Organ Systems Physiological Changes: Skeletal Muscle
Forty percent of the body mass is made up of some three hundred and fifty skeletal muscles with each muscle composed of hundreds of thousands of cells, termed fibers. Each fiber consists of overlapping thick and thin protein filaments organized longitudinally in repeating patterns. Muscle fibers have the unique capacity to utilize energy in the form of adenosine triphosphate (ATP) to force the thick and thin filaments to slide past one another and contract, or shorten (Vander et al.). The fibers in each muscle are organized in motor units composed of a motor nerve and the branches of the nerve to individual muscle fibers. Motor units range in size from only a few fibers for units required for fine motor control of fingers or eyes to many hundreds of fibers for control of large movements of arms, legs, or torso. Within a single motor unit, all of the fibers are of the same type: slow-fatigue resistant (SFR), fast-fatigue resistant (FFR), or fast-fatigable (FF). The designation of motor units as fast or slow is based on the velocity of shortening of the fibers with FF units contracting four times faster than SFR units and FFR units intermediate between the other two (Kadhiresan et al.). Consequently, for a given mass of muscle, FF units are four times as powerful as units.
The fatigability of fibers is a function of the rate of energy use (power) and the rate of energy production. For muscle fibers, the mitochondrial density in a fiber and the rate of delivery of oxygen to the fiber determines the rate of energy production (ATP). FF fibers fatigue quickly, because they develop high power, but have low rates of energy production. SFR fibers have a high level of endurance (low fatigability) with low power, but relatively high energy production. FFR fibers are intermediate in both categories. The contractions of individual muscles are controlled in intensity and duration by signals, termed action potentials, from the motor cortex of the brain (Vander et al.).
From birth to maturity, skeletal muscles become larger, stronger, more powerful, and more resistant to fatigue. These dramatic changes occur with no change in fiber number, but an increase in the fiber length, cross-sectional area of fibers, and the type of myosin in the thick filaments. During adulthood, atrophy and weakness may develop due to physical inactivity, immobilization by casting, bed rest, or diseases of muscle, such as muscular dystrophy (Grimby; Svanborg). Throughout the life span, an increase in physical activity will overcome the consequences of physical inactivity, but beyond forty years of age, even physically active people experience some degree of muscle atrophy, weakness, increased fatigability, and an increased susceptibility to injury (Faulkner et al.). After sixty-five years of age, the rate of decline accelerates dramatically. The losses in the structure and function of muscles associated with aging appear to be largely immutable in their progression and irreversible. In fact, beyond forty years of age the rates of decline in a wide variety of performances by highly conditioned athletes and unconditioned subjects show similar rates of decline (Holloszy).
For healthy eighty and ninety year olds, the decrease in muscle mass of approximately fifty percent results from a loss in the total number of fibers per muscle as well as a decrease in the mean cross-sectional area (CSA) of the remaining fibers (Lexell; Nair). Aging involves the progressive loss of whole FF motor units and denervation and subsequent loss of fibers in both FF and FFR motor units. Some of the denervated fast fibers are reinnervated by slow axons. For SR units, no change occurs in the number of motor units, but the number of fibers within SR motor units increases several-fold in old animals (Kadhiresan et al.). As a result of the motor unit remodeling, the proportion of slow to fast fibers increases considerably in muscles of old animals. The cause of the loss in motor units or the loss of fibers from within motor units is not known, but the immutable loss of fibers, frequently coupled with fiber atrophy, explain the loss of muscle mass with aging. Conditioning programs that maintain, or even increase, mean CSA of the remaining fibers can slow the atrophy to some extent (Grimby).
Maximum isometric force is developed by maximal activation of a muscle held at optimum length for force development. Maximum specific force (kN/m 2) is the maximum force normalized by the total muscle fiber cross-sectional area (CSA). The specific force developed by control muscles of adult animals is ~280 kN/m 2 (Faulkner et al.). For muscles of the oldest-old, compared with adult rats, the maximum force has decreased by 65 percent and the specific force by 46 percent. A lower specific force indicates a greater loss in force than in CSA. The weakness of muscles in old animals results in part from the presence of denervated fibers, as well as fibers with impaired force development. Less direct data on human beings are consistent with the data on rodents. The cause of the impaired force developed within single fibers of old animals has not been fully explained (Faulkner et al.). Absolute and normalized (watts/kg of muscle mass) power, a function of both force and velocity, are impaired to an even greater extent than force alone. For muscles in old compared with young animals, the greater impairment in power than in force alone arises from the greater proportion of slow fibers in muscles of old animals.
Muscles can be injured by their own contractions. Activities that require muscles to be stretched during contractions are most likely to injure muscles. The initial injury, which is mechanical in nature, is followed by a more severe inflammatory and free radical damage that result in late onset muscle soreness (Faulkner et al.). Throughout the life span, skeletal muscles are constantly undergoing contraction-induced injury of varying severity. In young active animals, muscle fibers are relatively resistant to injury and following injuries recover effectively, whereas fibers in muscles of old animals are more easily injured and recovery may be incomplete resulting in loss of fibers, muscle atrophy, and weakness (Faulkner et al.). Most activities include some stretching of muscles during contractions, but even in old animals, conditioning can protect muscles from injury.
With aging, skeletal muscle atrophy, weakness, fatigability, and injury impair performance of the activities of daily living, increase the incidence of falls and accidents, and impact the quality of life of old people (Holloszy). The degree to which these specific conditions are preventable or treatable is not known. Despite the lack of definitive answers to many questions regarding these conditions, the longer people can be motivated to maintain a physically active lifestyle, including brisk walking and the lifting of modest free weights, the higher will be the quality of their life in old age (Holloszy).
JOHN A. FAULKNER SUSAN V. BROOKS
FAULKNER, J. A.; BROOKS, S. V.; and ZERBA, E. "Muscle Atrophy and Weakness with Aging: Contraction-Induced Injury as and Underlying Mechanism." Journal of Gerontology 50 (1995): 124–129.
GRIMBY, G. "Muscle Performance and Structure in the Elderly as Studied Cross-sectionally and Longitudinally." Journal of Gerontology 50A (1995): 17–22.
HOLLOSZY, J. "Sarcopenia: Muscle Atrophy in Old Age." Journal of Gerontology 50A (1995A): 1–161.
KADHIRESAN, V. A.; HASSETT, C.; and FAULKNER, J. A. "Properties of Single Motor Units in Medial Gastrocnemius Muscles of Adult and Old Rats." Journal of Physiology (London) 493 (1996): 543–552.
LEXELL, J. "Human Aging, Muscle Mass, and Fiber Type Composition." Journal of Gerontology 50A (1995): 11–16.
NAIR, K. S. "Muscle Protein Turnover: Methodological Issues and the Effect of Aging." Journal of Gerontology 50A (1995): 107–112.
SVANBORG, A. "A Medical-social Intervention in a 70-year-old Swedish Population: Is It Possible to Postpone Functional Decline in Aging?" Journal of Gerontology 48 (1993): 84–88.
VANDER, A.; SHERMAN, J.; and LUCIANO, D. Human Physiology: The Mechanisms of Body Function, 8th ed. New York: McGraw Hill, 2001.
PHYSIOLOGICAL CHANGES: ORGAN SYSTEMS, SKIN
- Physiological Changes: Stem Cells - Embryonic Development And Mesengenesis, Adult Tissues, Bone Repair, Mesenchymal Stem Cell Numbers, Mesenchymal Stem Cells And Future Aging Therapies
- Organ Systems Physiological Changes: Cardiovascular - Heart Structure And Function At Rest, Reserve Capacity Of The Heart, Vascular Structure And Function At Rest
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