Heat stress continues to undermine efficient meat production and meat quality. It also jeopardizes human and animal health and wellbeing, regionalizes animal production, and threatens food security. Environmental models predict more frequent and severe heat waves, even in areas previously considered temperate indicating this problem will continue to have a progressively expanding, deleterious impact on agricultural productivity. Despite the broad, negative impact of heat stress little is known about underlying mechanisms leading to phenotypic outcomes. Because of its mass and energetic demands, skeletal muscle contributes greatly to regulation of systemic metabolism. We have discovered heat stress causes robust but transient oxidative stress and activation of apoptotic signaling in skeletal muscle in as little as two hours. Interestingly, these declined linearly through six hours concomitant with markers of increased autophagy and mitophagy, which would facilitate the removal of damaged mitochondria. Continued heating through 24 h causes a resumption of oxidative stress and autophagic dysfunction with an accumulation of autophagosomes and mitochondria. As mitochondrial injury and autophagic dysregulation appear to be key mediators of hyperthermic muscle dysfunction we propose a model that posits progressive mitochondrial injury leads to production of free radicals that overwhelms antioxidant systems and impairs autophagy facilitating accumulation of damaged, pro-oxidant mitochondria. Ultimately, these aforementioned changes may reduce efficient protein accretion. Our current work is focused on stimulating autophagy and protecting mitochondria during heat stress in an effort to maintain efficient muscle growth.
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