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Introduction: Collagen peptide supplementation in conjunction with exercise has been shown to improve structural and functional adaptations of both muscles and the extracellular matrix. This study aimed to explore whether specific collagen peptide (SCP) supplementation combined with a concurrent training intervention can improve muscular stress after exercise-induced muscle damage, verified by reliable blood markers. Methods: 55 sedentary to moderately active males participating in a concurrent training (CT) intervention (3x/week) for 12 weeks were administered either 15 g of SCP or placebo (PLA) daily. Before (T1) and after the intervention (T2), 150 muscle-damaging drop jumps were performed. Blood samples were collected to measure creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin (MYO) and high-sensitivity C-reactive protein (hsCRP) before, after, and at 2 h, 24 h and 48 h post exercise. Results: A combination of concurrent training and SCP administration showed statistically significant interaction effects, implying a lower increase in the area under the curve (AUC) of MYO (p = 0.004, ηp2 = 0.184), CK (p = 0.01, ηp2 = 0.145) and LDH (p = 0.016, ηp2 = 0.133) in the SCP group. On closer examination, the absolute mean differences (ΔAUCs) showed statistical significance in MYO (p = 0.017, d = 0.771), CK (p = 0.039, d = 0.633) and LDH (p = 0.016, d = 0.764) by SCP supplementation. Conclusion: In conclusion, 12 weeks of 15 g SCP supplementation combined with CT intervention reduced acute markers of exercise-induced muscle damage and improved post-exercise regenerative capacity, as evidenced by the altered post-exercise time course. The current findings indicate that SCP supplementation had a positive effect on the early phase of muscular recovery by either improving the structural integrity of the muscle and extracellular matrix during the training period or by accelerating membrane and cytoskeletal protein repair. Clinical trial registration: https://www.clinicaltrials.gov/study/NCT05220371?cond=NCT05220371&rank=1, NCT05220371.

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BACKGROUND: Although recent studies have investigated the effects of flywheel (FW) training on muscle function, the effects of transient FW exercise on jump performance in athletes are unknown. This study examined the effects of single and repeated bouts of FW squat exercises on jump performance and muscle damage in male collegiate basketball players. METHODS: The participants were 10 healthy college-age men (nonathletes) and 11 male basketball players (athletes). The intervention involved 100 squat exercises (10 repetitions × 10 sets) using an FW device. To examine the repeated-bout effects, the protocol was conducted again after a 2-week interval. Squat jumps, countermovement jumps, drop jumps, and rebound jumps were evaluated as jump performance, while isometric maximal voluntary contraction (MVC) torque in knee extension, muscle soreness, range of motion, thigh circumference, muscle thickness, and echo intensity were evaluated as markers of muscle damage. Measurements were taken at baseline, immediately after exercise, 24 h later, and 72 h later. RESULTS: The jump performance of nonathletes decreased after exercise (p < 0.05), while that of the athletes did not. The results were similar for muscle soreness. MVC torque decreased significantly after the first exercise in both groups (p < 0.05) and was significantly lower in the nonathletes versus athletes. Significant repeated-bout effects were found for muscle soreness in nonathletes but not athletes. CONCLUSIONS: These results suggest that a single bout of FW exercise reduces jump performance in male nonathletes but not basketball players.

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Delayed onset muscle soreness (DOMS) develops after performing unaccustomed eccentric exercises. Animal studies have shown that DOMS is mechanical hyperalgesia through nociceptor sensitization induced by nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) upregulated by cyclooxygenase-2 (COX-2). However, no previous study has investigated these in relation to DOMS in humans. This study compared the first and second bouts of one-leg eccentric cycling (ECC) for changes in NGF, GDNF, and COX-2 mRNA in the vastus lateralis (VL). Seven healthy adults (18-40 years) performed two bouts of ECC (10 sets of 50 contractions) with 80% maximal voluntary concentric peak torque separated by 2 weeks (ECC1, ECC2). Muscle soreness that was assessed by a visual analog scale and maximal voluntary isometric contraction (MVC) torque of the knee extensors were measured before, immediately after (MVC only), 24 and 48 h post-exercise. Muscle biopsy was taken from the VL before the first bout from nonexercised leg (control) and 24 h after each bout from the exercised leg, and analyzed for NGF, GDNF, and COX-2 mRNA. Peak DOMS was more than two times greater and MVC torque at 48 h post-exercise was approximately 20% smaller after ECC1 than ECC2 (p < 0.05), suggesting the repeated bout effect. NGF mRNA level was higher (p < 0.05) post-ECC1 (0.79 ± 0.68 arbitrary unit) than control (0.06 ± 0.07) and post-ECC2 (0.08 ± 0.10). GDNF and COX-2 mRNA did not show significant differences between control, post-ECC1, and post-ECC2. These results suggest that an increase in NGF is associated with the development of DOMS in humans.

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BACKGROUND:Unaccustomed exercise triggers skeletal muscle damage,but produces a specific training effect that reduces muscle re-injury to reduce pain-muscle memory. OBJECTIVE:Based on the etiology of delayed onset muscle soreness,to review the existence and possible mechanism of skeletal muscle memory in delayed onset muscle soreness and to present new insights into the prevention and treatment of delayed onset muscle soreness. METHODS:The first author searched in PubMed,Embase,Web of Science,CNKI and WanFang databases for relevant literature published from January 1990 to December 2022.The keywords were"DOMS,skeletal muscle memory,exercise skeletal muscle adaptation,repeat turn effect,exercise and autophagy,autophagy and inflammation"in English and Chinese,respectively.A total of 102 articles were finally included for review. RESULTS AND CONCLUSION:The etiology of delayed onset muscle soreness is currently believed to be an acute inflammatory response due to metabolic disorders,mechanical injury and oxidative stress,while exercise-induced skeletal muscle memory can reduce delayed onset muscle soreness and exercise re-injury.When the duration,frequency and intensity of centrifugal training are gradually increased,symptoms of the injury can be minimized or even avoided.Therefore,based on the mechanism of exercise-induced skeletal muscle memory,it is the future research direction to find more effective ways to prevent and alleviate exercise-induced muscle injury.This review aims to(1)clarify the existence of exercise-induced skeletal muscle memory;(2)explore the possible mechanisms of exercise-induced skeletal muscle memory and propose the relationship between this memory and skeletal muscle autophagy;and(3)provide new strategies for the prevention and treatment of delayed onset muscle soreness by improving the level of skeletal muscle autophagy.

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Introduction: It has been shown that short-term ingestion of collagen peptides improves markers related to muscular recovery following exercise-induced muscle damage. The objective of the present study was to investigate whether and to what extent a longer-term specific collagen peptide (SCP) supplementation combined with a training intervention influences recovery markers following eccentric exercise-induced muscle damage. Methods: Fifty-five predominantly sedentary male participants were assigned to consume either 15 g SCP or placebo (PLA) and engage in a concurrent training (CT) intervention (30 min each of resistance and endurance training, 3x/week) for 12 weeks. Before (T1) and after the intervention (T2), eccentric muscle damage was induced by 150 drop jumps. Measurements of maximum voluntary contraction (MVC), rate of force development (RFD), peak RFD, countermovement jump height (CMJ), and muscle soreness (MS) were determined pre-exercise, immediately after exercise, and 24 and 48 h post-exercise. In addition, body composition, including fat mass (FM), fat-free mass (FFM), body cell mass (BCM) and extracellular mass (ECM) were determined at rest both before and after the 12-week intervention period. Results: Three-way mixed ANOVA showed significant interaction effects in favor of the SCP group. MVC (p = 0.02, ηp2 = 0.11), RFD (p < 0.01, ηp2 = 0.18), peak RFD (p < 0.01, ηp2 = 0.15), and CMJ height (p = 0.046, ηp2 = 0.06) recovered significantly faster in the SCP group. No effects were found for muscle soreness (p = 0.66) and body composition (FM: p = 0.41, FFM: p = 0.56, BCM: p = 0.79, ECM: p = 0.58). Conclusion: In summary, the results show that combining specific collagen peptide supplementation (SCP) and concurrent training (CT) over a 12-week period significantly improved markers reflecting recovery, specifically in maximal, explosive, and reactive strength. It is hypothesized that prolonged intake of collagen peptides may support muscular adaptations by facilitating remodeling of the extracellular matrix. This, in turn, could enhance the generation of explosive force. Clinical trial registration: ClinicalTrials.gov, identifier ID: NCT05220371.

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The ability of skeletal muscle to adapt to eccentric contractions has been suggested to be blunted in older muscle. If eccentric exercise is to be a safe and efficient training mode for older adults, preclinical studies need to establish if older muscle can effectively adapt and if not, determine the molecular signatures that are causing this impairment. The purpose of this study was to quantify the extent age impacts functional adaptations of muscle and identify genetic signatures associated with adaptation (or lack thereof). The anterior crural muscles of young (4 mo) and older (28 mo) female mice performed repeated bouts of eccentric contractions in vivo (50 contractions/wk for 5 wk) and isometric torque was measured across the initial and final bouts. Transcriptomics was completed by RNA-sequencing 1 wk following the fifth bout to identify common and differentially regulated genes. When torques post eccentric contractions were compared after the first and fifth bouts, young muscle exhibited a robust ability to adapt, increasing isometric torque 20%-36%, whereas isometric torque of older muscle decreased up to 18% (P ≤ 0.047). Using differential gene expression, young and older muscles shared some common transcriptional changes in response to eccentric exercise training, whereas other transcripts appeared to be age dependent. That is, the ability to express particular genes after repeated bouts of eccentric contractions was not the same between ages. These molecular signatures may reveal, in part, why older muscles do not appear to be as adaptive to exercise training as young muscles.NEW & NOTEWORTHY The ability to adapt to exercise training may help prevent and combat sarcopenia. Here, we demonstrate young mouse muscles get stronger whereas older mouse muscles become weaker after repeated bouts of eccentric contractions, and that numerous genes were differentially expressed between age groups following training. These results highlight that molecular and functional plasticity is not fixed in skeletal muscle with advancing age, and the ability to handle or cope with physical stress may be impaired.

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Investigation of the contralateral repeated bout effect (CL-RBE) in women is scarce. Therefore, this study aimed at examining whether CL-RBE exists in women. Twelve healthy women (age: 20.9 ± 2.5 years) performed two bouts of maximal elbow flexor eccentric exercise (3 sets × 15 repetitions per bout) separated by 14 days, using the opposite arms. Surface Electromyography (EMG) was recorded during both exercise bouts. The isokinetic muscle strength (60°/s), muscle soreness, range of motion (ROM), limb girth, and blood creatine kinase activity were measured pre-exercise, and at 24 and 48 h post-exercise with the muscle strength being measured immediately post-exercise as well. Significant main effects of time were observed for muscle strength, muscle soreness and ROM (p < 0.05). There were no significant differences between bouts for all the measured variables including the EMG median frequency (p > 0.05). These results suggest that the CL-RBE of elbow flexors was not evident in young healthy women. This was because the mild muscle damage induced by the initial bout of exercise was either not enough to initiate the CL-RBE or the CL-RBE in women lasted shorter than two weeks. This study provides important information for future studies on CL-RBE in women.

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Purpose: This study aimed to examine the changes in skeletal muscle (SM) α-actin, myoglobin (Mb) and hydroxyproline (HP) in plasma and other indirect markers of muscle damage after repeated bouts of eccentric cycling. Methods: Ten healthy men (23.3 ± 2.8 years) performed two 30-min eccentric cycling bouts at 100% of maximal concentric power output (230.7 ± 36.9 W) separated by 2 weeks (ECC1 and ECC2). Maximal voluntary isometric contraction (MVIC) peak force of the knee extensor muscles, muscle soreness (SOR), pain pressure threshold (PPT) and plasma levels of SM α-actin, Mb, and HP were measured before, 0.5, 3, 24-168 h after each cycling bout. Results: MVIC peak force decreased on average 10.7 ± 13.1% more after ECC1 than ECC2. SOR was 80% greater and PPT was 12-14% lower after ECC1 than ECC2. Plasma SM α-actin levels increased at 0.5, 3, and 24-72 h after ECC1 (26.1-47.9%), and SM α-actin levels at 24 h after ECC1 were associated with muscle strength loss (r = -0.56, P = .04) and SOR (r = 0.88, P = .001). Mb levels increased at 0.5, 3, and 24 h after ECC1 (200-502%). However, Mb levels at 24 h after ECC1were not associated with muscle strength loss and SOR. HP levels remained unchanged after ECC1. ECC2 did not increase SM α-actin, Mb and HP levels. Conclusion: Our results indicate that α-actin could be used as a potential marker for the early identification of SM damage due to its early appearance in plasma and its association with other indirect markers of muscle damage.

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The purpose was to summarize the studies examining the contralateral protective effect on the maximal strength in the subsequent bout of muscle-damaging exercise. The literature search was conducted through CINAHL plus, SportDiscus, and PubMed. Hedge's g effect size (ES) and 95% confidence intervals (CIs) were computed using a random effects model. From 14 papers and 25 ESs, the mean ES for contralateral repeated bout effect (CL-RBE) on 1-, 2-, and 3-day post maximal strength were -0.61 (95% CI = -0.80, -0.41), -0.50 (95% CI = -0.67, -0.33), and -0.74 (95% CI = -1.01, -0.48), respectively. For moderator analyses, the mean ESs were not influenced by type (isometric vs. isokinetic) of strength, but CL-RBE on maximal strength was influenced by duration (≤6 weeks) between bouts. Therefore, the meta-analysis demonstrated that an initial bout of exercise induces the protective effect on contralateral limb muscles regardless of the different type of strength, but can be affected by different duration (≤6 weeks) between exercise bouts.

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To examine the repeated bout effect (RBE) following two identical resistance bouts and its effect on bowling-specific performance in male cricketers. Male cricket pace bowlers (N = 10), who had not undertaken resistance exercises in the past six months, were invited to complete a familiarisation and resistance maximum testing, before participating in the study protocol. The study protocol involved the collection of muscle damage markers, a battery of anaerobic (jump and sprint), and a bowling-specific performance test at baseline, followed by a resistance training bout, and a retest of physical and bowling-specific performance at 24 h (T24) and 48 h (T48) post-training. The study protocol was repeated 7-10 days thereafter. Indirect markers of muscle damage were lower (creatine kinase: 318.7 ± 164.3 U·L-1; muscle soreness: 3 ± 1), whilst drop jump was improved (~47.5 ± 8.1 cm) following the second resistance training bout when compared to the first resistance training bout (creatine kinase: 550.9 ± 242.3 U·L-1; muscle soreness: 4 ± 2; drop jump: ~43.0 ± 9.7 cm). However, sport-specific performance via bowling speed declined (Bout 1: -2.55 ± 3.43%; Bout 2: 2.67 ± 2.41%) whilst run-up time increased (2.34 ± 3.61%; Bout 2: 3.84 ± 4.06%) after each bout of resistance training. Findings suggest that while an initial resistance training bout reduced muscle damage indicators and improved drop jump performance following a second resistance training bout, this RBE trend was not observed for bowling-specific performance. It was suggested that pace bowlers with limited exposure to resistance training should minimise bowling-specific practice for 1-2 days following the initial bouts of their resistance training program.

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To examine the contralateral repeated bout effect (CL-RBE) on muscle damage markers and motor unit (MU) control strategies, seventeen healthy adults performed two bouts of 60 eccentric contractions with elbow flexor (EF group; n â€‹= â€‹9) or index finger abductor (IA group; n â€‹= â€‹8) muscles, separated by 1 week. All participants randomly performed eccentric exercise on either the right or left arm or hand muscles, and muscle damage markers and submaximal trapezoid contraction tests were conducted pre, post, 1- and 2-day post eccentric protocol. One week after the first bout, the same exercise protocol and measurements were performed on the contralateral muscles. Surface electromyographic (EMG) signals were collected from biceps brachii (BB) or first dorsal interosseous (FDI) during maximal and submaximal tests. The linear regression analyses were used to examine MU recruitment threshold versus mean firing rate and recruitment threshold versus derecruitment threshold relationships. EMG amplitude from BB (bout 1 vs. bout 2 â€‹= â€‹65.71% â€‹± â€‹22.92% vs. 43.05% â€‹± â€‹18.97%, p â€‹= â€‹0.015, d â€‹= â€‹1.077) and the y-intercept (group merged) from the MU recruitment threshold versus derecruitment threshold relationship (bout 1 vs. bout 2 â€‹= â€‹-7.10 â€‹± â€‹14.20 vs. 0.73 â€‹± â€‹16.24, p â€‹= â€‹0.029, d â€‹= â€‹0.513) at 50% MVIC were significantly different between two bouts. However, other muscle damage markers did not show any CL-RBE in both muscle groups. Therefore, despite changes in muscle excitation and MU firing behavior, our results do not support the existence of CL-RBE on BB and FDI muscles.

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An acute bout of eccentric exercise affects insulin sensitivity and lipid profile, but how the magnitude of muscle damage affects them is not clear. We compared changes in blood insulin sensitivity and lipid markers after the first (EC1) and second (EC2) eccentric exercise bouts. Fifteen sedentary young men performed arm, leg and trunk muscle eccentric exercises, and repeated them 2 weeks later. Fasting blood samples were taken before, 2 h and 1-5 days after each exercise bout to analyze plasma creatine kinase (CK) activity, serum glucose (GLU), insulin, homeostasis model assessment (HOMA), triacylglycerols (TG), total (TC) and low- (LDLC) and high-density lipoprotein cholesterol (HDLC) concentrations as well as TC/HDLC ratio. Changes in these measures were compared between bouts and relationships to peak plasma CK activity were analyzed. Plasma CK activity increased (p < 0.05) after EC1 (peak: 101,668 ± 58,955 IU/L) but not after EC2. The magnitude of changes in GLU (peak after EC1: 26 ± 10% vs. EC2: 7 ± 6%), insulin (46 ± 27% vs. 15 ± 8%), HOMA (86 ± 48% vs. 24 ± 15%), TC (-20 ± 5% vs. -6 ± 4%), TG (-32 ± 11% vs. -6 ± 3%), LDHC (-47 ± 15% vs. -12 ± 9%), HDLC (35 ± 26% vs. 7 ± 4%), and TC/HDLC ratio (-139 ± 13% vs. -11 ± 7%) were significantly greater after EC1 than EC2. Peak plasma CK activity was significantly (p < 0.05) correlated with the peak changes in blood insulin sensitivity and lipid markers for the combined data of EC1 and EC2. These results suggest that the greater the magnitude of muscle damage, the greater the magnitude of changes in the insulin sensitivity to a negative direction and lipid markers to a positive direction.

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Eccentric exercise is discussed as a treatment option for clinical populations, but specific responses in terms of muscle damage and systemic inflammation after repeated loading of large muscle groups have not been conclusively characterized. Therefore, this study tested the feasibility of an isokinetic protocol for repeated maximum eccentric loading of the trunk muscles. Nine asymptomatic participants (5 f/4 m; 34±6 yrs; 175±13 cm; 76±17 kg) performed three isokinetic 2-minute all-out trunk strength tests (1x concentric (CON), 2x eccentric (ECC1, ECC2), 2 weeks apart; flexion/extension, 60°/s, ROM 55°). Outcomes were peak torque, torque decline, total work, and indicators of muscle damage and inflammation (over 168 h). Statistics were done using the Friedman test (Dunn's post-test). For ECC1 and ECC2, peak torque and total work were increased and torque decline reduced compared to CON. Repeated ECC bouts yielded unaltered torque and work outcomes. Muscle damage markers were highest after ECC1 (soreness 48 h, creatine kinase 72 h; p<0.05). Their overall responses (area under the curve) were abolished post-ECC2 compared to post-ECC1 (p<0.05). Interleukin-6 was higher post-ECC1 than CON, and attenuated post-ECC2 (p>0.05). Interleukin-10 and tumor necrosis factor-α were not detectable. All markers showed high inter-individual variability. The protocol was feasible to induce muscle damage indicators after exercising a large muscle group, but the pilot results indicated only weak systemic inflammatory responses in asymptomatic adults.

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The present study compared the first (EC1) and second (EC2) bouts of whole-body eccentric exercises to examine the effects of the magnitude of muscle damage on changes in blood bone markers. Fifteen sedentary young men performed nine eccentric exercises of arm, leg, and trunk muscles, and repeated them 2 weeks later. Blood samples were taken before and 2 h and 1-5 days following each bout to analyze plasma creatine kinase (CK) activity and myoglobin concentration, serum tartrate-resistant acid phosphatase (TRAP), type 1 C-terminal telopeptide (CTX-1), procollagen type I N-terminal propeptide (P1NP), bone-specific alkaline phosphatase (BAP), undercarboxylated-osteocalcin (ucOCN), carboxylated-osteocalcin (cOCN), and leptin concentrations. All except ucOCN changed significantly (p < 0.05) after both bouts. When comparing bouts for peak changes, P1NP (bone formation marker) and CTX-1 (bone resorption marker) increased less after EC2 (peak: 137±96% and 7±6%, respectively) than after EC1 (146 ± 80% and 30 ± 21%, respectively), whereas BAP (bone formation marker) increased more after EC2 (18 ± 16%) than after EC1 (4 ± 15%) (p < 0.05). Leptin (49 ± 58%) and cOCN (14 ± 10%) increased more (p < 0.05) after EC2 than after EC1 (-30 ± 15%, 9 ± 26%). Significant (p < 0.05) correlations were evident between peak CK activity and peak CTX-1 (r = 0.847), P1NP (r = 0.815), BAP (r = -0.707), ucOCN (r = 0.627), cCON (r = -0.759), and leptin (r = -0.740) changes after EC1, but many of these correlations disappeared after EC2. This was also found for the relationships between other muscle damage markers (myoglobin, muscle soreness, and muscle strength) and the bone markers. It was concluded that bone turnover was affected by eccentric exercise, but muscle damage was unfavorable for bone formation.

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Post orgasmic illness syndrome is a rare, mysterious condition with an unknown pathomechanism and uncertain treatment. The symptoms of post orgasmic illness syndrome last about 2-7 days after an ejaculation. The current hypothesis proposes that the primary injury in post orgasmic illness syndrome is an acute compression proprioceptive axonopathy in the muscle spindle, as is suspected in delayed onset muscle soreness. The terminal arbor degeneration-like lesion of delayed onset muscle soreness is theorized to be an acute stress response energy-depleted dysfunctional mitochondria-induced impairment of Piezo2 channels and glutamate vesicular release. The recurring symptoms of post orgasmic illness syndrome after each ejaculation are suggested to be analogous to the repeated bout effect of delayed onset muscle soreness. However, there are differences in the pathomechanism, mostly attributed to the extent of secondary tissue damage and to the extent of spermidine depletion. The spermidine depletion-induced differences are as follows: modulation of the acute stress response, flu-like symptoms, opioid-like withdrawal and enhanced deregulation of the autonomic nervous system. The longitudinal dimension of delayed onset muscle soreness, in the form of post orgasmic illness syndrome and the repeated bout effect, have cognitive and memory consequences, since the primary injury is learning and memory-related.

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PURPOSE: Controversy remains about whether exercise-induced muscle damage (EIMD) and the subsequent repeated bout effect (RBE) are caused by the stretching of an activated muscle, or the production of high force at long, but constant, muscle lengths. The aim of this study was to determine the influence of muscle fascicle stretch elicited during different muscle contraction types on the magnitude of EIMD and the RBE. METHODS: Fourteen participants performed an initial bout of lower limb exercise of the triceps surae. One leg performed sustained static contractions at a constant long muscle length (ISO), whereas the contralateral leg performed a bout of eccentric heel drop exercise (ECC). Time under tension was matched between the ECC and ISO conditions. Seven days later, both legs performed ECC. Plantar flexor twitch torque, medial gastrocnemius (MG) fascicle length and muscle soreness were assessed before, 2 h and 2 days after each exercise bout. MG fascicle length and triceps surae surface electromyography were examined across the bouts of exercise. RESULTS: We found that both ECC and ISO conditions elicited EIMD and a RBE. ISO caused less damage 2 h after the initial bout (14% less drop in twitch torque, P = 0.03) and less protection from soreness 2 days after the repeated bout (56% higher soreness, P = 0.01). No differences were found when comparing neuromechanical properties across exercise bouts. CONCLUSION: For MG, the action of stretching an active muscle seems to be more important for causing damage than a sustained contraction at a long length.

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The purposes of this study were to investigate the muscle-tendon unit stiffness response and to compare the stiffness with those of other indirect markers induced by two bouts of unaccustomed eccentric exercise. Eleven untrained men performed two bouts of 200 maximal eccentric contractions of the right quadriceps 4 weeks apart. Changes in stiffness, pain evoked by stretching and pressure, plasma creatine kinase (CK) activity, and muscle thickness were followed for 7 days after each bout. Stiffness and pain peaked immediately and 1 day after the first exercise bout, whereas CK and thickness were highest 4 and 7 days after the first exercise bout, respectively (p < 0.05 for all). Muscular pain, thickness, and stiffness responses were lower by 53.3%, 99%, and 11.6%, respectively, after the repeated bout compared to after the first bout (p < 0.05 for all), while CK activity response did not differ significantly between bouts. High responders for an increase in muscle-tendon unit stiffness showed a repeated-bout effect for stiffness, pain, and CK activity (by 29%, 65%, and 98%, p < 0.05 for all), but the repeated-bout effect was not that clear in low responders. These findings suggest that a repeated eccentric exercise bout effect on stiffness in quadriceps is mostly not associated with muscle pain and CK activity, but there are large individual differences.

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High-intensity eccentric exercise can lead to muscle damage and weakness. The 'repeated bout effect' (RBE) can attenuate these impairments when performing a subsequent bout. The influence of eccentric exercise-induced muscle damage on low-frequency force production is well-characterized; however, it is unclear how eccentric exercise and the RBE affect torque production across a range of stimulation frequencies (i.e., the torque-frequency relationship). We investigated the influence of an initial (Bout 1) and repeated bout (Bout 2) of eccentric exercise on the elbow flexor torque-frequency relationship. Eleven males completed two bouts of high-intensity eccentric elbow flexions, 4 weeks apart. Torque-frequency relationships were constructed at baseline and 0.5, 24, 48, 72, 96, and 168 h following both bouts via percutaneous stimulation at 1, 6, 10, 20, 30, 40, 50, and 100 Hz. Serum creatine kinase activity, self-reported muscle soreness, and isometric maximum voluntary contraction torque indirectly inferred the presence of muscle damage following Bout 1, and attenuation of muscle damage following Bout 2. Torque amplitude at all stimulation frequencies was impaired 30 min following eccentric exercise, however, torque at lower (1-10 Hz) and higher frequencies (40-100 Hz) recovered within 24 h while torque across the middle frequency range (20-30 Hz) recovered by 48 h. No between-bout differences were detected in absolute or normalized torque at any stimulation frequency, indicating no protective RBE on the elbow flexor torque-frequency relationship.

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Delayed onset muscle soreness (DOMS) is hypothesized to be caused by glutamate excitotoxicity-induced acute compression axonopathy of the sensory afferents in the muscle spindle. Degeneration of the same sensory afferents is implicated in the disease onset and progression of amyotrophic lateral sclerosis (ALS). A series of "silent" acute compression proprioceptive axonopathies with underlying genetic/environmental factors, damaging eccentric contractions and the non-resolving neuroinflammatory process of aging could lead to ALS disease progression. Since the sensory terminals in the muscle spindle could not regenerate from the micro-damage in ALS, unlike in DOMS, the induced protective microcircuits and their long-term functional plasticity (the equivalent of the repeated bout effect in DOMS) will be dysfunctional. The acute stress invoking osteocalcin, bradykinin, COX1, COX2, GDNF, PGE2, NGF, glutamate and N-methyl-D-aspartate (NMDA) receptors are suggested to be the critical signalers of this theory. The repeated bout effect of DOMS and the dysfunctional microcircuits in ALS are suggested to involve several dimensions of memory and learning, like pain memory, inflammation, working and episodic memory. The spatial encoding of these memory dimensions is compromised in ALS due to blunt position sense from the degenerating proprioceptive axon terminals of the affected muscle spindles. Dysfunctional microcircuits progressively and irreversibly interfere with postural control, with motor command and locomotor circuits, deplete the neuroenergetic system, and ultimately interfere with life-sustaining central pattern generators in ALS. The activated NMDA receptor is suggested to serve the "gate control" function in DOMS and ALS in line with the gate control theory of pain. Circumvention of muscle spindle-loading could be a choice of exercise therapy in muscle spindle-affected neurodegenerative diseases.

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Nordic Hamstring Exercise (NHE) training improves eccentric hamstring strength and sprint performance. However, detraining causes rapid reductions of achieved adaptations. Furthermore, the transfer of improved hamstring capacity to swing phase mechanics of sprints is unknown. This longitudinal study aimed (a) to quantify NHE-induced adaptations by camera-based isokinetic assessments and sprint analyses, (b) to relate the magnitude of adaptations to the participants' initial performance level, (c) to investigate the transferability to sprints, and (4) to determine strength preservations after 3 months. Twelve sprinters (21 years, 1.81 m, 74 kg) were analyzed throughout 22 weeks. They performed maximal sprints and eccentric knee flexor and concentric knee extensor tests before and after a 4-week NHE training. Sprints and isokinetic tests were captured by ten and four high-speed cameras. The dynamic control ratio at the equilibrium point (DCRe) evaluated thigh muscle balance. High-intensity NHE training elicited significant improvements of hamstring function (P range: <.001-.011, d range: 0.44-1.14), thigh muscle balance (P < 0.001, d range: 0.80-1.08) and hamstring-related parameters of swing phase mechanics (P range: <0.001-0.022, d range: 0.12-0.57). Sprint velocity demonstrated small increases (+1.4%, P < 0.001, d = 0.26). Adaptations of hamstring function and thigh muscle balance revealed moderate to strong transfers to improved sprint mechanics (P range: <0.001-0.048, R2 range: 34%-83%). The weakest participants demonstrated the highest adaptations of isokinetic parameters (P range: 0.003-0.023, R2 range: 42%-62%), whereas sprint mechanics showed no effect of initial performance level. Three months after the intervention, hamstring function (+6% to +14%) and thigh muscle balance (+8% to +10%) remained significantly enhanced (P < 0.001, ƞp 2 range: 0.529-0.621). High-intensity NHE training induced sustained improved hamstring function of sprinters, which can be transferred to swing phase mechanics of maximal sprints. The initial performance level, NHE training procedures and periodization should be considered to optimize adaptations.

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