The deterioration of skeletal muscle with advancing age has long been anecdotally recognized and has been of scientific interest for more than 150 years. Over the past several decades, the scientific and medical communities have recognized that skeletal muscle dysfunction (e.g., muscle weakness, poor muscle coordination, etc.) is a debilitating and life-threatening condition in the elderly. For example, the age-associated loss of muscle strength is highly associated with both mortality and physical disability. It is well-accepted that voluntary muscle force production is not solely dependent upon muscle size, but rather results from a combination of neurologic and skeletal muscle factors, and that biologic properties of both of these systems are altered with aging. Accordingly, numerous scientists and clinicians have used the term “muscle quality” to describe the relationship between voluntary muscle strength and muscle size. In this review article, we discuss the age-associated changes in the neuromuscular system—starting at the level of the brain and proceeding down to the subcellular level of individual muscle fibers—that are potentially influential in the etiology of dynapenia (age-related loss of muscle strength and power).

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4. MODELS OF MUSCLE FORCE AND FATIGUE 4.1. Introduction vii 4.2. Hill model 4.3. Huxley model 4.4. Zahalak models 4.5. Ding models 4.5.1. Force model 4.5.2. Fatigue model 4.5.3. The nature of the problem with the Ding models 4.5.4. Criticism of statistical methods 5. A THEORY OF CALCIUM CURRENT IN PARALYZED MUSCLE 113 5.1. A mathematical construct of growth, diffusion, and decay in muscle 5.1.1. A theory of diffusion 5.1.2. Riccati-Bass diffusion function 5.2. The role of calcium in force and fatigue in paralyzed muscle 126 5.2.1. An early model of calcium current in skeletal muscle 5.2.2. The relationship of calcium-troponin binding, calcium channel activation, and voltage sensitivity to force generation in paralyzed muscle 5.2.3. The roles of inactivation of excitationcontraction coupling and voltage sensitivity in decreased force-generating ability, and increased fatigability, in paralyzed muscle 6. METHODS 6.1.