercise (r = �0.63, P < 0.05). This may be related to the ultra-structure damage induced by eccentric exercise, especially for fasttwitch fiber damage, which made the frequency shift to the left.Greater declines in ZCR were associated with greater CK leakedfrom damaged muscle. Comparing the correlation analysis results,the index of sEMG for the slow isokinetic test was better than thatfor the fast test.

After the endurance exercise, EMG signals and serum CK sug-gested that muscle fatigue was not serious and there was littlemuscle damage. The peak CK and AREA of sEMG were negativelycorrelated after endurance exercise; however, this result was notstatistically significant. In contrast, the MPF and ZCR of sEMG at6 h post exercise were positively correlated with the peak CK value(r = 0.73 and 0.69, P < 0.05) for the fast isokinetic test. That indi-cates that the higher frequency features of sEMG during fast testafter endurance exercise were associated with more CK leakagefrom the muscle. However, it is not fully understood why the peakCK was positively correlation with MPF and ZCR during the fastisokinetic contractions at 6 and 24 h. It may be due to a selectivefatigue of the slow twitch fibers that are more susceptible to dam-age in endurance exercise. During fast isokinetic contraction, morefast twitch fibers can remain recruited after endurance exercise,which preserves the conduct velocities and higher frequency(Turner et al., 2008), and means that more slow twitch fibers aredamaged.

There are many factors that affect the process of exercise-in-duced muscle damage and the content of serum CK, such as theelevated intracellular [Ca2+]i (Zhang et al., 2008), the immuneinflammatory response (Hirose et al., 2004; Suzuki et al., 1999),and CK clearance rate (Volfinger et al., 1994), etc. All of these willcause prediction errors. Therefore, the serum CK level at exerciseslater 24 or 48 h were not only relevant to the features of recruit-ment and fire rate.

5. Conclusion

It was possible to predict the delayed peak value of serum CKwith the EMG before and after exercise. The exercise-induced mus-cle damage measured by serum CK was associated with the AREAand ZCR of sEMG during slow isokinetic contractions after eccen-tric exercise. The MPF and ZCR of sEMG during fast isokinetic con-tractions were good predictors of muscle damage after enduranceexercise.

Acknowledgments

The authors would like to acknowledge those subjects that par-ticipated in this study. This work was supported by the NationalNatural Science Foundation of China (Grant No. 30570896) andthe Foundation of Doctor Degree Thesis from the Ministry of Edu-cation of China (Grant No. 20060043002).

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Yue Zhou earned a PhD degree in exercise physiologyfrom Beijing Sport University in 2005. He is currently anAssociate Professor in the Sport Science College of Bei-jing Sport University. His research focuses on influenceof exercise on the structure and function of muscle.

Yang Li earned his M.S. in exercise physiology fromBeijing Sport University, and is currently an AssociateResearcher in Chinese Winter Sport Federation. Hisresearch focuses on the monitoring and assessment ofathlete performance.

Ruiyuan Wang earned a PhD degree in exercise physi-ology from Beijing Sport University. He is currently aProfessor in the Graduate School of Beijing Sport Uni-versity. His research focuses on influence of exercise onthe structure and function of muscle.