Absorption function loss due to the history of previous ankle sprain explored by unsupervised machine learning.

BACKGROUND: Ankle sprains are common and cause persistent ankle function reduction. To biomechanically evaluate the ankle function after ankle sprains, the ground reaction force (GRF) measurement during the single-legged landing had been used. However, previous studies focused on discrete features of vertical GRF (vGRF), which largely ignored vGRF waveform features that could better identify the ankle function. PURPOSE: To identify how the history of ankle sprain affect the vGRF waveform during the single-legged landing with unsupervised machine learning considering the time-series information of vGRF. METHODS: Eighty-seven currently healthy basketball athletes (12 athletes without ankle sprain, 49 athletes with bilateral, and 26 athletes with unilateral ankle sprain more than 6 months before the test day) performed single-legged landings from a 20 centimeters (cm) high box onto the force platform. Totally 518 trials vGRF data were collected from 87 athletes of 174 ankles, including 259 ankle sprain trials (from previous sprain ankles) and 259 non-ankle sprain trials (from without sprain ankles). The first 100 milliseconds (ms) vGRF waveforms after landing were extracted. Principal component analysis (PCA) was applied to the vGRF data, selecting 8 principal components (PCs) representing 96% of the information. Based on these 8 PCs, k-means method (k = 3) clustered the 518 trials into three clusters. Chi-square test assessed significant differences (p < 0.01) in the distribution of ankle sprain and non-ankle sprain trials among clusters. FINDINGS: The ankle sprain trials accounted for a significantly larger percentage (63.9%) in Cluster 3, which exhibited rapidly increased impulse vGRF waveforms with larger peaks in a short time. SIGNIFICANCE: PCA and k-means method for vGRF waveforms during single-legged landing identified that the history of previous ankle sprains caused a loss of ankle absorption ability lasting at least 6 months from an ankle sprain.

Icing after skeletal muscle injury decreases M1 macrophage accumulation and TNF-α expression during the early phase of muscle regeneration in rats.

Following skeletal muscle injury, both myogenic and immune cells interact closely during the regenerative process. Although icing is still a common acute treatment for sports-related skeletal muscle injuries, icing after muscle injury has been shown to disrupt macrophage accumulation and impair muscle regeneration in animal models. However, it remains unknown whether icing shortly after injury affects macrophage-related phenomena during the early stages of muscle regeneration. Therefore, we focused on the distribution of M1/M2 macrophages and cytokines expressed predominantly by macrophages during the early stages of muscle regeneration after muscle crush injury. Icing resulted in a decrease, not retardation, in the accumulation of M1 macrophages, but not M2 macrophages, in injured muscles. Consistent with the decrease in M1 macrophage accumulation, icing led to a reduction, instead of delay, in the level of tumor necrosis factor-α (TNF-α) expression. Additionally, at subsequent timepoints, icing decreased the number of myogenic precursor cells in the regenerating area and the size of centrally nucleated regenerating myofibers. Together, our findings suggest that icing after acute muscle damage by crushing disturbs muscle regeneration through hindering tM1 macrophage-related phenomena.

Effect of the foot-strike pattern on the sagittal plane knee kinetics and kinematics during the early phase of cutting movements.

Anterior cruciate ligament (ACL) injury occurs soon after foot-strike. Cutting with a shallow flexed knee is considered a risk factor for ACL injury; however, how foot-strike patterns (forefoot strike [FFS] vs. rearfoot strike [RFS]) affect sagittal plane knee kinetics and kinematics after a foot-strike, is unknown. This study aimed to investigate the effect of foot-strike patterns on the sagittal plane knee kinetics and kinematics during cutting. Twenty-three males performed 45° cutting under RFS and FFS conditions. The marker position data on the lower limb, and the ground reaction force (GRF) data were collected and time-normalized (0-100%) during the stance phase. The knee flexion angle, shank and GRF vector inclination angle relative to the global vertical axis, knee flexion/extension moment, and anterior/posterior component of GRF relative to the shank segment were calculated and compared between foot-strike patterns using statistical parametric mapping paired t-test (p < 0.0071). The knee flexion angle was smaller in RFS than in FFS in the initial 40% of the stance phase. In the RFS condition, the GRF vector was directed anteriorly to the shank segment, and the knee extension moment was produced by GRF in 0-7% of the stance phase, while these results were not observed in the FFS condition. These results suggest that compared to FFS, RFS induces a shallow flexed knee with an anterior-directed GRF component in the early stance phase and might potentially provoke a risk of ACL injury.

Icing after eccentric contraction-induced muscle damage perturbs the disappearance of necrotic muscle fibers and phenotypic dynamics of macrophages in mice.

Icing is still one of the most common treatments to acute skeletal muscle damage in sports medicine. However, previous studies using rodents reported the detrimental effect of icing on muscle regeneration following injury. This study aimed to elucidate the critical factors governing the impairment of muscle regeneration by icing with a murine model of eccentric contraction-induced muscle damage by electrical stimulation. Because of icing after muscle injury, the infiltration of polynuclear and mononuclear cells into necrotic muscle fibers was retarded and attenuated, leading to the persistent presence of necrotic cellular debris. These phenomena coincided with the delayed emergence and sustained accumulation of Pax7+ myogenic cells within the regenerating area. In addition, due to icing, delayed and/or sustained infiltration of M1 macrophages was noted in accordance with the perturbed expression patterns of inflammation-related factors, including tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). The key myogenic regulatory factors (i.e., MyoD and myogenin) involved in the activation/proliferation and differentiation of myogenic precursor cells were not altered by icing during the regenerative process. A detailed analysis of regenerating myofibers by size distribution at day 14 after muscle damage showed that the ratio of small regenerating fibers to total regenerating fibers was higher in icing-treated animals than in untreated animals. These findings suggest that icing following muscle damage blunts the efficiency of muscle regeneration by perturbing the removal of necrotic myofibers and phenotypic dynamics of macrophages rather than affecting myogenic factors.NEW & NOTEWORTHY Icing blunted the muscle regeneration by perturbing the infiltration of polynuclear and mononuclear cells into necrotic myofibers and the phenotypic dynamics of macrophages rather than affecting the myogenic regulatory factors. Because of icing, the disappearance of necrotic muscle debris was retarded, coinciding with the delayed emergence and sustained accumulation of Pax7+ cells within the regenerating area. The expression patterns of TNF-α and IL-10 were altered by icing consistent with the perturbation of the macrophage phenotype.

Unloading during skeletal muscle regeneration retards iNOS-expressing macrophage recruitment and perturbs satellite cell accumulation.

After skeletal muscle injury, unloading disturbs the regenerative process of injured myofibers, in a manner highly attributed to impairment of macrophage functions. However, the effect of unloading on the spatiotemporal context of proinflammatory macrophage recruitment and satellite cell accumulation within the damaged area remains unclear. This study focused on macrophages expressing inducible nitric oxide synthase (iNOS) that synthesize nitric oxide, a key regulator of muscle regeneration, and compared the continuous hindlimb unloading (HU) by tail suspension versus weight-bearing (WB) after skeletal muscle crush injury in rats. We found that in the WB group, the recruitment of iNOS+ proinflammatory macrophages into the injured site gradually increased until their peak number at 48 h post-injury. In the HU group, the accumulation of iNOS+ macrophages until 48 h after injury was significantly less than that in the WB group and continued to increase at 72 h. In accordance with attenuated and/or delayed iNOS+ macrophage recruitment, whole iNOS expression at 24 and 48 h after injury was weakened by unloading. Additionally, in the HU group, satellite cell content of dystrophin-positive non-injured areas diminished at 48 h after injury, and the numbers of activated satellite cells within the regenerating area at 72 and 96 h post-injury were significantly smaller than those in the WB group. These findings suggest that muscle regeneration under unloading conditions results in attenuated and/or delayed recruitment of iNOS+ macrophages and lower iNOS expression in the early phase after muscle injury, leading to perturbed satellite cell accumulation and muscle regeneration.

Inhibition of the migration of MCP-1 positive cells by icing applied soon after crush injury to rat skeletal muscle.

Migration of the macrophages to the injured site soon after the skeletal muscle injury is crucial for subsequent regeneration of the muscle fibers. The Monocyte chemoattractant protein-1 (MCP-1) is important chemokine for regulating migration of the monocytes/macrophages. Earlier reports have discussed that icing applied soon after muscle crush injury retards muscle regeneration through retardation of macrophage migration. The MCP-1+ cells and neutrophils might promote the migration of the macrophages. To test the hypothesis that icing soon after the skeletal muscle injury affects MCP-1+ cells and neutrophils, we examined the effect of icing on MCP-1+ cells and neutrophils after crush injury to skeletal muscle in rats. Owing to the icing application for 20 min soon after the injury, accumulation of the macrophages was inhibited until 12 h after injury. Numbers of the neutrophils at 3 h after the injury and the MCP-1+ cells at 6 h and later after the injury in the icing group were significantly lower than those in the non-icing group, suggesting that these phenomena contribute to the retardation of macrophage migration.