Abstract
This study was designed to examine the potential involvement of reactive oxygen species in skeletal muscle dysfunction linked with stretching in a mouse model and to explore the effects of combined antioxidant intake on peripheral leukocyte apoptosis following eccentrically-biased downhill runs in human subjects. In the mouse model, diaphragmatic muscle was stretched by 30% of its optimal length, followed by 5-min contraction. Muscle function and extracellular reactive oxygen species release was measured ex vivo. In human models, participants performed two trials of downhill running either with or without antioxidant supplementation, followed by apoptotic assay of inflammatory cells in the blood. The results showed that stretch led to decreased muscle function and prominent ROS increase during muscle contraction. In human models, we observed an elevation in circulating leukocyte apoptosis 24–48 hours following acute downhill runs. However, there is an attenuated leukocyte apoptosis following the second bout of downhill run. Interestingly, the combination of ascorbic acid (vitamin C) and α-tocopherol (vitamin E) supplementation attenuated the decrease in B-cell lymphoma 2 (Bcl-2) at 24 hours following acute downhill running. These data collectively suggest that significant ROS formation can be induced by muscle-lengthening associated with eccentric exercise, which is accompanied by compromised muscle function. The combination of antioxidants supplementation appears to have a protective role via the attenuation of decrease in anti-apoptotic protein.
Highlights
Eccentric exercise-induced muscle damage is characterized by decreased muscle contractile force, muscle stiffness, swelling, delayed-onset muscle soreness, and histological alterations involving myofilament, extracellular matrix (ECM), and epimysium [1]
We identified the involvement of extracellular reactive oxygen species (ROS) in stretching-induced muscle force decline
Reactive oxygen species in stretched muscle associated with eccentric contractions
Summary
Eccentric exercise-induced muscle damage is characterized by decreased muscle contractile force, muscle stiffness, swelling, delayed-onset muscle soreness, and histological alterations involving myofilament, extracellular matrix (ECM), and epimysium [1]. As seen during eccentric exercise, is generally associated with muscle damage due to non-uniform stretching of the sarcomeres [2]. Since sarcomeres are arranged in series, the damage induced by extended sarcomeres can propagate longitudinally, collectively resulting in reduced production of force during the contraction [3]. Skeletal muscle exhibits a greater adaptive ability to stretching than myocardium through sarcomerogenesis and hypertrophy [2, 5], the disruption of sarcomere stability inadvertently impairs muscle force development. It is postulated that muscle damage resulting from eccentric exercise is associated with disrupted sarcomeres and subsequent excitation-contraction coupling dysfunction. Sarcomere lengthening is considered an initiative event for a muscle-damaging processes during eccentric contractions [6]
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