There is a long-time discussion going on among scientists, coaches and athletes about the nature of muscle growth in humans.
One school of thought claims that increases in the lean muscle mass are only from increased thickness of individual muscle fibers (hypertrophy).
The competing opinion claims that human muscle fibers are basically of the same size in trained and untrained individuals and that the increased number of fibers is the reason of muscle mass increases.
Strangely enough, scientific research is inconclusive.
The 1994 paper by Abernethy & colleagues states that: “Increments in the cross-sectional area of muscle after resistance training can be primarily attributed to fibre hypertrophy. However, there may be an upper limit to this hypertrophy. Furthermore, significant fibre hypertrophy appears to follow the sequence of fast twitch fibre hypertrophy preceding slow twitch fibre hypertrophy. Whilst some indirect measures of fibre number in living humans suggest that there is no interindividual variation, postmortem evidence suggests that there is. There are also animal data arising from investigations using resistance training protocols which suggest that chronic exercise can increase fibre number. Furthermore, satellite cell activity has been linked to myotube formation in the human. However, other animal models (i.e. compensatory hypertrophy) do not support the notion of fibre hyperplasia. Even if hyperplasia does occur, its effect on the cross-sectional area of muscle appears to be small.”
Studies supporting the hyperplasia theory
1997 paper by Tamaki & colleagues (http://ajpcell.physiology.org/content/273/1/C246.short ) concludes that after resistance training, muscle hyperplasia occurred in rats.
In 1999, Fawzi Kadi & colleagues published a study concluding that “The presence of small diameter fibres expressing markers for early myogenesis indicates the formation of new muscle fibres.” This statement was based on the observation of the biopsies of ten elite power lifters and a control group of untrained males. (http://www.springerlink.com/content/t1yk0cm2pacx3yr7/ )
In 1988 a team of scientists led by H.J. Appell of the German Sports University, Cologne, took biopsies from persons subject to 6 week-long aerobic training on stationary bicycle. The conclusion was that: “In some cases very small myofibers with central nuclei were found. At the ultrastructural level, these fibers turned out to be myotubes. The satellite cells occasionally appeared to be activated and to fuse with muscle fibers. It was concluded that these observations represented evidence for the development of new muscle fibers.” (http://www.ncbi.nlm.nih.gov/pubmed/3182162 )
In 1986, W.J. Gonyea & colleagues published the results of their study with cats. The animals were subject to resistance exercise of one leg only for 101 weeks. At the end of this period, the trained leg had 9% more muscle fibers than the untrained leg. (http://www.springerlink.com/content/h18807t1286807l2/ ) The results of this study were confirmed by another study by Giddings and Gonyea in 1992. (http://onlinelibrary.wiley.com/doi/10.1002/ar.1092330203/abstract )
P.A. Tesch and L. Larsson observed biopsies of bodybuilders and weight lifters. Their paper, published in 1982 is considered by some as a proof that hyperplasia takes place in trained human muscle. (http://www.ncbi.nlm.nih.gov/pubmed/6890445 )
Studies supporting the hypertrophy theory
In their 1984 article Muscle fiber number in biceps brachii in bodybuilders and control subjects, J.D. MacDougall & colleagues came to conclusion that no hyperplasia takes place in human muscle: “We conclude that in humans, heavy resistance training directed toward achieving maximum size in skeletal muscle does not result in an increase in fiber numbers.” The study calculated mean fibre area and collagen volume density from needle biopsies of three groups: top bodybuilders, intermediate bodybuilders and untrained males. (http://jap.physiology.org/content/57/5/1399.short )
A paper by Taylor and Wilkinson published in 1986 (Exercise-induced skeletal muscle growth. Hypertrophy or hyperplasia?) also states: “It was concluded that hyperplasia is not yet substantiated, and that new fibres, if present, may be the result of the development of satellite cells.”
The reason why some other studies concluded that hyperplasia does occur is – according to authors – incorrect counting of muscle fibers: “In studies of muscle cross-sectional area, errors are created by fibres terminating intrafascicularly. Longitudinal growth of such fibres result in an overestimation of fibre number, and with the use of penniform muscles where fibres do not run parallel to the longitudinal axis of the muscle, the error is compounded.” (http://www.ncbi.nlm.nih.gov/pubmed/3520748 )
George Kelley published a meta-analysis in 1996 on muscle hyperplasia in animals. 17 different studies had been analyzed and following conclusion drawn: “The results of this study suggest that in several animal species certain forms of mechanical overload increase muscle fiber number.”
As for muscle hyperplasia in humans, no such authoritative paper exists. It seems we will live in darkness for another couple of years until the final word will be said on this topic.