Comparisons of exercise-induced muscle damage after two closely scheduled sprinting exercises

2.1 Subjects

Fourteen healthy college-aged men (mean ± SD age = 21.67 ± 1.90 years; height = 174.0 ± 5.49 cm; body mass = 70.61 ± 13.85 kg) voluntarily participated in this study. Prior to any experimental procedures, each subject completed an informed consent and a health and exercise status questionnaire, which indicated no current or recent neuromuscular or musculoskeletal injuries of the lower body. In addition, all subjects were physically active (performed resistance exercises at least once per week, and aerobic exercises at least twice per week 6 months leading up to this study) but were not familiar with the sport-specific sprinting protocol involved in this study. During the consenting process, the subjects were instructed to maintain their normal habits regarding dietary intake, hydration status, and sleep during the study. Extra effort was made to conduct testing at roughly the same time of the day with the same arousal levels. In addition, the subjects were instructed to avoid any vigorous physical activity 72 hours prior to the beginning of this study and during the entire experimental period. This study was approved by the University Institutional Review Board (Approval Number: c104038), and the protocols conform with The Code of Ethics of the World Medical Association (Declaration of Helsinki), printed in the British Medical Journal (18 July 1964). All subjects were informed of the risks and benefits of the study and then gave written informed consent to participate.

2.2 Design

To examine the effects of the second bout of maximal sprinting exercise on muscle damage markers four days after the identical initial bout, nine separate visits to the laboratory were required to complete this study (Fig. 1). After the first visit as the familiarization, the following eight visits were conducted on eight consecutive days, during which the two identical muscle-damaging maximal sprinting exercise bouts were performed with 96 hours apart (Visit 2 and Visit 6). All dependent variables (muscle damage markers) were measured before (PRE), 24 (D1), 48 (D2), and 72 (D3) hours after both bouts of sprints on the dominant side of the subjects’ thigh muscles based on their kicking preferences. In addition, the sprint-related variables were also measured during both sprinting bouts.

2.3 Procedures

During the familiarization visit (Visit 1), all subjects visited the laboratory to receive instructions and to participate in a familiarization trial specifically to practice isokinetic strength tests. At least 24 hours after the familiarization, the subjects returned to the laboratory for the purpose of getting the PRE-measurements, followed by performing the first bout of sport-specific sprints. Upon arrival, the subjects were asked to perform 5 minutes of jogging at a self-selected speed. Following the warm-up exercise, dependent variable measurements were taken by the investigators with the order of hip flexion flexibility, muscle soreness, plasma creatine kinase (CK), and isokinetic knee flexion eccentric strength. Following the completion of the PRE-measurements, the subjects were asked to perform a 5-minute dynamic sprint drills which consisted of several running bouts at 60%–100% of perceived maximum speed, high knees, heel-flicks, and walking lunges. In addition, the subjects also performed self-administered static stretching exercises specifically targeting the gluteus, psoas, adductors, hamstrings and quadriceps muscles. The maximal sprinting protocol began 5 minutes following the final set of sprint drill or static stretches. Specifically, 15 sets of 30-m maximal intermittent sprints were performed by the subjects on the concrete floor, with a 10-m acceleration and a 15-m deceleration for each sprint set. The rest interval between consecutive sprint sets were 60 seconds. Each subject was verbally encouraged to give a maximal effort during every sprint set. For the sprint-related variables, the time to complete each sprint (time trial) was measured through a FitLight device (FitLight Corp., ON, Canada). The peak heart rate (HR) was recorded through a heart rate monitor (Polar RS 800, Polar Electro Inc., Kempele, Finland) during each sprint set. In addition, the rating of perceived exertion (RPE) was recorded using the Borg Rating of Perceived Exertion Scale [10] at the end of each spring set. Twenty-four (D1), 48 (D2), and 72 (D3) hours after the sprints, dependent variables were measured again with the same order and manner as they were measured at the PRE. Separated by four days from the first bout, the second bout of the sprinting exercise with its associated measurements (PRE, D1, D2, and D3) were performed with the exact same manner as they were performed for the initial bout.

2.4 Dependent variables

2.5 Statistical analyses

To compare the sprint-related performance variables between all 15 sets from the first and the second sprinting bouts, separate two-way repeated-measures (bout [initial vs. second] × sprint set [set 1 vs. set 2 vs…set 15]) analyses of variance (ANOVAs) were conducted. For the dependent variables, separate two-way repeated-measures (bout [initial vs. second] × time [PRE vs. D1 vs. D2 vs. D3]) ANOVAs were used to examine potential changes across time between two sprinting bouts. Follow-up statistical tests included one-way repeated measures ANOVAs and pairwise comparisons with Bonferroni adjustments. Mean ± standard deviations (SD) was used to describe all variables. All statistical tests were conducted using IBM SPSS Statistics 24.0 (IBM Corp., Armonk, NY, USA), with the alpha set at 0.05. Effect sizes Cohen’s d [11] was calculated for each pairwise comparison.

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Figure 2.

Sprint-related variables at each sprint set during two sport-specific maximal intermittent sprint bouts. Sub-figure A, B, and C are demonstrating Mean ± Standard Error Mean (SE) of the time trial, instantaneous heart rate, and rating of perceived exertion (RPE) across the entire 15 sprinting protocol for both bouts. †: significant difference between the mean marginal values of initial and the second bout (collapsed across time).

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Figure 3.

The responses of Mean ± SE muscle soreness (A) and plasma creatine kinase (B) before (PRE), 24 hours after (D1), 48 hours after (D2), and 72 hours after (D3) both initial and second sprinting bouts. *: significantly different from the value at PRE after the initial bout ( 0.05). †: significant difference between values of initial and the second bouts.

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Figure 4.

The responses of Mean ± SE knee flexion eccentric peak torque (A) and angle of knee flexion eccentric peak torque (B) before (PRE), 24 hours after (D1), 48 hours after (D2), and 72 hours after (D3) both initial and second sprinting bouts. *: significantly different from the value at PRE after the initial bout ( 0.05). **: significantly different from the value at PRE after the second bout ( 0.05). †: significant difference between values of initial and the second bouts.

3.1 Sprint-related variables between the initial and second sprinting bouts

For all the sprint-related performance variables (time trial, HR, and RPE for each sprint set), the results from the 2-way repeated-measures ANOVAs indicated that there were no bout × sprint set interactions. However, there was a main effect of sprint set for all variables ( 0.001 for all three variables). After collapsing across bout, the follow-up one-way repeated-measures ANOVAs showed significant differences among 15 sets, with greater values for the later sets than for the earlier sets (Fig. 2). In addition, there was also a main effect of bout for RPE ( p = 0.013). When collapsed across the sprint set, the follow-up paired samples t-test showed that the marginal mean RPE was significantly greater for the initial bout than for the second bout (mean ± SD: initial bout vs. second bout = 12.7 ± 2.0 vs. 11.1 ± 2.8; d = 0.65; Fig. 2C).

3.2 The comparisons of muscle damage markers’ responses after initial and second sprint bouts

To determine whether there was a potential prophylactic effect from the exposure to the initial muscle-damaging sport-specific sprinting bout, comparisons of muscle damage indices were made between the two bouts across time (PRE, D1, D2, and D3):

4.1 Performance comparisons between the initial and the second sprint bouts

With the presence of EIMD and its prolonged symptoms, which could be detrimental to the subsequent performance, it was also important to compare the sprint-related variables between the two exercise bouts separated by 96 hours. Based on our findings, all the variables (time trial, HR, and RPE for each sprint set) gradually increased throughout the 15-set intermittent maximal sprinting protocol. This indicates that the intermittent maximal sprints imposed greater physiologic stress, resulting in continued decrements in performance (longer time to complete each sprint set) throughout the sprint bout [14]. When comparing the performance and physiologic parameters between two bouts, no difference was found for the time trial or the HR, but interestingly, the RPE was generally lower by a 2-point scale during the second bout than the initial bout of the sprints. These findings are in agreement with the ones from Leeder et al. [7], where 5 sets of intensity-varying 15-minute Loughborough Intermittent Shuttle Test were performed by well-trained national or college athletes. It is worth mentioning that the training statuses (physically active men vs. well-trained national or college athletes), the running protocols (15 sets of 30-m intermittent maximal sprints vs. 5 sets of intensity-varying 15-minute Loughborough Intermittent Shuttle Test), as well as the rest periods between two bouts (4 days vs. 14 days) are different between these experiments. Even with all these differences, however, it is likely that the initial sprinting bout-induced muscle damage did not affect the second bout’s sprint time performance, given the 4-day rest period. Moreover, since the subjects were not accustomed to the intermittent maximal sprint exercise, the reduced RPE during the second bout was likely due to the habituation to the level of exertion [7], given that the second bout of sprints induced similar physiologic stress (heart rate responses) as the initial one did.

4.2 The protective effect from the initial bout?

Based on the results, lower levels of muscle soreness were found at both D1 and D2 after the second bout, when compared to the initial one. In fact, the muscle soreness scores were not elevated after the second sprinting bout, primarily due to the fact that 9 of the subjects reported “not sore at all” (muscle soreness = 0) during this time period. In addition, similar blunted responses were found for the knee flexion eccentric peak torque and angle of peak torque: even though both variables did not return to the baseline prior to the second sprinting bout, they recovered much faster after the second bout. Therefore, these results indicated certain adaptations from the exposure to the initial muscle-damaging exercise bout, making the subjects less susceptible to the potential muscle damage induced by the second sprinting bout. However, contrasting to the above-mentioned damage indices was the circulating CK concentration, which rose and remained at a higher level after the second bout of sprints than after the initial one, potentially suggesting a greater loss of sarcolemma integrity following the second bout of exercise [2, 15].

It is important to mention that the responses of different muscle damage markers do not necessarily correlate with each other in terms of magnitude and time-course after a muscle-damaging exercise bout [12]. Generally speaking, the blood CK activity increases dramatically 1–2 days and may reach the peak within 4–5 days after muscle-damaging exercises [16]. As shown from our data, the CK level was still elevated 3 days after the sport-specific sprints, it was possible therefore, the CK response after the second sprinting bout might still have partly represented EMID from the initial muscle-damaging bout. In addition, just like previous literature suggested [12], our CK data also showed large inter-subject variation especially after the second sprint bout, which challenges its use as a meaningful marker of EIMD. In contrast, muscle soreness develops at 1 day and peaks 2–3 days after muscle-damaging exercises [16]. Indeed, it is possible that the dampened muscle soreness response after the second bout could be attributed to familiarization to the sensation of pain [17]. However, previous review has suggested that muscle soreness can be a result of the increase of the inflammatory-induced tissue osmotic pressure, which triggers nociceptors to induce the pain sensation [18]. Regardless, our finding regarding the muscle soreness response was accompanied by the faster recoveries of both knee flexion peak torque and angle of peak torque after the second sprint bout, indicating the recovery of the muscle fiber membrane damage. Therefore, the protective effect from the exposure to the initial sport-specific sprint was positive, even when the second bout was performed only 4 days after.

4.3 Limitations

With some novel findings which can potentially provide practical information for sports performance and training purposes, this study however, does have some worth-mentioning limitations. Primarily, without a control group (only performing the initial sprints but getting muscle damage markers measured for the next 7 days) for the study, it was impossible to monitor how long the sport-specific sprints-induced muscle damage truly would have lasted, because some damage markers (plasma CK, knee flexion peak torque, and angle for peak torque) did not return to the baseline at the onset of the second sprint bout. That being said, this could have influenced the second sprint bout’s performance and physiologic variables as well as the subsequent muscle damage markers’ responses. Regardless, the second sprinting bout’s performance was not affected, and more importantly, there were evidences showing the protective effect from the previous muscle-damaging sprints. Second, when interpreting the results of the current study, it is important to be aware that these findings were based on healthy and physically-active individuals, meaning the related protective effect may or may not be observed in different populations (e.g., high-trained athletes who normally sprint during competitions or training). Thus, future studies are still needed to shed light onto this topic in a variety of populations.

In conclusion, for healthy physically-active young men who are not accustomed to maximal intermittent sport-specific sprints, performing a sport-specific sprinting exercise induced muscle damage. Even though some muscle damage markers (e.g., knee flexor strength) were not recovered to the baseline 4 days after the initial bout, the subjects’ performance and heart rate responses during the exact same second sprints were not affected. In addition, less muscle soreness and greater strength performance recovery following the second bout of sprints suggested a protective effect from the exposure to the initial muscle-damaging sprints. The current study suggests that repeated exposure of sport-specific maximal intermittent sprints even within a relatively short time period (e.g., 4 days) can positively influence symptoms of muscle damage, recovery, and adaptation, without sacrificing the sports performance. Therefore, training strategies can be specifically developed for specific individuals for the purposes of attenuating muscle damage and enhancing recovery between closely scheduled training sessions.