Do not let high temperature to lower down the production

The weather constitutes a complex system, which acts upon the bird & exert various detrimental effects on neuroendocrine, cardiorespiratory system. Rearing birds out of their thermal comfort zone could mean failing to leverage full genetic potential. Poultry production in the tropical and subtropical regions having biggest environmental challenge is heat stress which could reduce productivity and even increase the mortality tolls due to depressed immunity.

If the ambient temperature changes gradually, birds adapt to the changes, but if the changes are rapid and especially accompanied with high relative humidity, they induce heat stress (R. Mearns).

Complex interplay exists between the environment and reproductive performance of the poultry. Heat stress may influence the rate of secretion of hormones and their metabolic clearance rate. In addition, it may affect the sensitivity of gonads to metabolic hormones by altering the receptor numbers. (J.O Ayo).

Cytokine IL-1 stimulates hypothalamic-pituitary-adrenal axis and inhibits hypothalamic-pituitary-gonadal functions. Temperatures disturb the pulsatile gonadotrophin-releasing hormone generation frequency, which in turn compromises reproductive functions due to heat-induced impairment in the secretion of FSH & LH in laying birds. (Dantzer and Kelly). It also results in lipid peroxidation of cytomembranes due to excessive free radical generation. (Kronenberg & Williams).

Heat stress causing 20% feed reduction & calcium-estrogen homeostasis got imbalanced. It results in decrease egg production and egg shell quality. Stress also increases the free radicals thus lowered the Haugh unit of the albumen and depresses yolk size. Reproductive losses due to heat stress are manifested in the percentage of culled birds and mortality due to heat stroke. (Ayo et al & Mahmoud et al).

The broiler breeder contributed more to heat-induced infertility than the female. (McDaniel et al, 1996].

Heat stress affects all phases of semen production in breeder cocks. Serum calcium and phosphorus levels were observed to be significantly lowered in heat-stressed birds. Inhibition of calcium and potassium ion exchange significantly decreased spermatogenesis.[Schreiber et al, 1998].

Heat stress may be responsible for the inhibition of osmotic equilibrium and ionic channels that are key elements in the interplay between spermatozoa, its environment, and the egg, thus disrupting semen quality [Darszon et al, 1999].

Heat stress in the rooster retards or even prevents important physiological mechanisms, such as sperm-uterine epithelial cells interaction, capacitation, acrosome reaction, and zonal vesicle binding, resulting in depression in fertility. This is, apparently, due to a depletion of endogenous antioxidant present in semen, leading to speedy exhaustion of spermatozoa energy reserves. (Taylor et al, 2009).

Male fertility declined to 42% and in vivo sperm-egg penetration declined to 52%, compared to males that were maintained at thermoneutral zone.

Chicken spermatozoa composed of high proportion of polyunsaturated fatty acids such as arachidonic acids [Surai et al, 2002]. Reactive oxygen species generated during stress attack polyunsaturated fatty acids in the cell membranes, which leads to a sequential chemical reactions called lipid peroxidation & thus damage the spermatozoa.[ Surai et al, 2001].

Breeder hens inseminated in the morning hours had a significantly higher fertility and hatchability than those obtained in inseminated hens during the afternoon hours. The reason for this finding may be due to the association between semen production and rhythmic changes in metabolic rate; the rate of spermatogenesis may vary with diurnal changes in body temperature.

It has been shown that a constant incubation temperature of 37.80C is best for embryo development and hatchability. Any marginal deviation from this fragile balance is detrimental to the developing embryo [Lourens et al].

Dead embryos occurred soon after subjecting them to heat stress, especially on days 7 and 19. This implies that embryos at these stages of development may be very sensitive to all types of stress, including heat stress, which could be related to the chorioallantoic membrane susceptibility to environmental stress. It may be due to increased endogenous (metabolic) heat production.

Hyperthermia inhibited embryonic growth rate, which resulted in increased incidence of malformation and lowered hatch weight. Heat stress during incubation depressed liver function and development. High environmental temperatures were shown to induce high mortality due to ascites [Meijerhof and Albers]. Other consequences are disproportionate development, circulation disruption, abnormalities. (Ande and Wilson).