Abstract
In mammalian taxonomy, skeletal muscle constitutes a remarkable tissue not only in its innate capacity to generate force while shortening, remaining isometric, or lengthening, but in its capacity to adapt through atrophy or hypertrophy in response to decreased or increased loads, respectively and regenerate when injured. The chapter begins with Section 1 on the Structure of Skeletal Muscles and Skeletal Muscle Fibers. Section 2 describes Types of Contractions, shortening, isometric, and lengthening and the differences in the force development by each. The interactive roles of decreased usage and aging are covered in Section 3: Age-Related Muscle Wasting and Muscle Weakness and the condition of physical frailty is discussed. Section 4 focuses on Late-Onset Muscle Soreness described by Hough in 1902 and gaining widespread attention in the 1980s. The development of the concepts: Contraction-Induced Injury and Force Deficit are discussed in Section 5. Section 6 clarifies The Cause of the Contraction Induced Injury as a function of interactions between homogeneity of sarcomere strengths within a muscle and the severity of lengthening contraction protocols. Section 7 elaborates on the significance of the stability of the sarcomeres within fibers and the Contribution of Lateral Transmission of Force to Contraction-Induced Injury. Section 8, the Role of Contraction-Induced Injury in Wasting and Weakness contrasts the impact of contraction-induced injury on young and healthy and on elderly and frail subjects. The final Section 9: Measures to Prevent Contraction-Induced Injury emphasizes the positive aspects of utilizing lengthening contractions in training programs for both young and old participants.
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Faulkner, J.A., Mendias, C.L., Davis, C.S., Brooks, S.V. (2011). Role of Contraction-Induced Injury in Age-Related Muscle Wasting and Weakness. In: Lynch, G. (eds) Sarcopenia – Age-Related Muscle Wasting and Weakness. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9713-2_16
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DOI: https://doi.org/10.1007/978-90-481-9713-2_16
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