Effect of Eccentric Exercise and Vitamin E Supplementation on Indices of Lipid Peroxidation, Muscle Damage and Muscle Soreness

1994 ◽  
Vol 87 (s1) ◽  
pp. 83-83
Author(s):  
AMcE Jenkinson ◽  
C Riddoch ◽  
RJ Maughan ◽  
PC Morrice ◽  
KM Brown ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Muscle Soreness ◽  
Vitamin E Supplementation

scholarly journals Efectos de la suplementación con vitamina E en la reducción del dolor muscular de inicio retardado. Una revisión narrativa.

2019 ◽  
Vol 21 (2) ◽  
pp. 219-227
Author(s):  
Héctor Fuentes-Barria ◽  
Raúl Aguilera-Eguia ◽  
Catalina González-Wong ◽  
Aylinne Schramm-Saavedra ◽  
Denisse Muñoz-Peña
Keyword(s):  
Vitamin E ◽  
Muscle Damage ◽  
Muscle Soreness ◽  
Delayed Onset Muscle Soreness ◽  
Estrés Oxidativo ◽  
Delayed Onset ◽  
Vitamin E Supplementation

Antecedentes: actualmente existe un creciente interés en investigar métodos que logren disminuir el dolor muscular de inicio retardado. Se ha postulado que antioxidantes como las vitaminas C y E pueden atenuarlo. Objetivo: evaluar la efectividad de vitamina E en la atenuación del dolor muscular de inicio retardado. Materiales y métodos: se realizó una búsqueda bibliográfica en las bases de datos Medline, Registro Central Cochrane, Scopus, SportDiscus y SciELO, utilizando los términos: “vitamin e supplementation”, “muscle damage” y “delayed onset muscle soreness”. Resultados: se revisaron estudios en diversos grupos poblacionales, con diferentes métodos de evaluación y diversas dosis de vitamina E. Los resultados obtenidos fueron controversiales, en algunos casos se demostró un efecto atenuante del dolor muscular de inicio retardado y en otros casos no. Conclusiones: la vitamina E produce una disminución del estrés oxidativo y estabilización el sarcolema; no obstante, faltan pruebas concluyentes para afirmar que la vitamina E tenga el efecto de generar mejoras en los biomarcadores asociados al dolor muscular de inicio retardado.

Vitamin E supplementation inhibits muscle damage and inflammation after moderate exercise in hypoxia

2016 ◽  
Vol 29 (4) ◽  
pp. 516-522 ◽  
Author(s):  
S. A. Santos ◽  
E. T. Silva ◽  
A. V. Caris ◽  
F. S. Lira ◽  
S. Tufik ◽  
...  
Keyword(s):  
Vitamin E ◽  
Muscle Damage ◽  
Moderate Exercise ◽  
Vitamin E Supplementation

scholarly journals Muscle Damage Indicated by Maximal Voluntary Contraction Strength Changes From Immediately to 1 Day After Eccentric Exercise of the Knee Extensors

2021 ◽  
Vol 12 ◽  
Author(s):  
Mikio Shoji ◽  
Ryoichi Ema ◽  
Kazunori Nosaka ◽  
Akihiro Kanda ◽  
Kosuke Hirata ◽  
...  
Keyword(s):  
Shear Modulus ◽  
Muscle Damage ◽  
Eccentric Exercise ◽  
Recovery Rate ◽  
Muscle Soreness ◽  
Knee Extensors ◽  
Significant Group ◽  
Post Exercise ◽  
Significant Difference ◽  
Recovery Group

The present study examined if the magnitude of changes in indirect muscle damage markers could be predicted by maximal voluntary isometric contraction (MVIC) torque changes from immediately to 1 day after eccentric exercise. Twenty-eight young men performed 100 maximal isokinetic (60°/s) eccentric contractions of the knee extensors. MVIC torque, potentiated doublet torque, voluntary activation (VA) during MVIC, shear modulus of rectus femoris (RF), vastus medialis and lateralis, and muscle soreness of these muscles were measured before, immediately after, and 1–3 days post-exercise. Based on the recovery rate of the MVIC torque from immediately to 1-day post-exercise, the participants were placed to a recovery group that showed an increase in the MVIC torque (11.3–79.9%, n = 15) or a no-recovery group that showed no recovery (−71.9 to 0%, n = 13). No significant difference in MVIC torque decrease immediately post-exercise was found between the recovery (−33 ± 12%) and no-recovery (−32 ± 9%) groups. At 1–3 days, changes in MVIC torque (−40 to −26% vs. −22 to −12%), potentiated doublet torque (−37 to −22% vs. −20 to −9%), and proximal RF shear modulus (29–34% vs. 8–15%) were greater (p < 0.05) for the no-recovery than recovery group. No significant group differences were found for muscle soreness. The recovery rate of MVIC torque was correlated (p < 0.05) with the change in MVIC torque from baseline to 2 (r = 0.624) or 3 days post-exercise (r = 0.526), or peak change in potentiated doublet torque at 1–3 days post-exercise from baseline (r = 0.691), but not correlated with the changes in other dependent variables. These results suggest that the recovery rate of MVIC torque predicts changes in neuromuscular function but not muscle soreness and stiffness following eccentric exercise of the knee extensors.

Is isometric strength loss immediately after eccentric exercise related to changes in indirect markers of muscle damage?

2006 ◽  
Vol 31 (3) ◽  
pp. 313-319 ◽  
Author(s):  
Kazunori Nosaka ◽  
Dale Chapman ◽  
Mike Newton ◽  
Paul Sacco
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Elbow Joint ◽  
Muscle Soreness ◽  
Correlation Coefficients ◽  
Strength Loss ◽  
Isometric Strength ◽  
Joint Angles ◽  
Arm Circumference ◽  
Strong Correlate

This study tested the hypothesis that the magnitude of maximal isometric strength (MVC) loss immediately following eccentric exercise (MVC-post) would relate to changes in other indirect markers of muscle damage following exercise. Eighty-nine men were recruited from the same student population and performed 24 maximal eccentric actions of the elbow flexors. Commonly used markers of muscle damage such as relaxed and flexed elbow joint angles, range of motion (ROM), upper-arm circumference, muscle soreness, and plasma creatine kinase (CK) activity were measured before, immediately after, and 1-4 d after exercise. Pearson's product-moment correlation coefficients (r) between change in MVC-post and other markers of muscle damage, as well as MVC during recovery days, were calculated. Changes in MVC-post ranged from -72.8% to -17.6%, and correlated significantly (p < 0.01) with MVC at 1 (r = 0.59), 2 (0.63), 3 (0.61), and 4 (0.62) d after exercise. Reduction in MVC-post also correlated significantly (p < 0.05) with changes in relaxed (r = 0.50) and flexed elbow joint angles (-0.40), ROM (0.55), arm circumference (-0.45), peak palpation (-0.34) and extension muscle soreness (-0.48), and peak CK activity (-0.59). However, the r values were not necessarily high, and MVC-post poorly reflected the distribution of some measures, such as peak CK activity (124 - 50 440 IU·L-1). These results suggest that MVC-post is not a strong correlate of the changes in markers of muscle damage following eccentric exercise of the elbow flexors.Key words: maximal isometric strength, plasma CK activity, ROM, swelling, muscle soreness.

Vitamin E decreases hepatic levels of aldehyde-derived peroxidation products in rats with iron overload

1996 ◽  
Vol 270 (2) ◽  
pp. G376-G384 ◽  
Author(s):  
S. Parkkila ◽  
O. Niemela ◽  
R. S. Britton ◽  
K. E. Brown ◽  
S. Yla-Herttuala ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Iron Overload ◽  
Kupffer Cells ◽  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Alpha Tocopherol ◽  
Confocal Laser ◽  
Hepatocellular Injury ◽  
Vitamin E Supplementation

Hepatic iron overload can cause lipid peroxidation with the formation of aldehydic products, hepatocellular injury, and fibrosis. Vitamin E (alpha-tocopherol) may prevent peroxidation-induced hepatic damage. We used confocal laser scanning microscopy, digital image analysis, and immunohistochemical methods to quantitate aldehyde-derived peroxidation products in the liver of rats with experimental iron overload with or without supplemental vitamin E. A strong autofluorescent reaction colocalizing with iron deposits was present in the livers of iron-loaded rats. Fluorescent granules were unevenly distributed in the cytosol of both hepatocytes and Kupffer cells in the periportal regions. Immunohistochemical studies revealed the presence of malon-dialdehyde adducts in the periportal regions of the ironloaded rats. Vitamin E supplementation markedly reduced the fluorescence intensity and the amount of aldehyde-derived peroxidation products and changed the distribution of stainable iron and iron-associated peroxidation products such that their levels were much decreased in Kupffer cells. These results indicate that aldehyde-derived covalent chemical addition products are formed in the liver in iron overload. Vitamin E supplementation markedly reduces the amount of these compounds and changes their cellular distribution. These findings should be implicated in the role of antioxidant therapy in conditions causing iron overload and lipid peroxidation.

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