eccentric contraction
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It is well-known that unusual exercise, especially eccentric contraction (ECC), could cause delayed-onset muscle soreness. However, the factors related to the loss of muscle strength and range of motion (ROM) caused by eccentrically damaged muscle, such as increases in muscle soreness, tissue hardness, and pain threshold, have not been investigated in detail. Thus, this study was conducted to investigate the factors related to the loss of muscle strength and ROM caused by eccentrically damaged muscle in a large sample. Fifty-six sedentary healthy young male volunteers were instructed to perform 60 repetitions of ECC exercise. The outcome variables were measured before and 48 h after the ECC exercise. The results showed that a decrease in ROM was correlated to an increase in tissue hardness, whereas a decrease in muscle strength was correlated to an increase in muscle soreness. Our results suggested that tissue hardness must be controlled for ROM loss, and muscle soreness must be controlled for muscle-strength loss.

Background: Triceps tendon ruptures typically result from a forceful elbow eccentric contraction. The goal of a distal triceps tendon repair is to reattach the torn tendon back to the olecranon. Surgery is indicated for patients with complete rupture of the triceps tendon or symptomatic partial tears with failed conservative management. The complication rate occurs in 22% of patients postoperatively; however, only 0% to 4% of patients suffer a re-rupture of the tendon. Indications: We present a case of a highly active 38-year-old right-hand dominant man with acute onset of left posterior elbow pain following 1-handed pushup resulting in a complete distal triceps avulsion with 1.5 cm retraction. Technique: The distal triceps avulsion was repaired in a double row fashion using 2 double-loaded all-suture anchors in the medial row and anchor in the lateral row through a posterior approach. Results: Full anatomic footprint coverage was able to be achieved intraoperatively, and gentle range of motion from 0 to 90 degrees of flexion did not result in gap formation. Discussion/Conclusion: Successful outcomes with full anatomic footprint coverage of the distal triceps tendon can be achieved through a double row repair configuration.

Although several studies have reported the effect of exercise therapy for adhesive capsulitis (AC), studies on the comparison of different exercise types on shoulder muscle strength and function in patients with AC are lacking. This study aimed to investigate the effect of different exercise types on shoulder muscle strength and function in patients with AC. Thirty female patients with AC were categorized into an eccentric contraction exercise group (ECG, n = 15; age, 51.53 ± 4.73 years) and a concentric contraction exercise group (CCG, n = 15; age, 52.40 ± 4.03 years). The participants in each group performed a different exercise program three times per week for 60 min per session for 12 weeks. The range of motion (ROM) of the shoulder joint, visual analog scale, shoulder muscle strength, and Constant–Murley score (CMS) were measured before the intervention and after 12 weeks of the exercise intervention. Shoulder ROM in flexion (increase of 31%) and external rotation (ER) (increase of 54%) showed a significant improvement in the ECG (p < 0.05). Muscle strength in ER was significantly different between the two groups (p < 0.05). Pain severity showed improvement in the ECG (decrease of 61%) after the intervention (p < 0.01). The CMS in the ECG (increase of 48%) showed a greater improvement than that in the CCG after the intervention (p < 0.01). This study showed that eccentric contraction exercise had a more beneficial effect than concentric contraction exercise for improving shoulder muscle strength and function in females with AC.

Duchenne muscular dystrophy is caused by the absence of the protein dystrophin from skeletal muscle and is characterized by progressive cycles of necrosis/regeneration. Using the dystrophin deficient mdx mouse model, we studied the morphological and contractile chronology of dystrophic skeletal muscle pathology in fast-twitch Extensor Digitorum Longus muscles from animals 4–22 months of age containing 100% regenerated muscle fibers. Catastrophically, the older age groups lost ∼80% of their maximum force after one eccentric contraction (EC) of 20% strain with the greatest loss of ∼92% recorded in senescent 22-month-old mdx mice. In old age groups, there was minimal force recovery ∼24% after 120 min, correlated with a dramatic increase in the number and complexity of branched fibers. This data supports our two-phase model where a “tipping point” is reached when branched fibers rupture irrevocably on EC. These findings have important implications for pre-clinical drug studies and genetic rescue strategies.

We performed X-ray diffraction analyses on rat plantaris muscle to determine if there are strain-specific structural changes at the molecular level after eccentric contraction (ECC). ECC was elicited in situ by supramaximal electrical stimulation through the tibial nerve. One hour after a series of ECC sessions, the structural changes that remained in the sarcomere were evaluated using X-ray diffraction. Proteins involved in cell signaling pathways in the muscle were also examined. ECC elicited by 100, 75, and 50 Hz stimulation respectively developed peak tension of 1.34, 1.12 and 0.79 times the isometric maximal tetanus tension. The series of ECC sessions phosphorylated the forkhead box O proteins (FoxO) in a tension-time integral-dependent manner, as well as phosphorylated the mitogen-activated protein kinases (MAPK) and a protein in the mammalian target of rapamycin (mTOR) pathway in a maximal tension dependent manner. Compared to isometric contractions, ECC was more efficient in phosphorylating the signaling proteins. X-ray diffraction revealed that the myofilament lattice was preserved even after intense ECC stimulation at 100 Hz. Additionally, ECC < 75 Hz preserved the molecular alignment of myoproteins along the myofilaments, while 75-Hz stimulation induced a slight but significant decrease in the intensity of meridional troponin reflection at 1/38 nm−1, and of myosin reflection at 1/14.4 nm−1. These two reflections demonstrated no appreciable decrease with triple repetitions of the standard series of ECC sessions at 50 Hz, suggesting that the intensity decrease depended on the instantaneous maximal tension development rather than the total load of contraction, and was more likely linked with the phosphorylation of MAPK and mTOR signaling proteins.

The purpose of this study was to explore reliability and differences of jump kinetics related to different training load in college male athletes. The subjects were required to perform countermovement jump (CMJ) and loaded countermovement jump (LCMJ-0%, LCMJ-20% and LCMJ-80% of one-repetition maximum squat) three times for each load which were recorded by a force plate. One-way repeated measures ANOVA and the LSD post hoc method were employed to evaluate the results. The results reveled that jump kinetics-related parameters increased/decreased by the load. Compared with the loading jumps, the CMJ incorporate with an arm swing directly led to an increase in eccentric contraction duration during jumping. Most of the jump mechanical parameters under substantially different load conditions fall within the good to excellent reliability. It appears that the CMJ and CMJ with extra load were reliable in explore the kinetics related parameters. Keywords: countermovement jump, one-repetition maximum, arm swing, eccentric contraction

Background: Eccentric muscle contractions are commonly used in exercise regimens, as well as in rehabilitation as a treatment against muscle atrophy and weakness. If repeated multiple times, eccentric contractions may result in skeletal muscle injury and loss of function. Skeletal muscle possesses the remarkable ability to repair and regenerate after an injury or damage; however, this ability is impaired with aging. Phytoecdysteroids are natural plant steroids that possess medicinal, pharmacological, and biological properties, with no adverse side effects in mammals. Previous research has demonstrated that administration of phytoecdysteroids, such as 20-hydroxyecdysone (20E), leads to an increase in protein synthesis signaling and skeletal muscle strength.Methods: To investigate whether 20E enhances skeletal muscle recovery from eccentric contraction-induced damage, adult (7–8 mo) and old (26–27 mo) mice were subjected to injurious eccentric contractions (EC), followed by 20E or placebo (PLA) supplementation for 7 days. Contractile function via torque-frequency relationships (TF) was measured three times in each mouse: pre- and post-EC, as well as after the 7-day recovery period. Mice were anesthetized with isoflurane and then electrically-stimulated isometric contractions were performed to obtain in vivo muscle function of the anterior crural muscle group before injury (pre), followed by 150 EC, and then again post-injury (post). Following recovery from anesthesia, mice received either 20E (50 mg•kg−1 BW) or PLA by oral gavage. Mice were gavaged daily for 6 days and on day 7, the TF relationship was reassessed (7-day).Results: EC resulted in significant reductions of muscle function post-injury, regardless of age or treatment condition (p &lt; 0.001). 20E supplementation completely recovered muscle function after 7 days in both adult and old mice (pre vs. 7-day; p &gt; 0.05), while PLA muscle function remained reduced (pre vs. 7-day; p &lt; 0.01). In addition, histological markers of muscle damage appear lower in damaged muscle from 20E-treated mice after the 7-day recovery period, compared to PLA.Conclusions: Taken together, these findings demonstrate that 20E fully recovers skeletal muscle function in both adult and old mice just 7 days after eccentric contraction-induced damage. However, the underlying mechanics by which 20E contributes to the accelerated recovery from muscle damage warrant further investigation.

The present study aimed to investigate the relationship between linear deceleration performance and explosive strength capacity of the knee muscles. Fourteen female professional soccer players completed the maximal sprint deceleration tests and knee flexor (KF) and knee extensor (KE) isokinetic concentric (240° and 60°.s−1) and eccentric contractions (30°.s−1). Linear deceleration performance was evaluated from horizontal breaking force (FH), power (PH), and impulse (IH) during a maximal linear deceleration. The peak torque (PT) of KF and KE, PT ratio between KF and KE (conventional and functional H/Q ratio), rate of torque development (RTD) for each muscle group, and RTD between KF and KE (RTD H/Q) were extracted from the isokinetic contractions. Pearson’s correlation coefficients revealed that the eccentric (30°.s−1) and concentric (60°.s−1, 240°.s−1) KE peak torque, and the concentric KF peak torque (240°.s−1) were significantly correlated with FH, PH, and IH (−0.75&lt;r&lt;−0.54). Moreover, a significant correlation was found between KE RTD during eccentric contraction and FH, PH, and IH (−0.63&lt;r&lt;−0.54). Besides, a significant correlation was observed between RTD H/Q at 60°.s−1 and PH, IH (−0.61&lt;r&lt;−0.57). No significant relationship was observed between the H/Q ratio, KF RTD and deceleration performance. These main findings indicated the importance of the ability to quickly produce high KE eccentric torque, contributing to braking force production. Meanwhile, RTD H/Q should be assessed for its essential role in knee joint dynamic stability and can be a relevant index to determine deceleration performance.

ABSTRACTThe common null polymorphism (R577X) in the ACTN3 gene is present in over 1.5 billion people worldwide and results in the absence of the protein α-actinin-3 from the Z-discs of fast-twitch skeletal muscle fibres. We have previously reported that this polymorphism is a modifier of dystrophin deficient Duchenne Muscular Dystrophy. To investigate the mechanism underlying this we use a double knockout (dk)Actn3KO/mdx (dKO) mouse model which lacks both dystrophin and sarcomere α-actinin-3. We used dKO mice and mdx dystrophic mice at 12 months (aged) to investigate the correlation between morphological changes to the fast-twitch dKO EDL and the reduction in force deficit produced by an in vitro eccentric contraction protocol. In the aged dKO mouse we found a marked reduction in fibre branching complexity that correlated with protection from eccentric contraction induced force deficit. Complex branches in the aged dKO EDL fibres (28%) were substantially reduced compared to aged mdx EDL fibres (68%) and this correlates with a graded force loss over three eccentric contractions for dKO muscles (∼35% after first contraction, ∼66% overall) compared to an abrupt drop in mdx upon the first eccentric contraction (∼73% after first contraction, ∼89% after three contractions). In dKO protection from eccentric contraction damage was linked with a doubling of SERCA1 pump density the EDL. We propose that the increased oxidative metabolism of fast-twitch glycolytic fibres characteristic of the null polymorphism (R577X) and increase in SR Ca2+ pump proteins reduces muscle fibre branching and decreases susceptibility to eccentric injury in the dystrophinopathies.

ABSTRACTDuchenne muscular dystrophy is caused by the absence of the protein dystrophin from skeletal muscle and is characterized by progressive cycles of necrosis/regeneration. Using the dystrophin deficient mdx mouse model we studied the morphological and contractile chronology of dystrophic skeletal muscle pathology in fast twitch EDL muscles from animals 4-22 months of age containing 100% regenerated muscle fibers. Catastrophically, the older age groups lost ∼80% of their maximum force after one eccentric contraction of 20% strain, with the greatest loss ∼93% recorded in senescent 22 month old mdx mice. In old age groups there was minimal force recovery ∼24% after 120 minutes, correlated with a dramatic increase in the number and complexity of branched fibers. This data supports our two-stage model where a “tipping point” is reached when branched fibers rupture irrevocably on eccentric contraction. These findings have important implications for pre-clinical drug studies and genetic rescue strategies.