Muscles-Archilles Tendonitis

1. DESCRIPTION AND FUNCTION OF MUSCLES

A muscle is a primary tissue consisting predominantly of highly specialized contractile cells which may be classified as skeletal muscle, cardiac muscle, or smooth muscle.

The skeletal muscles are the effector organs of the locomotor system. They are under voluntary control, although much of their activity is subconsciously regulated. Skeletal muscle and cardiac muscle are both described as striated muscle because of their striped microscopic appearance. This appearance results from the ordered and regular arrangement of the sub-cellular contractile elements. Unlike cardiac muscle, skeletal muscle has no intrinsic spontaneous activity because it lacks the ion channels responsible for spontaneous membrane depolarization. Therefore, the stimulus for physiological skeletal muscle activity is always derived from a nerve impulse. The great majority of skeletal muscle fibers receive their nerve inputs at single central swellings of the fibres known as motor endplates. A few muscles, notably some of the facial muscles, are more diffusely innervated along the length of their fibres; such multifocal innervation may explain why these muscles respond with a more pronounced initial increase in tension after administration of succinylcholine.

However, irrespective of the type of innervation, the charge density arriving at the motor nerve terminal is insufficient to directly activate the much larger muscle fibres. The electrical neuronal impulse is amplified at the neuromuscular junction, the mechanism of which is beyond the remit of this review. The resulting generation of the endplate potential is the first step in muscle contraction.

KEY POINTS TO NOTE:

Skeletal muscle constitutes 40% of muscle mass. Derangement of muscle function can have profound systemic effects.

Physiological skeletal muscle contraction requires generation and spread of a membrane action potential, transduction of the electrical energy into an intracellular chemical signal that, in turn, triggers myofilament interaction.

Intracellular cytoskeletal proteins, cell membrane structures and the associated glycoprotein extracellular matrix are important for maintenance of cell architecture and force transmission.

Smooth and graded changes in force of contraction are achieved through summation of responses to successive stimuli and recruitment of motor units.

Sustained muscle contraction requires de novo synthesis of ATP, which is principally aerobic or anaerobic depending on muscle fibre type.

2. EFFECT OF AGE ASSOCIATED WITH MUSCLES

As the body ages, the size and power of all muscle tissues decrease. The effects on the muscular system can be summarized as follows:

* Skeletal muscle fibers become smaller in diameter. This reduction in size reflects primarily a decrease in the number of myofibrils. In addition, the muscle fibers contain smaller ATP, CP, and glycogen reserves and less myoglobin. The overall effect is a reduction in skeletal muscle size, strength, and endurance, combined with a tendency to fatigue rapidly. Because cardiovascular performance also decreases with age, blood flow to active muscles does not increase with exercise as rapidly as it does in younger people. These factors interact to produce decreases in anaerobic and aerobic performance of 30-50 percent by age 65.

* Skeletal muscles become less elastic. Aging skeletal muscles develop increasing amounts of fibrous connective tissue, a process called fibrosis. Fibrosis makes the muscle less flexible, and the collagen fibers can restrict movement and circulation.

* Tolerance for exercise decreases. A lower tolerance for exercise results in part from the tendency for rapid fatigue and in part from the reduction in thermoregulatory ability. Individuals over age 65 cannot eliminate the heat their muscles generate during contraction as effectively as younger people can and thus are subject to overheating.

* The ability to recover from muscular injuries decreases. The number of satellite cells steadily decreases with age, and the amount of fibrous tissue increases. As a result, when an injury occurs, repair capabilities are limited. Scar tissue formation is the usual result.

Age-related muscle loss is also called sarcopenia, which means "vanishing flesh." The rate of decline in muscular performance is the same in all individuals, regardless of their exercise patterns or lifestyle. Therefore, to be in good shape late in life, you must be in very good shape early in life. Regular exercise helps control body weight, strengthens bones, and generally improves the quality of life at all ages. Extremely demanding exercise is not as important as regular exercise. In fact, extreme exercise in the elderly can damage tendons, bones, and joints. Although it has obvious effects on the quality of life, there is no clear evidence that exercise prolongs life expectancy.

3. HOW POOR DIET AND LACK OF EXERCISE AFFECT MUSCLES

It's no surprise that exercise has numerous benefits such as keeping off excess weight, making your bones strong and keeping your heart healthy, but not exercising can actually make your bones and some organs weaker. Lack of exercise can also cause you to gain weight and develop a variety of obesity-related medical conditions such as high cholesterol, diabetes and hypertension.

Muscle Atrophy

Muscle atrophy is the medical term that describes the process of your muscles breaking down or wasting away. When your muscles aren't exercised to their full capacity, they begin to break down, according to the American Council on Exercise. Not only do you lose lean muscle, you gain fatter tissue after your muscle has broken down. Muscle burns fat, but when your body doesn't have muscle, your metabolism slows and you begin to gain even more fat.

Inactivity on the job, inactivity at leisure and decreased activity with age all contribute to loss of muscle mass and muscle tone. Despite the fact that some muscle atrophy occurs naturally with age, even this can be significantly offset with exercise, especially weight-lifting exercises. Immobilization, such as that imposed by a severely broken limb or limbs, also can lead to disuse atrophy.

Mechanism Behind Atrophy

The physiological mechanisms that cause the decrease in muscle mass and water retention due to disuse are not entirely understood, as put forth by Wilmore's "Physiology

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