Nutrition: Protein, building the rumen in kids, etc.

Discussion in 'Health & Wellness' started by, Jun 10, 2008.

  1. New Member

    Calf Note #27 – How Calf Starter Intake Drives Rumen Development
    Introduction. Development of the rumen generally occurs during the first 4 to 8 weeks of a calf's
    life. The process of rumen development is driven primarily by consumption of dry feed. If calves
    have feed - particularly calf starter - available from an early age, then the development of the rumen
    will begin within a couple weeks of birth.
    There are 5 requirements (or "ingredients") for rumen development. These include the presence of
    bacteria, availability of liquid in the rumen, rumen motility, absorptive ability of the rumen
    epithelium and availability of calf starter. Bacteria, liquid, rumen motility, and absorptive ability are
    established prior to rumen development, or develop rapidly when the calf begins to consume dry
    There are five requirements for ruminal development. They are:
    • Establishment of bacteria in the rumen
    • Liquid in the rumen
    • Outflow of material from the rumen (muscular action)
    • Absorptive ability of the tissue
    • Substrate
    A number of other metabolic changes occur during ruminal development in the rumen and other
    tissues, but we will consider the above requirements for the rumen to begin to function.
    Bacteria. When the calf is first born, the rumen is sterile - there are no bacteria present. However,
    by one day of age, a large concentration of bacteria can be found which are mostly aerobic (or
    oxygen-using) bacteria. Thereafter, the numbers and types of bacteria change as dry feed intake
    occurs and the substrate available for fermentation changes. The change in bacterial numbers and
    types is almost always a function of intake of substrate. Prior to consumption of dry feeds, bacteria
    in the rumen exist by fermenting ingested hair, bedding, and milk that flows from the abomasum
    into the rumen. The substrate ingested will also affect the types of ruminal bacteria that flourish in
    the young rumen. For example, calves fed mostly hay develop a different flora from those fed
    mostly grain.
    Liquid in the Rumen. To ferment substrate (grain and hay), rumen bacteria must live in a water
    environment. Without sufficient water, bacteria cannot grow and ruminal development is slowed.
    Most of the water that enters the rumen comes from free water intake. If water is offered to calves
    from an early age, this is not usually a problem; unfortunately, many producers in the U.S. do not
    provide free water to their calves until calves reach 4 or more weeks of age. Offering water in the
    winter can be a significant challenge in Canada and the northern U.S. However, calves still need
    water, even when it is cold. Sometimes, it may be necessary to bring warm water at an additional
    Calf © 2001 by Dr. Jim Quigley Page 2
    feeding to ensure that calves have enough liquid water available. Free water has been shown to
    increase rate of body weight gain and reduce scours.
    Milk or milk replacer does not constitute "free water". Milk or milk replacer will by-pass the rumen
    by closure of the esophageal (reticular) groove. Closure of the groove is a neural response to feeding.
    Free water does not stimulate closure of the groove, so water enters the rumen. Feeding water can
    increase body weight gain, starter intake, and reduce scours score.
    Outflow of Material from the Rumen. Proper ruminal development requires that material entering
    the rumen must be able to leave it. Measures of ruminal activity include rumen contractions, rumen
    pressure, and regurgitation (cud chewing). At birth, the rumen has little muscular activity, and few
    rumen contractions can be measured. Similarly, no regurgitation occurs in the first week or so of life.
    With increasing intake of dry feed, rumen contractions begin. When calves are fed milk, hay, and
    grain from shortly after birth, rumen contractions can be measured as early as 3 weeks of age.
    However, when calves are fed only milk, rumen contractions may not be measurable for extended
    periods. Cud chewing has been observed as early as 7 days of age, and may not be related to ruminal
    development per se. However, calves will ruminate for increasing periods when dry feed (particularly
    hay) is fed.
    Absorptive Ability of the Rumen Tissue. The absorption of end-products of fermentation is an
    important criterion of ruminal development. The end-products of fermentation, particularly the
    volatile fatty acids (VFA; acetate, propionate, and butyrate) are absorbed into the rumen epithelium,
    where propionate and butyrate are metabolized in mature ruminants. Then, the VFA or endproducts
    of metabolism (lactate and ß-hydroxybutyrate) are transported to the blood for use as
    energy substrates. However, there is little or no absorption or metabolism of VFA in neonatal
    calves. Therefore, the rumen must develop this ability prior to weaning.
    The rumen wall consists of epithelial and muscular layers. Each layer has its own function and
    develops as a result of different stimuli. The muscle layer provides support for the interior (epithelial
    layer) and moves ruminal contents in the rumen. The epithelial layer is the absorptive layer of tissue
    inside the rumen which is in contact with rumen contents. This tissue contains many small fingerlike
    projections called papillae. These papillae provide the absorptive surface for the rumen. At birth,
    the papillae are small and non-functional. They absorb little and do not metabolize significant VFA.
    Many researchers have evaluated the effect of various compounds on the development of the
    epithelial tissue in relation to size and number of papillae and their ability to absorb and metabolize
    VFA. Results of these studies indicate that the primary stimulus to development of the epithelium
    are the VFA - particularly propionate and butyrate. Milk, hay, and grain added to the rumen
    are all fermented by the resident bacteria to these acids; therefore, they contribute VFA for
    epithelial development. Plastic sponges and inert particles - both added to the rumen to provide
    "scratch" - did not promote development of the epithelium. These objects could not be fermented
    to VFA, and thus did not contribute any VFA to the rumen environment. Therefore, rumen
    development (defined as the development of the epithelium) is primarily controlled by chemical, not
    physical means. This is further support for the hypothesis that ruminal development is primarily
    driven by the availability of dry feed, but particularly starter, in the rumen.
    Availability of Substrate. Bacteria, liquid, rumen motility, and absorptive ability are established
    prior to rumen development, or develop rapidly when the calf begins to consume dry feed. Thus,
    the primary factor determining ruminal development is dry feed intake. To promote early
    Calf © 2001 by Dr. Jim Quigley Page 3
    rumen development and allow early weaning, the key factor is early consumption of a diet to
    promote growth of the ruminal epithelium and ruminal motility. Because grains provide fermentable
    carbohydrates that are fermented to propionate and butyrate, they are a good choice to ensure early
    rumen development. On the other hand, the structural carbohydrate of forages tend to be fermented
    to a greater extent to acetate, which is less stimulatory to ruminal development.
    In conclusion, the primary factor determining ruminal development is dry feed intake. To promote
    early rumen development and allow early weaning, the key factor is early consumption of a diet to
    promote growth of the ruminal epithelium and ruminal motility. Because grains provide nonstructural
    carbohydrates that are fermented to propionate and butyrate, they are a good choice to
    ensure early rumen development. On the other hand, the structural carbohydrates in forages tend to
    be fermented to a greater extent to acetate, which is less stimulatory to ruminal development.
  2. New Member

    Feeding too much protein causes too high of a pH in the rumen and blood. Feeding commercial feed, which often has molasses, and "cheap highs" in the form of processed grains and byproducts causes too low of a pH, leading to acidosis. It is the molasses and high carbs that make for an acidic rumen, not protein. And as Vicky said, too much protein means too much urea in urine, and too much uric acid.

    Protein interaction is different in kind from mineral interaction in hypocalcemia. There are two parts to consider, one: the role of feed and how that feed and its calcium/phosphorus ratio and mineral content affect the ability to digest calcium and use it and store it for later in blood serum, and in bone, and two: the role of mineral balance and more importantly parathyroid hormone activity during actual onset of hypocalcemia. The two factors are interrelated, as I'll try to explain. But they combine in many ways to produce perhaps a half dozen or more possible causes of a hypocalcemic condition. Some are more likely than others in goats especially.

    In the first case, when feed causes a basic condition, more calcium is excreted as waste. The rumen pH and total acid affect the balance of calcium that is in ionic form, and readily absorbable, and in protein-bound form. The lower the pH, the more calcium is in ionic form. This is why a very slightly acidic rumen, as occurs with a raw grain 12% ration is good. But, here it gets tricky because there's a sort of tipping point and balance. Acid is produced from sugars and carbs, whereas protein produces ammonia (which raises pH). That ammonia must be metabolized both in the rumen, hopefully by the yeast population there, and by the liver. When the liver metabolyzes it, it uses up energy. Energy that can be better used elsewhere. A long-term high-protein diet causes long-term poor absorption of calcium. I think, more importantly, it negatively affects the body's capacity to respond to severe events that draw on massive reserves, like during birth and milking. When the calcium mechanisms only know one way to function, throwing something extreme at them likely will not produce a rapid enough response to meet the new demands.

    In the first case also, the mineral balance affects a similar mechanism as with acidosis, which is available ionic calcium. Other minerals can bind up calcium and precipitate it. Interestingly enough, phytic acid (in fiber), oxalic acid (in some greens like spinach and rhubarb), and sodium (in salt an bicarb), can cause precipitation. Similar story with phosphorus and potassium.. but those are more about cell membrane pumps and more complex biological reactions than straight precipitation.

    In the second case of the actual causes of hypocalcemia, it gets interesting. The mechanism by which it occurs is that the parathyroid gland produces a hormone (parathyroid hormone, PTH), which regulates the level of ionic calcium in the blood. The activity of this gland is influenced by a hodgepodge of things. Vitamin D, magnesium (this is part of why we give CMPK), and calcitonin play the major roles here. It's a complex interaction, no time to talk about it now, but the major point is that when does kid, their bodies release massive amounts of PTH, to trigger the bones (the osteoclasts in bone) to release calcium and use up those reserves. PTH also ups ionic calcium absorption, and increases vitamin D activation (Vit D is a calcium/phosphorus regulator)

    So what happens if something is off? Well:
    -not enough Vit D (with not enough sunshine from having no windows in the barn, for example) means no way to regulate the calcium, the PTH hormone doesn't work in time, bones don't give off calcium (they actually become resistant, it's like they "see" the PTH which wants to borrow some calcium, and the osteoclasts say "eh, maybe later"), and the overall calcium balance is disrupted.
    - Too much protein? Pure and simple, calcium is peed out, causing not enough reserves on bones, and more importantly for milkers, not enough long-term calcium, causing subclinical hypocalcemia that is undetected, and then presents itself in birth. It also taxes the liver and kidneys. It also causes this imbalance between the protein-bound calcium and ionic calcium, which combined with a PTH inefficiency is not good... means intermediate term calcium in the blood in the form of protein-bound calcium can't be accessed.
    - Not enough magnesium or other minerals? Improper parathyroid function, too slow, can't respond to body hormonal triggers, etc.
    - Too much grain or too many grain byproducts or molasses? Long-term acidosis, which at first is fine, because it actually makes more calcium available, but, it sets the stage for long term failure. Ability to absorb calcium is decreased due to damage to cells, rumen microflora isn't balanced, cell ionic active transport mechanisms aren't used to a more normal, moderate protein diet, like what you get from high quality alfalfa.

    Back to work, but that's the gist of it.

    Well, maybe one more word. If anyone is feeding a 16% dairy ration, along with high quality alfalfa, unless you know what you're doing, you are slowly killing your does with protein. Sure, they'll perform for a while, and die at 8 or 9, and have health issues in the meantime. The many recommendations here for a 12% ration of whole grain at no more than 1.5% of body weight are very well founded in nutritional science. Same thing for many commercial feeds, especially ones with molasses. If you don't balance those with a high quality calcium supplement (like Techmaster), and alfalfa or something similar for the right calcium/phosphorus balance, you are slowly killing your does. Commercial dairies sometimes do it because a certain rate of mastitis, and a certain rate of hypocalcemia are expected as normal, and because they push for milk production and milk stars. Neither should be normal with good management. The common cause of mastitis, for example, is not keeping things clean, and more so, bad teat management by not using the right inflations, not having air inlet at the claw to help avoid backsplashing, not configuring pulsators properly, not cleaning, etc. But, there I go on my soapbox again.

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    Pav in Redmond, WA
    Own Mini-LaManchas, hope to breed new mini-LaMancha line.