Effects of Energy Intake on Performance, Mobilization and Retention of Body Tissue, and Metabolic Parameters in Dairy Cows with Special Regard to Effects of Pre-partum Nutrition on Lactation - A Review -

Abstract

The present review focuses on the effects of energy intake on performance, changes in body tissue during lactation, and metabolic parameters in dairy cows. Especially, pre-partum nutrition and its influence on lactation are emphasized. In recent decades the increase in genetic potential of dairy cows has increased milk yield. This fact sharpens the problem of a negative energy balance in early lactation because the amount of energy required for maintenance and milk production exceeds the amount of energy cows can consume. Around parturition, reduced feed intake reinforces the situation. Continuing negative energy balance causes decreasing milk yield, fertility problems, and incidence of metabolic diseases. Hence, the cow has to rely on body reserves that were stored in late lactation and the dry period. It is evident that the nutritional status pre-partum acts as the key factor for milk yield and fertility parameters in the following lactation. Cows overfed during the foregoing gestation and which have gained large quantities of body fat have lower dry matter intake along with the need to mobilize larger quantities of body reserves in lactation. The milk yield in the following lactation is lower than in cows fed according to their requirements. Cows restrictively fed in late gestation have a higher feed intake in lactation and a lower mobilization of body reserves. The effect of energy intake post-partum plays only a minor role for performance parameters in lactation. Lipid mobilized from body reserves makes a substantial contribution to the energetic cost of milk production in early lactation and adipose tissue undergoes specific metabolic alterations. Adipose tissue is degraded to free fatty acids, which are used in liver for energy purposes. High lipid mobilisation promotes the development of a fatty liver and therefore a reduced gluconeogenesis.