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Although performance-enhancing substances often do improve performance, most are banned by governing bodies in sports and are illegal for nonmedical purposes. Their use to enhance performance raises ethical issues of cheating because they give users an unfair advantage over nonusers. A greater concern, however, is that their use carries serious health risks. The side effects of these substances are often significant, nonreversible, and in some cases fatal. The physiological strain caused by these substances is often greater than what the body can handle, leading to effects that are unpredictable and dangerous. Anabolic steroid use has been linked to infertility, aggressive behavior, cardiovascular disease, and brain cancer.

Similarly, some athletes have used creatine to increase power output. Creatine phosphate provides quick bursts of ATP to muscles in the initial stages of contraction. Increasing the amount of creatine available to cells is thought to produce more ATP and therefore increase explosive power output, although its effectiveness as a supplement has been questioned.

Everyday connection

Aging and muscle tissue

Although atrophy due to disuse can often be reversed with exercise, muscle atrophy with age, referred to as sarcopenia, is irreversible. This is a primary reason why even highly trained athletes succumb to declining performance with age. This decline is noticeable in athletes whose sports require strength and powerful movements, such as sprinting, whereas the effects of age are less noticeable in endurance athletes such as marathon runners or long-distance cyclists. As muscles age, muscle fibers die, and they are replaced by connective tissue and adipose tissue ( [link] ). Because those tissues cannot contract and generate force as muscle can, muscles lose the ability to produce powerful contractions. The decline in muscle mass causes a loss of strength, including the strength required for posture and mobility. This may be caused by a reduction in FG fibers that hydrolyze ATP quickly to produce short, powerful contractions. Muscles in older people sometimes possess greater numbers of SO fibers, which are responsible for longer contractions and do not produce powerful movements. There may also be a reduction in the size of motor units, resulting in fewer fibers being stimulated and less muscle tension being produced.

Atrophy

This image shows muscle atrophy. The left panel shows normal muscle and the right panel shows atrophied muscle.
Muscle mass is reduced as muscles atrophy with disuse.

Sarcopenia can be delayed to some extent by exercise, as training adds structural proteins and causes cellular changes that can offset the effects of atrophy. Increased exercise can produce greater numbers of cellular mitochondria, increase capillary density, and increase the mass and strength of connective tissue. The effects of age-related atrophy are especially pronounced in people who are sedentary, as the loss of muscle cells is displayed as functional impairments such as trouble with locomotion, balance, and posture. This can lead to a decrease in quality of life and medical problems, such as joint problems because the muscles that stabilize bones and joints are weakened. Problems with locomotion and balance can also cause various injuries due to falls.

Chapter review

Hypertrophy is an increase in muscle mass due to the addition of structural proteins. The opposite of hypertrophy is atrophy, the loss of muscle mass due to the breakdown of structural proteins. Endurance exercise causes an increase in cellular mitochondria, myoglobin, and capillary networks in SO fibers. Endurance athletes have a high level of SO fibers relative to the other fiber types. Resistance exercise causes hypertrophy. Power-producing muscles have a higher number of FG fibers than of slow fibers. Strenuous exercise causes muscle cell damage that requires time to heal. Some athletes use performance-enhancing substances to enhance muscle performance. Muscle atrophy due to age is called sarcopenia and occurs as muscle fibers die and are replaced by connective and adipose tissue.

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Source:  OpenStax, Anatomy & Physiology. OpenStax CNX. Feb 04, 2016 Download for free at http://legacy.cnx.org/content/col11496/1.8
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