Changes in Passive Muscle Stiffness Following Biceps Femoris Strain Injury in Track‐and‐Field Athletes: Cross‐Sectional and Longitudinal Analyses

ABSTRACT

A history of muscle strain injury has consistently been identified as one of the strongest risk factors for future muscle strain injuries. However, information on the characteristics associated with a history of muscle strain injury is limited. This study aimed to examine whether passive muscle stiffness changes following biceps femoris long head (BFlh) strain injury in track‐and‐field athletes through cross‐sectional and longitudinal analyses. In Study 1 (cross‐sectional), 13 male track‐and‐field athletes with unilateral BFlh strain injury history underwent passive BFlh stiffness assessment using ultrasound shear wave elastography of previously injured and uninjured limbs. In Study 2 (longitudinal), seven athletes who sustained BFlh strain injury during the competitive season were followed from pre‐injury baseline through return‐to‐sport. Passive BFlh stiffness was assessed in both limbs at baseline, acute phase, rehabilitation phase, and return‐to‐sport phase. In Study 1, passive BFlh stiffness was significantly greater in the previously injured limb than in the uninjured limb (p = 0.001). In Study 2, a significant limb × time interaction was observed (p = 0.001). In the injured limb, passive BFlh stiffness at the rehabilitation phase was significantly greater than at baseline and remained elevated at return‐to‐sport, whereas it returned to baseline in the uninjured limb. Passive BFlh stiffness increases following strain injury and persists through return‐to‐sport. These findings reveal that strain injury leads to lasting increases in passive muscle stiffness, which may have implications for post‐injury muscle function.

1. Introduction

Hamstring strain injury (HSI) is one of the most common sports injuries in sprint‐demanding sports, such as track‐and‐field [1], soccer [2], and rugby [3]. The biceps femoris long head (BFlh) accounts for the majority of sprint‐type HSIs [4], and recurrence rates remain high despite advances in rehabilitation [5, 6]. Previous injury is consistently identified as the strongest risk factor for future strain injury [7, 8], suggesting that the initial injury induces lasting alterations in muscle structure or mechanical properties. Histological studies have reported structural changes such as collagen remodeling and extracellular matrix alterations following muscle injury [9, 10]. However, the accompanying mechanical adaptations at the muscle level remain insufficiently understood.

Among potentially modifiable risk factors for muscle strain injuries, passive muscle stiffness has gained increasing attention [11, 12, 13]. Post‐injury tissue remodeling, including scar formation, may increase stiffness of the muscle, predisposing it to reinjury. Thus, elucidating whether and how passive muscle stiffness changes could help shift “history of strain injury” from a non‐modifiable to a potentially modifiable risk factor through targeted interventions. However, accurate assessment of muscle‐specific stiffness remains technically challenging.

Conventional measures such as joint range‐of‐motion or joint stiffness tests assess composite mechanical behavior of multiple tissues, including muscles, tendons, fasciae, and ligaments rather than the mechanical characteristics of individual muscles [14, 15, 16]. These measures are also affected by subjective factors such as pain perception and stretch tolerance [17, 18]. Moreover, these methods cannot distinguish individual muscles within the hamstring group, even though the BFlh is the muscle most frequently injured [4]. These methodological constraints may explain the inconsistent findings when comparing previously injured and uninjured limbs using conventional assessments [19, 20].

Ultrasound shear wave elastography (SWE) has emerged as a technique to address these limitations by quantifying tissue stiffness in vivo. This technique measures shear wave propagation speed, which increases with tissue stiffness [21]. Thus, SWE enables assessment of individual muscles' stiffness, independent of examiner technique or participant tolerance [16, 18]. In the present study, taking these advantages of SWE, we conducted two studies: first, a cross‐sectional comparison of passive BFlh stiffness between previously injured and contralateral uninjured limbs in athletes with unilateral HSI history; second, recognizing that retrospective analyses cannot establish temporal relationships, a prospective longitudinal study investigating passive BFlh stiffness from pre‐injury baseline through injury occurrence to return‐to‐sport.

2. Methods

2.1. Study Design

Our research consisted of two studies: a cross‐sectional analysis (Study 1) and a longitudinal analysis (Study 2). In both studies, ultrasound SWE was employed to assess passive BFlh stiffness. In Study 1, we measured passive BFlh stiffness in athletes with a unilateral history of BFlh strain injury, comparing the previously injured limb with the uninjured contralateral limb. In Study 2, passive BFlh stiffness was longitudinally assessed in athletes who sustained BFlh strain injury, measuring both the injured and uninjured limbs from pre‐injury baseline through return‐to‐sport (defined as the ability to perform maximal sprinting without pain and clearance for full participation in training and competition). In both Study 1 and Study 2, participants were classified as Tier‐2 or Tier‐3 track‐and‐field (sprint and jump event) athletes according to the framework of McKay et al. [22], and competed at the collegiate, regional, or national level. Prior to the main studies, a preliminary reliability study was conducted by the same examiner on 12 participants to establish inter‐day reliability of SWE measurements. The experimental setup and procedures were identical to those described below. Reliability was evaluated using the within‐subject coefficient of variation (CV), intraclass correlation coefficient (ICC [95% confidence interval]), standard error of measurement (SEM), and minimal detectable change (MDC). All participants in both Study 1 and 2 were fully informed of the purpose and experimental procedures. Written informed consent was obtained from each participant. Both studies were approved by the institutional review board of the Research Ethics Committee of Juntendo University (E22‐0345) and conducted in accordance with the Declaration of Helsinki.

2.2. Study 1

2.2.1. Participants

Thirteen young male track‐and‐field athletes with a history of unilateral BFlh strain injury were recruited (174.8 ± 4.3 cm, 68.8 ± 3.8 kg, 20.4 ± 1.6 years). All participants had sustained their BFlh injury within the previous 12 months and had already returned to training and competition in track‐and‐field events and were asymptomatic (defined as the absence of pain or discomfort during activities of daily living and sport‐specific movements) at the time of testing. All BFlh strain injuries were confirmed through magnetic resonance imaging at the time of initial diagnosis. Inclusion criteria required that the injury site was classified as muscular/musculotendinous (site “b”) according to the British Athletics Muscle Injury Classification (BAMIC) [23], which included grade 1b (n = 6), 2b (n = 6), and 3b (n = 1). None of the participants reported leg pain on the day of testing. Participants were instructed to refrain from warm‐up or stretching activities before testing.

2.2.2. Experimental Setup and Procedure

BFlh stiffness was evaluated using established ultrasound SWE protocols [11, 12, 13, 24, 25]. Participants were positioned seated with the hip maintained at 70° flexion (with 0° representing the anatomically neutral position), the knee in complete extension, and the ankle positioned at approximately neutral position (Figure 1). This position was chosen so that the hamstring could be stretched to a lengthened state without pain for all participants and that muscle stiffness could be assessed at a certain angle common to all participants [15]. An ultrasound SWE system (Aixplorer Ver.12, Supersonic Imagine, France) was used with SWE mode (preset: MSK, persistence: off, smoothing: level 5), paired with a linear transducer (SL10‐2, Supersonic Imagine, France). The transducer was positioned at the midpoint of thigh length, measured from the greater trochanter to the popliteal crease. Transducer alignment was adjusted to visualize multiple BFlh fascicles and the proximal intramuscular tendon (i.e., intermediate aponeurosis) clearly within the B‐mode image (Figure 2). The probe was held manually in direct contact with the skin, with a layer of ultrasound gel applied between the probe and the skin to ensure optimal signal transmission. The examiner took care to minimize pressure on the skin as much as possible during the measurements. Throughout SWE measurements, participants were instructed to fully relax their legs and the examiner visually monitored participants for any signs of muscle activation or discomfort. SWE measurements were performed three times (i.e., three images were acquired). All SWE measurements were performed by a single examiner with more than 7 years of experience. The reliability of passive BFlh stiffness measurements by this examiner in this protocol has been previously established [25].

FIGURE 1.

Experimental setup for shear wave elastography measurements.

FIGURE 2.

Typical example of ultrasound shear wave elastographic image of the biceps femoris long head. The colored region represents the shear wave speed map with a scale at the bottom of the figure.

The acquired SWE images were exported as DICOM files and processed using a custom‐written MATLAB algorithm on a personal computer. Mean shear wave speed (SWS) of the BFlh was calculated over the region of interest (ROI). The ROI was manually selected to be as large as possible while excluding other tissues (e.g., fascia and subcutaneous fat). In the calculation of BFlh SWS, only pixels with a quality index (information in DICOM data) of ≥ 0.7 (out of the maximum of 1.0) were included [11, 25]. We confirmed that no pixels in the ROI reached the saturation limit of SWS for the SWE system (16.3 m/s). Shear modulus can be derived from SWS using tissue density × SWS². However, tissue density following strain injury may be altered by hemorrhage, edema, and subsequent tissue remodeling, and whether density returns to baseline during recovery is unknown. Additionally, the conversion from shear modulus to Young's modulus assumes tissue isotropy, an assumption that does not hold for skeletal muscle due to its anisotropic fiber structure. To avoid these potentially invalid assumptions, we reported the squared‐value of the SWS as an index of stiffness, consistent with previous ultrasound SWE studies in this field [11, 26]. The average value of the squared‐SWS from three images was adopted for statistical analysis.

2.2.3. Statistical Analysis

When a priori sample size calculation was conducted beforehand, there were no direct data from previous studies to be referred to because the present study is the first to examine passive BFlh stiffness using ultrasound SWE between legs with and without strain injury history in a lengthened muscle position. Consequently, the necessary sample size was calculated based on the results of our preliminary experiment (n = 4, effect size of Cohen's d for paired t‐test ≥ 1.080), using G*Power (Düsseldorf, Germany) with an assumed type 1 error of 0.05 and statistical power (1−β) of 0.80 to find a significant difference for the squared‐SWS of the BFlh in the established position. The minimum sample size was estimated as nine. Thus, 13 participants in this study satisfied the minimum sample size.

The normal distribution of the data was confirmed using the Shapiro–Wilk normality test. A paired t‐test was performed to compare the legs with and without a history of the BFlh strain injury. The significance level for all tests was set at p = 0.05. Statistical analyses were conducted using statistical software (SPSS Statistics Ver. 29, IBM Japan, Japan). Descriptive data are presented as mean and standard deviation. Cohen's d was reported as effect size.

2.3. Study 2

2.3.1. Participants

Seven track‐and‐field athletes (174.7 ± 6.3 cm, 66.3 ± 4.4 kg, 19.9 ± 1.2 years) who underwent preseason passive BFlh stiffness assessment and subsequently sustained a BFlh strain injury during the competitive season were enrolled in Study 2. Inclusion criteria required that athletes had no history of BFlh strain injury in the previous 12 months and could be followed at regular intervals (every 1–3 weeks) from injury through return‐to‐sport. Pre‐injury baseline measurements were collected during the preseason period when all athletes were asymptomatic and fully training. Data collection was conducted between February and October 2025.

2.3.2. Experimental Procedure

Following injury, all athletes underwent a structured rehabilitation program tailored to injury severity. Passive BFlh stiffness measurements commenced once athletes could tolerate the standardized testing position without pain. This typically occurred 1–3 weeks post‐injury, depending on injury severity. All measurements were performed using the same testing position, ultrasound equipment, and SWE protocol as described in Study 1. Measurements were repeated every 1–3 weeks, with both injured and uninjured limbs assessed at each time point. The same experienced examiner performed all measurements to ensure consistency across the longitudinal assessment period. Athletes were tracked until they achieved full return to unrestricted training and competition.

2.3.3. Statistical Analysis

A two‐way repeated measures analysis of variance (ANOVA: limb × time) was performed. Time points were defined as: baseline, acute phase (first measurement post‐injury), rehabilitation phase (approximately midpoint between injury and return‐to‐sport), and return‐to‐sport. When significant interactions were observed, post hoc pairwise comparisons were conducted with Bonferroni correction. Additionally, to address potential variability in inflammatory responses, Pearson correlation coefficients were calculated to examine the relationship between the timing of acute phase measurements (days post‐injury) and both the absolute passive BFlh stiffness at acute phase and its percentage change from baseline in the injured limb.

Given the small sample size of Study 2 (n = 7) and the limited power of normality tests under such conditions, sensitivity analyses were conducted using nonparametric methods to assess the robustness of the primary findings. Specifically, the Friedman test was used as a nonparametric alternative to the repeated measures ANOVA, followed by Wilcoxon signed‐rank tests with Bonferroni adjustment for post hoc comparisons where appropriate. In addition, Spearman's rank correlation coefficients were calculated as a nonparametric alternative to Pearson correlation analyses. The significance level was set at p = 0.05. All statistical analyses were performed using SPSS Statistics Ver. 29 (IBM Japan, Japan).

3. Results

3.1. Reliability Test

The preliminary reliability study demonstrated good to excellent inter‐day reliability for SWE measurements (ICC = 0.975, [95% CI: 0.918–0.993]). The within‐subject CV was 3.13%, with an SEM of 0.188 m²/s² and MDC of 0.520 m²/s².

3.2. Study 1

Figure 3 shows passive BFlh stiffness with and without a history of BFlh strain injury. A paired t‐test revealed that passive BFlh stiffness was significantly greater in the leg with a history of strain injury than in the leg without a strain injury history (p = 0.001, Cohen's d = 1.189 [95% CI: 0.456–1.893]).

FIGURE 3.

Passive muscle stiffness (assessed as squared‐value of shear wave speed) of the biceps femoris long head (BFlh) of the uninjured and previously injured limbs. *p < 0.05 vs. uninjured limb.

3.3. Study 2

Table 1 presents the injury severity classifications and time to return‐to‐sport for Study 2 participants. The mean period between injury and return‐to‐sport was 60.1 ± 23.4 days. Based on BAMIC, three athletes sustained myofascial injuries (grades 1a or 2a), one sustained a muscular/musculotendinous injury (grade 1b), and three sustained intratendinous injuries (grades 2c or 3c). The rehabilitation phase measurements were performed 27.6 ± 7.3 days after injury.

TABLE 1.

Injury grade and days between injury and return‐to‐sport of participants in Study 2.

Subject no.	Grade of injury	Days to return‐to‐sport
1	1a	74
2	1a	24
3	2a	40
4	1b	45
5	2c	79
6	2c	68
7	3c	91

Note: Subject 1 required 74 days to return‐to‐sport despite sustaining a grade 1a injury. This prolonged duration was athlete‐driven rather than medically indicated; the attending physician had cleared the athlete for return at an earlier stage based on MRI and clinical assessment, but the athlete chose to delay return due to persistent subjective discomfort.

Figure 4 shows passive BFlh stiffness in the uninjured and injured limbs. Two‐way ANOVA revealed a significant limb × time interaction (p = 0.001, partial η ² = 0.598 [95% CI: 0.214–0.761]). Post hoc Bonferroni tests demonstrated that in the uninjured limb, passive BFlh stiffness at the acute phase was significantly greater than that at baseline, rehabilitation, and return‐to‐sport phases (acute vs. baseline: p < 0.001, Cohen's d = 5.165 [95% CI: 2.233–8.098]; acute vs. rehabilitation: p = 0.007, Cohen's d = 2.170 [95% CI: 0.743–3.556]; acute vs. return‐to‐sport: p = 0.001, Cohen's d = 3.214 [95% CI: 1.286–5.119]). In the injured limb, passive BFlh stiffness at the rehabilitation phase was significantly greater than that at baseline (p = 0.049, Cohen's d = 1.465 [95% CI: 0.343–2.537]), while the difference at the return‐to‐sport phase approached but did not reach statistical significance (p = 0.094, Cohen's d = 1.261 [95% CI: 0.219–2.252]). Between‐limb comparisons revealed that at the rehabilitation phase, the difference approached significance (p = 0.057, Cohen's d = 0.890 [95% CI: −0.023–1.755]), while at the return‐to‐sport phase, the injured limb was significantly greater (p = 0.017, Cohen's d = 1.231 [95% CI: 0.200–2.211]). No significant between‐limb difference was observed at baseline or acute phase.

FIGURE 4.

Time‐course changes in passive muscle stiffness (assessed as squared‐value of shear wave speed) of the biceps femoris long head (BFlh) in response to sustaining strain injury. Data are shown for uninjured and injured limbs at baseline, acute phase, rehabilitation (Rehab) phase, and return‐to‐sport (RTS) phase. *p < 0.05 vs. acute phase; ^† p < 0.05 vs. baseline; ^a p < 0.05 vs. uninjured limb. Individual data points are color‐coded by injury type: Myofascial injuries (grades 1a, 2a) in blue, muscular/musculotendinous injury (grade 1b) in red, and intratendinous injuries (grades 2c, 3c) in green.

To assess the robustness of the primary findings, sensitivity analyses using nonparametric tests were conducted. For the uninjured limb, the Friedman test followed by Wilcoxon signed‐rank post hoc comparisons showed a pattern largely consistent with the parametric analyses. Significant differences were observed between the acute phase and baseline (p < 0.001), as well as between the acute phase and return‐to‐sport (p = 0.023). In contrast, the comparison between the acute phase and rehabilitation phase did not reach statistical significance (p = 0.078). For the injured limb, the Friedman test and subsequent post hoc comparisons identified significant differences between baseline and rehabilitation phase (p = 0.038) and between baseline and return‐to‐sport (p = 0.038). Although some comparisons that showed only a trend toward significance in the parametric analyses reached statistical significance in the nonparametric tests, the overall pattern of temporal changes was consistent across analytical approaches. These findings suggest that the main conclusions were not materially affected by the choice of statistical method. In addition, between‐limb comparisons using the Wilcoxon signed‐rank test at each time point showed no significant differences at baseline or acute phase, a trend toward significance at the rehabilitation phase (p = 0.063), and a significant difference at return‐to‐sport (p = 0.028). Taken together, these findings suggest that the main conclusions were not materially affected by the choice of statistical method.

The timing of acute phase measurements (days post‐injury) showed no significant correlation with either absolute passive BFlh stiffness (Pearson: r = 0.523 [95% CI: −0.380 to 0.915], p = 0.229; Spearman: ρ = 0.162 [95% CI: −0.689 to 0.825], p = 0.728) or its percentage change from baseline (Pearson: r = 0.076 [95% CI: −0.718 to 0.784], p = 0.872; Spearman: ρ = 0.090 [95% CI: −0.725 to 0.800], p = 0.848).

4. Discussion

The present study examined cross‐sectionally and longitudinally how muscle strain injury influences muscle stiffness in track‐and‐field athletes. In Study 1 (cross‐sectional analysis), passive muscle stiffness was higher in the previously injured BFlh than in the uninjured BFlh. In Study 2 (longitudinal analysis), the increased passive BFlh stiffness at the rehabilitation phase persisted through the return‐to‐sport phase in the injured limb, while passive BFlh stiffness returned to baseline in the uninjured limb. These findings provide evidence that muscles can stiffen after sustaining strain injury, as suggested in previous studies [27, 28].

The passive BFlh stiffness in the previously injured limb was higher than that in the contralateral uninjured limb in Study 1. Although injury locations were identified using MRI, the ultrasound SWE measurement sites may not have precisely matched the actual injury sites. This is because MRI‐based identification of the exact injury site is inherently difficult due to edema extending beyond the primary lesion and overlap with unaffected tissue, making precise targeting of the same site with two‐dimensional ultrasound imaging even more challenging. Nevertheless, it is theoretically reasonable that high stiffness in one area of a muscle forces other areas of the muscle to produce most of the strain during lengthening, resulting in those areas exhibiting higher stiffness [29]. That is, if a previously injured area within the muscle becomes stiffer, it would increase the overall passive muscle stiffness, even though passive muscle stiffness measurements were not performed at the exact injury site. However, the temporal relationship between a history of strain injury and passive muscle stiffness remained unclear due to the retrospective design of Study 1.

To overcome this limitation of the retrospective (cross‐sectional) analysis in Study 1, passive BFlh stiffness was longitudinally assessed before and after sustaining strain injury until return‐to‐sport in Study 2. In the uninjured limb, passive BFlh stiffness increased at the acute phase, which aligns with the previous finding that passive BFlh stiffness increased after 2 weeks of training cessation in highly trained sprinters [25]. This increase is thought to result from the cessation of eccentric and plyometric training as well as conditioning activities such as stretching, which are known to reduce passive muscle stiffness; discontinuing these activities would therefore lead to increased passive muscle stiffness. In contrast, passive BFlh stiffness in the injured limb did not increase at the acute phase. This may be attributed to the combined effects of the training cessation‐induced increase in passive muscle stiffness [25] and the decrease in passive muscle stiffness associated with hemorrhage following strain injury [30], although the influence of hemorrhage at the injury site on stiffness measured at other locations within the same muscle is not fully understood. Subsequently, during the rehabilitation phase, passive BFlh stiffness in the uninjured limb decreased to baseline, whereas passive BFlh stiffness in the injured limb increased compared with baseline. Furthermore, during the rehabilitation phase, passive BFlh stiffness in the injured limb tended to be greater than that in the uninjured limb, although this difference did not reach statistical significance (p = 0.057). This increase in passive BFlh stiffness in the injured limb may be attributed not only to the resolution of hemorrhage but also to post‐injury tissue remodeling, including scar formation [27]. Moreover, this increase did not diminish over time and passive BFlh stiffness remained elevated at the return‐to‐sport phase. Moreover, passive BFlh stiffness in the injured limb showed a tendency to remain elevated at the return‐to‐sport phase compared with baseline, although this difference did not reach statistical significance in the parametric analysis (p = 0.094). Of note, nonparametric sensitivity analysis indicated a significant difference (p = 0.038), and the between‐limb comparison confirmed significantly greater stiffness in the injured limb at return‐to‐sport (p = 0.017). Taken together, the significant limb × time interaction, the significant increase from baseline to the rehabilitation phase in the injured limb, and the significant between‐limb difference at return‐to‐sport are consistent with a temporal relationship between strain injury and increased passive muscle stiffness, corroborating the cross‐sectional findings of Study 1. Nevertheless, when individual responses were examined by injury type (Figure 4), participants with myofascial (grades 1a, 2a) and muscular/musculotendinous (grade 1b) injuries consistently demonstrated elevated BFlh stiffness at return‐to‐sport. In contrast, responses among participants with intratendinous injuries (grades 2c, 3c) were more heterogeneous, with some cases showing no increase in stiffness at return‐to‐sport. Although formal subgroup analysis was not feasible due to the limited sample size, this observation warrants further investigation in larger cohorts.

Recent studies have examined passive muscle stiffness between limbs with and without an injury history [31, 32, 33]. However, no longitudinal study has included pre‐injury baseline measurements. The present study is the first to examine post‐injury changes in passive muscle stiffness with comparison to baseline values. Even when limited to retrospective studies comparing previously injured and uninjured limbs, there is no consensus regarding strain injury‐induced changes in passive muscle stiffness, including the present findings [31, 32, 33]. One of the reasons for this inconsistency would be the differences in SWE measurement positions among studies. We assessed passive BFlh stiffness in a lengthened position rather than shortened positions such as the lying position. This approach was chosen because passive muscle stiffness is strongly influenced by the extracellular matrix (including perimysial and endomysial collagen fibers), and its characteristics are more apparent when the muscle is stretched [34, 35]. Indeed, effects of various interventions (e.g., stretching exercise [36, 37, 38] and supplementation [39]) and age‐associated differences in passive muscle stiffness [40] have been detected only in stretched positions, not in shortened positions. Based on these considerations and the present findings, muscle conditions for strain injury prevention and rehabilitation should be assessed in lengthened positions.

Another reason for the inconsistent findings among studies may be the failure to identify injury grade (location and severity). In the present study, based on MRI diagnosis and BAMIC, Study 1 included only athletes with a history of muscular/musculotendinous injury (i.e., grade 1b, 2b, or 3b). In contrast, Study 2 included athletes who sustained BFlh strain injuries of various grades (locations and severities). This represents a limitation of the present study, as the number of athletes who sustained muscular/musculotendinous injuries (i.e., the same injury type as in Study 1) was insufficient for the longitudinal analysis. Nevertheless, despite including participants with various injury grades, Study 2 yielded results supporting the findings of Study 1. However, when examining the data by injury location (myofascial vs. muscular/musculotendinous vs. intratendinous), athletes with myofascial and muscular/musculotendinous injuries showed increased passive muscle stiffness at return‐to‐sport, whereas some cases of intratendinous injury did not show increased passive BFlh stiffness at return‐to‐sport (Figure 4). Therefore, future studies should examine how passive muscle stiffness changes according to injury grade (location and severity).

The findings obtained in the present study have practical implications for understanding the potential mechanisms underlying increased risk in muscles with a history of strain injuries. A history of HSI has consistently been identified as one of the strongest risk factors for future HSI in the same leg [7, 8]. Additionally, high passive muscle stiffness assessed using ultrasound SWE has recently been suggested as a risk factor for strain injuries [12, 24]. Considering these findings together with the present findings, it is plausible that the increased passive BFlh stiffness following strain injury increases the likelihood of sustaining a new strain injury (including reinjury). Exploring potential interventions to manage increases in passive muscle stiffness induced by strain injuries is an important area for future research. Such studies may contribute to understanding whether the notion of HSI history as a “non‐modifiable” risk factor could be revisited.

Besides the presence of injury‐induced scar tissue, the difference between measurement and injury sites, and the varied injury grades in Study 2, which have already been discussed above, the present study has other limitations. First, the sample size in Study 1, although satisfying the minimum sample size calculated through a priori power analysis, is still relatively small. Similarly, Study 2, although yielding significant interactions, had a small sample size. Second, the present study included only male track‐and‐field athletes. While this homogeneous sample reduces confounding factors and strengthens internal validity, it limits generalizability. Estrogen and other female hormones are thought to reduce passive muscle stiffness, and passive muscle stiffness in females is lower than in males [18]. Therefore, it remains unclear whether passive muscle stiffness increases following strain injury in female athletes. Third, although participants were instructed to fully relax their legs and we visually monitored participants for any signs of muscle activation or discomfort during measurements, muscle activity was not monitored using electromyography. Normalizing electromyography amplitude to maximal voluntary contraction is required to objectively confirm muscle relaxation. However, maximal voluntary contraction testing was considered impractical, especially during the acute and rehabilitation phases due to pain and functional limitations associated with injury. Consequently, the actual level of relaxation and its potential influence on the results remain unclear. Larger studies including female participants, with objective confirmation of muscle relaxation using methods applicable across all recovery phases, are needed to confirm the present findings and improve generalizability to broader athletic populations.

In conclusion, the present study provides both cross‐sectional and longitudinal findings that strain injury leads to persistent increases in passive BFlh stiffness. These findings reveal that strain injury leads to lasting increases in passive muscle stiffness, a biomechanical change that persists at return‐to‐sport and may have implications for post‐injury muscle function.

5. Perspective

The present findings indicate several directions for future research. First, larger‐scale studies should examine whether post‐injury changes in passive muscle stiffness differ according to injury grade, including location and severity. Second, prospective cohort studies are warranted to investigate whether strain injury‐induced increases in passive muscle stiffness elevate subsequent injury risk. Third, intervention studies targeting post‐injury passive muscle stiffness may help determine whether this factor is modifiable. These lines of research could advance our understanding of whether HSI history might shift from a non‐modifiable to a potentially modifiable risk factor.

Funding

This work was supported by JSPS KAKENHI (grant number JP19H04005).

Ethics Statement

This study was approved by the ethics committee (No. E22‐0345) of Juntendo University.

Consent

Written informed consent was obtained from all participants prior to data collection.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.