Date of Award
Master of Science
Genetics and Genomics
Prolonged exposure to elevated environmental temperature can result in heat stress. Heat stress has negative effects on human health, animal health and wellbeing, and brings economic losses related to agricultural production. While clinical symptoms of heat stress are well studied, intracellular mechanisms of heat stress-induced injury require further investigation and are essential for development of etiological treatment of heal illness. Skeletal muscle dysfunction is one of the major pathologies associated with heat stress in both humans and animals. This thesis was aimed to determine changes in major pathways involved in the skeletal muscle response to short-term hyperthermic exposure. It has been established that redox balance plays a crucial role in heat stress injury as an exposure to elevated temperature leads to mitochondrial respiratory dysfunction via disruption of the mitochondrial electron transport chain. Dysfunctional mitochondrial respiration, in turn, leads to increased production of reactive oxygen species and oxidative stress. Further, heat stress activates inflammatory signaling pathways in skeletal muscle. To determine changes in heat stress sensitive pathways, this thesis was divided into three research chapters. The first research chapter includes results from pigs exposed to heat stress for 2 h, 4 h, or 6 h. We found that heat stress resulted in decreased abundance of oxidative stress indicators likely due to elevations in antioxidant activity. These changes were independent of mitochondrial content and mitochondrial biogenesis. In the second research chapter we found activation of AP-1 signaling pathway following 4 h of heat stress, while initial signs of NF-κB activation occurred following 6 h of heat stress. Inflammatory signaling activation was associated with decreased protein abundance of cytokine IL-6. In the final research chapter we aimed to determine the extent to which short-term heat stress altered mitochondrial function and confirm a reductive shift in redox balance in murine skeletal muscle. Mice exposed to elevated temperature for 6 h had mitochondrial function similar to animals kept under thermoneutral conditions. In conclusion, short-term heat stress shifts redox balance and activates inflammatory signaling but has little effect on mitochondrial content, biogenesis, or function.
Volodina, Olga, "Early chronology of heat stress-induced alterations in skeletal muscle" (2016). Graduate Theses and Dissertations. 16530.