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Cow Physiology-Based Phase Feeding Revisited

 

Cow Physiology-Based Phase Feeding Revisited

PHASE feeding is a concept introduced in the early 1980s that is centered around diet modifications based on the relationship among milk production, feed intake and bodyweight change occurring throughout the cow's lactation cycle.

It was an economically driven, evolutionary step in feed management as dairy herds became larger and cow grouping more feasible. Having recently reread several papers from Michigan State University researchers on the hepatic oxidation (HO) theory of feed intake, it occurred to me that phase feeding might need rejuvenating based on a much-improved understanding of the physiological changes cows undergo from prepartum through late lactation.

Intake drivers

Most nutritionists were trained to think about feed intake as a function of bodyweight, production demand, weather conditions, feeding frequency and sequencing, particle size, specific gravity, physical fill and fermentability of starch and fiber. The current National Research Council's Nutrient Requirements of Dairy Cattle (2001) also makes limited references to metabolic feedback factors and oxygen consumption theories for predicting intake.

More recently, physiological-based explanations such as the HO theory are providing yet more insight into the various factors that need to be considered to maximize intakes.

The HO theory suggests that the oxidation of fatty acids, propionate, lactate and amino acids in the liver is an important driver of feed intake. The production of adenosine triphosphate (ATP) appears to influence the firing rate of the hepatic vagus nerve, triggering either satiety (increased oxidation and ATP production) or hunger (reduced oxidation and ATP production).

What makes this difficult to research is that the pattern of liver oxidation on a minute-to-minute basis is critical to feeding behavior because the amount of oxidation studied over longer periods of time (hours or days) is relatively constant and is determined by the energy requirement of the liver (Allen and Bradford, 2009a).

The physiological signals driving intake change from transition cows to late-lactation cows. It appears that controlling feed intake is heavily influenced by liver oxidation of non-esterified fatty acids (NEFAs) during the transition phase, by ruminal distention in peak-lactation cows and by propionate production in late-lactation animals (Allen and Bradford, 2009a). Rethinking the concept of phase feeding with these factors in mind may help nutritionists better formulate diets that optimize dry matter intake.

Transition to early lactation

Elevated NEFA levels from mobilized body fat suppress both intake and immune function during the transition period. Controlling the mobilization of body fat during transition and early lactation is essential to maximizing intake.

Plasma insulin concentrations and insulin tissue sensitivity - both of which contribute to increased fat mobilization - begin declining several weeks prepartum. Despite lower intakes, this helps the transition cow maintain a constant plasma glucose concentration due to the glucose-sparing result from maternal and fetal tissue utilization of the circulating NEFAs (Allen and Bradford, 2009a).

Plasma insulin concentrations and tissue sensitivity remain low in early lactation, thus elevating NEFA levels. The length of time NEFAs remain elevated varies among cows and depends upon the rate of fat mobilization and removal rates by the liver and mammary gland. NEFA utilization by the mammary gland serves to lower NEFA levels.

However, elevated NEFA oxidation in the liver reduces feed intake, increases the potential for fatty liver and increases the export of ketones when the liver's ability to completely oxidize fatty acids is limited (Allen and Bradford, 2009a).

Reduced feed intake from elevated NEFA levels will delay the increase in plasma glucose concentrations, resulting in lower milk yield due to reduced lactose production. Thus, it is desirable to increase glucose concentrations in early lactation because it stimulates insulin secretion from the pancreas.

One study (Dann et al., 1999) has shown a positive intake response during the first 63 days of lactation by feeding a low concentration of highly fermentable starch in the prepartum diet, which initiated an increase in plasma insulin and a decrease in plasma NEFA concentrations.

Limiting dietary starch fermentability can enhance intake during early lactation. Propionate, the primary end product of starch digestion, is absorbed at high rates and rapidly taken up in the liver to produce glucose. If propionate is absorbed faster than it can be utilized to produce glucose, it will be oxidized, yielding ATP and signaling satiety to the brain.

This is typically not a problem in early-lactation cows due to the fact that the liver increases significantly in size after calving and limiting liver enzymes are up-regulated in response to the increased production demand for glucose. However, propionate also stimulates oxidation of acetyl co-enzyme A (CoA), which is typically elevated in early-lactation cows from partial oxidation of NEFAs, and that can also result in increased ATP production and signal satiety to the brain (Allen and Bradford, 2009a).

The need for propionate to produce glucose, stimulate insulin, reduce fat mobilization and increase intake must be balanced against its potential to send satiety signals to the brain due to ATP production from direct propionate oxidation or stimulation of acetyl CoA oxidation. Altering starch fermentability in transition and early-lactation diets appears to be a more desirable strategy than replacing starch with digestible fiber sources.

Supplemental fat should not be fed during the transition phase due to the intake suppression from gut peptide release that affects insulin and glucagon concentrations and also increases the supply of fatty acids (Allen and Bradford, 2009a).

Nutritionists might consider these options (Allen and Bradford, 2009a) for limiting dietary starch fermentability in fresh cows:

  1. Manipulate the grain particle size or use dry corn rather than high-moisture corn to shunt more starch digestion post-ruminally, where it is digested to glucose and oxidized to lactate by tissue and intestinal microbes;
  2. Supply other glucose precursors with less of a stimulatory effect on acetyl CoA oxidation such as glycerol from biofuel production or fructose, and
  3. Use additives such as monensin (to drive propionate production), niacin (to reduce lipolysis) or chromium (to increase tissue insulin sensitivity).

Peak lactation

As cows approach peak milk yield, increasing plasma glucose stimulates insulin production, thus reducing lipolysis and both plasma NEFA and liver acetyl CoA concentrations. A reduction in acetyl CoA coupled with increased production demand for glucose reduces liver oxidation and satiety signals to the brain.

The best indicator that HO is becoming less of an intake driver is observed increases in intake along with reduced plasma NEFA and ketone concentrations. The focus should now be on concentration, digestibility and fragility of forage neutral detergent fiber to formulate diets with relatively low gut fill and high fiber fermentability (Allen and Bradford, 2009a).

During this phase, when ruminal distension (gut fill) becomes more of an intake inhibitor, the inclusion of highly fermentable, non-forage fiber sources such as beet pulp or soy hulls as a substitute for dietary grains may be a better strategy than replacing the grain with forage, depending on cost.

Rates of starch digestion can also be manipulated, which is likely why many nutritionists prefer to feed some dry corn (shunted post-ruminally) to supplement the starch in highly rumen-fermentable starch sources like well-processed corn silage or high-moisture corn. Decreasing the rate of propionate production and absorption will likely increase meal size and possibly intake because when propionate is absorbed faster than it can be utilized to produce glucose, it will be oxidized, yielding ATP and signaling satiety (Allen and Bradford, 2009b).

Late lactation

As energy requirements decrease after peak milk yield, the impact of gut fill diminishes, and intake is again regulated more by HO. Diets fed during this phase should provide more gut fill and be limited in starch fermentability as glucose demand for milk production declines and as increases in both plasma insulin concentration and tissue sensitivity lead to greater propionate oxidation and ATP-induced satiety signals to the brain.

This approach will promote increased intake and provide a more consistent source of energy, reducing insulin and partitioning more energy to milk than body condition (Allen et al., 2009).

The Bottom Line

Many environmental, dietary and physiological factors influence feed intake in the dairy cow. Savvy nutritionists may already be formulating diets consistent with recommendations from Michigan State University, but now we have a better idea of the physiological basis for the success of these diets.

The future looks promising for refining approaches to phase feeding dairy cows now that commercial laboratory methods are becoming available to better quantify factors, like rumen fermentability, that have such a big impact on the physiological response formulated diets elicit.

References

Allen, M.S., and B.J. Bradford. 2009a. Strategies to optimize feed intake in lactating cows. WCDS Advances in Dairy Technology. 21:161-172.

Allen, M.S., and B.J. Bradford. 2009b. Nutritional control of feed intake in dairy cattle. Proceedings of the 20th Annual Florida Ruminant Nutrition Symposium. Feb. 10-11. Gainesville, Fla.

Allen, M.S., B.J. Bradford and M. Oba. 2009. Board invited review: The hepatic oxidation theory of the control of feed intake and its application to ruminants. J. Anim. Sci. 87:3317-3334.

Dann, H.M., G.A. Varga and D.E. Putnam. 1999. Improving energy supply to late gestation and early postpartum dairy cows. J. Dairy Sci. 82:1765-1778.

National Research Council. 2001. Nutrient requirements of dairy cattle. Seventh revised edition. National Academy Press, Washington, D.C.


This article was originally published in the February 2011 Feedstuffs issue, and is reproduced with their permission.

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