Rumen Physiology
This microbial population allows cattle to digest cellulose.
Anaerobic rumen microbes (bacteria, protozoa, fungi)
The primary VFA produced on high-forage diets.
Acetate
Dietary nitrogen source used by rumen microbes to synthesize amino acids.
Rumen degradable protein (RDP)
TDN primarily estimates this nutritional component.
Energy
Energy balance state of early lactation cows.
Negative energy balance
The primary site of VFA absorption in the ruminant stomach.
Rumen (via ruminal papillae)
High-grain diets increase this VFA, predisposing to milk fat depression.
Propionate
Non-protein nitrogen commonly added to cattle diets.
Urea
Net energy for lactation accounts for losses via feces, urine, and this process.
Heat increment
Excessive early-lactation BCS loss predisposes to this liver disorder.
Fatty liver disease
Low rumen pH favors proliferation of this bacterial group.
Lactic acid–producing bacteria (e.g., Streptococcus bovis)
Physically effective fiber is required to stimulate this reflex.
Rumination (chewing and saliva production)
Another term for bypass protein.
Rumen undegradable protein (RUP)
Primary gluconeogenic VFA in ruminants.
Propionate
Ideal BCS at calving (1–5 scale).
3.0–3.5
Hypocalcemia reduces rumen motility because calcium is required for this process.
Smooth muscle contraction
Excessive production of this acid is central to acute ruminal acidosis.
Lactic acid
Excess rumen ammonia is converted in the liver to this compound.
Urea
Elevated NEFA are converted in the liver into this ketone body.
Beta-hydroxybutyrate (BHB)
DCAD diets manipulate these minerals to prevent hypocalcemia.
Calcium and phosphorus (via cation–anion balance)
Explain how rapid grain introduction can lead to laminitis.
Rapid fermentation → excess lactic acid → ↓ rumen pH → rumen epithelial damage → endotoxin/histamine release → vasoconstriction in the corium → laminitis
Describe how subacute ruminal acidosis decreases milk fat percentage.
↓ rumen pH alters biohydrogenation → ↑ trans-fatty acids → inhibit mammary fat synthesis → milk fat depression
Why can milk production be limited despite adequate crude protein intake?
Inadequate RDP limits microbial protein synthesis → reduced metabolizable protein supply
Describe the endocrine changes driving negative energy balance postpartum.
↓ insulin, ↑ growth hormone → increased lipolysis → ↑ NEFA → hepatic ketogenesis
Why are overconditioned cows predisposed to fatty liver?
Excess adipose → increased NEFA mobilization → hepatic triglyceride accumulation