The Breakdown of Skeletal Muscle in Dairy Cows During Peak Lactation
Gray, T. S. (2008). The Breakdown of Skeletal Muscle in Dairy Cows During Peak Lactation (Thesis, Master of Science (MSc)). The University of Waikato, Hamilton, New Zealand. Retrieved from http://hdl.handle.net/10289/2249
Permanent Research Commons link: http://hdl.handle.net/10289/2249
The decline in fertility in dairy cows is of international concern. Since 1950, milk production demands have increased while first service rates of conception have decreased. It is unclear why fertility has decreased, however current dairy management practice requires cows to be kept on a tight yearly calving schedule to ensure maximum milk production over the lifetime of the cow. The current postulate suggests that this regime places a high metabolic burden on the cows, which in turn requires the breakdown of tissues such as fat and muscle to provide substrates to meet the increased energy demands of lactation. Immediately after calving, dairy cows enter a state of negative energy balance (EB), as they cannot consume enough energy to sustain lactation. During this period of negative EB, fat is mobilised in the form of non-esterified fatty acids to help supply the body with the extra energy it needs, but fat mobilisation decreases after four weeks while cows remain in a state of negative EB for several more weeks. It is unclear whether or not muscle breakdown occurs and plays a role in the restoration of EB in lactating cows during peak lactation. I hypothesized that the breakdown of muscle does occur in cows during peak lactation, and that it occurs to a greater extent in cows producing higher amounts of milk. Dairy cows from three strains, NZL, NZH and OSH, representing cows with differing milk production abilities (low, intermediate and high, respectively), were studied for 12 weeks postpartum. Blood was drawn at weekly intervals and muscle biopsies taken at -1, 1, 4, 8, and 12 weeks postpartum. Analysis of plasma revealed an increase in the abundance of troponin I-fs (a marker of muscle breakdown) over the period of study, suggesting that breakdown of skeletal muscle was occurring. Real-time polymerase chain reaction analysis showed that expression of the ubiquitin-proteasome (UbP) ligases atrogin-1 (atro1) and muscle ring finger protein 1 (murf1) increased initially, but returned to normal levels by four weeks postpartum. Concentration of mRNA of the lysosomal proteases, cathepsin B, D, H and L, did not change over the period of study. Therefore, the UbP pathway may contribute to the breakdown of muscle detected by troponin I-fs in plasma. Proteins involved in translation initiation were examined by Western blotting. The ratio of phosphorylated over total eIF2alpha and 4E-BP1 remained unchanged throughout the study, indicating that the breakdown of muscle was not a result of decreased protein synthesis. However, there was a greater ratio of phosphorylated to total eIF2alpha in NZL cows compared with NZH and OSH, suggesting that protein synthesis was less overall in NZL cows than other strains. Measurement of myosin heavy chain composition indicated there was no change in the abundance of type I and type IIx muscle fibres and plasma myostatin levels did not change over the period of study. However, the OSH cows had less myostatin in their plasma than the NZL and NZH cows, suggesting that there may be inhibition of muscle growth occurring in this strain. The results of this study suggest that breakdown of muscle could be important in restoring the EB in high-producing dairy cows during peak lactation. Upregulation of the UbP pathway during the first four weeks of lactation may contribute to this muscle breakdown. However, it remains unclear what processes then continue to regulate breakdown of skeletal muscle to maintain the elevated abundance of troponin I-fs in plasma from four to 12 weeks postpartum in lactating dairy cows.
The University of Waikato
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- Masters Degree Theses