Factors that alter the growth and development of ruminants.

F N Owens, P Dubeski and C F Hanson

J ANIM SCI 1993, 71:3138-3150.

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Factors that Alter the Growth and Development of Ruminants1f2

F. N. Owens*, P. Dubeski"~3,and C. F. Hansont
Departments of *Animal Science and +Nutritional Science, Oklahoma State University,
Stillwater 74078

ABSTRACT:

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 ( a s 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.

Key Words: Growth, Body Composition, Beef Cattle, Hormones

J. h i m . Sci. 1993. 71:3138-3150

Introduction
Animal growth has been the topic of a number of
symposia sponsored by the American Society of
Animal Science (1974, 1987, 1988) and textbooks
(Berg and Butterfield, 1976; Rechcigl, 1981). Although animal growth encompasses many diverse
fields (biochemistry, physiology, endocrinology, genetics, and animal management), this paper will emphasize factors that limit growth, and the effects of

'Presented a t a symposium titled "Raising Replacement Stock

(Dairy, Sheep, Beef) in the South-Birth to Parturition" a t the 1992
Southern Section ASAS Annu. Mtg., Lexington, KY in conjunction
with the SAAS 89th Annu. Mtg. and the Southern Branch ADSA
Annu. Mtg.
'Paper no. 6205 of the Oklahoma Agric. Exp. Sta.
'Present address: National Animal Disease Lab., PO Box 70,
Ames, IA 50010.
Received April 28, 1992.
Accepted June 21, 1993.

growth rate on protein (lean tissue) deposition, the

primary goal of meat animal production. Related
papers at this symposium discussed matching the
quality and quantity of forage produced in the
southern United States to needs for growing
ruminants from birth to puberty.

Definitions
Growth usually is defined as production of new
cells. But because growth typically is measured as an
increase in mass, growth includes not only cell
multiplication (hyperplasia) but also cell enlargement
(hypertrophy) and incorporation of specific components from the environment (e.g., apatite deposition).
By definition, growth includes deposition of fat even
though muscle mass is of primary interest in meat
production. Mature size generally is considered the
point at which muscle mass reaches a maximum.
During embryonic development, all tissues grow by

3138
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RUMINANT GROWTH

hyperplasia, but as mammals mature, specialized cells

(e.g., nerves, skeletal muscle cells) lose their ability
to replicate and grow only by hypertrophy o r incorporation of satellite cells. Other tissues (e.g., blood cell
precursors, hair follicles, gastrointestinal epithelia,
digestive tract organs, ectoderm) continue to divide
throughout life. In humans, DNA measurements
indicate that cells divide 42 times before birth but
only five times postnatally (Batt, 1980). This figure
varies markedly among tissues as noted above. If all
cells replicated once more before birth, dystocia would
be prevalent, but postnatal growth rate and mature
mass probably could be increased greatly!
Net growth is the difference between synthesis and
degradation of body tissue. Both are continuous
processes; total protein synthesis is 6 to 10 times net
retention of protein (Eisemann et al., 1989; Bergen
and Merkel, 1991). Most mammals are born with
nearly their full complement of skeletal muscle fibers.
Muscle hyperplasia occurs primarily prenatally (Allen
et al., 19791, and muscle fiber numbers increase only
slightly postnatally (Bergen and Merkel, 1991).
Postnatal growth of muscle mass occurs through
hypertrophy and through satellite cell replication and
incorporation (Goldspink, 1962, 1968, 1991). Numerous factors have been elucidated that regulate the
number of muscle fibers and of nuclei (Goldspink,
1991).
Certain tissues associated with digestion (e.g.,
gastrointestinal tract and liver) have faster protein
and cell turnover than skeletal muscle does. Fractional protein synthesis in the ruminant gastrointestinal tract ranges from 10 to 30% daily (McBride and
Kelly, 1990) and the digestive tract alone can account
for 28 to 46% of whole-body protein synthesis. By
comparison, half-life for myofibrillar protein generally
ranges from 18 to 50 d (Swick and Song, 1974). Thus,
despite its mass, skeletal muscle may not be the
primary site of protein synthesis even in rapidly
growing ruminants.
Organs and tissues do not mature simultaneously
(Figure 1).Based on relative growth rates of various
tissues, a general gradient in orgadmuscle formation
from head to tail and from extremities t o the core is
apparent. Thus, body shape changes over time;
deposition of certain internal muscle components (e.g.,
loin, intramuscular fat [marbling]) is more extensive
later in life.
Cumulative weight plotted against animal age
follows a sigmoid curve; this curve is composed of the
prepubertal, self-accelerating phase and the postpubertal, self-inhibiting phase (Figure 2 ). Reasons for
deceleration postpubertally are not well understood
despite years of study with isolated muscle or bone
cultures. Transformed muscle cell culture studies
suggest that growth inhibition is due either to a
limitation in resources (space, nutrient supply,
growth factors) or to accumulation of products or

3139

tl

Age, from conception to maturity2

Neck
Eona
Tibia-fibula
Intermuscular far

H M
Enin
M-WS

Kidnav fat

3
Thorax
Muscle
Farnur
Subcuranaourfar

Loin

Far
Pelvis
lnmrnuacularla1

Figure 1. Growth rates of various tissues and various

sites in animals fed for a) rapid or b) slow rates of
growth. The sequence remains the same despite rate of
growth or maturation. Modified from Batt (1980).

inhibitory factor(s) that restrict cell division. Specific

blood serum proteins can stimulate or inhibit in vitro
muscle cell proliferation (Hathaway et al., 1990;
Dayton and Hathaway, 1991). Because growth rate is
retarded when substrate (energy or protein supply) is
limited, some researchers have speculated that growth
deceleration is due simply to reduced intake of energy
above maintenance. However, if this were true, forced
feeding should increase lean body mass of maturing
animals. In most force-feeding studies, protein deposition has not increased. Instead, excess nutrients were
either converted to lipid, excreted, or catabolized. This

1I

c d

[Age;
I

I
I

I
II

Figure 2. Growth curve for lambs showing a

characteristic sigmoid form. Points represent a) conception, b) birth, c) self-accelerating phase, d) inflection
point often associated with puberty, e) self-retarding
phase, and f ) maturity. Modified from Batt (1980).

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3140

OWENS ET AL.

indicates that factors in addition to nutrient supply

must inhibit protein deposition.
Growth must be differentiated from development.
In mammals, chronological, physiological, social, mental, and emotional development proceed at different
rates. Asynchrony among these processes in different
species and individuals makes it difficult to assess
stage of development quantitatively. Based on the
diversity of these indicators of development, it is not
surprising that physiological responses to specific
nutrient deficiencies and environmental factors often
are inconsistent.
Mathematical equations can be developed to characterize growth of individual species, organs, or tissues.
When discussing growth responses and maturity,
measurements and equations must be clearly defined.
For example, the mathematical formula used to
calculate growth rate can alter interpretation of data
(e.g., absolute vs relative growth rate) as discussed
and appraised by Taylor (1980).
Brody ( 1964) developed the classical empirical
equation to predict BW of many different species at
various ages. This equation was based on three
parameters (viz, mature BW, growth deceleration rate
[kl, and age beyond conception [tl). His equation is as
follows: Weight = Mature weight ( 1 - e-kt). Effects of
altering these three factors by 10% from the coefficients defined by Brody (1964) on rate of gain from
200 to 500 kg in Hereford-Shorthorn steers are
presented in Figure 3. An increase in mature weight of
10% will increase daily gain by 15%,whereas decreasing the deceleration factor by 10% will increase daily
gain by 10%.A decrease in the deceleration factor will
increase the rate of maturation as discussed and
modeled by Doren et al. (1989) and Erlinger et al.
(1990).
A heavy mature weight is correlated with increased
birth weight and increased dystocia. Birth weight is
altered extensively by environmental factors. Because
birth weight at term is well correlated with gestation
length, selection for decreased gestation length seems
desirable. Thus, to increase rate of gain and mature
weight but avoid dystocia, one can select for shorter
gestation length simultaneously with a high mature
weight. Novel, yet practical solutions t o this genetic
dilemma (twinning, Caesarean section, hormonal
therapy to control parturition date, or pre- or postpartum growth) need further exploration.
Many researchers have assumed that the factors of
the Brody equation are fixed genetically and cannot be
altered. However, malnutrition retards growth. The
extent of retardation depends on the stage of development and severity of the nutritional insult (McCance
and Widdowson, 1962). The smaller weight and
height of many children in developing countries is well
documented (Martorell, 1985; Waterlow, 1986). Early
malnutrition impedes cell division and the animal
may never recover, but some recovery is expected
when growth retardation occurs at later stages of

growth (Winick and Noble, 1966). Feed restriction in

heifers can reduce birth weight and decrease gestation
length (Warrington et al., 1988). Even season of birth
has been reported to alter mature size of cattle in
developing countries (Abassa, 1987). These observations indicate that both mature size and the deceleration factors in the growth equation can be altered at
various stages of life by nutritional or hormonal
factors even though genetics are important. Heritabilities of mature weight have been estimated in various
species to be low t o high (.28 in mice, Kachman et al.,
1988; .30 in Chios sheep, Mavrogenis and Constantinou, 1990; .29 in Landrace ewes, Nasholm and
Danell, 1990; .82 in cows, Humes and Munyakazi,
1989). These values indicate that environment can
play an important role in determining mature weight.
The definition of mature weight is not standardized,
even among simulation models (Arnold and Bennett,
1991). For discussion here, mature size (weight) will
be considered the point of maximum protein mass
despite the increased fat deposition that can occur
beyond this point.
The relationship between frame size and mature
weight usually is direct, but depending on muscling
characteristics, the relationship is far from perfect.
Frame size or skeletal size usually is measured as
length of specific bones or wither height; in contrast,
weight is a mass measurement, not a linear measurement. For animals with different frame sizes and
presumably different mature weights, Fox and Black
(1984) estimated fat content at various empty BW.
These are plotted together with estimated fat content
at mature weight in Figure 4. In this case, mature BW
was calculated as the empty BW above which energy
content of gain was > 8 kcaVg and thereby should not
include protein (NRC, 1984). Fat content at the point
at which protein mass was maximum was surprisingly
constant (34 to 37% of empty BW) for all the classes
examined. This indicates that mature weight for
animals of different frame size might be defined as the
weight at which fat content of the empty body reaches
34 to 37%.
Below mature weight, the lower slope for large
animals indicates that fat deposition is a lower
proportion of weight gained. The steeper slope beyond
mature empty BW indicates that all added weight is
fat. Averaged across classes, an equation for fat
content can be derived as follows: Fat(% EBW) = 3.42
+ 31.55*(EBW/MBW) in which EBW is empty BW
and MBW is mature empty BW. This means that body
composition at a specific fraction of mature wight is a
constant. If this relationship is valid, one should be
able to calculate the mature empty BW for a young
animal once fat content and empty BW are known. It
is very convenient and comforting to assume that
empty body composition at a specific fraction of
mature weight is constant, although Korver et al.
( 1987 ) indicated that composition of the carcass
differed among breed groups even after adjusting for

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3141

RUMINANT GROWTH

500--

450-400--

350-300250--

200

10

12

14

16

18

20

STEER AGE, MONTHS

Figure 3. Effect of altering components of Brody's growth curve equation on weights at specific ages. Equation is
as follows: body weight = mature weight*[1 - e(deceleration*agefrom conception]].

degree of maturity. Nevertheless, if values are relatively constant, body composition measurement at any
slaughter weight would permit one to predict mature
BW. This should interest scientists who find it costly
to feed animals long enough to measure mature
weight directly. Mature weight of sheep is reached at
approximately 5 yr, but it can be estimated from serial
weights < 30 mo of age according to Nasholm (1990).

Factors that Affect Body Composition

and Growth Rate
Mature Body Size. Although the maximum body
size is genetically determined, it can be altered by
nutritional and hormonal factors. Differences between
breeds in size are due to differences in size of the
skeleton and in the number but not the size of muscle
cells (Hammond, 1961). Early fetal growth largely is
genetically regulated, although blood flow later in
pregnancy will alter fetal weight and maturity.
Growth rate at later fetal stages and after birth but
before maturity can be influenced greatly by factors
such as plane of nutrition, hormonal status, and
environment (Widdowson, 1980; Gluckman, 1986).
Such factors may inhibit cell division to the point that
mature body size is below the genetically determined
maximum.
Whether mature size of cattle can be altered readily
by nutritional restriction remains debated. Depending
on the severity of the restriction and the specific

nutrient involved, size of an animal when it becomes

mature has been reported variously to be decreased,
unchanged, or increased. Discrepancies among reports
may relate to the timing or severity of deprivation or
the nutrient involved. Very severe nutrient restriction,
especially for protein, reduces mature size of swine
and cattle (Berg and Butterfield, 1976; Pond et al.,
1990; Widdowson and Lister, 1991). However, a
moderate degree of restricted feeding during growth
failed to alter composition of rib sections of the carcass
(Winchester and Howe, 1955; Winchester and Ellis,
1956). Based on the relationship of fat percentage to
degree of maturity discussed above, this means that
restricted feeding did not alter mature weight of
finished steers. Echoing this theme, Long (1988)
stated that the "genetic potential of cattle dictates
their carcass composition at any weight regardless of
whether they reach that weight in a short or a long
period of time." In contrast, several researchers (Lake
et al., 1974; Lewis et al., 1990b) have reported that
restricting energy intake during the late prepubertal
or early postpubertal period markedly reduces fat
content of finished steers at a specific weight. Again,
this composition change could be interpreted to imply
that restricting growth INCREASED mature weight.
By altering the length and age of restriction, livestock
producers may be able to alter the mature weight of
animals to meet specifications of packing plants and
consumers for carcass composition and weight of meat
cuts.
Nutrition, Tissues grow and develop chronologically
in specific "growth waves." Certain tissues grow and

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OWENS ET AL.

3 142

55
50--

45--

40--

w!

35--

30-25--

SFH=SMALL FRAME HEIFER

MFH=MEDIUM FRAME HEIFER
SFS=SMALL FRAME STEER
LFH=LARGE FRAME HEIFER
MFS=MEDIUM FRAME STEER
LFS=LARGE FRAME STEER

20--

15I

EMPTY BODY WEIGHT, K G

Figure 4.Fat content of empty body weight (EBW)at various body weights for small-, medium-, and large-framed
size heifers and steers. Calculated from Fox and Black (1984).

mature before others; growth starts with neural tissue

and proceeds to bone, muscle tissue, and finally
adipose tissue (Figure 1 ) . Within each of these
tissues, development can be early, medium, or late
depending on its location in the body. For example,
deposition of fat near the kidney precedes deposition
at intermuscular, subcutaneous, and intramuscular
sites. Hence, body shape and composition change as an
animal matures. Supply of dietary nutrients must be
coordinated with this progression to maintain optimum growth rates.
The concept of attempting to alter body composition
via altering mature size is applied by commercial
cattle feeders. As indicated by Greathouse (19851,
when earlier maturing cattle (small-framed cattle and
heifers) were fed high-energy diets as calves, they
exhibited enhanced fattening and reduced slaughter
weight at a specified fat thickness. Similarly, Nour
and Thonney (1987) indicated that at any carcass
weight, smaller mature weight breeds of cattle had
more lipid in soft tissue. Because light-weight carcasses are discounted at slaughter, a growing (often
pasture) period is interposed between weaning and
entry into a feedlot. This delays fat deposition so that
carcasses of animals with enough intramuscular fat to
grade Choice will have greater and thereby more
acceptable carcass weights. Larger framed animals do
not require this growing period. These observations
indicate that mature size can be reduced by an oversupply of energy during the middle phase of growth.
Perhaps some signal from lipid mass decreases the

rate of protein deposition. In contrast, the reduction in

mature size due to a severe restriction of energy or
protein intake during the early, hyperplastic phase of
growth presumably is due to some permanent reduction in either nutrient supply (damage to the digestive tract as from parasites or viruses) or in satellite
cell or muscle fiber number.
Biochemical studies (Bergen, 1974) suggest that
the rate of protein synthesis during growth can be
limited by an inadequate supply of substrate (amino
acids, ATP). In turn, nutrient supply regulates the
amount of protein synthesis machinery (RNA).
Total protein deposition can be limited by nutrient
supply, but with high intakes of a well-balanced diet,
the maximum rate of protein deposition seems to be
limited by concentrations of growth-stimulating hormones.
Hormones. As outlined in various symposia (ASAS,
1974, 1987, 19881, specific hormones or growth factors
alter growth rate or body composition. Endogenous
(e.g., insulin, somatotropin, IGF-I and IGF-11) and
exogenous hormones promote translation, transcription, and amino acid uptake. With an insulin deficiency, the number of polysomes in muscle is
decreased, whereas with growth hormone deficiency,
both number and activity of ribosomes is decreased
and DNA production by muscle tissue ceases. Cessation of protein growth occurs simultaneously with
decreases in ribosomal and total RNA.
Responses to hormone administration can differ
with species and organ of the body. Direct

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RUMINANT GROWTH

administration of growth hormone (somatotropin) has

improved growth rate and gain:feed ratio of pigs,
lambs, and cattle and decreased fat content of pig and
lamb carcasses. In steers, growth hormone administration has expanded the size of internal organs
(Early et al., 1990) and increased feed intake.
Cascades of hormones may be involved with growth.
Growth hormone effects seem to be indirect and
dependent on locally produced somatomedins (IGF-I
and 11). The IGF response to growth hormone is
dampened when nutrient status or insulin levels are
low. For example, estradiol administration increased
the IGF-I concentration in serum of cows with
moderate body energy stores but not in cows with low
body energy stores (Richards et al., 1991). A number
of growth promoters or inhibitors (differentiation
inhibitor, transferrin, fibroblast growth factor) are
involved in controlling muscle growth or satellite cell
incorporation into muscle fibers (Dayton, 1988).
Another class of chemicals that can alter tissue
growth and composition are the &adrenergic agonists.
These compounds structurally are related to
epinephrine and norepinephrine. When activated, 0receptors in adipose tissue stimulate lipolysis (Muir,
1988) and in muscle tissue they decrease protein
degradation (Morgan et al., 1989) either transiently
or continuously. Fat deposition is decreased and net
protein deposition may be increased in poultry, swine,
sheep and, to a lesser extent, in cattle.
Other Factors. Besides nutrient supply, hormonal
or environmental factors may indirectly or directly
alter growth rate. Precisely how factors such as
environmental temperature, day length, breed type,
parasites, disease, competition, and exercise influence
size of specific organs and site of lipid deposition
during growth or at maturity remain largely unknown. Some may act through controlling feed intake
of animals and the supply of nutrients above maintenance; others may alter blood hormone concentrations, blood flow, and nutrient supply to specific body
organs or locations.
Compensatory Growth. If the nutrient intake of
growing animals is restricted, growth rate is subnormal. For such animals, rate of weight gain during
realimentation usually is greater than for companions
that never were restricted. Called compensatory
growth, this growth rebound presumably represents
rapid hypertrophy of muscle tissue. The extent of
compensatory growth is greater when it follows energy
restriction rather than protein restriction (Drouillard
et al., 1991a,b).
Compensatory growth often is measured by determining the change in BW of animals over several
weeks. Unfortunately, BW is an imprecise, inaccurate,
and often biased predictor of lean body mass. By
extrapolating from weights taken before and after a
specified diet change, Tolley et al. (1988) concluded
that differences in digesta alone could account fully for

3 143

the compensatory growth phenomenon. Weight of

digestive tract contents can change within minutes or
days; weight of the empty digestive tract plus liver can
change within a few weeks (Williams et al., 1992).
Carstens et al. (1991) reported that accretion rates
for carcass protein, water, ash, and fat were no greater
for steers exhibiting compensatory growth than for
steers continuously growing even though at 450 kg
empty BW, steers making compensatory growth contained more protein and less fat. Instead, changes in
fill and size of the digestive tract accounted for most of
the compensatory weight and protein gain. Deposition
rate for noncarcass protein was increased during
compensatory growth. This contradicts earlier suggestions that compensatory growth was due primarily to
hypertrophy of muscle and thereby lean tissue.
Because ruminants usually are bought and sold on the
basis of live weight, compensatory weight gain can
have a sizeable economic effect on livestock production. However, if compensatory growth does not
represent lean carcass mass, it should be irrelevant for
animals sold on a carcass value-based marketing
system.
As reviewed by Moran and Holmes (1978) and
Hogg (1991), the magnitude of compensatory growth
depends on a number of factors. These include age
when restriction begins; the severity, duration, and
nature of undernutrition; the realimentation diet and
time; and the breed type. Compensatory growth seems
to alter composition most during growth but has
limited effect on body composition at maturity.

Measurements of Growth and Development

Total Muss. Full, shrunk, and empty BW can
change independently of muscle mass. Alterations in
digestive tract fill and in body composition make full
weight alone imprecise as an indicator of growth.
Shrunk weight will partly remove digestive tract fill
although the extent of shrink varies with diet (Tolley
et al., 1988) and type of diet or forage fed (Waldo et
al., 1990; Williams et al., 1992). Measurement of
empty body mass is preferable to shrunk or full BW,
although an increase in empty body mass need not
represent an increase in empty body protein. Using
isotope dilution procedures, Laurenz et al. ( 1992)
reported that during the summer months, mature
Simmental cows, while losing 5.4 kg of empty body
protein, gained 5.6 kg of empty BW because of
deposition of added fat (30.1 kg). In other studies,
animals have lost fat while gaining protein. This
demonstrates how changes in live weight or even
empty body mass may not fully reflect changes in
protein (and presumably lean) mass or body energy
content.
Lean Mass. Some workers reserve the term growth
for increases in protein mass or lean body mass. These

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OWENS ET AL.

two terms are not synonyms because digestive tract

and liver protein stores may increase independently of
carcass lean mass during compensatory gain (Carstens et al., 1991) and growth hormone administration (Early et al., 1990). If mature weight is the point
of maximum lean body mass, additional weight gain
beyond this point is fat. This means that weight of
mature animals alone may not reflect mature weight.
If fat content is constant in nonstarved animals a t a
specific fraction of mature empty BW by the equation
discussed previously, mature lean body mass can be
predicted at commercial slaughter weights.
Stature. Sometimes growth is measured as size or
stature (wither height; long bone length); fatness or
muscling are judged subjectively. Because long bones
cease to increase in length after epiphyseal closure,
linear bone growth presumably stops when closure
occurs. Hormones and nutrient intake can influence
the age at epiphyseal closure (Oberbauer et al.,
1989). Hence, closure need not correspond to a specific
animal age even though closure is used commercially
as an index of maturity in slaughter lambs.
Sexual Maturity. Reproductive characteristics have
been used widely as indicators of development and
maturation in heifers and bulls. Years ago, Brody
(1964) concluded that puberty is the point at which
self-accelerating growth changes to self-inhibiting
growth and that weight at puberty occurs at approximately 60% of mature weight in all species. Puberty
has been variously estimated as the age of first estrus,
conception, or sperm production. Although puberty is
related t o weight in some species and to age in others,
for cattle, weight and age both are important in
determining the age at puberty (Yelich et al., 1992).
Certain environmental factors (temperature, day
length, specific nutrients) also can influence age and
weight at puberty.
The effect of estrogenic implants on mature weight
seem contradictory. In a study lasting 486 d, repeated
implants of an estrogenic substance (diethylstilbestrol) increased mature size of steers by 15% (Preston,
1978j. Estrogens presumably act through enhancing
secretion of growth hormone (Beitz, 1985), which
should increase mature size. An increase in mature
size automatically reduces fat content and increases
growth rate at a specified weight as has been observed
typically with estrogen administration. In contrast, by
hastening closure of the growth plate and increasing
ossification, estrogens should limit mature size. This
could explain the smaller stature of females of many
species. Field et al. (1990) found that closure in
lambs occurred so late that mature size of wether
lambs was not altered by estrogenic implants.
Growth Rate Measurements. Rate of gain usually is
calculated as change in weight during a specified time
interval. Even when weight is measured numerous
times during a study, weight change from the initial to
the final date typically is used to calculate growth

rate. In contrast to calculating rate of gain from only

two fixed time points, regression across the various
time points smooths the growth curve (Tolley et al.
1988). Because pasture conditions and the animal's
nutrient requirements can change over time, it often
proves informative to subdivide experiments into
specified time periods to determine when treatment
responses are evident. One convenient way to appraise
responses during various time intervals is to calculate
and plot weight gain as a percentage of the control in
several sequential time periods.
Voluntary feed intake above maintenance, and
thereby rate of gain of an animal, changes as animals
mature and tends to reach a plateau at mature BW.
Based on records from feedlot cattle differing in body
composition, D. R. Gill (personal communication)
indicated that energy intake was directly proportional
to empty body protein mass but inversely related to
rate of fat deposition. Cattle entering a feedlot at a
heavier weight generally have greater feed intake,
especially if they have a large frame size or mature
body weight; feed intakes decline as fat mass increases, as occurs late in the finishing period.
Alternatives to Linear Measurement. Selection of
animals for a rapid growth rate or low fat content
often results in increased mature body weight. This is
because at any specified weight, animals with a large
skeletal mass and large mature weight are earlier ( a t
a steeper phase) in their growth curve and contain
less lipid. Large mature size is desirable to enhance
efficiency of production of lean tissue and to reduce fat
content of animals at a specific slaughter weight
(Greathouse, 1986). However, a large mass increases
both birth weight (and dystocia) and the cost of
maintenance.
One method to circumvent the problem of selecting
animals for larger mature size when selecting for
growth rate is to calculate growth rate on a relative
(fractional) rather than an absolute basis. This is
based on the premise that growth rate of animal
tissues, like that of microbes, depends on the initial
number of cells available. Mathematically, the natural
logarithm of final weight minus the log of initial
weight divided by time interval yields fractional
growth rate. Although both relative and absolute
growth rate measurements proved equally effective
indices for selecting bulls for rapid growth postweaning (Brown et al., 1988), selection based on relative
rather than absolute growth rate might enhance
metabolic efficiency at other stages of growth. Another
index, growth rate as a fraction of mature weight,
might prove preferable to both absolute and relative
growth rate. Calculated by dividing growth rate
during a period by mature BW, this index should
avoid the bias associated with leaner mass at a given
weight of animals with greater mature body size and
thereby be more precise as an index of metabolic
efficiency.

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RUMINANT GROWTH

The extent to which selection and growth

stimulants act through increasing mature body weight
has not been explored fully. In contrast with its effects
on nonruminants, estrogen administration consistently has increased protein and decreased fat deposition for growing cattle (Lemieux et al., 1990).
However, estrogens implanted in animals that are
losing weight may accelerate their weight loss, perhaps though increasing maintenance requirements.
Effects of testosterone or the synthetic anabolic agent,
trenbolone acetate, are synergistic with estrogen for
enhancing deposition of lean tissue, again potentially
through increasing mature body size.
Considering that maintenance energy requirements
and age at puberty both increase with mature weight
(Koch et al., 19891, growth retardation rather than
stimulation might be preferable for heifers destined to
be herd replacements. Specific chemicals to inhibit
growth could prove useful for beef cow replacements,
although adverse effects on pubertal age and
reproductive performance need close scrutiny. Fiss
and Wilton ( 1989) noted that heavier body weight
within a breed of cattle slightly increased age at first
calving and days to pregnancy, but these factors were
not detectably altered by mature weight. In contrast,
certain breeds of cattle, particularly those with a high
mature weight, reach puberty at a very late age
(Patterson et al., 1991).
Live vs Shrunk vs Carcass Weight. Body mass is
composed of the salable product plus other components
of the carcass, the digestive tract and its contents, and
offal (hide, blood, etc). Hence, animal weight is not
always well correlated with the quantity of salable
product.
To attain a more reliable estimate of empty body
mass, animals often are shrunk by depriving them of
feed and water for a period of time (e.g., overnight or
for 24 h). This reduces the weight of digestive tract
contents, but shrink often is greater for cattle fed
concentrate than for cattle fed roughage, whereas
weight of digestive tract contents is greater for those
fed roughage. For animals of similar weight fed a
single diet, shrunk BW (24 h without feed) gives
reasonably accurate estimates of empty BW (Reid et
al., 1968). Traditionally, shrunk weight is taken after
a period of feed withdrawal (24 h 1 but with access to
water. Transport of animals will decrease weight
further. Weighing animals at the same time on several
consecutive days also has been used to estimate full
BW; this decreases the variation associated with
recent consumption of feed and water and aids in
detecting mistakes involved with reading balances.
Dressing percentage is weight of the carcass as a
fraction of live weight, although live weight in this
case can be either full or shrunk. Dressing percentage
increases with maturation both because fat deposition
is greater and because the proportion of BW that
consists of the digestive tract and its contents

3145

decreases (Berg and Butterfield, 1976; Waldo et al.,

1990; Williams et al., 1992). Diet can markedly
influence dressing percentage. For cattle fed higher
levels of roughage, dressing percentage is markedly
lower at similar live weights (62.8 vs 65.9 and 65.3%
for steers fed diets composed of 75, 30, and 14% corn
silage in high-moisture corn diets; Gill et al., 1976).
To circumvent effects of digestive tract fill on final live
weight and thereby on performance and efficiency,
many researchers calculate final live weight from
carcass weight. Carcass weight for each animal is
divided by one constant value, typically the mean
dressing percentage for all cattle.
Short-Term Variations in Weight. Body mass fluctuates within a day due to consumption and excretion
patterns of animals, largely due to changes in the
mass of digesta within the tract. Zinn (1990) indicated that weight of feedlot cattle early in the day
(before they had consumed water) was more repeatable than weights taken later in the day.
Longer-Term Variation in Body Weight. In addition
to accretion of body tissue during normal growth, body
mass will fluctuate over a period of weeks as plane of
nutrition is changed due both to the mass of digesta
within the tract and to expansion or contraction of
organs involved with digestion and metabolism, particularly the liver and digestive tract. A number of
recent studies (Koong et al., 1982; Ferrell et al., 1986;
Drouillard et al., 1991b) have demonstrated that the
mass of visceral organs vanes in weight roughly in
proportion to nutrient (energy) intake. As mass of the
digestive tract and liver increases, an animal's maintenance energy requirement increases. In contrast,
reduction in the mass of these rapid-turnover organs
(liver and small and large intestines) may explain
why maintenance energy requirements decline during
several weeks or months of low energy intake.
Visceral mass also differs among breed (Olthoff and
Dickerson, 1989). Smaller, more prolific breeds of
sheep had a higher percentage of their empty BW in
visceral organs, gastrointestinal tract, and internal
fat. A large digestive tract and visceral mass is a
mixed blessing. Although a large digestive tract may
increase capacity to consume roughage, the digestive
tract and visceral mass has a large maintenance
requirement. Benefits from a large digestive tract
thereby would differ for feast and famine vs stable
nutritional environments and for roughage vs concentrate diets.
We have observed that cattle that had grazed
during the summer, when placed into the feedlot, ate
much more feed but had much lower gain:feed ratios
(much poorer than NE equations predict) than cattle
that had been placed in the feedlot at weaning.
Heavier initial weight and size of the animals that
grazed plus weighing conditions could explain only a
portion of this effect. Grazing for several months
before finishing could be deleterious to feedlot

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3146

OWENS ET AL.

performance if grazing expands internal organs,

decreases digestibility, or increases maintenance requirements. A protein deficiency during the grazing
period was especially deleterious to subsequent performance (Drouillard et al., 1991a,b).
Carcass weights often are considered to be the
ultimate weight measurement. Even with this measurement, whether the carcass is weighed hot or cold,
washed or unwashed, and with the kidneys present or
absent ( a s used in some countries) will alter carcass
weight. Trimming of bruises or excess fat from the
carcass reduces carcass weight. Compared with
weights obtained at other ages, carcass weight or
weight of wholesale cuts should more precisely estimate salable product. Even beyond wholesale cut
weight, most cuts have external fat trimmed before
sale. If animals were marketed on a lean carcass
weight basis, producers would have greater incentive
to produce lean mass.
Lean or Empty Body Mass Estimation. The comparative slaughter procedure combined with direct
chemical analysis or specific gravity measurement is
the ultimate index to quantify growth rate of animals
or specific tissues. Other procedures based on correlations of lean body mass with body water (potassium40, pyridine, urea, deuterium oxide, electrical conductivity) may prove useful for evaluating single animals
repeatedly during growth. For estimating lean mass in
slaughtered animals, scanning or tomographic procedures as used in human research offer promise.
To measure rate of protein synthesis and degradation more directly, isotope flooding procedures can be
employed (Morgan et al., 1989). Such measurements
can help to determine whether a given growth
modifier enhances protein mass by increasing net
protein synthesis or by decreasing net protein degradation. This in turn helps researchers judge whether
different modifiers act through the same mechanism,
and thereby may not be additive. Certain &agonists
seem to enhance carcass protein by decreasing the
rate of muscle turnover (Morgan et al., 1989) without
altering energetic efficiency (Rikhardsson et al.,
1991). In contrast, growth hormone administration
increases both digestive tract size and total protein in
cattle (Early et al., 1990) and thereby would be
expected to increase requirements for nutrients and
energy.

Effects of Altered Growth Rates

Adverse Effects o f Accelerated Growth. An increase
in udder size can be good or bad. An increase in the
amount of secretory tissue may increase milk production. However, if udder size increases due to deposition of lipid, secretory cells are displaced and milk
production may be decreased. Rapid growth and
fattening of dairy and beef calves can increase the

amount of lipid deposited within the udder and reduce

milk production (Sejrsen et al., 1982). Concerns about
excessive fat deposition in the udder with high planes
of nutrition has led producers to restrict rates of gain
for replacement heifers. Often, beef replacement
heifers are selected for rapid preweaning growth rate
based on the premise that growth rate is limited by
genetic potential and maternal milk supply. However,
if preweaning growth rate is rapid, fat deposition in
the udder of heifers may be excessive, which in turn
limits potential milk production. In this manner,
selection of replacement beef heifers based on high
weaning weights alone may prove fruitless. To avoid
excess fat deposition, developing heifers should not be
given ad libitum access t o high-concentrate diets.
Although high-concentrate diets are implicated with
greater fat deposition in the udder, exactly what
component is responsible is not clear. The effect may
be merely quantitative (excess energy from any
source) or dependent on the type of nutrient (e.g.,
more propionate) absorbed from high-concentrate
diets with subsequent changes in hormone concentrations. This question could be explored by limit feeding
high-concentrate diets to growing heifers.
Sejrsen et al. (1986) and McFadden et al. (1990)
found that bovine somatotropin administration enhanced interstitial tissue growth (but not fat) in the
mammary glands of heifer calves. Early production
studies show no evidence that the bovine somatotropin
( o r IGF-1)-induced enlargement of the mammary
glands increases potential milk yield.
Supply of specific nutrients also can alter mammary
growth. McFadden et al. (1990) indicated that
mammary development in lambs was stimulated by
polyunsaturated fat but not by a moderately high
plane of nutrition. Specific tissue level effects of
individual nutrients need further study to determine
their activity and their modes of action.
Adverse Effects o f Retarded Growth. Effects of
retarding growth rate of calves during winter on
subsequent performance during grazing (Lewis et al.,
1990a; McCollum et al., 1991) or even later in a
feedlot have been appraised in several studies
(Owensby, 1986; Lewis et al., 1990b; McLean et al.,
1990; Gill et al., 1991; D. R. Gill, personal communication). Summer grazing can compensate for large
differences in rate of gain of wintering calves (Lewis
et al., 1990a; McCollum et al., 1991). Compared with
calves placed directly in a feedlot, those grown more
slowly on plant residues or pasture usually have
heavier slaughter weights at a similar degree of
fatness (Figure 51, consistently consume more feed
(average of 22% more in six comparisons), and may or
may not gain more rapidly (average of 1%more in six
comparisons). At equal external fat thickness, slaughter weights for cattle placed in the feedlot at 3 mo
(early weaned), at 8 mo (normal weaning time), after
wheat pasture grazing or after grazing grass pastures

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3 147

RUMINANT GROWTH

OFAT-STARTING

STEERS

+ +

BPROTEIN-FINISHED STEERS

t+

STEERS

3
0
0

00

0
0
F

20--

BB

I
I

ws

I
I

I N,I

ws,

Figure 5. Weight of protein ( 0 , m) and fat (0, 4 ) in the empty body of steers at entry ( 0 , 0) or exit (m, 4 ) from the
feedlot after early weaning (E) at 3.5 mo of age, weaning at normal (N)age of 7.9 mo, normal weaning age but after
grazing of wheat pasture (W) for 112 d, or after wintering on native range and grazing of grass pasture for either 68
(S) or 122 d(L). From D. R. Gill, personal communication.

for a short or a long period differed markedly. Based

on fat and empty BW, mature weights for these cattle
were calculated from the equation discussed previously. These estimated mature weights were 474, 542,
743, 711, and 686 kg for the various backgrounds,
respectively, indicating that mature BW was reduced
by > 30% by feeding young calves a high-concentrate,
feedlot diet. Older and heavier cattle consistently have
had poorer feedlot feed efficiency (average of 22%
worse in six comparisons from the literature). Adjusting for mean weight differences may reduce this
difference, but on a NE, basis, cattle placed in the
feedlot at weaning were 2 10% more efficient in the
feedlot than cattle that had grazed. Whether the
decreased efficiency is due to greater visceral mass
and metabolic rate, to reduced digestion due to less
extensive chewing or a faster passage, or to age and
reduced growth potential has not been defined.
Nutrient restriction, particularly protein restriction, can reduce mature body size and increase fat
content of the carcass. Retarded growth also may
delay puberty (and thereby partition) so that lifetime
cow productivity is reduced. This problem is more
prevalent with cattle with very large frame size or
with Brahman genetics. Supplemental feeding of
postpubertal heifers to attain a greater weight at
breeding generally can solve this problem. Again,

specific nutrients or metabolites may be involved in

signalling puberty and might be used to accelerate
reproductive maturity. Randel ( 199 0 ) noted that
feeding protected lipids to growing heifers delayed
puberty. In contrast to its effects with heifers, feeding
calcium soaps or protected lipids to lactating cows
shortened the postpartum interval, possibly through
decreasing the energy deficit (Randel, 1990; Hightshoe et al., 1991). Randel (1990) also noted that
feeding ionophores, possibly through increasing insulin and blood glucose levels, accelerated puberty in
growing heifers. Meinert et al. (1992) noted similar
effects with younger age at first breeding and calving
in Holstein heifers fed monensin despite no change in
body compositions and weight. Again, further study of
specific nutrients involved with age at puberty should
prove rewarding.

Implications
Growth rate can be defined mathematically in
terms of mature size, the rate of growth deceleration,
and age. Although maximum growth rate is set
genetically, nutritional and hormonal factors can limit
growth rate and, by altering mature size, may reduce
or increase fat content of the carcass at a given

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3 148

OWENS ET AL.

weight. Heavy mature weights are not desirable for

ruminants maintained for reproduction. Growth
stimulants or depressants and &agonists that alter
body size and composition may prove as useful to
enhance production efficiency in the cow herd as in
finishing animals.

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