Eccentric contractions have been demonstrated to be a potent stimulus to induce gains to the neuromuscular system (12), and are routinely used by athletic populations within training regimens; however, when unaccustomed, eccentric muscle actions often lead to temporary exercise-induced muscle damage (EIMD), which is manifested as muscle soreness and a reduction in muscle function that may last for several days after exercise (14,20).
In recent years, there has been growing body of literature examining the possible physiological mechanisms responsible for muscle damage (4,24), adaptation (14), and interventions to reduce the negative effects of damaging eccentric exercise (13). Many protocols induce damage to the knee extensors and elbow flexors using isokinetic dynamometry (14) or specifically designed instruments (24), whereas some other investigations have successfully employed downhill ambulatory protocols (1,5,9,21) and plyometric exercises (16,29). Although the results from this research have provided an insight of the complex events surrounding EIMD, the extent of damage arising from more sport-specific exercise regimens is not well documented.
Sports such as rugby, soccer, and field hockey require periods of high-intensity, repeated sprint activity interspersed with short distances of deceleration in order to stop or change direction (23,25). The movement pattern characteristics of field-based team sports were evaluated by Spencer et al. (26), who ascertained that mean sprint duration in such activities is generally 2-3 seconds, equating to a maximum sprint distances of no more than 22 m and average rest times of approximately 2 minutes. However, other investigations (8,19,25) also noted that players often conduct multiple sprints (>12) and exceed these mean sprint distances; up to 30 m with durations exceeding 4 seconds and rest periods of more than 1 minute. This information should have particular bearing in the design of physiological testing protocols if they are to be sport specific (26).
Thompson et al. (27) identified that during sprinting, significant mechanical stress is imposed on the quadriceps and hamstrings as they try to decelerate the body's mass, which accounted for an increase in blood markers of muscle damage and soreness, which has since been further supported (22,29). Other research has suggested that high-force, high-velocity eccentric contractions such as those employed in sprinting strides increase the extent of muscle damage (3) and hence significantly reduces the performance of skeletal muscle (4,17,24).
It has been documented that an intermittent sprinting protocol results in muscle damage (28); however, there is limited research investigating the magnitude of damage that arises from more sport-specific activities that replicate intermittent sprint sports. Lakomy and Haydon (15) showed that a significant performance decrement arises from employing rapid deceleration following repeated 40-m sprints; they also reported anecdotally that muscle damage was present. Consequently, there is a requirement for a sport specific damaging protocol that may provide a suitable model to examine EIMD, adaptation, and interventions to reduce EIMD. Such a protocol may provide a) a useful model to examine muscle damage from a sport specific task, and b) an insight into the magnitude of muscle damage and the recovery time course of muscle function, which may provide practical implications for coaches, strength and condition specialists, and athletes when participating in such activities. Therefore the aim of this investigation was to examine the extent of damage precipitated from a sport-specific, repeated sprint protocol and therefore elucidate its suitability as an appropriate model to investigate EIMD.
Experimental Approach to the Problem
This investigation examined a repeated sprint protocol based on the documented demands of repeated sprint (8,19,25,26), field sports-specifically 15 × 30 m sprints interspersed by 60 seconds of rest. In addition, a rapid deceleration was enforced within 10 m from the finish line in order to further replicate the demands of these sports and to elicit high force eccentric contractions in the lower limbs. Longitudinal measures of maximal voluntary contraction (MVC), creatine kinase (CK), muscle soreness, and lower limb girth were taken at the same time of day (±1 hour), to elucidate the magnitude and time course of muscle damage; these were taken at pre-exercise, and at 24 hours, 48 hours, and 72 hours postexercise. These measures are commonly used indirect markers of muscle damage and provide an indication of the magnitude of EIMD.
Following ethical approval from the Universities Research Ethics Committee in accordance with Helsinki Declaration, 20 male subjects (mean ± SD age 22 ± 2 years, height 178 ± 6.6 cm, and mass 84.6 ± 13.6 kg) were recruited and asked to complete informed consent forms and medical screening questionnaires prior to participation. All participants regularly participated in collegiate field-based team sports-specifically soccer (n = 5), rugby (n = 11), and field hockey (n = 4), all of which were in their competitive season. Typically, participants did sport-specific training on at least 4 occasions per week and played competitively once per week, during the competitive season. For the duration of the study, participants were asked to abstain from competition, resistance exercise, and avoid the ingestion of alcohol, nutritional supplements, and nonsteroidal anti-inflammatory drugs.
A 30-m section of a 400-m running track was marked using cones and two sets of light timing gates (Brower, Utah, USA), one set at each end of the start and finish line. A further 10-m deceleration zone was also marked at the end of the 30-m sprint track. The environmental conditions during the test days were dry with an ambient temperature of between 17°C and 19°C.
Firstly, a warm-up was performed, consisting of 400 m self-selected pace jogging, a series of dynamic sprint drills (high-knees, heel-flicks, and walking lunges), and sprints at 60%, 80%, and 100% of perceived maximum speed. Immediately following the warm-up, subjects were given 5 minutes to stretch and prepare themselves for the protocol (11). Participants stood 30 cm from the start line to avoid premature triggering of the timing system and completed 15 × 30 m sprints with 60 seconds of rest between repetitions. Subjects were instructed to sprint maximally between the light gates and stop within the 10-m deceleration zone, which was laid out immediately after the 30-m sprint zone. When the repetition was completed (i.e., the subject had come to a halt), the rest period was initiated. Standardized verbal encouragement was provided throughout the protocol.
Maximum Voluntary Contraction
Maximum isometric voluntary contraction (MVC) in the nondominant leg was determined using isokinetic dynamometry (Kin-Com, Chattanooga, TN, USA). The dynamometer was set up according to manufacturer's instructions; the joint angle was set at 70° of flexion and gravity compensation was employed to allow for inter subject variations in moment acting upon limb weight (6). Following a standardized warm-up consisting of 10 isokinetic contractions (60°·s−1) at 70% of the participants' maximum, all participants completed three isometric MVCs of 3 seconds duration, which were separated by 60 seconds of recovery; standardized verbal instructions and encouragement were provided throughout the protocol. The peak MVC from the three contractions was used for data analysis; coefficient of variation (CV) for this procedure was established at 6.1%.
Creatine kinase (CK) was determined using capillary puncture from the earlobe. A sample of whole fresh blood was analysed immediately using a colorometric assay procedure (Reflotron Plus, Roche Diagnostics, UK). The resting normal expected values for CK using this instrument are between 50 and 200 IU·L−1. The intra-assay reliability for this method is a CV of <3%.
Perceived Muscle Soreness Measurement
Participants were asked to complete a 200-mm visual analogue scale while squatting at a knee angle of approximately 90° to determine muscle soreness in the lower limb with “no soreness” at one end and “unbearably painful” at the other (14). In addition to the perceived soreness rating, a diagram was provided for subjects to indicate the areas where muscle soreness was present. This method was previously employed by Thompson et al. (27) and provided a useful indicator of localised muscle soreness.
Muscle swelling was measured at the mid thigh (2). This was determined by marking the midpoint between the inguinal crease and the superior border of the patella with a pen to ensure consistency in the measurement site on consecutive days; intra-examiner technical error of measurement (TEM) was established at 1.98%.
All statistical analyses were conducted using SPSS for Windows (v.15, SPSS Inc., Chicago, IL, USA). Fatigue (10), fastest sprint time, and mean sprint time and 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 (10).
For the purposes of data analysis, MVC and limb girth were normalized and expressed as a percentage change from pre-exercise to account for intersubject variability. All data are displayed as mean ± SD. A repeated measures analysis of variance was used to determine differences over time; assumptions of sphericity were tested using Mauchly's test of sphericity and any violations were corrected using the Greenhouse-Geisser correction factor. Significant effects were followed up using Tukey's post-hoc analysis and all significance levels were at α = 0.05.
The repeated sprint protocol group mean for fastest and mean times were 4.33 ± 0.21 seconds and 4.49 ± 0.09 seconds, respectively. The group mean fatigue score was 4.51 ± 1.72%. There was a significant time effect (F = 52.268, p < 0.001) for MVC (Figure 1) and post-hoc analysis showed a decline at 24 hours and 48 hours postexercise (p < 0.001). Force production demonstrated a mean decline of 28% from pre-exercise (828 ± 187 N) to 24 hours postexercise (594 ± 150 N). Force recovered somewhat at 48 hours (672 ± 114 N) and was close to full recovery at 72 hours postexercise (791 ± 160 N). CK (Figure 2) was within the normally expected resting values pre-exercise (158 ± 56 IU·L−1). There was a significant increase over time from pre-exercise levels after the damaging bout (F = 60.688, p < 0.001) and peaked at 24 hours (p < 0.001) to a level of 776 ± 312 IU·L−1. Although still elevated at 48 hours (p < 0.001), CK made some recovery towards basal level at 72 hours (p < 0.004).
Muscle soreness (Figure 3) showed a significant effect over time (F = 201.853, p < 0.001), peaking at 48 hours postexercise and remaining significantly elevated above pre-exercise levels for 72 hours (p < 0.001). Incidentally, subjects reported muscular soreness predominantly from in the quadriceps, calf, and hamstring muscle groups, although 8 out of the 20 subjects also reported muscle soreness in the gluteal, lumbar, and abdominal regions. Limb girth (Figure 4) was also significantly elevated over time (F = 32.427, p < 0.001) and peaked at 24 hours (p < 0.001) to 3% greater than baseline. Girth remained elevated at 48 hours postexercise (p = 0.005); although slightly elevated, post-hoc analysis showed no significant difference at 72 hours from baseline.
The aim of this investigation was to determine the magnitude of muscle damage following a repeated sprint protocol and hence elucidate its suitability as a sport-specific model to examine EIMD. In the days following the repeated sprints and rapid decelerations, there was a decrease in knee extensor strength and increases in muscle soreness, CK efflux, and limb girth, which collectively demonstrate that this bout of exercise is effective in inducing muscle damage.
The mechanisms governing the change in dependent variables have been extensively debated in the literature and are not discussed here; for a detailed overview of these potential mechanisms, the reader is directed to reviews (4,7). The sprint times and percentage fatigue showed there was little fatigue during the protocol, indicating that sufficient rest was given between repetitions to allow for perimaximal effort on subsequent sprints. This is important when inducing damage, as a faster sprint speed requires greater breaking forces to be applied in the deceleration zone and may consequently assist in maximising the damage response.
All dependent variables showed a significant change over time, indicating that muscle damage was successfully induced as a result of the repeated sprint protocol, which has been demonstrated following eccentric based exercise (14,20). Although this protocol is not inherently eccentric based, it does contain a heavy eccentric component, particularly in the forced 10-m deceleration zone. Some investigators (4) have documented that high eccentric forces generated during sprinting strides accentuate the damage response. However, it is in the 10-m deceleration zone where it is most likely to have precipitated to the lion's share of damage, which concurs with previous investigations reporting damage from repeated sprints (22,27) and performance decrements from forced deceleration (15). Thompson et al. (27) examined the damage response following the Loughborough intermittent shuttle test, which consisted of a 90-minute bout of shuttle running at different speeds that was designed to replicate field sports such as soccer. Although determined in the days following the exercise bout, CK efflux and soreness was of a similar magnitude and showed a similar time course as those of the current study. Interestingly, the rise in soreness that peaked at 48 hours postexercise mirrors that observed in many other damage models (14,29); however, it did not exclusively occur in the quadriceps, calf, and hamstrings as one might have expected. Some subjects (40%) also reported localized soreness occurring in the gluteal, lumbar, and abdominal muscles, which has been previously reported following longer duration shuttle running (27) and should be considered in future investigations that implement this type of exercise in a damage-treatment model.
All the subjects were competitive collegiate field sportsmen who regularly participated in competition (usually once per week) during the academic semester. Intuitively, there may be an expectation for them to exhibit a protective effect or repeated bout effect from prior bouts of repeated sprints; a phenomenon that has been extensively shown to occur from prior bouts of eccentric exercise in other damage models (12,14,17) and results in little or no damage on subsequent bouts of exercise (12,14,17,18). It is not clear why these subjects showed such a marked damage response; although it is possible that the surface used in this investigation (a running track) was sufficiently different from their normal playing surface (grass and artificial turf) to induce a damage response. Another possibility is that the exercise intensity and volume were possibly greater than they were accustomed to, thereby causing sufficient overload to precipitate damage. Traditionally, most muscle damage research utilises untrained subjects in order to observe a large damage response; based on this observation it seems that future investigations could recruit relatively well trained individuals to participate in muscle damage studies and still see a marked response, which may help provide greater external validity of research findings to a sporting context.
Most of the documented literature that examined exercise-induced muscle damage has used isolated muscle groups to examine the response from eccentric based exercise (12,13,14,17,20). Some investigations have attempted to make the mode of damaging exercise more specific by utilising downhill running (1,5,9,21) and plyometric exercises (16,29), however these protocols still lack specificity and direct application to field sports. This investigation has utilised a sport specific protocol based on sprint movement patterns observed in field based team sports (8,19,25,26). It has also provided a valuable insight in to the magnitude of damage that can be precipitated from such activity and has demonstrated that repeated sprints with a rapid deceleration zone can be successfully used as a suitable model for examining exercise-induced muscle damage.
Exercise-induced muscle damage is a popular area of investigation to model the response, adaptation, prevention, and treatment of damaging exercise; however, many damaging protocols lack sport specificity. This study demonstrates that muscle function is significantly reduced following a sport-specific repeated sprint session with rapid deceleration and therefore coaches, strength and condition specialists, and athletes should be mindful that performance in subsequent sessions may be compromised for 48 hours or more following training of this nature. Additionally, the damage model examined in this investigation provides a viable sport-specific alternative for researchers to examine the damage response in repeated sprint field sports such as soccer, rugby, and field hockey.
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