Growth is defined as an increase in tissue mass. Mass increases by hyperplasia early in life and hypertrophy later in life, although hyperplasia of adipose tissue continues throughout life. The growth curve, being mass or cumulative weight plotted against age, is sigmoid, consisting of a prepubertal accelerating phase plus a postpubertal decelerating phase. Mathematically, this curve can be described as a function of mature mass, fractional growth rate, and age. At a specific fraction of mature mass, body composition seems to be constant, but the degree to which nutrition can alter mature mass is not certain. If mature mass is altered, body composition at any given mass will be altered. Mature mass can be decreased by starvation or protein deficiency early in life. Alternatively, retarding the deposition of fat or the administration of estrogenic compounds may increase mature protein mass. Many of the advances in rate and efficiency of growth and in reduced fat of meat cuts can be explained by increased mature protein mass of ruminants. Animals with higher mature weight require more energy for maintenance and reach puberty later in life, so a larger mature mass is not desirable for the breeding herd. Indeed, smaller replacement heifers would prove economical if reproduction were not decreased. A period of restricted growth and fat deposition (as on pasture) can increase the slaughter weight of small cattle into a more desirable range, presumably through increasing mature protein mass. However, calves with retarded growth often make less efficient feedlot gains than do calves finished immediately after being weaned. For growing large-framed heifers, pasture alone often provides an inadequate energy supply for early puberty, but excessive amounts of supplemental feed can enhance fat deposition in the udder, which subsequently decreases milk production. By manipulating the supply of specific nutrients and hormones, it may prove feasible in the future to reduce fat deposition in specific tissues and to alter mature body protein mass.

Digesta markers are used routinely to calculate fecal output and to estimate kinetics within the digestive tract. A marker suitable for estimating fecal output may not be a suitable kinetic marker because of problems with marker migration, phase separation, inhibition of digestion, osmotic effects within the gut, and quantitation. Marker validity should be checked when possible based on alternative methods (e.g., fecal output and ruminal evacuation). Certain parameters, such as pool size and passage rate, that can be estimated with markers cannot be measured by other noninvasive procedures. Nevertheless, only when marker results are verified by other methods can one evaluate the magnitude of error associated with assumptions inherent in marker mathematics (steady state, instantaneous mixing, and first-order kinetics). When marker results do not meet expectations, marker failure, rather than inadequate knowledge of gastrointestinal function or analytical difficulties, is blamed. No marker is ideal, but research to compare markers is useless if results are not related to direct flow or output measurements. Marker results often are adjusted for marker recovery based on the premise that analysis is precise and that losses are constant. Such adjustment is appropriate only if the error is analytical and proportional. Despite imprecision in marker procedures, inherent variation may be small relative to other sources of variation (e.g., gut physiology, diet, environment, and feed intake). Even though absolute values may be imprecise and inaccurate, marker-based estimates usually provide reliable information about the direction and extent of kinetic changes induced by treatments.

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