Fig 1.
Schematic representation of treatments for 10 generations of Japanese quail.
Table 1.
Sample size of individually housed birds for treatment x length of exposure x sex for body weight and all i-STAT1 measurements.
Fig 2.
Body weight2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Body weight was compared across treatment, length of exposure1, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-d Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).
Table 2.
Percentage of infertile, embryo death, deformed/twins1 at the 10th generation of Japanese quail of respective treatments1.
Table 3.
FCR1 within treatments.
Fig 3.
Blood pH2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Blood pH (scale as 0 to 9) were compared across treatment, length of exposure2, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-b Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).
Fig 4.
Blood base excess2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Blood base excess (mmol/L) were compared across treatment, length of exposure2, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-c Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).
Table 4.
Blood gases1 of quail exposed to acute2 and chronic2 temperatures.
Table 5.
Blood electrolytes1 of quail exposed to acute and chronic2 temperatures.
Fig 5.
Blood glucose2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Blood glucose was compared across treatment, length of exposure2, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-d Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).
Fig 6.
Hematocrit2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Hematocrit was compared across treatment, length of exposure2, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-c Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).
Fig 7.
Hemoglobin2 of quail exposed to acute and chronic3 temperatures.
1 Four treatments were: (1) thermoneutral controls (22.2˚C, TN), (2) thermoneutral siblings (22.2˚C, TNS), (3) heat stress (31.1˚C, HS), and (4) heat stressed siblings (31.1˚C, HSS) TN and HS were obtained through generational mating at 22.2˚C and 31.1˚C, respectively. TNS and HSS were obtained by mating males and females from TNS and dividing their offspring evenly into chambers at 22.2˚C (TNS) and 31.1˚C (HSS). Only families from TNS that had high fitness in HSS were mated. 2 Hemoglobin was compared across treatment, length of exposure2, sex, and their interactions. 3 Acute, exposure to respective temperature for 4 hours; chronic, exposure to respective temperatures for 3 weeks. a-c Superscripts indicate significant differences at P≤0.05. Means are presented with standard deviations (SD).