How does a muscle grow? First take a closer look at a slice of muscle tissue taken from your arm or leg, you'd see that it's made up of many smaller muscle fibers. Each fiber constitutes one muscle cell. A large fiber is comparable in thickness to that of a fine human hair. Smaller fibers cannot be seen by the naked eye.
Filling the inside of these fibers are myofibrils. Deeper inside the muscle, you'll find the myofibrils' tiny component units, called sarcomeres. Within each sarcomere are many proteins, including myosin, actin, troponin and several others. They're linked end to end to make up a myofibril.
Muscles get bigger when these individual fibers become thicker. This is called hypertrophy. One way this is caused is by the creation of new myofibrils. Myofibrillar hypertrophy describes the enlargement of the muscle fiber as it gains more myofibrils and, correspondingly, more actin and myosin. In an extremely complex process that is still poorly understood, the stress that exercise exerts on tendons and other structures connected to the muscle cause the muscle cells to make more proteins.
To produce all this protein requires more nuclei. Genes are located in the nuclei, which are the brain centers of cells. Muscle cells, unlike most cells in the body, contain many nuclei. This increases their capacity to produce more proteins. The new nuclei are donated by satellite cells. Satellite cells proliferate in response to the stresses and wear and tear of exercise. Scientists think that exercise inflicts tiny microtears in muscle fibers, which attracts satellite cells.
Satellite cells incorporate themselves into the muscle tissue and begin producing proteins to fill the gap. Their nuclei become indistinguishable from the muscle cell's other nuclei. With these additional nuclei, the fiber is able to produce more proteins and create more myofibrils. Gradually, as more microtears are repaired in this manner, the muscle fiber grows. Some researchers believe that sarcoplasmic hypertrophy also occurs. The sarcoplasm is the fluid part of the muscle fiber in which the myofibrils are embedded. Sarcoplasmic hypertrophy is characterized by the growth of sarcoplasm and noncontractile proteins that don't contribute directly to the production of muscle force. Myofibrillar hypertrophy is typically found in elite weight lifters, whereas sarcoplasmic hypertrophy is typically seen in bodybuilders.
Although it's still an active area of research, some researchers believe that hyperplasia — an increase in the number of muscle fibers — also makes a contribution to gains in muscle size. But it's extremely difficult to determine the extent to which fiber size and fiber number contributes to muscle growth. See:
Kadi, F., Bonnerud, P., Eriksson, A., & Thornell, L.E. (2000). The expression of androgen receptors in human neck and limb muscles: effects of training and self-administration of androgenic-anabolic steroids. Histochemistry and Cell Biology, 113, 25-29
Kadi F, Eriksson A, Holmner S, Butler-Browne GS, Thornell LE. (1999). Cellular adaptation of the trapezius muscle in strength-trained athletes. Histochemistry and Cell Biology, 111, 189-195
Kadi, F., Eriksson, A., Holmner, S., & Thornell, L.E. (1999). Effects of anabolic steroids on the muscle cells of strength-trained athletes. Medicine and Science in Sports and Exercise, 31, 1528-1534
Russell, B., Motlagh, D., & Ashley, W.W. (2000). Form follows function: how muscle shape is regulated by work. Journal of Applied Physiology, 88, 1127-1132
Filling the inside of these fibers are myofibrils. Deeper inside the muscle, you'll find the myofibrils' tiny component units, called sarcomeres. Within each sarcomere are many proteins, including myosin, actin, troponin and several others. They're linked end to end to make up a myofibril.
Muscles get bigger when these individual fibers become thicker. This is called hypertrophy. One way this is caused is by the creation of new myofibrils. Myofibrillar hypertrophy describes the enlargement of the muscle fiber as it gains more myofibrils and, correspondingly, more actin and myosin. In an extremely complex process that is still poorly understood, the stress that exercise exerts on tendons and other structures connected to the muscle cause the muscle cells to make more proteins.
To produce all this protein requires more nuclei. Genes are located in the nuclei, which are the brain centers of cells. Muscle cells, unlike most cells in the body, contain many nuclei. This increases their capacity to produce more proteins. The new nuclei are donated by satellite cells. Satellite cells proliferate in response to the stresses and wear and tear of exercise. Scientists think that exercise inflicts tiny microtears in muscle fibers, which attracts satellite cells.
Satellite cells incorporate themselves into the muscle tissue and begin producing proteins to fill the gap. Their nuclei become indistinguishable from the muscle cell's other nuclei. With these additional nuclei, the fiber is able to produce more proteins and create more myofibrils. Gradually, as more microtears are repaired in this manner, the muscle fiber grows. Some researchers believe that sarcoplasmic hypertrophy also occurs. The sarcoplasm is the fluid part of the muscle fiber in which the myofibrils are embedded. Sarcoplasmic hypertrophy is characterized by the growth of sarcoplasm and noncontractile proteins that don't contribute directly to the production of muscle force. Myofibrillar hypertrophy is typically found in elite weight lifters, whereas sarcoplasmic hypertrophy is typically seen in bodybuilders.
Although it's still an active area of research, some researchers believe that hyperplasia — an increase in the number of muscle fibers — also makes a contribution to gains in muscle size. But it's extremely difficult to determine the extent to which fiber size and fiber number contributes to muscle growth. See:
Kadi, F., Bonnerud, P., Eriksson, A., & Thornell, L.E. (2000). The expression of androgen receptors in human neck and limb muscles: effects of training and self-administration of androgenic-anabolic steroids. Histochemistry and Cell Biology, 113, 25-29
Kadi F, Eriksson A, Holmner S, Butler-Browne GS, Thornell LE. (1999). Cellular adaptation of the trapezius muscle in strength-trained athletes. Histochemistry and Cell Biology, 111, 189-195
Kadi, F., Eriksson, A., Holmner, S., & Thornell, L.E. (1999). Effects of anabolic steroids on the muscle cells of strength-trained athletes. Medicine and Science in Sports and Exercise, 31, 1528-1534
Russell, B., Motlagh, D., & Ashley, W.W. (2000). Form follows function: how muscle shape is regulated by work. Journal of Applied Physiology, 88, 1127-1132
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