Heat stress decreases metabolic flexibility in skeletal muscle of growing pigs

Author:

Zhao Lidan1,McMillan Ryan P.2,Xie Guohao1,Giridhar Samantha G. L. W.1,Baumgard Lance H.3,El-Kadi Samer1,Selsby Joshua3,Ross Jason3,Gabler Nicholas3,Hulver Matthew W.24,Rhoads Robert P.1ORCID

Affiliation:

1. Department of Animal and Poultry Sciences, Virginia Tech University, Blacksburg, Virginia

2. Virginia Tech Metabolic Phenotyping Core, Virginia Tech University, Blacksburg, Virginia

3. Department of Animal Science, Iowa State University, Ames, Iowa

4. Department of Human Nutrition, Foods and Exercise, Virginia Tech University, Blacksburg, Virginia

Abstract

Heat-stressed pigs experience metabolic alterations, including altered insulin profiles, reduced lipid mobilization, and compromised intestinal integrity. This is bioenergetically distinct from thermal neutral pigs on a similar nutritional plane. To delineate differences in substrate preferences between direct and indirect (via reduced feed intake) heat stress effects, skeletal muscle fuel metabolism was assessed. Pigs (35.3 ± 0.8 kg) were randomly assigned to three treatments: thermal neutral fed ad libitum (TN; 21°C, n = 8), heat stress fed ad libitum (HS; 35°C, n = 8), and TN, pair-fed/HS intake (PF; n = 8) for 7 days. Body temperature (TB) and feed intake (FI) were recorded daily. Longissimus dorsi muscle was biopsied for metabolic assays on days −2, 3, and 7 relative to initiation of environmental treatments. Heat stress increased TBand decreased FI ( P < 0.05). Heat stress inhibited incomplete fatty acid oxidation and glucose oxidation ( P < 0.05). Metabolic flexibility decreased in HS pigs compared with TN and PF controls ( P < 0.05). Both phosphofructokinase and pyruvate dehydrogenase (PDH) activities increased in PF ( P < 0.05); however, TN and HS did not differ. Heat stress inhibited citrate synthase and β-hydroxyacyl-CoA dehydrogenase (β-HAD) activities ( P < 0.05). Heat stress did not alter PDH phosphorylation or carnitine palmitoyltransferase 1 abundance but reduced acetyl-CoA carboxylase 1 (ACC1) protein abundance ( P < 0.05). In conclusion, HS decreased skeletal muscle fatty acid oxidation and metabolic flexibility, likely involving β-HAD and ACC regulation.

Funder

USDA AFRI

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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