Abstract
The dairy industry depends upon a successful cow lactation for economic profitability. Heat stress is documented to have a significant impact on the economic sustainability of the dairy industry as it significantly alters production parameters such as milk yield and reproduction. Heat stress has been documented to alter highly conserved lactation nutrient sparing strategies, such as the mobilization of fatty acids to support the energetic demands on extramammary tissues. If a cow is unable to maintain metabolic homeorhesis, lactation performance is impacted and there is an increased risk for developing metabolic disorders. Mitochondria provide the energetic foundation to enable a myriad of metabolic processes and changes in an organism’s metabolism are accomplished through adaptations in mitochondrial behavior. There is evidence that links mitochondrial metabolism adaptation as a response to the increased energy needs of lactation in the mammary gland and extramammary tissues. Additionally, mitochondria act as primary stress responses and coordinate the body’s response to stress. They integrate endocrine signals into the cellular stress response and, through mito-nuclear communication, modulate the energetic response to stress. In-vitro heat insults affect mitochondria through a compromise in mitochondrial integrity, which is linked to a decrease in mitochondrial function. However, limited evidence exists linking the in-vivo metabolic effects of heat stress with parameters of mitochondrial behavior and function in lactating dairy cattle. Through this thesis research, I seek to characterize how in-vivo heat stress affects mitochondrial function and behavior. Moreover, I seek to utilize these measures to possibly explain the cellular underpinnings of the heat-stress induced lactation depression commonly observed in dairy cows. Briefly, through a pair-feeding heat stress experimental design, we found that our heat stress model induced a mild and chronic heat stimulus in which we observed a reduction in milk yield. Further, this stimulus had an effect on mitochondrial biogenesis and mitochondrial number, in mammary tissue. Thus, our data suggest that, even mild heat stress stimuli can have an effect on mitochondrial behavior.