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. 2022 Dec 1;17(12):e0277949.
doi: 10.1371/journal.pone.0277949. eCollection 2022.

Neuromuscular characteristics of agonists and antagonists during maximal eccentric knee flexion in soccer players with a history of hamstring muscle injuries

Affiliations

Neuromuscular characteristics of agonists and antagonists during maximal eccentric knee flexion in soccer players with a history of hamstring muscle injuries

Ramona Ritzmann et al. PLoS One. .

Abstract

Background: Muscle strain injuries (MSIs) in the hamstrings are among the most prevalent injuries in elite soccer. We aimed to examine the relation between biomechanical maladaptation in eccentric strength and neuromuscular factors separated by their time and frequency domains.

Methods: 20 elite soccer players with a previous history of unilateral MSI in the M. biceps femoris (BF) long head and 20 without MSI participated. Knee flexion torques, rate of torque development (RTD) and electromyographic signals (EMG) of the BF, the M. semitendinosus (SMT) and knee extensors were obtained during unilateral maximal eccentric knee flexions performed at slow (30°/s) and fast (120°/s) angular speeds. Root mean squares and mean power frequency (MF) was calculated.

Results: In the group with a history of MSI, reduced maximal eccentric flexion torque (slow eccentrics -8±11, p<0.05; fast eccentrics -18±13 N*m, p<0.05) and RTD (-33±28 N*m/s, p<0.05; -95±47 N*m/s, p<0.05) concomitantly occurred with diminished agonistic myoelectrical activities (-4±5% of MVC, p<0.05; -10±7% of MVC, p<0.05) and MFs (-24±13 Hz, p<0.05; -24±18 Hz, p<0.05) in the BF. Simultaneously, antagonistic myoelectric activity was elevated (+4±3% of MVC, p<0.05; +3±3% of MVC, p<0.05) in MSI affected legs as compared to unaffected legs for both eccentric contractions. Deficits in myoelectrical activity (r2 = 0.715, p<0.05; r2 = 0.601, p<0.05) and MF (r2 = 0.484, p<0.05; r2 = 0.622, p<0.05) correlated with deficits in maximal torque in the affected leg in the MSI group. Analysis of SMT demonstrated no significant differences.

Conclusion: Positive relationships between neuromuscular deficits and the reduced eccentric strength profile underpin neuronal inhibition after MSI. This persistent involvement of dysfunctional synergist and antagonist neural hamstring function in strength weakness is of clinical relevance in sports medicine for prevention and rehabilitation.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. CONSORT flow chart diagram.
Enrollment procedures and sample size.
Fig 2
Fig 2. Raw tracings of isokinetic knee torque and electromyogram (EMG).
They obtained in a male elite soccer player in the paradigm of maximal eccentric knee flexion contraction during joint movements performed at slow (A) and fast (B) joint angular speeds (30°/s and 120°/s, respectively) illustrated for the unaffected leg (left) and the affected leg with a history of MSI. Range of joint motion was from 90° to 0° (0° = full knee extension). Upper tracings display the joint torque and position signal. Lower tracings display raw EMG signals recorded from the biceps femoris (BF), semitendinosus (ST), vastus medialis (VM), and rectus femoris (RF) muscles. EMG was lower in the MSI affected compared with the unaffected leg, suggesting significant neural inhibition after MSI. Note the appearance of large EMG amplitude spikes separated by short inter spike periods of high neuromuscular activity in the BF and SMT of the unaffected leg as compared to the affected leg. Furthermore, torque and EMG amplitudes were diminished on the MSI affected side, especially during eccentric and fast concentric contractions (B).
Fig 3
Fig 3
A illustrates the MSI group with previous unilateral hamstring strain injuries experienced in the M. biceps long head (left) and the healthy CONTROL group with bilateral healthy legs. Graphs B–E illustrate changes in joint torques and impulses: B displays differences in the peak knee flexion joint torque (ordinate) and the corresponding knee flexion angle as well as the joint torques at 30ms, 50ms 100ms and 200ms after the movement onset of the lever arm at 30°/s speed for both groups. Graph C displays differences in the total impulse and impulses calculated for the intervals 0–50ms, 0–100ms and 0–200ms after movement onset of the lever arm at 30°/s speed. Joint torques at 120°/s are illustrated in graph D. Joint Impulses at 120°/s are illustrated in graph E. Values are means ± SD; § indicates significant group * leg interaction effects; * symbolizes significant pairwise differences.
Fig 4
Fig 4. Grand means of myoelectrical activities.
A illustrates Biceps femoris myoelectrical activity as the root mean square normalized to MVC and B the median frequency at 30°/s during the eccentric knee flexion for the MSI and CONTROL group. Grands means for myograms are illustrated across the entire range of motion and the intervals 0–50ms, 0–100ms and 0–200ms after movement onset of the lever arm at 30°/s speed. C illustrates Biceps femoris myoelectrical activity and D the median frequency at 120°/s during the eccentric knee flexion for the MSI and CONTROL group. Not the reduced myoelectrical activities and frequencies for the affected leg of the MSI groups as compared to the healthy contralateral side or the CONTROL group. Values are means ± SD; § indicates significant group * leg interaction effects; * symbolizes significant pairwise differences.
Fig 5
Fig 5. Scatter plots with regression lines.
They are illustrated for differences (Δ) between the unaffected leg and the affected leg with MSI history in the biceps femoris long head (BF) muscles of the MSI group (n = 20) for the slow (30°/s, black) and fast (120°/s, grey) eccentric contraction. A illustrates the plot for maximal torque and BF EMGRMS (normalized to MVC) for the entire range of motion. B illustrates maximal torque and BF EMGRMS for the interval 0–200ms after contraction onset. Graph C illustrates the plot for maximal torque and the corresponding the medium frequency. Regressions A–C are significantly positive.

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