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Muscle Damage Response in Female Collegiate Athletes After Repeated Sprint Activity

Keane, Karen M.; Salicki, Rebecca; Goodall, Stuart; Thomas, Kevin; Howatson, Glyn

Journal of Strength and Conditioning Research: October 2015 - Volume 29 - Issue 10 - p 2802–2807
doi: 10.1519/JSC.0000000000000961
Original Research

Keane, KM, Salicki, R, Goodall, S, Thomas, K, and Howatson, G. Muscle damage response in female collegiate athletes after repeated sprint activity. J Strength Cond Res 29(10): 2802–2807, 2015—Exercise-induced muscle damage (EIMD) is a well-investigated area, however there is a paucity of data surrounding the damage response in females. The aim of this study was to examine the damage responses from a sport-specific bout of repeated sprints in female athletes. Eleven well-trained females (mean ± SD; age: 22 ± 3 years; height: 166.6 ± 5.7 cm; mass: 62.7 ± 4.5 kg) in the luteal phase of the menstrual cycle completed a repeated sprint protocol designed to induce EIMD (15 × 30 m sprints). Creatine kinase, countermovement jump height, knee extensor maximal voluntary isometric contraction (MVIC) force, delayed onset muscle soreness (DOMS), 30-m sprint time, and limb girth were recorded before, after, 24, 48, and 72 hours after exercise. Creatine kinase was elevated at 24, 48, and 72 hours (p ≤ 0.05), peaking at 24 hours (+418%) and returning toward baseline at 72 hours. Countermovement jump height was reduced immediately after, 24, and 48 hours (p ≤ 0.05). Sprint performance was also negatively affected immediately after, 24, 48, and 72 hours after exercise. Muscle soreness peaked at 48 hours (p < 0.01) and remained significantly elevated at 72 hours after exercise (p < 0.01). Limb girth and MVIC did not alter over time. This study provides new information on the EIMD response in trained females after a sport-specific bout of repeated sprints. Importantly, this damage response has the potential to negatively affect performance for several days after exercise.

1Department of Sport, Exercise and Rehabilitation, Northumbria University, Newcastle, United Kingdom; and

2Water Research Group, School of Environmental Sciences and Development, Northwest University, Potchefstroom, South Africa

Address correspondence to Glyn Howatson, glyn.howatson@northumbria.ac.uk.

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Introduction

Exercise-induced muscle damage (EIMD) is a popular area of investigation. Numerous signs and symptoms are associated with EIMD, including elevated muscle soreness, inflammation, systemic appearance of intramuscular proteins, and a concurrent decrement in physical performance (1). These indices can persist for several days and are precipitated by an initial mechanical disruption of the contractile apparatus during the damaging exercise and a secondary inflammatory response (18). The damage response has been well established in male populations (5,15,17,19,33); however, there is a paucity of literature investigating EIMD in females.

Various factors could potentially modulate the EIMD response in females, including oral contraceptive use, and the potential protective effect of estrogen (10,23,29,31,37,42). There is some evidence suggesting that females are less fatigable than males (20) and the subsequent recovery after damaging exercise is known to be quicker (7). The faster recovery from damaging exercise has largely been attributed to the protective effect of estrogen, but there has been no attempt to control for the menstrual cycle where large changes in sex hormones can be seen throughout the course of the menstrual cycle (9). This could potentially influence both the damage response and recovery process. It therefore makes the expectation tenable that the damage response in females could be somewhat different to the well-established response in males. However, it is critical to understand the damage-recovery response with control over the menstrual cycle to ascertain the implications of damaging exercise in female athletes.

In addition to the lack of data on the damage response in female athletes, much of the existing literature investigating EIMD uses damage protocols that lack specificity to a sporting context and are often eccentric biased (3,5,6,8,17,38,40), and in isolated muscle groups (3,5,6,9,19). Intermittent sports, such as soccer, rugby, and basketball that require periods of high intensity, repeated sprint activity, and changes of velocity (4) and direction (39), elicit significant muscle damage and prolonged decrements in function. Given the prevalence of both male and female participation in sports of this nature, further research is warranted with more sport-specific damage models to better understand the consequences of damaging repeated sprint activity (17). Establishing these responses in female athletes in particular will provide new important information on the damage response in this population that could influence recovery strategies and exercise prescription. Consequently, the aim of this study was to examine the magnitude of damage after a sport-specific repeated sprint protocol in females. We hypothesized that a repeated sprint exercise protocol would induce muscle damage in females and negatively affect performance in the subsequent days.

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Methods

Experimental Approach to the Problem

This investigation used a repeated sprint protocol with forced deceleration actions, which has previously been successfully used to induce muscle damage (17). A commonly used battery of muscle damage indices were measured before, immediately after, and 24, 48, and 72 hours after muscle damage; these were lower limb girth, muscle soreness (DOMS), total creatine kinase (CK) activity, countermovement jump (CMJ) height, maximal voluntary isometric contraction (MVIC), and sprint performance.

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Subjects

After ethical approval from the University Research Ethics Committee in accordance with Helsinki declaration, 11 female athletes (mean ± SD; age: 22 ± 3 years; age range 18–30 years, height: 166.6 ± 5.7 cm; mass: 62.7 ± 4.5 kg) were recruited and informed of the benefits and risks of the investigation before signing an institutionally approved informed consent document to participate in the study. All participants regularly participated in premier league collegiate or national league field-based team sports, specifically rugby union (n = 2), soccer (n = 8), and netball (n = 1). A menstrual cycle questionnaire was also completed to determine menstrual cycle phase; all testing took place during the early/mid luteal phase. Participants were free of injury and testing took place out of season. Participants were asked to refrain from strenuous exercise, alcohol, caffeine, nutritional supplements, and any anti-inflammatory drugs or alternative treatments for the duration of the study.

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Procedures

A 30-m section of an environmentally controlled (19° C and 70% RH) 60-m indoor running track was marked using cones and 2 sets of light timing gates (Brower Timing Systems, Brower, UT, USA). A further 10-m deceleration zone was also marked at the end of the 30-m section. Participants first completed a warm-up consisting of 400-m self-paced jogging, a series of dynamic sprint drills including high knees, heel flicks, and walking lunges, which were conducted over a measured 10-m section of the aforementioned indoor running track. This was followed by a series of 3 practice sprints at the participants perceived 60, 80, and 100% of maximum speed. After the warm-up, the participants were given 5 minutes to prepare themselves for the repeated sprint protocol, during which time, no static stretching was performed. Participants then stood 30 cm from the start line to avoid premature triggering of the timing system and completed 15 × 30 m sprints departing every 65 seconds with gates set up to record in the reverse order for the next sprint. Participants were told that all efforts must be maximal, and they were instructed to stop within the 10-m deceleration zone. The rest period was initiated when participants came to a complete halt and the repetition was completed. Standardized strong verbal encouragement was provided throughout the protocol.

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Limb Girth

Lower limb girth was measured at the midcalf. This was determined at baseline by the largest girth on the right leg while the subject remained standing in anatomical zero. The location was marked with permanent marker to ensure consistency on subsequent days. The mean of 2 measures at each site was used for analysis; the intrarater coefficient of variation (CV) for this procedure was <1.0%.

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Muscle Soreness

Subjective muscle soreness (DOMS) was measured using a 200-mm visual analog scale (VAS) with “no soreness” at one end and “unbearably painful” at the other and was a reflection of global soreness of the thigh. Soreness was indicated on the VAS after the participant performed a squat to a knee angle of approximately 90° with the feet shoulder width apart and then returning to the standing position.

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Creatine Kinase

Creatine kinase was determined using a capillary blood sample from the fingertip. A sample of whole fresh blood was analyzed immediately using a colorimetric assay procedure (Reflotron Plus; Roche Diagnostics, West Sussex, United Kingdom). The resting normal expected values for CK when using this equipment are between 50 and 200 IU·L−1; the CV for this instrument was <3%.

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Countermovement Jump Height

Countermovement jump height was assessed using a light timing system (Optojump; Microgate, Bolzano, Italy). Participants were instructed to squat down and jump vertically, with their hands on their hips throughout. Participants were advised that all jumps must be a maximal effort. Three trials with a 60-second rest were performed and the peak jump height was used for analysis.

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Maximum Voluntary Contraction

Maximal voluntary isometric contraction force of the nondominant knee extensor musculature was determined using a strain gauge (MIE Digital Myometer; MIE Medical Research Ltd., Leeds, United Kingdom). The knee joint angle was set before each contraction at 90° using a goniometer to minimize for error derived from alteration in muscle length (27,28,45). All participants completed 3 isometric MVICs of 3 seconds duration, separated by 60 seconds. The peak MVIC from the 3 contractions was used for analysis; the CV for this variable was <5%.

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Thirty-Meter Sprint Time

Participants completed a single maximal effort 30-m sprint where sprint time was recorded. The sprint was initiated from a line 30 cm behind the start line to prevent false triggering of the timing gates (Brower).

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Statistical Analyses

Statistical analyses were performed using PASW Statistics 21.0 for Windows (SPSS, Inc., Chicago, IL, USA). Descriptive statistics are reported as mean ± SD. Fatigue, fastest sprint time, and mean sprint time were calculated for the repeated sprint protocol: Fatigue = (100 × [total sprint time ÷ ideal sprint time]) – 100, in which total sprint time = sum of sprint times from all sprints and ideal sprint time = the number of sprints × fastest sprint time (17). For illustrative purposes, and to account for interindividual variability, CMJ height and sprint performance were presented in figure format as a change from baseline. The absolute scores were analyzed using a 1-way analysis of variance (ANOVA) with repeated measures and are presented in Table 1. Mauchly's test of sphericity was used to check homogeneity of variance for all variables; where necessary, any violations of the assumption were corrected using the Greenhouse-Geisser adjustment. Significant effects were followed up using Tukey post hoc analysis. The alpha level for statistical significance was set at p ≤ 0.05 a priori.

Table 1

Table 1

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Results

The repeated sprint protocol fastest and mean times were 4.93 ± 0.23 and 5.12 ± 0.23 seconds, respectively. The mean fatigue score was 4 ± 1%. All dependent variables with the exception of limb girth and MVIC showed significant time effects following the repeated sprints protocol (p ≤ 0.05), illustrating a muscle damage response. DOMS was elevated over time (F = 26.86, p < 0.001; Figure 1); post hoc analyses revealed elevations at 24 and 72 hours post, with a peak at 48 hours (Table 1). Creatine kinase was elevated (F = 13.34, p ≤ 0.05), at every time point compared with preexercise (Table 1; Figure 2). For muscle function measures, there was a significant main effect for 30-m sprint time (F = 8.29, p = 0.001; Figure 3B) and CMJ height (F = 9.78; p < 0.005, Figure 3A), but not for MVIC (Table 1). Decrements in sprint performance were evident across all time points (p ≤ 0.05). Countermovement jump height was reduced immediately after, 24, and 48 hours after exercise (p ≤ 0.05) but had returned to near baseline at 72 hours.

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

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Discussion

The aim of this study was to ascertain the magnitude of EIMD indices following a repeated sprint protocol in an athletic female population. Results demonstrated that the repeat sprint protocol induced muscle damage with increases in DOMS, plasma CK, sprint time, and reductions in CMJ height and 30-m sprint time, all of which persisted for several days after the exercise insult. These data are broadly in agreement with the literature reporting that EIMD in males is evident soon after strenuous exercise, peaks at 24–48 hours after exercise, and remains elevated for several days (7,18,41). Similar results have also been shown with exercise with a high eccentric component, such as downhill running (24) and plyometric jumps (15). However, this is the first study to specifically document the signs and symptoms of muscle damage in a female athletic population following a sport-specific EIMD protocol.

To date, the majority of research investigating EIMD has used male volunteers and the differences between the sexes are largely overlooked. There remains some controversy concerning the presence of sex differences in the response to damaging exercise in humans, whereas the animal literature clearly shows that females experience less damage than males (10,29,37). The pattern and magnitude of EIMD was somewhat different in our female sample when compared with previous research in males (17,26). First, lower peak CK values were observed in this study (307 ± 92 IU·L−1) in comparison with previous research using 100 drop jumps (16) and the Loughborough Intermittent Shuttle Test (28), which showed peak values in excess on 1,000 IU·L−1; and an identical repeated sprint protocol (17) using the same CK analyzer method, but in male volunteers (776 ± 312 IU·L−1). Despite this lower CK response, soreness levels reported in females in this study were higher than those previously reported in males (17) across all time points. However, detriments in muscle function after damaging exercise were not as substantial, with no change in MVIC and a return of CMJ toward basal levels by 48 hours. In contrast to previous work that showed decreases in knee extension force that extended to up to and beyond 48 hours, after damaging exercise (17,40), there was no change in this study. However, CMJ was reduced at 24 hours and sprint time was still effected up to 72 hours after EIMD. There is little doubt that training status and the degree to which participants are accustomed to the exercise insult will affect the damage-recovery profile (18) because of the presence of a repeated bout effect (19,30). Although it is beyond the scope of the current work to elucidate the time course differences in muscle function between studies, we speculate (based on previous work) that the preferential recruitment (12,32) and preferential damage of type 2 fibers (4,13) during heavy eccentric contractions led to an inability to generate “power,” which is an integral component of dynamic explosive activity, such as CMJ and sprint performance. Collectively, these data suggest that the magnitude and pattern of the functional, physiological, and perceptual response to EIMD in female athletes might be different to their male counterparts. However, further work is required to confirm our observations and to elucidate the possible reasons underpinning these responses in muscle function.

There is evidence to suggest that estrogen may have a protective effect against EIMD by stabilizing membrane properties (43). Estrogen has been suggested to have the ability to interact with the phospholipid double layer on the cell membrane thus stabilizing the membrane (11). This interaction has led to a suggestion that the hormone estrogen might alleviate muscle damage after a strenuous bout of exercise (7). This potential attenuation of membrane disruption might account for some of the steroid hormone's mitigating effects on CK and muscle function. Moreover, it has been suggested that females have a higher CK clearance rate from the blood, which might further explain why CK levels were lower in this study in comparison with past studies (17,26). Although CK release from the muscles is not a direct indicator of muscular damage, it is still recognized as a surrogate indicator of damage and a loss of sarcolemma integrity (36,46).

Another plausible mechanism that could explain the lower degree of damage is the difference in strength, power, speed, and potentially fatigue resistance, between the sexes (20,44). Male soccer players are relatively stronger, quicker, and more powerful than females (44), and during repeated sprint exercise, men experience a greater decline in performance compared with women (25), which is associated with the initial higher power (2). Males will therefore typically generate more force during repeated sprint exercise, experience greater fatigue, and potentially cause greater disturbance to homeostasis and greater EIMD as a result. Further support for this idea arises from observations that women are more fatigue resistant than men during isometric (14) and dynamic contractions (34), but not when matched for initial strength level, at least for sustained submaximal contractions (21,22). Differences in strength, power, speed, and fatigue resistance might explain the lower CK values and faster return of muscle function observed in females in this study compared with previous literature in males. Further research is warranted to determine sex difference in the damage response to exercise, particularly between men and women matched for initial strength level.

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Practical Applications

Our results demonstrate that a bout of sport-specific exercise induces muscle damage and affects functional performance on subsequent days in females. The data provides new information for athletes, coaches, scientists, and practitioners to better understand the consequences of females engaging in strenuous exercise of this nature. The ability to balance the consequences of training and competition and optimize recovery time to be well prepared for subsequent training and competition and to reduce the likelihood of injury is a constant dichotomous battle when performance schedules are so heavy. Clearly, there is a requirement for further research to examine the damage responses in this population after strenuous exercise paradigms and, importantly, if the EIMD response is modulated differently through phases of the menstrual cycle. Previously, Rampinini et al. (35) proposed that 48 hours is adequate recovery time after a simulated soccer game; based on observations from this study, more time is required before full recovery is reached after repeated sprint activity in female athletes.

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Acknowledgments

The authors thank the participants in this study for their participation.

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References

1. Assumpção Cde O, Rabello Lima LC, Dias Oliveira FB, Greco CC, Denadai BS. Exercise-induced muscle damage and running economy in humans. ScientificWorldJournal 2013. doi: 10.1155/2013/189149.
2. Billaut F, Bishop DJ. Mechanical work accounts for sex differences in fatigue during repeated sprints. Eur J Appl Physiol 112: 1429–1436, 2012.
3. Bowtell JL, Sumners DP, Dyer A, Fox P, Mileva KN. Montmorency cherry juice reduces muscle damage caused by intensive strength exercise. Med Sci Sports Exerc 43: 1544–1551, 2011.
4. Byrne C, Eston R. The effect of exercise-induced muscle damage on isometric and dynamic knee extensor strength and vertical jump performance. J Sports Sci 20: 417–425, 2002.
5. Chen TC, Chen H-L, Pearce AJ, Nosaka K. Attenuation of eccentric exercise-induced muscle damage by preconditioning exercises. Med Sci Sports Exerc 44: 2090–2098, 2012.
6. Chen TC, Lin K-Y, Chen H-L, Lin M-J, Nosaka K. Comparison in eccentric exercise-induced muscle damage among four limb muscles. Eur J Appl Physiol 111: 211–223, 2011.
7. Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. Am J Phys Med Rehabil 81: S52–S69, 2002.
8. Cockburn E, Robson-Ansley P, Hayes PR, Stevenson E. Effect of volume of milk consumed on the attenuation of exercise-induced muscle damage. Eur J Appl Physiol 112: 3187–3194, 2012.
9. Dannecker EA, Liu Y, Rector RS, Thomas TR, Filingim RB, Robinson ME. Sex differences in exercise-induced muscle pain and muscle damage. J Pain 13: 1242–1249, 2012.
10. Enns DL, Tiidus PM. Estrogen influences satellite cell activation and proliferation following downhill running in rats. J Appl Physiol (1985) 104: 347–353, 2008.
11. Enns DL, Tiidus PM. The influence of estrogen on skeletal muscle sex matters. Sports Med 40: 41–58, 2010.
12. Enoka RM. Eccentric contractions require unique activation strategies by the nervous system. J Appl Physiol (1985) 81: 2339–2346, 1996.
13. Friden J, Sjostrom M, Ekblom B. Myofibrillar damage following intense eccentric exercise in man. J Sports Med 4: 170–176, 1983.
14. Guenette JA, Romer LM, Querido JS, Chua R, Eves ND, Road JD, McKenzie DC, Sheel AW. Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes. J Appl Physiol (1985) 109: 35–46, 2010.
15. Highton JM, Twist C, Eston RG. The effects of exercise-induced muscle damage on agility and sprint running performance. J Exerc Sci Fit 7: 24–30, 2009.
16. Howatson G, Hoad M, Goodall S, Tallent J, Bell PG, French DN. Exercise-induced muscle damage is reduced in resistance-trained males by branched chain amino acids: A randomized, double-blind, placebo controlled study. J Int Soc Sports Nutr 8: 9, 2012.
17. Howatson G, Milak A. Exercise-induced muscle damage following a bout of sport specific repeated sprints. J Strength Cond Res 23: 2419–2424, 2009.
18. Howatson G, van Someren KA. The prevention and treatment of exercise-induced muscle damage. Sports Med 38: 483–503, 2008.
19. Howatson G, Van Someren K, Hortobagyi T. Repeated bout effect after maximal eccentric exercise. Int J Sports Med 28: 557–563, 2007.
20. Hunter SK. Sex differences in human fatigability: Mechanisms and insight to physiological responses. Acta Physiol 210: 768–789, 2014.
21. Hunter SK, Critchlow A, Enoka RM. Influence of aging on sex differences in muscle fatigability. J Appl Physiol (1985) 97: 1723–1732, 2004.
22. Hunter SK, Critchlow A, Shin IS, Enoka RM. Fatigability of the elbow flexor muscles for a sustained submaximal contraction is similar in men and women matched for strength. J Appl Physiol (1985) 96: 195–202, 2004.
23. Iqbal S, Thomas A, Bunyan K, Tiidus PM. Progesterone and estrogen influence postexercise leukocyte infiltration in overiectomized female rats. Appl Physiol Nutr Metab 33: 1207–1212, 2008.
24. Kirwan JP, Hickner RC, Yarasheski KE, Kohrt WM, Wiethop BV, Holloszy JO. Eccentric exercise induces transient insulin resistance in healthy individuals. J Appl Physiol (1985) 72: 2197–2202, 1992.
25. Laurent CM, Green JM, Bishop PA, Sjökvist J, Schumacker RE, Richardson MT, Curtner-Smith M. Effect of gender on fatigue and recovery following maximal intensity repeated sprint performance. J Sports Med Phys Fitness 50: 243–253, 2010.
26. Leeder J, Gissane C, van Someren K, Gregson W, Howatson G. Cold water immersion and recovery from strenuous exercise: A meta-analysis. Br J Sports Med 46: 233–240, 2012.
27. Leeder J, van Someren KA, Bell PG, Spence JR, Jewell AP, Gaze D, Howatson G. Effects of seated and standing cold water immersion on recovery from repeated sprinting. J Sport Sci 2015. Epub ahead of print. doi: 10.1080/02640414.2014.996914.
28. Leeder J, van Someren KA, Gaze D, Jewell A, Deshmukh NI, Shah I, Barker J, Howatson G. Recovery and adaptation from repeated intermittent-sprint exercise. Int J Sports Physiol Perform 9: 489–496, 2014.
29. McCormick KM, Burns KL, Piccone CM, Gosselin LE, Brazeau GA. Effects of ovariectomy and estrogen on skeletal muscle function in growing rats. J Muscle Res Cell Motil 25: 21–27, 2004.
30. McHugh MP. Recent advances in the understanding of the repeated bout effect: The protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports 13: 88–97, 2003.
31. Moran AL, Warren GL, Lowe DA. Removal of ovarian hormones from mature mice detrimentally affects muscle contractile function and myosin structural distribution. J Appl Physiol (1985) 100: 548–554, 2006.
32. Nardone A, Romano C, Schieppati M. Selective recruitment of high-threshold human motor units during voluntary isotonic lengthening of active muscles. J Appl Physiol (1985) 409: 451–471, 1989.
33. Nosaka K, Sakamoto K, Newton M, Sacco P. The repeated bout effect of reduced-load eccentric exercise on elbow flexor muscle damage. Eur J Appl Physiol 85: 34–40, 2001.
34. Pincivero DM, Gandaio CB, Ito Y. Gender-specific knee extensor torque, flexor torque, and muscle fatigue responses during maximal effort contractions. Eur J Appl Physiol 89: 134–141, 2003.
35. Rampinini E, Bosio A, Ferraresi I, Petruolo A, Morelli A, Sassi A. Match-related fatigue in soccer players. Med Sci Sports Exerc 43: 2161–2170, 2011.
36. Sayers SP, Peters BT, Knight CA, Urso ML, Parkington J, Clarkson PM. Short-term immobilization after eccentric exercise. Part I: Contractile properties. Med Sci Sports Exerc 35: 753–761, 2003.
37. Schneider BSP, Fine JP, Nadolski T, Tiidus PM. The effects of estradiol and progesterone on plantarflexor muscle fatigue in ovariectomized mice. Biol Res Nurs 5: 265–275, 2004.
38. Sipaviciene S, Daniuseviciute L, Kliziene I, Kamandulis S, Skurvydas A. Effects of estrogen fluctuation during the menstrual cycle on the response to stretch-shortening exercise in females. Biomed Res Int 2013. doi: 10.1155/2013/243572.
39. Sirotic AC, Coutts AJ. Physiological and performance test correlates of prolonged, high-intensity, intermittent running performance in moderately trained women team sport athletes. J Strength Cond Res 21: 138–144, 2007.
40. Starbuck C, Eston RG. Exercise-induced muscle damage and the repeated bout effect: Evidence for cross transfer. Eur J Appl Physiol 112: 1005–1013, 2012.
41. Tee JC, Bosch AN, Lambert MI. Metabolic consequences of exercise-induced muscle damage. Sports Med 37: 827–836, 2007.
42. Tiidus PM, Deller M, Liu XL. Oestrogen influence on myogenic satellite cells following downhill running in male rats: A preliminary study. Acta Physiol Scand 184: 67–72, 2005.
43. Tiidus PM. Estrogen and gender effects on muscle damage, inflammation, and oxidative stress. Can J Appl Physiol 25: 274–287, 2000.
44. Turner E, Munro AG, Comfort P. Female soccer: Part 1-A needs analysis. J Strength Cond Res 35: 51–57, 2013.
45. Warren GL, Lowe DA, Armstrong RB. Measurement tools used in the study of eccentric contraction-induced injury. Sports Med 27: 43–59, 1999.
46. Warren GL, O'Farrell L, Rogers KR, Billings KM, Sayers SP, Clarkson PM. CK-MM autoantibodies: Prevalence, immune complexes, and effect on CK clearance. Muscle Nerve 34: 335–346, 2006.
Keywords:

females; muscle function; recovery; exercise-induced muscle damage

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