The Physiology of Heat Stress: A Shift in Metabolic Priorities at the Systemic and Cellular Levels

Authors

  • Robert P. Rhoads Virginia Tech University
  • Lance H. Baumgard Iowa State University
  • Lidan Zhao Virginia Tech University

DOI:

https://doi.org/10.5377/ceiba.v54i1.2778

Keywords:

Heat load, metabolism, metabolic modifiers, sweating rate.

Abstract

At the onset of heat stress, cattle initiate a series of whole body adaptations in an effort to cope with and dissipate additional heat load. These include well-known physiological changes such as increased respiration rate and sweating rate and decreased feed intake. Environmentally induced hyperthermia in ruminants depresses production as a consequence of reduced feed intake but it is unclear how shifts in metabolism may further affect production performance and physiological acclimation. Our evidence indicates that cattle experiencing heat stress do not appear to engage metabolic and glucose-sparing adaptations consistent with their plane of nutrition. In this context, the liver is uniquely positioned to direct exogenously and endogenously derived nutrients for use by other metabolically active tissues such as the mammary gland and skeletal muscle. Despite the prominent role of the liver in whole-body metabolism, alterations in the molecular mechanisms leading to hepatic adaptation during heat challenge are unclear. We are using management tools and metabolic modifiers, such as bovine somatotropin, in an attempt to better understand and improve hepatic function during heat stress. Because a large proportion of an animal’s mass is comprised of skeletal muscle, alterations in skeletal muscle metabolism and function can have a profound impact on whole-animal energy metabolism and nutrient homeostasis especially during periods of stress.  We have initiated studies to understand how hyperthermia influences the set points of several metabolic pathways within skeletal muscle. It appears that during heat stress bovine skeletal muscle experiences mitochondrial dysfunction leading to impaired cellular energy status. Finally, investigations into adipose tissue metabolism demonstrate impaired lipolytic functions likely due to a refractory nature to adrenergic stimuli. Taken together, this may have broad implications for the reduced production and heat intolerance seen during heat stress especially if tissue(s) are not able to make necessary contributions to whole-body energy homeostasis. Accurately understanding the biological mechanism(s) by which thermal stress reduces animal performance is critical for developing novel approaches (i.e. genetic, managerial and nutritional) to preserve growth and lactation especially given the critical importance of nutrients, such as glucose, to animal production and well being in these situations.

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Author Biographies

Robert P. Rhoads, Virginia Tech University

Dept. of Animal and Poultry Sciences

Lance H. Baumgard, Iowa State University

Dept. of Animal Science

Lidan Zhao, Virginia Tech University

Dept. of Animal and Poultry Sciences

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Published

2016-08-03

How to Cite

Rhoads, R. P., Baumgard, L. H., & Zhao, L. (2016). The Physiology of Heat Stress: A Shift in Metabolic Priorities at the Systemic and Cellular Levels. Ceiba, 54(1), 50–58. https://doi.org/10.5377/ceiba.v54i1.2778

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