Nutritional agents that are capable of metabolic optimization of the ECM and the connective tissue components of muscle and its myotendinous junctions have the potential to provide safe and cost-effective tools that can aid in the recovery from intense or unaccustomed exercise bouts. 6 More studies need to be conducted, particularly in humans, to further the understanding of specific agents or conditions that enhance the role of the musculoskeletal ECM in mechanotransduction and force transmission and in the RBE (ie, the protective effect that a novel exercise bout has on subsequent exercise sessions). This protective effect occurred against different types of the second EIMD. In a rat model, RBE was shown to occur as early as 2 days after the first bout of contractions of the dorsiflexor muscles in the left hind limbs, and it persisted for several weeks.
4, 6, 7 For example, compared with a novel bout of eccentric exercise that causes muscle damage and loss of strength, a subsequent bout of eccentric exercise, when performed days or even weeks later, is associated with less loss of contractile force, a decreased soreness, and a reduction in the amount of muscle proteins in the blood, the biomarkers of tissue disruption, when compared with the first bout of exercise. Hence, although high-force eccentric contractions are associated with EIMD and microtrauma or injury, they are also known to provide, paradoxically, significant protection against future injury through what is known as the repetitive bout effect (RBE).
The resulting biochemical and molecular responses within both skeletal muscles and tendons promote adaptation to mechanical loading and physical activity. A substantial body of evidence has demonstrated that exercise leads to local enhancement of metabolic activity, circulatory responses, and collagen turnover, together with an elevated expression of growth factors, such as insulin growth factor 1 (IGF-1) and transforming growth factor β (TGF-β). It is well established that ECMs of both the muscles and tendons are sensitive to the mechanical stimuli and tension generated by muscular contractions, particularly by a lengthening or eccentric muscle action against resistance from either isotonic, isometric, or isokinetic modalities. 4, 5 This structural alteration of the skeletal muscle tissue is known to limit performance in repetitive activities due to a decreased range of motion, decreased force production, and pain. 2, 3 However, it is clear that shear stress and injury to other extramuscular elements of connective tissue (extracellular matrix proteins basal lamina types 1, 3, 4, and 6 collagen proteoglycan/glycosoaminoglycans epimysium/perimysium/endomysium and tendon)-are also involved. 1 Traditionally, DOMS has largely been explained by myogenic factors associated with structural alteration of the sarcolemmal membrane, damage to Z disks of sarcomeres and disruption of cytoskeletal proteins (ie, dystrophin, desmin, titin, integrins, and fibronectin). EIMD results in delayed-onset muscle soreness (DOMS) in association with an increased presence of muscle-specific proteins in the blood, muscle edema, and fiber swelling. The use of mechanical stressors that overload skeletal muscle and associated connective tissue often result in some degree of exercise-induced muscular damage (EIMD).
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