A requisite step in the development of effective therapies is an appreciation of pathologic changes caused by heat stress. Given this, we are particularly interested in improving our mechanistic understanding of pathological changes in skeletal muscle caused by prolonged heat stress.  At the whole muscle level heat stress antagonizes muscle growth and protein accretion.  Furthermore, application of in utero heat stress causes offspring to have less lean tissue.  This is in stark contrast to brief exposure to heat, which results in enhanced muscle growth and even blunts atrophy caused by unweighting or disuse.  Hence, we are also interested in discerning molecular events that distinguish therapeutic hyperthermia from pathological heat stress.  Gaining this mechanistic understanding of heat stress is necessary for the development of therapies to protect human patients from injury as well as maintain efficient meat production in an agricultural setting.  We are currently exploring the role of mitochondrial injury and dysfunction of autophagy in heat stressed muscle as well as how sex impacts the severity of heat stress.