| Commercial AA broilers and local Beijing-You chickens were used in two experiments to study theeffects of chronic heat exposure on meat quality and fat deposition. The mechanisms underlying thesechanges in response to heat stress were also studied.Trial 1: Male chickens (5wk old) from a fast-growing strain (Arbor Acres, AA) and a local slow-growingbreed (Beijing-You, BJY) were transferred to three temperature-controlled chambers, where the 108from each type were equally distributed to 3 treatments with 6 replicates each of 6 birds: constantoptimal ambient temperature at 21C with ad libitum feeding (21AL), constant high ambient temperatureat 34C with ad libitum feeding (34AL), and constant optimal ambient temperature at 21C but pair-fed tothe amount consumed by the 34AL group (21PF). At 8 wk of age, 18 birds from each treatment wereweighed, blood sampled, and slaughtered. The results showed that: 1) feed intakes were decreased(P＜0.001) by heat exposure in both types of chickens. Compared to 21A1, AA broilers in 34ALexhibited greatly decreased weight gain (P＜0.001), breast proportion ofBW (P＜0.05) and fat deposition,L~* values and drip loss increased but insine monphosphate (IMP) decreased in breast muscles. Whencomparing 21PF to 34AL AA broilers, heat stress enhanced abdominal fat and intermuscular fatdeposition (P＜0.01). For BJY chickens,, pair-feeding decreased weight gain and breast proportion(P＜0.05), but heat exposure had no significant influence on weight gain, breast proportion and meatquality when compared to 21AL. Heat-exposed BJY chickens showed higher feed efficiency than didbirds in 21AL, and higher abdominal fat deposition than those in both 21AL and 21PE The mortalitywas 36％in AA broilers and 0 in BJY chickens when they were chroniclly exposed to high ambienttemperature. 2) Heat exposure had no effect on malondiadehyde (MDA) concentration, activities ofsuperoxide dismutase (SOD) and creatine kinase (CK) in plasma, and activity of hepaticglutamate-oxalacetate transaminase (GOT) in BJY chickens. Activity of CK in plasma and GOT in liverwere enhanced significantly in heat-stressed AA broilers. 3) Activities of fat acid synthase (FAS) andmalic enzyme (ME) in liver had no significant difference between 34A1 and 21AL AA broilers or BJYchickens. These activities increased in heat-exposed birds when compared to 21PF birds. Increasedactivities of lipoprotein lipase (LPL) in abdominal fat (P＜0.01) and plasma level of nonesterified fattyacid (NEFA) (P＜0.05) were measured in 34AL BJY chickens. Heat exposure of AA broilers increasedthe concentration of glucose in plasma (PG), but had no obvious effect on blood level of very lowdensity lipoproteins (VLDL) or insulin (INS). 4) Eexpressions of FAS and ME genes tended to decreasein heat-exposed BJY chickens but in increased in heat-exposed AA broilers.Trial 2: Male BJY chickens (n=72, 80d of age) were equally distributed to 21PF and 34A1 treatments, asdescribed above, for a 20 d period of study. The results showed that the final weight, daily weight gain,feed conversion, carcass traits and fat deposition did not filer significantly between the 2 groups. ForBJY chickens, heat-exposed at this older age, L~* values increased (P＜0.05) and IMP content decreased(P＜0.01) significantly in breast muscles; MDA concentration (P＜0.05) and CK activity (P＜0.01) inplasma increased; LPL activities in both subcutaneous (P＜0.01) and intermuscular fats (P＜0.05)increased; Concentration of NEFA in plasma decreased (P＜0.05); there were no differences between thetreatments in PG, VLDL and INS, nor in the activities and transcript aboundance of FAS and ME in liver.The results from this study demonstrate the following: 1) the responses to heat stress in broilers differswith breeds and age; younger BJY chickens were less affected and maintained normal growth and meat quality despite the heat; resistance to heat was reduced in older BJY chickens, feed intake decreasedmore and resulted in lower performance; AA broilers were more sensitive, heat exposure with strikinglynegative effects on survival, growth performance, breast yield, and meat quality. 2) The higher feedefficiency and enhanced abdominal fat deposition would account for the high adaptability to extremeheat in 35-56d BJY chickens. The lipid metabolism of adipose tissues in heat-exposed younger BJYchickens was enhanced, suggesting that this represents a high priority use of energy. Consequently,plasma fatty acid uptake and storage in adipose tissue would have been facilitated, resulting in greaterfatness. 3) Enhancement of fat deposition may be an adaptive strategy in heat-stressed chickens. Similarchanges were apparent even in AA broilers, but enhancement in lipogenesis was counteracted bydecreased feed intake when these birds were exposed to heat. The activity of LPL in adipose tissues wasincreased and lipid catabolism was reduced in older heat-exposed BJY chickens, presumably to maintainthe maximal energy storage. 4) The activity of LPL in adipose tissues and plasma concentration ofNEFA maybe be useful as indices when attempting to control fatness of broilers under hot conditions.
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