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At the dawn of the 20th century, seminal studies revealed that muscle fibers produce less heat and generate greater force during elongation than during shortening actions, laying the foundation for contemporary research on eccentric exercise. Today, eccentric exercise is widely used by athletes to enhance strength and by older adults to maintain functional capacity, yet it may cause muscle damage, particularly in unaccustomed muscles. Despite more than a century of investigation, the precise mechanisms of eccentric exercise-induced muscle damage remain incompletely resolved. Nevertheless, eccentric exercise serves as a valuable model for studying muscle injury and repair and adaptation. This review organizes current evidence into nine key themes: (1) eccentric exercise-induced muscle damage and flawed biomarkers, (2) satellite cell-mediated and alternative repair pathways, (3) high-force, low-cost contractions and metabolic impact, (4) repeated bout effect and protective adaptations, (5) architectural remodeling of fascicles, sarcomeres and tendon, (6) distinct neural control, proprioception, and cross-education adaptations, (7) mitochondrial, sarcoplasmic reticulum, and cytoskeletal stress remodeling, (8) connective tissue perturbation, remodeling, and joint stability, and (9) targeted, cautious use of antioxidant supplementation. Rather than offering a comprehensive overview, this review highlights pivotal experiments, concepts, and controversies within these themes to guide readers to the most impactful discoveries in eccentric exercise and muscle damage.

Background: Type 2 diabetes mellitus (T2DM) is linked to accelerated losses in muscle function. The aim of the present investigation was to evaluate the effect of chronic higher-protein intake on isokinetic knee performance in the older adults with type 2 diabetes mellitus (T2DM). Methods: Thirty adults (15 men and 15 women) aged 60–80 years with non-insulin-treated T2DM and sarcopenia-related deficits were randomized for 12 weeks to a higher-protein diet (1.2–1.5 g·kg−1·day−1) or a recommended protein diet (0.8–1.0 g·kg−1·day−1), with meal plans designed to maintain body mass. Protein was increased mainly through Mediterranean-style protein sources while diet was monitored using repeated 3-day recalls. Isokinetic knee extensors and flexors peak torque (angular velocity 60°/s) was assessed at baseline and at week 6 and at the end of the 12th week of intervention. Fatigability (20 maximal contractions at an angular velocity at 180°/s) and DXA body composition were assessed at baseline and at the end of the 12th week of intervention. Data were analyzed using two-way repeated-measures ANOVA with repeated measures on time (2 groups × 3 time points), followed by post hoc analysis when significant difference was occurred. Results: Thirty participants completed the trial. Energy intake and body mass remained stable in both groups. At the end of week 12, peak torque declined in the control group (p < 0.05) but remained stable in the higher-protein group. The fatigue index worsened over time in controls but was preserved in the higher protein group, resulting in a significant group d7 time interaction at week 12 (p < 0.05) (post hoc between-group difference at week 12, p < 0.05). Fat-free mass and blood pressure did not change. In fat mass, a decrease was observed with higher protein intake, whereas it remained stable in the control group. Conclusions: Higher protein intake for 12 weeks preserved knee muscle performance in older adults with T2DM without weight gain, supporting dietary protein optimization to counter functional decline.

The aim of this study was to determine the effects of a simulated one-day Greco-Roman wrestling tournament on selected performance and inflammatory status indices. Twelve competitive wrestlers (22.1 ± 1.3 years) completed five matches according to the official Olympic wrestling tournament regulations following a ~6% weight loss. Performance measurements, muscle damage assessment, and blood sampling were performed before and following each match. Performance and inflammatory markers were not affected by weight loss. Mean wrestling heart rate reached ~85% of maximal and lactate concentration exceeded 17 mM. Fatigue rating demonstrated a progressive rise ( P  < 0.05) throughout the tournament, peaking in match 4. Performance demonstrated a progressive deterioration ( P  < 0.05) throughout the tournament, especially in the last two matches ( P  < 0.05), with upper-body measures exhibiting a greater decline ( P  < 0.05) and remaining below baseline ( P  < 0.05) until the end of the tournament. Muscle damage markers increased during the course of the tournament with upper limbs affected more. Creatine kinase activity, CRP levels, IL-6 concentration, and leukocyte counts increased ( P  < 0.05) progressively throughout the tournament, peaking in the last two matches. Cortisol, epinephrine and norepinephrine increased ( P  < 0.05) after each match, but testosterone declined ( P  < 0.05) progressively, reaching a nadir before the last match. This inflammatory response was accompanied by a marked increase ( p  < 0.05) in lipid peroxidation, protein oxidation, and antioxidant status markers indicating the development of oxidative stress. These results suggest that a one-day wrestling tournament may induce significant physiological demands on wrestlers that may adversely affect their performance and inflammatory status especially during the later stages of the tournament.

Hypertension and arterial stiffness are significant factors contributing to cardiovascular disease. L-citrulline, a nitric oxide precursor, has been proposed as a nutritional, non-pharmacological blood pressure-lowering intervention. This study aimed to investigate the impact of L-citrulline on central and peripheral blood pressure, pulse wave reflection, and central arterial stiffness at rest and during an isometric knee extension exercise protocol. Twelve older males received 6 g of L-citrulline or a placebo for six days using a double-blind crossover design. Blood hemodynamics parameters (i.e., aortic and brachial systolic and diastolic blood pressure, mean arterial pressure, pulse pressure, heart rate), pulse wave reflection (i.e., augmented pressure, augmentation index, forward/backward wave pressure), and arterial stiffness (i.e., carotid–femoral pulse wave velocity) were measured at baseline, post-supplementation, and during isometric exercise. No significant effects of L-citrulline supplementation were observed at rest or during exercise on blood pressure, pulse wave reflection, or arterial stiffness. Both central and peripheral blood pressure were increased during the exercise, which is consistent with isometric contractions. The results of the present study do not support any blood pressure-lowering effect of short-term L-citrulline at rest or during low-intensity isometric exercise compared to the pre-exercise values in older males.

A novel automatic escalator was designed, constructed and used in the present investigation. The aim of the present investigation was to compare the effect of two repeated sessions of stair descending versus stair ascending exercise on muscle performance and health-related parameters in young healthy men. Twenty males participated and were randomly divided into two equal-sized groups: a stair descending group (muscle-damaging group) and a stair ascending group (non-muscle-damaging group). Each group performed two sessions of stair descending or stair ascending exercise on the automatic escalator while a three week period was elapsed between the two exercise sessions. Indices of muscle function, insulin sensitivity, blood lipid profile and redox status were assessed before and immediately after, as well as at day 2 and day 4 after both exercise sessions. It was found that the first bout of stair descending exercise caused muscle damage, induced insulin resistance and oxidative stress as well as affected positively blood lipid profile. However, after the second bout of stair descending exercise the alterations in all parameters were diminished or abolished. On the other hand, the stair ascending exercise induced only minor effects on muscle function and health-related parameters after both exercise bouts. The results of the present investigation indicate that stair descending exercise seems to be a promising way of exercise that can provoke positive effects on blood lipid profile and antioxidant status.

PurposeAcute high-intensity unaccustomed eccentric exercise performed by naive subjects is accompanied by disturbances in muscle damage biomarkers. The aim of the study was to investigate whether a causal relationship indeed exists between eccentric exercise and muscle damage.MethodsTwenty-four men randomly assigned into a concentric only or an eccentric-only training group and performed 10 weeks of isokinetic resistance exercise (one session/week of 75 maximal knee extensors actions). Physiological markers of muscle function and damage (i.e., range of motion, delayed onset muscle soreness, isometric, concentric and eccentric peak torque) were assessed prior to and 1–3 and 5 days post each session. Biochemical markers of muscle damage (creatine kinase) and inflammation (C-reactive protein) were measured prior and 2 days post each session.ResultsAfter the first bout, eccentric exercise induced greater muscle damage compared to concentric exercise; however, during the nine following sessions, this effect progressively diminished, while after the 10th week of training, no alterations in muscle damage biomarkers were observed after either exercise protocol. Additionally, strength gains at the end of the training period were comparable between the two groups and were mode-specific.Conclusion(1) eccentric exercise per se does not affect muscle damage biomarkers; (2) muscle damage occurs as a result of muscle unaccustomedness to this action type; (3) exercise-induced muscle damage is not a prerequisite for increased muscle strength. Collectively, we believe that muscle unaccustomedness to high-intensity eccentric exercise, and not eccentric exercise per se, is the trigger for muscle damage as indicated by muscle damage biomarkers.

There is a lack of consensus on optimal timing to assess redox biomarkers post‐exercise, limiting methodological standardisation and linking oxidative stress to physiology. We determined optimal post‐exercise oxidative stress assessment times using three redox biomarkers: glutathione, F 2 ‐isoprostanes and protein carbonyls. Standardised mean differences were calculated using random‐effects models, with 95% confidence and prediction intervals. Risk of bias was assessed via RoB2 and ROBINS‐I tools. Egger's test and funnel plots evaluated publication bias. Certainty of evidence was rated using GRADE. PROSPERO preregistration: CRD42024508049. A total of 103 studies ( n  = 1418) were included. Glutathione levels decreased immediately ( g  = −0.70; 95% CI: −0.96, −0.44; P  < 0.001), at 30 min to 2 h ( g  = −0.81; 95% CI: −1.19, −0.43; P  < 0.001), and 48 h post‐exercise ( g  = −0.98; 95% CI: −1.50, −0.46; P  < 0.01). F 2 ‐isoprostanes increased immediately post‐exercise ( g  = 1.01; 95% CI: 0.70, 1.33; P  < 0.001) and at 30 min to 2 h ( g  = 0.46; 95% CI: 0.23, 0.69; P  < 0.001). Protein carbonyls increased at all time points, especially at 48 h post‐exercise ( g  = 1.17; 95% CI: 0.73, 1.60; P  < 0.001), peaking at 72 h ( g  = 1.33; 95% CI: 0.52, 2.14; P  = 0.0048). Subgroup analyses revealed that non‐muscle‐damaging exercise elicits responses immediately after exercise or within the first 2 h, while muscle‐damaging exercise induces peaks at 48 and 72 h post‐exercise. Egger's test indicated publication bias for F 2 ‐isoprostanes ( P  = 0.017) and protein carbonyls ( P  = 0.031) post‐exercise. Risk of bias was moderate in randomised controlled trials and serious in non‐randomised studies. Certainty of evidence ranged from moderate to high. In conclusion, non‐muscle‐damaging exercise elicits early responses within hours, while muscle‐damaging protocols produce delayed peaks at 48–72 h. These findings support methodological consistency and are useful for optimising study design, sample size estimation and providing links between redox biology and physiological outcomes. What is the topic of this review? The optimal timing to assess exercise‐induced oxidative stress in humans, via a systematic review and meta‐analysis of three commonly used redox biomarkers: glutathione (antioxidant), F 2 ‐isoprostanes (lipid peroxidation product) and protein carbonyls (protein oxidation product). What advances does it highlight? It delineates biomarker‐ and protocol‐specific kinetics: non‐muscle‐damaging exercise peaks immediately/within 2 h, while muscle‐damaging protocols peak at 48–72 h. It offers specimen guidance, quantifies effect sizes, grades evidence and provides practical standards for study design.

PURPOSE: It has been suggested that part of the failure of antioxidant supplementation to reduce oxidative stress and promote health is that it has been administered in humans with normal levels of antioxidants. METHODS: To test this hypothesis, we screened 100 males for vitamin C baseline values in blood. Subsequently, the 10 individuals with the lowest and the 10 with the highest vitamin C values were assigned in two groups. Using a placebo-controlled crossover design, the 20 selected subjects performed aerobic exercise to exhaustion (oxidant stimulus) before and after vitamin C supplementation for 30 days. RESULTS: The low vitamin C group had lower VO₂max values than the high vitamin C group. Vitamin C supplementation in this group marginally increased VO₂max. Baseline concentration of F₂-isoprostanes and protein carbonyls was higher in the low vitamin C group compared to the high vitamin C group. Vitamin C supplementation decreased the baseline concentration of F₂-isoprostanes and protein carbonyls in both groups, yet the decrease was greater in the low vitamin C group. Before vitamin C supplementation, F₂-isoprostanes and protein carbonyls were increased to a greater extent after exercise in the high vitamin C group compared to the low vitamin C group. Interestingly, after vitamin C supplementation, this difference was narrowed. CONCLUSION: We show for the first time that low vitamin C concentration is linked with decreased physical performance and increased oxidative stress and that vitamin C supplementation decreases oxidative stress and might increase exercise performance only in those with low initial concentration of vitamin C.

The present study aimed to investigate whether acute L-citrulline supplementation would affect inspiratory muscle oxygenation and respiratory performance. Twelve healthy males received 6 g of L-citrulline or placebo in a double-blind crossover design. Pulmonary function (i.e., forced expired volume in 1 s, forced vital capacity and their ratio), maximal inspiratory pressure (MIP), fractional exhaled nitric oxide (NO•), and sternocleidomastoid muscle oxygenation were measured at baseline, one hour post supplementation, and after an incremental resistive breathing protocol to task failure of the respiratory muscles. The resistive breathing task consisted of 30 inspirations at 70% and 80% of MIP followed by continuous inspirations at 90% of MIP until task failure. Sternocleidomastoid muscle oxygenation was assessed using near-infrared spectroscopy. One-hour post-L-citrulline supplementation, exhaled NO• was significantly increased (19.2%; p < 0.05), and this increase was preserved until the end of the resistive breathing (16.4%; p < 0.05). In contrast, no difference was observed in the placebo condition. Pulmonary function and MIP were not affected by the L-citrulline supplementation. During resistive breathing, sternocleidomastoid muscle oxygenation was significantly reduced, with no difference noted between the two supplementation conditions. In conclusion, a single ingestion of 6 g L-citrulline increased NO• bioavailability but not the respiratory performance and inspiratory muscle oxygenation.

In sports nutrition, nitric oxide (NO•) precursors such as L-citrulline are widely used to enhance NO• bioavailability, which is considered an ergogenic aid. Our study aimed to examine the effect of short-term L-citrulline supplementation on respiratory muscles’ performance, fatigue, and oxygenation in older adults. Fourteen healthy older males took 6 g of L-citrulline or a placebo for seven days in a double-blind crossover design. Pulmonary function via spirometry (i.e., forced expired volume in 1 s (FEV1), forced vital capacity (FVC), and their ratio)), fractional exhaled nitric oxide (NO•), maximal inspiratory pressure (MIP), rate of perceived exertion, and sternocleidomastoid muscle oxygenation (i.e., oxyhemoglobin (Δ[O2Hb]) and de-oxyhemoglobin (Δ[HHb]), total hemoglobin concentration (Δ[tHb]), and tissue saturation index (TSI%)) were evaluated at baseline, after seven days of L-citrulline supplementation, and after incremental resistive breathing to task failure of the respiratory muscles. The exhaled NO• value was only significantly increased after the supplementation (26% p < 0.001) in the L-citrulline condition. Pulmonary function, MIP, rate of perceived exertion, and sternocleidomastoid muscle oxygenation were not affected by the L-citrulline supplementation. In the present study, although short-term L-citrulline supplementation increased exhaled NO•, no ergogenic aids were found on the examined parameters at rest and after resistive breathing to task failure in older adults.