Types Of Muscle Hypertrophy
Muscle hypertrophy can be considered distinct and separate from muscle hyperplasia. During hypertrophy, contractile elements enlarge and the extracellular matrix expands to support growth. This is in contrast to hyperplasia, which results in an increase in the number of fibers within a muscle.
Contractile hypertrophy can occur either by adding sarcomeres in series or in parallel. The majority of exercise-induced hypertrophy subsequent to traditional resistance training programs results from an increase of sarcomeres and myofibrils added in parallel. When skeletal muscle is subjected to an overload stimulus, it causes perturbations in myofibers and the related extracellular matrix. This sets off a chain of myogenic events that ultimately leads to an increase in the size and amounts of the myofibrillar contractile proteins actin and myosin, and the total number of sarcomeres in parallel. This, in turn, augments the diameter of individual fibers and thereby results in an increase in muscle cross-sectional area. A serial increase in sarcomeres results in a given muscle length corresponding to a shorter sarcomere length.
Inseries hypertrophy has been shown to occur when muscle is forced to adapt to a new functional length. This is seen with limbs that are placed in a cast, where immobilization of a joint at long muscle lengths results in an increased number of sarcomeres in series, whereas immobilization at shorter lengths causes a reduction.
There is some evidence that certain types of exercise can affect the number of sarcomeres in series. Lynn and Morgan showed that when rats climbed on a treadmill (i.e., incline), they had a lower sarcomere count in series than those who descended (i.e., decline). This suggests that repeated eccentric-only actions lead to a greater number of sarcomeres in series, whereas exercise consisting solely of concentric contractions results in a serial decrease in sarcomere length.
It is hypothesized that hypertrophy may be augmented by an increase in various noncontractile elements and fluid. This has been termed ‘‘sarcoplasmic hypertrophy,’’ and may result in greater muscle bulk without concomitant increases in strength. Increases in sarcoplasmic hypertrophy are thought to be training specific, a belief perpetuated by studies showing that muscle hypertrophy is different in bodybuilders than in powerlifters.
Specifically, bodybuilders tend to display a greater proliferation of fibrous endomysial connective tissue and a greater glycogen content compared to powerlifters, presumably because of differences in training methodology. Although sarcoplasmic hypertrophy is often described as nonfunctional, it is plausible that chronic adaptations associated with its effects on cell swelling may mediate subsequent increases in protein synthesis that lead to greater contractile growth.
Some researchers have put forth the possibility that increases in cross-sectional area may be at least partly because of an increase in fiber number. A meta-analysis by Kelley found that hyperplasia occurs in certain animal species under experimental conditions as a result of mechanical overload. Increases in muscle fiber number were greatest among those groups that used an avian vs. a mammalian model, and stretch overload yielded larger increases in fiber count than exercise. However, subsequent research suggests that such observations may be erroneous, with results attributed to a miscounting of the intricate arrangements of elongating fibers as a greater fiber number. Evidence that hyperplasia occurs in human subjects is lacking and, if it does occur at all, the overall effects on muscle cross-sectional area would appear to be minimal.
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