Fiber number

Muscle fibers may be counted directly in small muscles or large muscles that have been longitudinally subdivided. In the large muscles of the carcass, fiber numbers may be estimated indirectly from representative samples but it is unlikely that the apparent number of fibers in a cross section will include all the real number of fibers in the whole muscle. This discrepancy may be caused by both fascicular arrangement and the presence of intrasfascicularly terminating fibers. MacCallum (a really bright guy) first demonstrated this problem in 1898 with reference to the determination of myoblast numbers in embryonic muscle, but the same principle exists in adult animals with intrafascicularly terminating muscle fibers.


Bendall (another really bright guy and great drinking companion, now sadly missed) estimated apparent fiber numbers in longissimus dorsi and semitendinosus muscles of Hereford and Friesian steers from 11 days to 2 years of age. The longissimus dorsi started with 75% of the peak postnatal number which was reached at 5 months. After 5 months, numbers declined sharply and later reached 50% of the peak number at 2 years. The semitendinosus started with its peak fiber number at 11 days, and then steadily lost fibers to drop below 60% of the initial peak number at 2 years. My guess is that most breeds would show similar changes, depending on frame size.

Double-muscled cattle

For many years, cattle with greatly enlarged muscles and a scarcity of adipose tissue have caught the attention of beef producers. The large superficial muscles of the shoulder and proximal hindlimb often are more enlarged than the distal limb muscles or deep muscles of the carcass. The condition has been given a number of other colloquial names apart from double-muscling, such as: doppellender (Germany), muscular hypertrophy (a misleading name), a groppa doppia (Italy), and culard (France).

The effect of double muscling on meat flavor and overall acceptibility usually is minor, if detectable at all.

Although the greatly increased yield of lean meat in double muscled animals is of considerable interest commercially, there is a long list of disadvantages and physiological abnormalities associated with the condition. These abnormalities do not necessarily prohibit the exploitation of double muscling, but they explain many of the past failures that have otherwise gone unrecorded.

This list looks terrible! But it's not really that bad. These are problems that should not be ignored, not problems that cannot be beaten.

The genetic basis of the condition is a single pair of autosomal genes. Heterozygous animals may range from normal to extremely double muscled phenotypes. Incomplete dominance, incomplete penetrance and modifier genes are the usual explanations proposed to explain the phenotypic range of heterozyous animals, but it is difficult to locate any proof that the range is due solely to genetic interactions at the DNA level. The gene for double muscling is also pleiotropic, and affects the numerous physiological and anatomical systems listed above. The expressivity of double muscling in heifers may be affected by their plane of nutrition. It is equally plausible, therefore, that incomplete dominance and pleiotropy might be a result of epigenetic interactions. Epigenetics is the science concerned with the causal analysis of development: it encompasses genetic interactions that are mediated by the interactions of gene products in the cells of the body tissues.

Double muscling is caused primarily by an increase in the apparent number of muscle fibers. As far as is known at present, the increase in apparent fiber numbers is based on an increase in real fiber numbers as well, but nothing is known for certain about the epigenetic development of double-muscling. The pleiotropic nature of the single gene involved, together with the considerable involvement of various types of connective tissues, suggests that the development of double-muscling may involve a shift in the programmed sequence of muscle cell differentiation. Since adipose cells and fibroblasts are both deficient in double-muscled cattle, an increase in the number of myoblasts appears to have been made at the expense of the fibroblast stem-cell population. Genes have been identified that may cause just such a shift. In addition to hyperplasia of extrafusal muscle fibers, double muscled cattle also may have an increase in the number of the intrafusal fibers in their neuromuscular spindles.


A problem with many studies on fiber numbers in porcine longissimus dorsi muscles is that they relate to apparent fiber numbers, not to real fiber numbers. If whole longissimus dorsi muscles are subdivided and the total apparent numbers of fibers is found, only a small, variable fraction (6 to 12%) of the total apparent number appears in the longissimus dorsi when it is transected in a single pork chop. Thus, factors that change the magnitude of this fraction are superimposed on what at first sight appears to be the number of fibers in the muscle. And the factor that causes most concern, since it varies postnatally, is muscle fiber length.

At the midlength of sartorius muscles of pigs, apparent fiber numbers may increase throughout fetal development and onwards during growth to market weight. Furthermore, if body growth is arrested by a low plane of nutrition, the increase in apparent fiber numbers is stopped or reversed.

However, there are other opinions on the subject apart from mine. There is a considerable difference of opinion on the interpretation of data on fiber numbers. One school of thought considers that real and apparent fiber numbers are fixed after birth. Another school considers that real fiber numbers reach their maximum early in development and that increases in fiber number after the neonatal period are restricted to changes in apparent numbers. A third school considers that both real and apparent numbers of fibers may continue to increase by the formation of new fibers for several years after birth. We should by now have reached agreement on this important point, but we have not. I support the second school of thought, but readers must judge for themselves, paying particular attention to sources of technical error in the original methodologies.


Sir John Hammond in 1932 speculated that muscle fiber numbers in some breeds of sheep had increased as a result of selective breeding for increased meat yield. One of his students was unable to account for the greater muscularity of male lambs relative to females on the basis of differences in fiber diameter and concluded that males had more muscle fibers. But, more recently. it has been shown that male lambs do develop larger diameter fibers than females when they reach live weights of 58.5 kg. It is quite likely that differences in fiber number are involved in explaining differences in muscularity between breeds of sheep, but there is no hard evidence that I am aware of yet (please e-mail me if you know of any!). Competition between twin and triplet fetuses produces a similar effect to a low maternal plane of nutrition and reduces apparent fiber numbers in sartorius muscles. Double-muscling has been reported in sheep, but it is very rare.


Differences in fiber numbers may account for differences in muscularity between breeds and types of poultry, but numbers may change after hatching, probably because of changes in the length of intrafascicularly terminating muscle fibers.