Muscle Damage Biomarkers Research Articles

Adding exercise training to rosuvastatin treatment: influence on serum lipids and biomarkers of muscle and liver damage

Statin treatment and exercise training can improve lipid profile when administered separately. The efficacy of exercise and statin treatment combined, and its impact on myalgia and serum creatine kinase (CK) have not been completely addressed. The purpose of this study was to determine the effect of statin treatment and the addition of exercise training on lipid profile, including oxidized low-density lipoprotein (oxLDL), and levels of CK and alanine transaminase. Thirty-one hypercholesterolemic and physically inactive subjects were randomly assigned to rosuvastatin (R) or rosuvastatin/exercise (RE) group. A third group of physically active hypercholesterolemic subjects served as an active control group (AC). The R and RE groups received rosuvastatin treatment (10 mg/d) for 20 weeks. From week 10 to week 20, the RE group also participated in a combined endurance and resistive exercise training program (3 d/wk). Lipid profile was determined for all subjects at week 0 (Pre), week 10 (Mid), and week 20 (Post). The CK and alanine transaminase levels were measured at the same time points in the RE and R groups and 48 hours after the first and fifth exercise bout in the RE group. Each RE subject was formally queried about muscle fatigue, soreness, and stiffness before each training session. Total, LDL, and oxLDL cholesterol was lower in the RE and R groups at Mid and Post time points when compared with Pre. Oxidized LDL was lower in the RE group compared with the R group at the Post time point. When treatment groups (R and RE) were combined, high-density lipoprotein levels were increased and triglycerides decreased across time. Creatine kinase increased in the RE group 48 hours after the first exercise bout, but returned to baseline levels 48 hours after the fifth exercise bout. Rosuvastatin treatment decreased total, LDL, and oxLDL cholesterol. The addition of an exercise training program resulted in a further decrease in oxLDL. There was no abnormal sustained increase in CK or reports of myalgia after the addition of exercise training to rosuvastatin treatment.

Effect Of b-hydroxy-b-methylbutyrate On Biomarkers Of Muscle Damage After Prolonged Downhill Running

The leusine metabolite beta-hydroxy-beta-methylbutyrate (HMB) has been shown to increase muscle mass and strength following resistance training and has been also proposed to function as an anticatabolic agent and decrease exercise induced muscle damage. PURPOSE: The aim of this study was to investigate the effects of 14 days oral supplementation of HMB on muscle damage as a result of intense and prolonged uphill and downhill running. METHODS: Subjects (n=22) well trained endurance runners were randomly assigned to treatment of either HMB (3g/day) or a placebo for 2 weeks before race. They all run Olympus mountain marathon (44km) consisted of 21km uphill to 2700m altitude and 23km continuous downhill. Venous blood samples were obtained from the participants before, immediately after the race, also 3 and 7 days post race. They were analysed with standard methods for creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and myoglobin (MGL). RESULTS: Mean±sd (n=22) pre race CPK (149.55±21.47 U/L), MGL (32.31±4.00 mcg/l) and LDH (327.27±34.43 U/L) increased 5 (714.06±203.02U/L), 20 (662.06±260.99mcg/l) and 2 (698.06±107.84 U/L) fold (p<0.01) respectively immediately after the race. Mean CPK (256.93 U/L), MGL (61.64 mcg/l) and LDH (467.21 U/L) activities remained elevated 1.7, 1.9, and 2.1 fold (p<0.05) respectively 72 hours after the race. The placebo-supplemented group exhibited significantly greater (p<0.05) plasma concentration of CPK, LHD and MGL post race, 3 days and 7 days after the race than did the HMB supplemented group. Placebo-supplemented group presented also greater (p<0.05) mean difference (post race minus pre race values) in muscle damage biomarkers. CONCLUSIONS: The results of this study indicate that 2 weeks dietary supplementation of 3.0g HMB/day in endurance runners resulted in decreased CPK, LDH and MGL, after a very prolonged run. The finding agree with the hypothesis that HMB supplemented athletes experienced less muscle damage and also recovered at a faster rate.

The Effects Of Green Tea Extract Supplementation On Markers Of Muscle Injury And Oxidative Stress.

Reactive oxygen species (ROS) are key biologic radical species that oxidize molecules and impair their function. Exercise involving repeated lengthening muscle contractions (i.e. downhill running) has been shown to result in the generation of ROS. ROS are also thought to be involved in the inflammatory response to exercise. In addition, some markers of ROS induced damage exhibit a delayed response, 24 to 48 hr post-exercise, and have been correlated with delayed onset muscle soreness (DOMS). Green tea polyphenols possess antioxidant properties and have been used to counteract ROS production. PURPOSE: To test the hypothesis that the antioxidants in green tea will reduce biomarkers of oxidative stress and mechanical muscle damage following a downhill run. METHODS: Participants were young, healthy males (21 - 25 y/o) who reported running 3 - 5 days/wk. Participants were randomly assigned to a placebo (n = 6), green tea pre-exercise group (n = 5), or green tea post-exercise group (n = 5). Subjects performed a 45-min downhill treadmill run (-10°) at 60 - 65% of their VO2max. Measurements of muscle soreness (7 point Likert scale) and blood samples for the measurement of oxidative stress (malondialdehyde-MDA) and muscle damage (creatine kinase-CK) were obtained pre-exercise, immediately post-exercise, and 24 hr post-exercise. RESULTS: CK levels and muscle soreness were significantly elevated in all 3 groups at 24 hr post-exercise (p <.05). Green tea supplementation did not affect muscle damage as there were no differences in CK or soreness between the groups at any time point (p >.05). There were no significant differences (p >.05) in MDA between pre, post, and 24 hr samples for any group, however, a 36% and 24% increase in MDA occurred in the placebo and supplemented groups respectively at 24 hr post-exercise. CONCLUSIONS: This pilot study suggests that: 1) downhill running is not associated with increased oxidative stress, although there was a trend for increased MDA in the placebo group, and 2) green tea supplementation is ineffective in reducing muscle soreness/injury in response to downhill running.

Influence of acute physical exercise on emerging muscular biomarkers

Although there is comprehensive information on traditional biomarkers of muscle and cardiac damage following exercise, less is known on the kinetics of innovative markers, including ischemia modified albumin (IMA), glycogen phosphorylase isoenzyme BB (GPBB), carbonic anhydrase III (CAIII) and heart-type fatty acid-binding protein (H-FABP) in athletes performing a sub-maximal exercise. A total of 10 healthy trained Caucasian males performed a 21-km run. Blood samples were collected before the run, immediately after (post), 3, 6 and 24 h thereafter. Cardiac troponin I (cTnI), myoglobin, creatine kinase isoenzyme MB (CK-MB), GPBB, CAIII and H-FABP were assayed using a new diagnostic system based on protein biochip array technology. IMA was measured by a commercial colorimetric assay on a Roche Modular system P. Significant variations by one-way analysis of variance were observed for CK-MB (p=0.013), myoglobin (p<0.001), GPBB (p=0.029), H-FABP (p<0.001), CAIII (p=0.006), but not for cTnI (p=1.00) and IMA (p=0.881). In particular, values of all the biomarkers tested, but cTnI and IMA, increased significantly immediately after the run. GPBB and H-FABP values returned to baseline 6 and 3 h thereafter, those of CAIII, CK-MB and myoglobin remained significantly elevated from the pre-run value up to 24 h after the run. The major variation over pre-run values was recorded for myoglobin (nearly 4-fold increment), whereas CAIII, CK-MB, GPBB and H-FABP increased by 2.9-, 1.8-, 1.4- and 1.2-fold, respectively. We conclude that a sub-maximal aerobic exercise influences the concentration of several markers of muscle damage. Except for IMA, not one of the emerging biomarkers tested can be safely used to rule out myocardial damage as well as cardiospecific troponins in patients who had undergone recent physical activity.

Biomarkers of muscle and cartilage damage and inflammation during a 200km run

Biomarkers of muscle and cartilage damage and inflammation during a 200km run

Acute variation of biochemical markers of muscle damage following a 21‐km, half‐marathon run

Objective. Although there is information on biochemical markers of muscle and cardiac damage following strenuous exercise, little is known about the kinetics of these markers in athletes performing sub‐maximal exercise. Material and methods. Fifteen healthy, trained, Caucasian males took part in a 21‐km run. Blood samples were collected before the run, immediately after (post), and 3 h, 6 h and 24 h thereafter. Biochemical markers of muscle and cardiac damage were evaluated on the Modular System, employing proprietary reagents. In no case did the concentration of troponin T increase by >0.03 ng/mL. The values of aspartate aminotransferase (AST), creatine kinase (CK), CK MB, lactate dehydrogenase (LDH) and myoglobin increased significantly immediately after the run and remained elevated 24 h thereafter. Results. The number of subjects with values above the upper limit of the relative reference ranges did not vary throughout the study period for AST and LDH, while it increased significantly for CK, CK MB and myoglobin. The major variation over the pre‐run value was recorded for myoglobin (3‐fold increment), whereas AST and LDH increased 1.1 and 1.3‐fold, respectively. Conclusions. The results suggest the hypothesis that sub‐maximal exercise influences the concentration of several biomarkers of muscle damage for up to 24 h with no biochemical signs of myocardial damage.

Biomarkers of muscle and cartilage damage and inflammation during a 200 km run

Ultra-marathon running is frequently associated with muscle fibre damage. However, ultra-marathon related information is scarce. The present study evaluated muscle and cartilage biomarkers, and cytokine secretion during a 200 km running event. Venous blood samples from 54 trained male ultra-marathon runners (mean +/- SD, 45.7 +/- 5.1 years). Plasma creatine phosphokinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate, glucose, high-sensitivity C-reactive protein (Hs-CRP), interleukin-6 (IL-6), TNF- proportional, variant and serum cartilage oligomeric matrix protein (COMP) content were determined before, midway and immediately after the race. CPK increased 90-fold (19-fold at 100 km) from pre-race value and LDH increased 3.7-fold (2.2-fold at 100 km). AST increased 15-fold (5-fold at 100 km) and ALT increased 3.9-fold (2-fold at 100 km). Blood lactate and glucose levels did not change significantly. Hs-CRP increased 23-fold (3-fold at 100 km) and IL-6 increased 121-fold at 100 km, and then remained stable up to 200 km, whereas TNF- proportional, variant did not change significantly. Serum COMP increased 3-fold (1.3-fold at 100 km). Post-run CPK was correlated with LDH (r = 0.62, P < 0.001), Hs-CRP (r = 0.45, P < 0.001), ALT (r = 0.89, P < 0.001), AST (r = 0.97, P < 0.001), and IL-6 (r = 0.61, P < 0.001). The present study demonstrated that blood biomarkers related to muscle and cartilage damage and inflammation were increased during a 200 km run and that this was particularly marked during the second half of the event. Ultra-marathon running clearly has a major impact on muscle and cartilage structures.

Blood oxidative stress, antioxidant enzymes and muscle damage biomarkers changes during a competitive season in soccer players

O exercício físico induz aumento no consumo de oxigênio bem como na demanda energética. O aumento no consumo de 0 2 induz aumento na produção de espécies reativas de oxigênio (EROs). Dependendo da sua concentração, as EROs reagem com estruturas celulares, oxidando-as. Altos níveis de oxidação alteram sua função e prejudicam a homeostase intracelular. Jogadores de futebol aumentaram o desempenho de forma significativa nas últimas décadas, pela intensificação do processo de treinamento e melhoria das capacidades físicas envolvidas na modalidade. Tal fato sugere um aumento na possibilidade destes atletas estarem mais susceptíveis ao ataque oxidativo de EROs, com conseqüente aumento nos níveis de estresse oxidativo. Por outro lado, o treinamento também age na modulação dos sistemas antioxidantes intracelulares, aumentando sua capacidade de remover EROs. O objetivo deste estudo foi analisar o comportamento de marcadores sangüíneos do sistema de defesa antioxidante, de ataque oxidativo, bem como dos níveis de alteração muscular ao longo de cinco meses de campeonato paulista de um time de futebol, categoria sub-20. Nossos resultados mostram que as enzimas antioxidantes glutationa redutase e catalase atingiram picos de atividade em momentos distintos da temporada, sugerindo uma ação complementar entre elas. Os marcadores de estresse oxidativo e lesão muscular analisados não mostraram alterações significativas ao longo do estudo. Esses dados sugerem que a capacidade de defesa antioxidante foi eficiente em tamponar o possível aumento na produção de EROs induzido pelos treinamentos e jogos da competição, impedindo a ocorrência de lesões musculares de origem oxidativa ao longo do campeonato

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Skeletal muscle damage is an often-occurring event. Diagnosis using the classic blood marker creatine kinase sometimes yields unsatisfactory results due to great interindividual variability. Therefore, the identification of reliable biomarkers is important. Our aim was to detect and characterize circulating miRNAs in plasma in response to acute notexin-induced muscle damage in rats. Real-time quantitative RT-PCR profiling led to the identification of miRNAs that were highly increased in plasma in response to notexin injection into several muscles, namely miR-1-3p, -133a-3p, -133b-3p, -206-3p, -208b-3p, and -499-5p, as well as miR-378a-3p and miR-434-3p. Peak values of miRNAs appeared 12 hours after injury, and were contained both in the vesicular and nonvesicular fractions of plasma. Receiver operating characteristic curve analysis showed that circulating miRNAs could accurately discriminate between damaged and nondamaged tissues. Furthermore, we tested the robustness of expression profiles in slow- and fast-type fibers. Upon inducing damage in slow- or fast-type muscle, we found that the damaged-muscle phenotype had a very limited impact on the miRNA response. Similarly, the circulating miRNAs selected were not affected by hemolysis or platelets, two pre-analytical factors known to affect plasma miRNA profiles. Taken together, our results show that circulating muscle-specific miRNAs, miR-378a-3p and miR-434-3p, are robust and promising biomarkers of acute muscle damage in rats.