Despite many challenges faced by animal producers, including environmental problems, diseases, economic pressure, and feed availability, it is still predicted that animal production in developing countries will continue to sustain the future growth of the world's meat production. In these areas, livestock performance is generally lower than those obtained in Western Europe and North America. Although many factors can be involved, climatic factors are among the first and crucial limiting factors of the development of animal production in warm regions. In addition, global warming will further accentuate heat stress-related problems. The objective of this paper was to review the effective strategies to alleviate heat stress in the context of tropical livestock production systems. These strategies can be classified into three groups: those increasing feed intake or decreasing metabolic heat production, those enhancing heat-loss capacities, and those involving genetic selection for heat tolerance. Under heat stress, improved production should be possible through modifications of diet composition that either promotes a higher intake or compensates the low feed consumption. In addition, altering feeding management such as a change in feeding time and/or frequency, are efficient tools to avoid excessive heat load and improve survival rate, especially in poultry. Methods to enhance heat exchange between the environment and the animal and those changing the environment to prevent or limit heat stress can be used to improve performance under hot climatic conditions. Although differences in thermal tolerance exist between livestock species (ruminants . monogastrics), there are also large differences between breeds of a species and within each breed. Consequently, the opportunity may exist to improve thermal tolerance of the animals using genetic tools. However, further research is required to quantify the genetic antagonism between adaptation and production traits to evaluate the potential selection response. With the development of molecular biotechnologies, new opportunities are available to characterize gene expression and identify key cellular responses to heat stress. These new tools will enable scientists to improve the accuracy and the efficiency of selection for heat tolerance. Epigenetic regulation of gene expression and thermal imprinting of the genome could also be an efficient method to improve thermal tolerance. Such techniques (e.g. perinatal heat acclimation) are currently being experimented in chicken.

Rapid growth rate has presented broiler chickens with serious difficulties when called on to thermoregulate efficiently in hot environmental conditions. Altering the incubation temperature may induce an improvement in the acquisition of thermotolerance (AT). This study aimed to elucidate the effect of thermal manipulations (TM) during the development of the thyroid and adrenal axis of broiler embryos on the potential of broilers to withstand acute thermal stress at marketing age. Cobb broiler embryos were subjected to TM at 39.5 degrees C and 65% RH from embryonic day 7 to 16 (inclusive), either continuously (24 h) or intermittently (12 h). After hatching chicks were raised under standard conditions to 35 d of age and then subjected to thermal challenge (35 degrees C for 5 h). Continuous TM caused a significant decline in hatchability, coupled with significantly lower BW and body temperature at hatching. The intermittent (12-h) chicks showed results similar to the controls but had significantly lower body temperature. Thermal challenge at marketing age demonstrated a significant improvement in AT in both the 12- and 24-h TM-treated broilers, which was characterized by a significantly lower level of stress (as evidenced by the level of plasma corticosterone) and rate of mortality. It was concluded that TM during the portion of embryogenesis when the thyroid and adrenal axis develop and mature had a long-lasting effect and improved the AT of broiler chickens. Whereas intermittent TM had no significant effect on hatchability and performance parameters, continuous TM negatively affected these parameters.

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Exposure of young chicks to thermal conditioning (TC; i.e., 37 degrees C for 24 h) resulted in significantly improved body and muscle growth at a later age. We hypothesized that TC causes an increase in satellite cell proliferation, necessary for further muscle hypertrophy. An immediate increase was observed in satellite cell DNA synthesis in culture and in vivo in response to TC of 3-day-old chicks to levels that were significantly higher than those of control chicks. This was accompanied by a marked induction of insulin-like growth factor-I (IFG-I), but not hepatocyte growth factor in the breast muscle. No significant difference between treatments in plasma IGF-I levels was observed. A marked elevation in muscle regulatory factors on day 5, followed by a decline in cell proliferation on day 6 together with continuous high levels of IGF-I in the TC chick muscle may indicate accelerated cell differentiation. These data suggest a central role for IGF-I in the immediate stimulation of satellite cell myogenic processes in response to heat exposure.

Chicks were conditioned by exposure to heat stress (36 +/- 1 C; to 80% RH) for 24 h at the age of 5, or 5 and 7 d. During conditioning, weight gain was depressed. Due to accelerated growth during the postconditioning period, a complete compensation for lost weight gain was achieved by the group conditioned at 5 d, but only a partial compensation was obtained in the group conditioned at both 5 and 7 d. At the age of 42 d, challenge with acute heat stress (35 +/- 1 C; 20 to 30% RH) resulted in a large increase in cloacal temperature of the controls and a more moderate increase in the conditioned chickens. Mortality during the thermal challenge was significantly higher in the control than that of the previously exposed (conditioned) groups. Conditioning at an early age resulted in hemodynamic changes (significant decrease in heart weight and hematocrit) and reduced plasma triiodothyronine (T3) concentration. The results suggest that reduced T3 and hemodynamic changes may be part of the mechanism associated with improved thermotolerance by early age temperature conditioning.

Genetic selection has significantly improved the muscle development of fast-growing broiler chickens in the last 50 yr. However, improvement in muscle growth has coincided with relatively poor development of visceral systems, resulting in impaired ability to cope with high environmental temperatures. The aim of this study was to elucidate the effects of thermal manipulation (TM) during different periods of embryogenesis on chick hatchability, BW and thermoregulation upon hatching, on their ability to cope with thermal challenge at 42 d of age, and on carcass and breast meat traits. Control embryos were incubated at 37.8 degrees C. The TM embryos were incubated at 37.8 degrees C and treated for 3 h at 39.5 degrees C on the following days of embryogenesis: E8 to E10 [early (EA)], E16 to E18 [late (LA)], and both E8 to E10 and E16 to E18 (EA-LA). Body weight and body temperature (T(b)) were measured at hatching and throughout the growth period as well as during exposure of 42-d-old chickens to a thermal challenge at 35 degrees C for 6 h. The LA and EA chicks exhibited significantly lower T(b) than control chicks (37.9 vs. 38.2 degrees C) at hatching, but during the growth period, differences in T(b) between treated and control chicks decreased with age. Significant hyperthermia (over 44 degrees C) was monitored in all groups during the thermal challenge, but mortality was higher in treated than in control chickens. No effect of treatments on BW was found during the entire growth period. However, breast yield was higher in LA chickens than in controls at slaughter. The EA and EA-LA treatments slightly decreased the ultimate pH of breast meat, whereas the LA treatment had no effect. In conclusion, none of the TM conditions tested in the present study were able to improve long-term thermotolerance in chickens. Late treatment favored breast muscle growth without affecting ultimate pH and drip loss of breast meat.

We investigated the cellular and molecular bases for the promotion of muscle development and growth by temperature manipulations (TMs) during late-term chick embryogenesis. We show that incubation at 39.5 degrees C (increase of 1.7 degrees C from normal conditions) from embryonic days 16 to 18 (E16 to E18) for 3 or 6 h daily increased diameter of myofibers as of day 13 of age and enhanced absolute muscle growth relative to controls, until day 35 of age. TMs had immediate (E17) and later (up to 2 wk posthatch) effects in elevating muscle cell proliferation relative to controls. This was indicated by higher DNA incorporation of thymidine and a higher number of cells expressing PCNA in intact muscle, accompanied by higher Pax7 levels, all reflecting a higher number of myogenic cells, and suggesting that the increased hypertrophy can be attributed to a higher reservoir of myogenic progeny cells produced in response to the TM. IGF-I levels were higher in the TM groups than in controls, implying a mechanism by which heat manipulations in chicks affect muscle development, with locally secreted IGF-I playing a major role. Whereas hypertrophy was similar in both TM groups, cell proliferation and Pax7 levels were more robust in the 6-h muscle, mainly posthatch, suggesting a differential effect of various TM periods on cell reservoir vs. hypertrophy and a high sensitivity of myoblasts to relatively small changes in heat duration with respect to these processes, which is manifested in the short and long term.

Thermal conditioning of chicks results in improvements in performance and thermotolerance at marketing age. Conditioning has been found to be a sensitive process, dependent on age and the temperature used. The objective of this study was to assess the optimal timing and temperature for the conditioning processes. Six separate trials were conducted on male broiler chickens: the first two aimed to find the optimal age for thermal conditioning (1 to 5 d of age); the other four evaluated the optimal thermal conditioning temperature between 36 and 40.5 C. At 42 d of age chickens were thermally challenged to evaluate their ability to cope with acute heat stress. The highest body weight was achieved when thermal conditioning had been applied at the age of 3 d, and it coincided with low feed intake and higher to significantly higher feed efficiency. These treated chickens showed relatively lower mortality rate under thermal challenge and lower to significantly lower Triiodothyronine (T3) concentration in Trial 2. Chicks that had been thermally conditioned at ambient temperatures (Ta) of 36 and 37.5 C at the age of 3 d demonstrated the best performance characteristics and the ability to reduce T3 concentration to the lowest levels during thermal challenge. It can be suggested, therefore, that a Ta between 36.0 and 37.5 C, applied at 3 d of age is optimum for thermal conditioning of broiler chickens.