Induced Muscle Damage Research Articles

Kinetics of recovery and normalization of running biomechanics following aerobic-based exercise-induced muscle damage in recreational male runners.

The study aimed to examine the effects of exercise-induced muscle damage on running kinetics. Twenty-six adult recreational male runners performed 60 min of downhill running (-10 %) at 65 % of maximal heart rate. Running gait changes, systemic and localized muscle damage markers were assessed pre - and post-exercise induced muscle damage protocol. Running gait was analyzed using a 3D treadmill at baseline, immediately post, 24 h, and 48 h to determine changes in running pressure sway and vertical ground reaction forces. Blood markers, subjective pain perception, and magnetic resonance imaging utilizing T2 relaxation time of the thigh muscles assessed systemic and localized damage. Linear mixed-effects models examined changes over time. Significant decreases were found in the left leg's first (-454.0 to -396.1, P < 0.05) and second (-532.8 to -498.2, P < 0.05) VGRF peaks across all time points compared to baseline. The right leg showed reductions in the first vertical ground reaction forced peak at immediately post (-348.4, P = 0.036) and the second peak at immediately post and 24 h (-467.4 and -396.8, P < 0.05). Creatine kinase increased significantly (P < 0.001) at 24 h and 48 h compared to baseline. The anterior thigh muscle compartment showed significant (P < 0.05) increases in mean T2 values 1 h following exercise protocol remained elevated up to 48 h. Negative correlations were identified between running biomechanics to local and systemic muscle damage markers. Running biomechanics remained impaired for up to 48 h following exercise induced muscle damage and correlated with markers of muscle damage using magnetic resonance imaging.

Effects of repeated isometric and eccentric contractions on active muscle stiffness.

Joint stiffness endurance is considered essential in many sports events. We previously reported that reduced joint stiffness due to repetitive hopping was associated with reduced active muscle stiffness. However, the determinants of active muscle stiffness endurance were unknown. This study aimed to compare the effects of repeated isometric contractions (ISO), which induced metabolic muscle fatigue, and repeated eccentric contractions (ECC), which induced muscle damage, on active muscle stiffness endurance. Fourteen males performed two kinds of fatigue tasks (ISO and ECC) using only ankle joint. Before and after the fatigue tasks, changes in estimated muscle force and fascicle length during fast stretching were used to calculate the active muscle stiffness of the medial gastrocnemius muscle. In addition, the thickness of the plantar flexor muscles was measured before and after fatigue tasks. After fatigue tasks, no difference in the relative increase of muscle thickness was found between ISO and ECC. The increase in torque during fast stretching did not change after both ISO and ECC. The increase in fascicle length during fast stretching significantly increased after ECC but not ISO. Active muscle stiffness significantly decreased after ECC but not ISO. Active muscle stiffness decreased after repeated eccentric contractions damaging fascicles and did not change with repeated isometric contractions causing metabolic fatigue. These results implied that the joint stiffness reduction due to repetitive stretch-shortening cycle exercises shown in previous studies involved a reduction in active muscle stiffness due to repeated eccentric contractions.

No effect of grape juice on exercise-induced muscle damage or performance in male runners: a randomized, placebo-controlled, triple-blind clinical trial.

This study aimed to verify the effect of grape juice (Vitis Labrusca) intake on exercise-induced muscle damage (EIMD) and exercise performance parameters (5-km running time-trial [TT], running economy, and countermovement jump [CMJ]). Twenty trained male runners were randomized into two blinded groups and consumed either placebo (n=9) or grape juice (n=11) for six consecutive days (600 mL/day). On the fourth day, the participants performed a downhill running (-15%) at speed that elicited 70% V̇O2max for 20 minutes, to induce muscle damage, followed by assessment of running economy, 5-km TT, and CMJ tests. Blood samples were obtained before and after the exercise tests for quantifying total phenols, creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). On the sixth day, blood parameters and CMJ were evaluated. A two-way ANCOVA mixed model was employed for data analysis, the effects were the juice groups, measurement and a interaction between the factors. EIMD was confirmed by increased levels of indirect markers (serum AST and LDH activities) and an impairment in TT and CMJ performances after 48 hours. The 5-km TT, economy, and CMJ were compromised after EIMD, to a similar extent in the groups. Blood concentrations of CK, LDH, AST, and total phenolic compounds presented similar time course behavior between the groups, showing no group × time interaction effects. In conclusion, grape juice consumption over six days did not attenuate EIMD markers or the impairment in running performance in trained male runners. (ReBEC number: RBR-9jkkvbb).

Recovery After Exercise Induced Muscle Damage In Subjects Following A Vegetarian Or Mixed Diet

Recovery After Exercise Induced Muscle Damage In Subjects Following A Vegetarian Or Mixed Diet

Update: Delayed Onset Muscle Soreness (DOMS) – Muscle Biomechanics, Pathophysiology and Therapeutic Approaches

The term Delayed Onset Muscle Soreness (DOMS) refers to a complex injury entity which is based on ultrastructural injury patterns. The injury is usually harmless and heals within a few days without sequelae. However, at the time of the manifestation there are (sometimes considerable) performance limitations and the risk of possible secondary injuries is increased. Thus, prevention and treatment of DOMS, especially in high-performance sports, are of particular value. Insights into muscle biomechanics are necessary to understand the background and mechanisms of DOMS. The definition and classification of overload-related muscle injuries has not yet been uniformly determined. Fluid transitions between physiological, metabolic and neuromuscular fatigue as well as the actual occurrence of injuries with clinical symptoms make clear delineation difficult. The “Munich Classification” terms Delayed Onset Muscle Soreness (DOMS) as Type 1b muscle injury, “delayed onset muscle pain”. The central target of prevention of DOMS is to prevent or alleviate the onset of the initial damage, known as “Exercise Induced Muscle Damage” (EIMD). In case of manifest DOMS, the intention is both to relieve the attendant symptoms and to promote rapid restoration of muscle function. In clinical practice as in scientific research, diverse procedures and interventions have proven valuable, whereby especially physical therapy procedures like cryotherapy, heat therapy or compression therapy show promising study results.

The Contrasting Effects of Two Distinct Exercise Training Modalities on Exhaustive Exercise-Induced Muscle Damage in Mice May Be Associated with Alterations in the Gut Microbiota.

Exhaustive exercise is known to induce muscle damage characterized by inflammation and oxidative stress. Although "regular" and "weekend warrior" exercise regimens have been shown to confer comparable health benefits in human studies, such as reduced risks of all-cause, cardiovascular disease (CVD), and cancer mortality, their differential impacts on muscle damage post-exhaustive exercise remain unclear. This study aimed to compare the effects of long-term, moderate-intensity (LTMI) and short-term, high-intensity (STHI) training modalities, matched for total exercise volume, on gut microbiota, short-chain fatty acids (SCFAs), and exhaustive exercise-induced muscle damage in mice, as well as to evaluate the correlation between these factors. LTMI is considered a regular exercise regimen, while STHI shares some similarities with the "weekend warrior" pattern, such as promoting exercise intensity and condensing training sessions into a short period. Our findings indicate that LTMI training significantly enhanced the abundance of SCFA-producing bacteria, including Akkermansia, Prevotellaceae_NK3B31_group, Odoribacter, Alistipes, and Lactobacillus, thereby increasing SCFA levels and attenuating muscle damage following exhaustive swimming. In contrast, STHI training increased the abundance of opportunistic pathogens such as Staphylococcus and Bilophila, without altering SCFA levels, and was associated with exacerbated muscle damage. Moreover, we observed a significant negative correlation between the abundance of SCFA-producing bacteria and SCFA levels with the expression of inflammatory cytokines in the muscle of mice post-exhaustive exercise. Conversely, the abundance of Staphylococcus and Bilophila showed a notable positive correlation with these cytokines. Additionally, the effects of LTMI and STHI on exhaustive exercise-induced muscle damage were transmissible to untrained mice via fecal microbiota transplantation, suggesting that gut microbiota changes induced by these training modalities may contribute to their contrasting impacts on muscle damage. These results underscore the significance of selecting an appropriate training modality prior to engaging in exhaustive exercise, with implications for athletic training and injury prevention.

Effect of different Volumes of exercise on skin temperature responses over the following 24 hours

Skin temperature responses have been advocated to indicate exercise-induced muscle soreness and recovery status. While the evidence is contradictory, we hypothesize that the presence of muscle damage and the time window of measurement are confounding factors in the skin temperature response. The objective was to determine whether skin temperature is influenced by different workloads and the time course of temperature measurements over the following 24 h. 24 trained male military were assigned to one of three groups: GC group (n = 8) serving as control not performing exercises, GE group (n = 8) performing a simulated military combat protocol in an exercise track with different obstacles but designed not to elicit muscle damage, and the GEMD group (n = 8) performing the simulated military combat protocol plus 5 sets of 20 drop jumps, with 10-sec between repetitions and with 2-min of rest between sets aiming to induce muscle damage. Skin temperature was measured using infrared thermography before exercise (Pre) and 4 (Post4h), 8 (Post8h) and 24h (Post24h) post-exercise. Perception of pain (DOMS) was evaluated Pre, Post24h, and Post48h, and countermovement jump height was evaluated at Pre and Post24h. DOMS did not differ between groups in the Pre and Post24h measures but GEMD presented higher DOMS than the other groups at Post48h (p < 0.001 and large effect size). Jump height did not differ for GEMD and GC, and GE presented higher jump height at Post24h than GC (p = 0.02 and large effect size). Skin temperature responses of GEMD and GG were similar in all measurement moments (p > 0.22), and GE presented higher skin temperature than the GC and the GEMD groups at Post24h (p < 0.01 and large effect sizes). In conclusion, although physical exercise elicits higher skin temperature that lasts up to 24 h following the efforts, muscle soreness depresses this response.

Changes in protein fluxes in skeletal muscle during sequential stages of muscle regeneration after acute injury in male mice

Changes in protein turnover play an important role in dynamic physiological processes, including skeletal muscle regeneration, which occurs as an essential part of tissue repair after injury. The inability of muscle tissue to recapitulate this regenerative process can lead to the manifestation of clinical symptoms in various musculoskeletal diseases, including muscular dystrophies and pathological atrophy. Here, we employed a workflow that couples deuterated water (2H2O) administration with mass spectrometry (MS) to systematically measure in-vivo protein turnover rates across the muscle proteome in 8-week-old male C57BL6/J mice. We compared the turnover kinetics of over 100 proteins in response to cardiotoxin (CTX) induced muscle damage and regeneration at unique sequential stages along the regeneration timeline. This analysis is compared to gene expression data from mRNA-sequencing (mRNA-seq) from the same tissue. The data reveals quantitative protein flux signatures in response to necrotic damage, in addition to sequential differences in cell proliferation, energy metabolism, and contractile gene expression. Interestingly, the mRNA changes correlated poorly with changes in protein synthesis rates, consistent with post-transcriptional control mechanisms. In summary, the experiments described here reveal the signatures and timing of protein flux changes during skeletal muscle regeneration, as well as the inability of mRNA expression measurements to reveal changes in directly measured protein turnover rates. The results of this work described here provide a better understanding of the muscle regeneration process and could help to identify potential biomarkers or therapeutic targets.

Indices of exercise induced muscle damage following low load resistance exercise with blood flow restriction in untrained males.

There is conflicting evidence regarding the presence and magnitude of exercise-induced muscle damage (EIMD) following low-load resistance training with blood flow restriction (LL+BFR), which may be related to the protocol implemented or exercise volume. Therefore, the purpose of this investigation was to examine the effects of a 75 repetition (BFR-75) (1×30, 3×15) and four sets to volitional failure (BFR-4x) protocols on indices of EIMD among untrained men. Twelve males with no history of lower-body resistance training during the previous six months volunteered for this investigation. One leg was randomly assigned to BFR-75, and the other to BFR-4x. Participants performed isokinetic, unilateral, concentric-eccentric, leg extension muscle actions at 30% of maximal strength with BFR. Indices of EIMD (limb circumference, perceived muscle soreness, pain pressure threshold [PPT], passive range of motion, and maximal strength [MVIC]) were recorded before exercise and 0, 24, 48, 72, and 96-hours post-exercise for each protocol. There were no significant changes (P>0.05) in limb circumference, PPT, passive range of motion, or MVIC. For both BFR-75 and BFR-4x, perceived muscle soreness increased (P<0.001) similarly 24- (2.5±1.7 AU) and 48-hours (1.9±1.7 AU) post-exercise. There was an increase in muscle soreness 24-48 hours post-exercise for both conditions, which may be due to metabolic stress, but this did not affect the force-generating capacity of the muscle (MVIC), suggesting minimal EIMD. The conflicting evidence of EIMD following LL+BFR may be related to differences in restriction time or overall exercise time.

시합 시즌 중 단주기 저강도 회복 운동 프로그램이 운동 유발성 근육 손상이 있는 엘리트 축구 선수들의 근육 조직 손상 생체지표에 미치는 영향

시합 시즌 중 단주기 저강도 회복 운동 프로그램이 운동 유발성 근육 손상이 있는 엘리트 축구 선수들의 근육 조직 손상 생체지표에 미치는 영향

Association between Serum Biomarkers of Muscle Damage after Isokinetic Eccentric Exercise in Trained Males and Females

Eccentric exercise is well-known to induce muscle damage, and biomarkers may be related to the magnitude of impact on muscle force and muscle soreness after exercise. However, this phenomenon still needs to be investigated in more detail. The present study aimed to analyze if a correlation between muscle force, soreness, and biomarkers after eccentric exercise exists in healthy, trained 11 males and females. Eleven volunteers with previous resistance training experience performed 6 x 10 maximal isokinetic eccentric contractions of the elbow flexors in the muscle performance laboratory up to 72 hours after exercise. Peak torque was measured by maximal voluntary isometric contractions (MVIC) and muscle soreness by visual analogic scale (VAS) before, 24h, 48h, and 72h after the isokinetic eccentric exercise protocol. A fluorescence immunoassay analyzer determined Myoglobin and C-reactive protein levels. The MVIC significantly decreased while muscle soreness increased 24h, 48h, and 72h post eccentric exercise. Myoglobin significantly increased 48h and 72h after exercise. Muscle soreness was inversely correlated with MVIC 24h, 48h, and 72h and positively correlated with myoglobin 48h and 72h after eccentric exercise. The myoglobin was not correlated with muscle force. No significant correlation between C-reactive protein and muscle soreness and MVIC was found. In conclusion, our data suggest that myoglobin could be a valuable biomarker to be assessed alongside exercise-induced muscle soreness.

Age-dependent loss of Crls1 causes myopathy and skeletal muscle regeneration failure

Skeletal muscle aging results in the gradual suppression of myogenesis, leading to muscle mass loss. However, the specific role of cardiolipin in myogenesis has not been determined. This study investigated the crucial role of mitochondrial cardiolipin and cardiolipin synthase 1 (Crls1) in age-related muscle deterioration and myogenesis. Our findings demonstrated that cardiolipin and Crls1 are downregulated in aged skeletal muscle. Moreover, the knockdown of Crls1 in myoblasts reduced mitochondrial mass, activity, and OXPHOS complex IV expression and disrupted the structure of the mitochondrial cristae. AAV9-shCrls1-mediated downregulation of Crls1 impaired muscle regeneration in a mouse model of cardiotoxin (CTX)-induced muscle damage, whereas AAV9-mCrls1-mediated Crls1 overexpression improved regeneration. Overall, our results highlight that the age-dependent decrease in CRLS1 expression contributes to muscle loss by diminishing mitochondrial quality in skeletal muscle myoblasts. Hence, modulating CRLS1 expression is a promising therapeutic strategy for mitigating muscle deterioration associated with aging, suggesting potential avenues for developing interventions to improve overall muscle health and quality of life in elderly individuals.

Pre-exercise hot water immersion increased circulatory heat shock proteins but did not alter muscle damage markers or endurance capacity after eccentric exercise

ABSTRACT Pre-exercise passive heating attenuates muscle damage caused by eccentric exercise in rats where the induction of heat shock proteins (HSPs) confers a myoprotective effect. We investigated whether pre-exercise hot water immersion (HWI) confers similar benefits in humans. Eleven recreational male athletes were immersed in 41°C water up to 60 min or until rectal temperatures reached 39.5°C. After a 6 h rest, the participants performed an eccentric downhill run for 1 h at −4% gradient to induce muscle damage. An endurance capacity test at 75% VO2max was conducted 18 h later. The control trial was similar except that participants were immersed at 34°C. Blood samples were collected to assess HSPs levels, creatine kinase, and lactate dehydrogenase activities. Plasma eHSP70 was higher post-immersion in HWI trials (1.3 ± 0.4 vs 1.1 ± 0.4; p = 0.005). Plasma eHSP27 was higher before (p = 0.049) and after (p = 0.015) endurance test in HWI. Leukocytic p-HSP27 was increased 18 h after HWI (0.97 ± 0.14 vs 0.67 ± 0.11; p = 0.04). Creatine kinase and lactate dehydrogenase activities were increased by 3-fold and 1.5-fold, respectively, after endurance test in HWI but did not differ across trials (p > 0.05). Mean heart rates were higher during eccentric run and endurance test in HWI as compared to control (p < 0.05). Endurance capacity was similar between trials (57.3 ± 11.5 min vs 55.0 ± 13.5 min; p = 0.564). Pre-exercise heating increased the expression of plasma eHSPs and leukocytic p-HSP27 but did not reduce muscle damage nor enhance endurance capacity.

A comparison of the effects of sheep's milk and cow's milk on recovery from eccentric exercise.

When consumed after eccentric exercise, cow's milk has been shown to improve recovery and alleviate symptoms of exercise induced muscle damage. Although currently less commercially available than cow's milk, sheep's milk may offer similar or greater benefits for recovery as it is higher in protein and energy; however, the effect of sheep's milk in any exercise context has not been explored. This study compared the effects of a sheep's milk beverage and a cow's milk beverage on recovery from strenuous eccentric exercise. Additionally, the effects of each beverage on satiety and gastrointestinal comfort were assessed. Ten healthy males completed baseline measures of perceived muscle soreness and maximal voluntary concentric, eccentric, and isometric quadriceps force of one leg before completing 200 maximal eccentric knee extensions on an isokinetic dynamometer. Measures were repeated 0.5, 24, 48 and 72 h post-eccentric exercise. After 0.5 h measures, participants consumed either 450 ml of chocolate flavored sheep's milk or chocolate flavored cow's milk. Following a washout period, participants completed a second trial on the contralateral leg and consumed the other beverage. Additionally, a satiety and gastrointestinal comfort questionnaire was completed before and after each beverage was consumed. Eccentric exercise brought about a significant decrease in muscle function over time (all P < 0.012). No difference between treatments (all P > 0.097) was found. Measures of muscle soreness increased over time (all P < 0.002), however no difference was observed between treatments (all P > 0.072). Only sheep's milk altered perceived satiety, however, only the response to "How full do you feel" differed between treatments (P = 0.04). The results of this study suggest that consuming sheep's milk may provide similar benefits as cow's milk when recovering from exercise-induced muscle damage. While these findings provide initial support for the use of sheep's milk in a muscle recovery context, further research is warranted to confirm these findings. Given its superior nutritional profile, greater impact on satiety and lower environment impact, sheep's milk may be a more efficient post-exercise recovery beverage, compared to cow's milk.

Acute effects of exercise-induced muscle damage on sprint and change of direction performance: A systematic review and meta-analysis.

The aim of this study is to determine the acute effects of resistance and plyometric training on sprint and change of direction (COD) performance in healthy adults and adolescents. A systematic literature search was conducted via Medline, Cinahl, Scopus and SportDiscus databases for studies that investigated: 1) healthy male, female adults, or adolescents; and 2) measured sprint or change of direction performance following resistance and plyometric exercises. Studies were excluded if: 1) resistance or plyometric exercises was not used to induce muscle damage; 2) conducted in animals, infants, elderly; 3) sprint performance and/or agility performance was not measured 24 h post muscle damaging protocol. Study appraisal was completed using the Kmet Quality Scoring for Quantitative Study tool. Forest plots were generated to quantitatively analyse data and report study statistics for statistical significance and heterogeneity. The included studies (n = 20) revealed sprint and COD performance was significantly impaired up to 72 hr following resistance and plyometric exercises; both protocols significantly increased creatine kinase (CK), delayed-onset muscle soreness (DOMS) and decreased countermovement jump (CMJ) up to 72 hr. The systematic review of 20 studies indicated that resistance and plyometric training significantly impaired sprint and COD performance up to 72 hours post-exercise. Both training protocols elevated exercise-induced muscle damage (EIMD) markers (CK, DOMS) and decreased CMJ performance within the same timeframe.

Association between Gray-Scale Ultrasound Imaging and Serological Creatine Kinase for Quantifying Exercise-Induced Muscle Damage: An Observational Study.

Limited evidence has verified if ultrasound imaging (US) can detect post-exercise muscle damage based on size, shape, and brightness metrics. This study aimed to analyze the correlation between creatine kinase (CK) concentration and (as a biomarker of muscle damage) changes in US gray-scale metrics after an exercise-induced muscle damage protocol. An observational study was conducted at a private university lab located in Madrid. Twenty-five untrained and asymptomatic volunteers were enrolled in this study. Baseline demographic data and body composition metrics were collected. In addition, the rectus femoris US data and CK concentration were assessed at baseline and after inducing muscle damage (24 and 48 h later). After calculating time differences for all the outcomes, the correlation between the changes observed with US and biomarkers was assessed. Significant CK concentration increases were found 24 h (p = 0.003) and 48 h (p < 0.001) after exercise. However, no significant changes in muscle size, shape, or brightness were found in any location (p > 0.05 for all). In addition, no significant associations were found between CK changes and US changes (p > 0.05 for all). Gray-scale US is not a sensitive tool for detecting muscle damage, as a protocol of exercise-induced muscle damage confirmed with CK produced no significant gray-scale US changes after 24 or 48 h. In addition, US and CK changes after 24 and 48 h were not associated with each other.

CAN ACUTE MUSCLE DAMAGE LEAD TO OSTEOARTHRITIS?

Abstract Skeletal muscles are crucial for maintaining musculoskeletal homeostasis, as they provide mechanical support, joint stability, and biochemical functions via myokine secretion. We investigated whether acute muscle damage or weakness could contribute to the development of osteoarthritis (OA). Using a chemical damage model, we induced muscle damage by injecting 1.2% barium chloride into the tibialis anterior muscle, resulting in an immune response characterized by a significant increase in the concentration of Prostaglandin E2 (PGE2) and other lipid mediators derived from the EPA and DHA signaling pathways, as quantified using our innovative lipidomics methods. The muscle damage was confirmed and visualized by muscle histomorphometry. The damage resulted in muscle weakness, detected by a significant decrease in grip strength at 4-days post-injury, but without changes in mice activity measured with force-plate actimeter. After 1-month post-injury, grip strength and muscle histology returned to normal, but histological changes were observed in the articulating cartilage, indicating surface erosion and cartilage matrix loss (OARSI grade 4). We used Raman Spectroscopy and micro-CT to confirm the joint alterations observed in the changes in subchondral bone and increased bone volume fraction in the cortical shell of the subchondral bone, respectively, features characteristic of OA in rodents and humans. These findings suggest that muscle weakness or imbalance due to injury can contribute to joint degeneration. This study highlights the significance of muscles in preventing OA and provides a novel approach for exploring the relationship between muscle damage and OA development. This new model could prove valuable for aging research.

Sodium salicylate ameliorates exercise-induced muscle damage in mice by inhibiting NF-kB signaling

BackgroundEccentric muscle contraction can cause muscle damage, which reduces the efficiency of exercise. Previous evidence suggested that Sodium salicylate (SS) could improve the repair of aged muscle. This study intends to investigate whether SS can impact skeletal muscle damage caused by eccentric exercise.MethodsEccentric treadmill exercise was performed to induce muscle damage in mice. Plasma levels of muscle damage markers were estimated. RT-qPCR was employed for detecting mRNA levels of proinflammatory mediators in murine gastrocnemius muscle. Immunofluorescence staining of laminin/DAPI was utilized for quantifying centrally nucleated myofibers in the gastrocnemius muscle. Western blotting was implemented to examine protein levels of mitsugumin 53 (MG53), matrix metalloproteinase (MMP)-2/9, and NF-κB signaling-related markers.ResultsSS administration reduced muscle damage marker production in the plasma and decreased the levels of proinflammatory mediators, MG53 and MMP-2/9 in mice after exercise. SS alleviated the severity of muscle damage in the gastrocnemius of mice after eccentric exercise. SS blocked NF-κB signaling pathway in the gastrocnemius muscle.ConclusionSS administration ameliorates skeletal muscle damage caused by eccentric exercise in the mouse model.

Re‑examining the mechanism of eccentric exercise‑induced skeletal muscle damage from the role of the third filament, titin (Review).

Intense and unaccustomed eccentric exercise has been extensively studied for its ability to induce muscle damage. However, the underlying mechanism of this phenomenon still requires further clarification. This knowledge gap arises from the need for explanation of the eccentric contraction through the sliding filament theory. The two-filament sarcomere model, which is consisted of thin and thick filaments, forms the basis of the sliding filament theory. The mechanisms of concentric and isometric contractions at the cellular and molecular levels are effectively described by this model. However, when relying solely on the cross-bridge swing, the sliding filament theory fails to account for specific observations, such as the stability of the descending limb of the force-length relationship curve. Recent evidence indicated that titin and the extracellular matrix (ECM) may play a protective role by interacting with the thick and thin filaments. During an eccentric contraction, titin serves as a third filament in the sarcomere, which helps regulate changes in passive force. The two-filament sarcomere model has limitations in explaining eccentric contraction, thus this compensates for those shortcomings. The present review explored the potential of replacing the two-filament sarcomere model with a three-filament sarcomere model, incorporating thin filaments, thick filaments and titin. This revised model offers a more comprehensive explanation of eccentric contraction phenomena. Furthermore, the sliding filament theory was investigated in the context of the three-filament sarcomere model. The double-layer protection mechanism, which involves increased titin stiffness and the ECM during eccentric contraction was explored. This mechanism may enhance lateral force transmission between muscle fibers and the ECM, resulting in sarcolemma and ECM shear deformation. These findings provided insight into the mechanism of eccentric exercise-induced skeletal muscle damage. Considering the three-filament sarcomere model and the double-layer protection mechanism, the present review offered a more logical and comprehensive understanding of the mechanism behind eccentric exercise-induced muscle damage.

Hypohydration induced by prolonged cycling in the heat increases biomarkers of renal injury in males

PurposeRecent studies have shown that hypohydration can increase renal injury. However, the contribution of hypohydration to the extent of renal injury is often confounded by exercise induced muscle damage. Therefore, the aim of the present study was to investigate the effect of manipulating hydration status during moderate-intensity cycling in the heat on biomarkers of renal injury.MethodsFollowing familiarisation, fourteen active males (age: 21 [20–22] y; BMI: 22.1 ± 1.9 kg/m2; V˙\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$ \\dot{V} $$\\end{document}O2peak: 55 ± 9 mL/kg/min) completed two experimental trials, in a randomised cross-over design. Experimental trials consisted of up to 120 min of intermittent cycling (~ 50% Wpeak) in the heat (~ 35 °C, ~ 50% relative humidity). During exercise, subjects consumed either a water volume equal to 100% body mass losses (EU) or minimal water (HYP; 75–100 mL) to induce ~ 3% body mass loss. Blood and urine samples were collected at baseline, 30 min post-exercise and 24 h post-baseline, with an additional urine sample collected immediately post-exercise.ResultsThirty minutes post-exercise, body mass and plasma volume were lower in HYP than EU (P < 0.001), whereas serum and urine osmolality (P < 0.001), osmolality-corrected urinary kidney injury molecule-1 concentrations (HYP: 2.74 [1.87–5.44] ng/mOsm, EU: 1.15 [0.84–2.37] ng/mOsm; P = 0.024), and percentage change in osmolality-corrected urinary neutrophil gelatinase-associated lipocalin concentrations (HYP: 61 [17–141] %, EU: 7.1 [– 4 to 24] %; P = 0.033) were greater in HYP than EU.ConclusionHypohydration produced by cycling in the heat increased renal tubular injury, compared to maintaining euhydration with water ingestion.