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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.

Fatouros, IG, Chatzinikolaou, A, Douroudos, II, Nikolaidis, MG, Kyparos, A, Margonis, A, Michailidis, Y, Vantarakis, A, Taxildaris, K, Katrabasas, I, Mandalidis, D, Kouretas, D, and Jamurtas, AZ. Time-course of changes in oxidative stress and antioxidant status responses following a soccer game. J Strength Cond Res 24(12)3278-3286, 2010-Exercise-induced muscle damage is associated with an acute-phase inflammatory response characterized by phagocyte infiltration into muscle and free radical production. Although soccer includes intense eccentric muscle actions that cause muscle damage, the oxidative stress responses after a soccer game are currently unknown. The present investigation attempted to determine the responses of circulating levels of oxidative stress and antioxidant status markers during recovery from a soccer game. Twenty soccer players (experimental group) were assigned to 2 different teams that competed against each other (2 × 45 minutes). Ten other players served as controls (rested). Creatine kinase (CK) activity, uric acid, leukocyte count, malondialdehyde (MDA), protein carbnyls (PC), reduced (GSH) and oxidized glutathione (GSSG), antioxidant capacity (TAC), catalase, glutathione peroxidase activity (GPX), delayed-onset of muscle soreness (DOMS), and anaerobic performance (speed, vertical jump performance) were measured before and following (immediately post, 24 hours, 48 hours, 72 hours) the game. Performance deteriorated (2-17%, p < 0.05) throughout recovery. Leukocytosis developed (p < 0.05) immediately following the game and at 24 hours. Both CK and DOMS (3-8-fold, p < 0.05) increased from baseline and remained elevated (p < 0.05) through 48 hours. Thiobarbituric acid reactive substances (TBARS), PC, uric acid, GPX, and TAC increased (13-67%, p < 0.05) throughout recovery, whereas catalase was elevated (38%, p < 0.05) only immediately after the game. GSH/GSSG declined (17-75%, p < 0.05) throughout recovery. Our results suggest that oxidative stress is markedly upregulated by a soccer game, probably as a part of the exercise-induced inflammatory response, and is accompanied by a marked deterioration of anaerobic performance for as long as 72 hours.

Without effective countermeasures, the musculoskeletal system is altered by the microgravity environment of long-duration spaceflight, resulting in atrophy of bone and muscle tissue, as well as in deficits in the function of cartilage, tendons, and vertebral disks. While inflight countermeasures implemented on the International Space Station have evidenced reduction of bone and muscle loss on low-Earth orbit missions of several months in length, important knowledge gaps must be addressed in order to develop effective strategies for managing human musculoskeletal health on exploration class missions well beyond Earth orbit. Analog environments, such as bed rest and/or isolation environments, may be employed in conjunction with large sample sizes to understand sex differences in countermeasure effectiveness, as well as interaction of exercise with pharmacologic, nutritional, immune system, sleep and psychological countermeasures. Studies of musculoskeletal biomechanics, involving both human subject and computer simulation studies, are essential to developing strategies to avoid bone fractures or other injuries to connective tissue during exercise and extravehicular activities. Animal models may be employed to understand effects of the space environment that cannot be modeled using human analog studies. These include studies of radiation effects on bone and muscle, unraveling the effects of genetics on bone and muscle loss, and characterizing the process of fracture healing in the mechanically unloaded and immuno-compromised spaceflight environment. In addition to setting the stage for evidence-based management of musculoskeletal health in long-duration space missions, the body of knowledge acquired in the process of addressing this array of scientific problems will lend insight into the understanding of terrestrial health conditions such as age-related osteoporosis and sarcopenia.

The present study aimed to investigate whether endurance exercise-induced changes in blood plasma composition may lead to adaptations in erythrocytes, skeletal muscle and liver. Forty sedentary rats were randomly distributed into two groups: a group that was injected with pooled plasma from rats that swam until exhaustion and a group that was injected with the pooled plasma from resting rats (intravenous administration at a dose of 2 mL/kg body weight for 21 days). Total antioxidant capacity, malondialdehyde and protein carbonyls were higher in the plasma collected from the exercised rats compared to the plasma from the resting rats. Νo significant difference was found in blood and tissue redox biomarkers and in tissue metabolic markers between rats that received the “exercised” or the “non-exercised” plasma (P > 0.05). Our results demonstrate that plasma injections from exercised rats to sedentary rats do not induce redox or metabolic adaptations in erythrocytes, skeletal muscle and liver.

This study aimed to assess the arterial pressure (AP) determinants during the muscle metaboreflex in boys and men and to investigate the contribution of baroreflex and sympathovagal function to the metaboreflex-induced responses. Fourteen pre-adolescent boys and 13 men performed a protocol involving: baseline, isometric handgrip exercise, circulatory occlusion, and recovery. The same protocol was repeated without occlusion. During baseline, boys had lower beat-to-beat AP, higher heart rate (HR), and lower low/high frequency HR variability. During exercise, a parasympathetic withdrawal was evident in both groups. In adults, HR was the key contributor to the pressure response, with no changes in stroke volume, whereas in boys, the lower HR increase was counterbalanced by an increase in stroke volume, resulting in similar relative increases in AP in both groups. In recovery, boys exhibited a faster rate of HR-decay, rapid vagal reactivation, and greater decrease in TPR than men. An overshoot in baroreceptor sensitivity was observed in men. The isolated metaboreflex resulted in a similar AP elevation in both age groups (by ~15 mmHg), and attenuated spontaneous baroreceptor sensitivity. However, during the metaboreflex, pre-adolescent males exhibited a lower increase in peripheral resistance and a greater bradycardic response than adults, and a fast restoration of vagal activity to non-occlusion levels. During metaboreflex, boys were capable of eliciting a pressure response similar to the one elicited by men; however, the interplay of the mechanisms underlying the rise in AP differed between the two groups with the vagal contribution being greater in the younger participants.

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.

Antioxidant supplementation has been suggested to prevent exercise-induced muscle injury, but the findings are inconsistent. The objective of this study was to investigate the potential protective role of vitamin E treatment against eccentric exercise-induced muscle injury by examining morphological and functional alterations in rat soleus muscle after downhill running as well as muscle injury markers in the blood. Sixty adult male Wistar rats were randomly assigned to vitamin E-treated or placebo-treated groups studied at rest, immediately post-exercise or 48 h post-exercise ( n  = 10 per group). Vitamin E was administered by daily intraperitoneal injections of 100 mg/kg body mass of dl -α-tocopheryl acetate for five consecutive days prior to exercise, resulting in the doubling of its plasma concentration. Downhill running resulted in significant ( P  < 0.05) changes in all injury markers for the placebo-treated rats at 0 and 48 h post-exercise. However, significantly smaller soleus muscle single-twitch tension ( P t ) and unfused (40 Hz) tetanic force, and greater plasma creatine kinase (CK) and lactate dehydrogenase (LD) activities compared with the control were found only immediately post-exercise for the vitamin E-treated rats ( P  < 0.05). Maximal tetanic force ( P o ) did not decline significantly compared to sedentary controls at neither time points measured. The vitamin E-treated rats had significantly ( P  < 0.05) higher soleus muscle P t immediately post-exercise than the placebo-treated rats as well as lower plasma CK and LD activity 48 h post-exercise. However, there was no difference in P o decline between groups at either time points measured. Vitamin E-treated rats had less pronounced morphological alterations in muscle in the immediate and 48-h post-exercise period. In conclusion, the effect of short-term vitamin E supplementation against eccentric exercise-induced muscle injury did not appear to be physiologically significant, because vitamin E failed to prevent the decline in the functional measure of P o compared to the placebo conditions.

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.

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 The purpose of the present study was to directly compare oxidative stress and inflammation responses between rats and humans. Methods We contrasted rat and human oxidative stress and inflammatory responses to exercise (pro-oxidant stimulus) and/or vitamin C (anti-oxidant stimulus) administration. Vitamin C was administered orally in both species (16 mg kg −1 of body weight). Twelve redox biomarkers and seven inflammatory biomarkers were determined in plasma and erythrocytes pre- and post-exercise or pre- and post-exercise combined with vitamin C administration. Results Exercise increased oxidative stress and induced an inflammatory state in rats and humans. There were only 1/19 significant species × exercise interactions (catalase), indicating similar responses to exercise between rats and humans in redox and inflammatory biomarkers. Vitamin C decreased oxidative stress and increased antioxidant capacity only in humans and did not affect the redox state of rats. In contrast, vitamin C induced an anti-inflammatory state only in rats and did not affect the inflammatory state of humans. There were 10/19 significant species × vitamin C interactions, indicating that rats poorly mimic human oxidative stress and inflammatory responses to vitamin C administration. Exercise after acute vitamin C administration altered redox state only in humans and did not affect the redox state of rats. On the contrary, inflammation biomarkers changed similarly after exercise combined with vitamin C in both rats and humans. Conclusions The rat adequately mimics human responses to exercise in basic blood redox/inflammatory profile, yet this is not the case after exercise combined with vitamin C administration.