The impact of antioxidant supplementation and short-term heat stress on lamb body weight gain, meat nutritional profile and functionality (storage stability of lipids and colour) of lamb meat was investigated. A total of 48 crossbred ((Merino × Border Leicester) × Dorset) lambs (42 ± 2 kg body weight, 7 mo age) were randomly allocated to three dietary treatments (n
= 16) by liveweight (LW) that differed in dosage of vitamin E and selenium (Se) in the diet. Vitamin E and Se levels in the control (CON), moderate (MOD) and supranutritional (SUP) dietary treatments were 28, 130 and 228 mg/kg DM as α-tocopherol acetate and 0.16, 0.66 and 1.16 mg Se as SelPlex™/kg DM, respectively. After four weeks of feeding in individual pens, including one week of adaptation, lambs were exposed to two heat treatments. Animals were moved to metabolism cages for one week and subjected to heat treatments: thermoneutral (TN; 18–21 °C and 40–50% relative humidity) and heat stress (HS; 28–40 °C and 30–40% relative humidity) conditions, respectively. Final LW and hot carcass weight were influenced by dietary treatments with higher final live weight (FLW) (p
= 0.05; 46.8 vs. 44.4 and 43.8 kg, respectively) and hot carcass weight (HCW) (p
= 0.01; 22.5 vs. 21.3 and 21.0 kg, respectively) recorded in lambs fed the SUP as opposed to the CON and MOD diets. Vitamin E concentration in the longissimus lumborum (LL) muscle tended to be higher in lambs fed MOD or SUP diets than the CON group. Lipid oxidation of aged meat at 72 h of simulated retail display was reduced by antioxidant supplementation. Short-term (one week) heat stress treatment significantly increased muscle linoleic acid and total omega-6 concentrations compared with the CON group. The results demonstrate that four-week antioxidant supplementation at the SUP level improved animal productivity by increasing LW and carcass weight and the functionality of meat exhibited by reduced lipid oxidation. An increase in muscle omega-6 fatty acid concentration from short-term heat stress may induce oxidative stress via proinflammatory action.
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