Model of Physiological Stress in Chickens 4. Digestion and Metabolism 1,2

Model of Physiological Stress in Chickens 4. Digestion and Metabolism 1,2 S. Puvadolpirod 3 and J. P. Thaxton 4 Department of Poultry Science, Mississippi State University, Mississippi State, Mississippi 39762 ABSTRACT Two similar experiments were conducted chicks were lower than CON through 1 wk after cessation to evaluate the effects of stress on growth and feed utilization of broiler chicks. Stress was induced by continuous of infusion of ACTH. Contrasted to effects during the stress period, after cessation of ACTH-treatment, absorption of all nutrients was reduced, and, during this delivery of adrenocorticotropin (ACTH) at 8 IU/kg BW/ d for 7 consecutive d. During the 7-d stress period, ACTHtreated chicks did not exhibit increases in feed intake, but poststress recovery period, digestion appeared to return to the range of CON values. Results indicate that all physiological parameters with the exceptions of reductions in increases in water intake concomitant with an increase BW and thymus weight returned to the range of CON in excreta output were recorded. The ACTH caused decreases in digestion of dry matter, proteins, gross energy, values within 1 wk after cessation of ACTH infusion. However, feed intake and absorption of energy dry matter and nitrogenous compounds remained lower than and carbohydrates, whereas fat digestibility was unaffected. Digestion of these nutrients was affected more CON at that time. Also, losses in skeletal muscle caused than absorption during the stress period. by prolonged gluconeogenesis apparently required extended By 1 wk poststress, all parameters were comparable with those of the control, except for feed intake, which was less than that of CON. The BW of ACTH-treated periods for complete recovery, as evidenced by stressed chicks that did not gain comparably to CON after a 1 wk cessation of ACTH delivery. (Key words: stress, adrenocorticotropin, digestion, metabolism, broilers) 2000 Poultry Science 79:383 390 INTRODUCTION Stress causes a general deterioration in the well-being of animals, and growth and reproduction are often compromised. Stressed chicks normally exhibit elevated plasma levels of corticosterone (CS), whether treated with adrenocorticotropin (ACTH) (Siegel, 1968; Davison et al., 1985; Davis and Siopes, 1989), CS (Siegel and Van Kampen, 1984; Donker and Beuving, 1989), or feed restriction (Weber et al., 1990). Elevated blood levels of CS, in turn, cause increased energy levels by acting on intermediary metabolism of carbohydrates, protein, and fats. One of the most important effects of CS is an increase in glucose production by catabolism of muscle protein. This catabolic turnover of muscle proteins is driven directly by CS-activated gluconeogenesis. Plasma Received for publication May 28, 1999. Accepted for publication November 11, 1999. 1 This is Journal Article No. J-9527 from the Mississippi Agricultural and Forestry Experiment Station supported by MIS-2903. 2 Use of trade names in this publication does not imply endorsement by the Mississippi Agricultural and Forestry Experiment Station of these products nor similar ones not mentioned. 3 Present address: Sukothai Thommathrirot Open University, Pogkred, Thailand. 4 To whom correspondence should be addressed: Poultry Science Department, Mississippi State University, Box 9665, Mississippi State, MS 39762-9665; E-mail: pthaxton@poultry.msstate.edu. glucose levels increase during gluconeogenesis, and concomitantly there is an increase in excretory uric acid (Brown et al., 1958; Siegel and Van Kampen, 1984; Davison et al., 1985). In addition to metabolic effects on carbohydrates and proteins, CS also influences fat metabolism. Siegel and Van Kampen (1984) demonstrated that during adrenocortical-mediated gluconeogenesis in chicks, as protein catabolism increased efficiency of energy absorption decreased because of increased energy retention. These workers defined efficiency of energy absorption as energy absorbed divided by total energy intake, while total energy absorbed was defined as total energy intake minus excretory loss of energy. If loss of urinary energy is ignored, then energy absorption can be equated to the better known term of ME. Therefore, during periods of stress, it is possible for decreases in growth to be accompanied by increases in body fat deposition (Brown et al., 1958; Nagra and Meyer, 1963; Siegel and Van Kampen, 1984). In previous reports (Puvadolpirod and Thaxton, 2000a,b,c), a model for studying ACTH-mediated stress in chicks has been described. The ACTH (8 IU/kg BW/ Abbreviation Key: ACTH = adrenocorticotropin; CON = control; CS = corticosterone; G/F = gain/feed intake; W/F = water/feed intake. 383

384 PUVADOLPIROD AND THAXTON d) was infused continuously for 7 d using a surgicallyimplanted mini-osmotic pump. Stress responses described in this model include increased plasma CS, glucose, cholesterol, triglycerides, high-density lipoproteins, total protein, relative liver weight and liver lipids, and an increased heterophil/lymphocyte ratio. Reductions in body and carcass weight, involution of immunobiological organs (spleen, thymus, and bursa of Fabricius), were also recorded. Additionally, chronology, magnitude, and duration of these stress responses were described in this model. One major aspect of the model is lacking, which is an understanding of the metabolic responses that support adaptive stress responses. Thus, the objective of this study was to assess metabolic responses of broilers during stress and after a period of recovery. MATERIALS AND METHODS Two experiments were conducted using Peterson Arbor Acre chicks. These chicks were reared in metal brooder batteries that were housed in an environmentally regulated laboratory animal facility. A brooding area was provided in each battery to insure a temperature of 38 C. The remainder of each battery was not heated. Ambient temperature was regulated at 27 ± 2C for the first 4 wk of each experiment; thereafter, it was 24 ± 2C. Feed and water were available ad libitum. For the first 4 wk, a starter diet containing 22.6% protein and 3,135 kcal ME/kg was fed; thereafter, a grower diet containing 20% protein and 3,190 kcal ME/kg was fed. These diets were described previously (Puvadolpirod and Thaxton, 2000a). A lighting schedule of 16 h light:8 h darkness was maintained. Light was provided by standard overhead fluorescent fixtures. At 4 wk of age, chicks were sexed, and only males were included in the experiments. Chicks were placed at random into 10 individual pens. In each experiment, five chicks were designated as controls (CON), and the other five were ACTH-treated chicks. All chicks were allowed 1 wk to acclimate to their experimental conditions before experimentation began. At 5 wk, chicks that had been designated for ACTH treatment received surgical implants of a mini-osmotic pump calibrated to deliver 8 IU ACTH/kg BW/d for 7 d. Puvadolpirod and Thaxton (2000a,b) have described this surgical procedure in detail. The pumps 5 delivered porcine ACTH. 6 Puvadolpirod and Thaxton (2000a) also demonstrated that chicks that were not handled were acceptable CON for the ACTH treatment. Therefore, nonhandled CON were employed in both experiments. In Experiment 1, parameters of measurement included BW, feed consumption, water consumption, and total 5 Alzet Model 2001, Alza Corp., Mountain View, CA 94039-7210. 6 Sigma Aldrich Fine Chemicals, St. Louis, MO 63103. 7 Parr Instrument Co., Moline, IL. excreta (feces and urine) output. Measurements of BW and feed and water consumption were determined daily for each bird at 1000 h. Pumps were implanted on Day 1. Excreta were collected twice daily and kept frozen ( 20 C) until further analysis. After the experiment was completed, samples of excreta from all ACTH-treated birds, as well as CON, were pooled over each 2-d period of the experiment. Pools consisted of samples taken on Days 1 to 2, 3 to 4, 5 to 6, 7 to 8, and 9 to 10. Each pool of excreta was dried to a constant weight in a forceddraft oven (70 C for 48 h). Since excreta data were pooled over each 2 d period, results of BW, feed consumption, and water consumption were likewise pooled over the same 2-d periods. Experiment 2 differed from Experiment 1 in several aspects. Specifically, the same parameters as in Experiment 1 were measured, but data were pooled such that measurements represented Days 1 to 2, 3 to 4, 5 to 8, 9 to 12, and 13 to 16. Additionally, feed and excreta were analyzed for gross energy with a Parr Model 1261 isoperibol bomb calorimeter; 7 total nitrogen was determined by the Kjeldahl procedure, and protein content was calculated. Lipid content was determined by extraction using ethyl ether, and ash content was determined gravimetrically after incineration (550 C for 24 h; AOAC, 1984). Carbohydrate content was calculated by subtracting protein, fat, and ash contents from dry matter content. After chemical analyses, several calculations were made using results of the above described measurements. Nutrient digestibility (%) was calculated by dividing nutrient intake per day by nutrient excreted per day, multiplying the qoutient by 100, and dividing by nutrient intake per day. Nutrient absorption (g or kcal) was calculated by subtracting weight of nutrient excreted per day (g or kcal) from weight of nutrient intake per day (g or kcal). Digestion and absorption or proteins could have been compounded by nonprotein nitrogen levels. Corrections for uric acid content in fecal matter were not attempted. Statistical analyses of all data of both experiments involved repeated measures design with treatments arranged in a completely randomized and split plot in time design. The general linear models procedure of the Statistical Analysis System (SAS, 1990) was employed, and means were partitioned by least-squares. Statements of significance were based on P 0.05. RESULTS The ACTH caused consistent depression in growth as evidenced by the BW data in Table 1. Additionally, as summarized in Table 2, during the early part of the stress period, BW of ACTH-treated chicks was approximately 4% less than that of CON. This percentage decrease in BW was exacerbated throughout the experimental period. In fact, by 1 wk poststress, BW of ACTH-treated chicks was approximately 20% less than CON. Gain was also adversely affected by ACTH treatment (Table 1).

STRESS, DIGESTION AND METABOLISM 385 TABLE 1. The effect of adrenocorticotropin (ACTH) on growth performance of broiler chicks 1 BW (g) Gain (g/d) Feed intake (g/d) G/F ratio Water intake (g/d) W/F ratio Days CON ACTH CON ACTH CON ACTH CON ACTH CON ACTH CON ACTH Experiment 1 1 2 1,666 ± 93 1,545 ± 73* 81 ± 11 32 ± 13* 133 ± 16 152 ± 24* 0.62 ± 0.06 0.19 ± 0.09* 259 ± 36 395 ± 42* 1.98 ± 0.16 2.78 ± 0.41* 3 4 1,827 ± 100 1,625 ± 111* 80 ± 6 39 ± 20* 143 ± 8 152 ± 21 0.56 ± 0.03 0.21 ± 0.12* 258 ± 43 445 ± 79* 1.78 ± 0.24 3.45 ± 1.19* 5 6 1,975 ± 97 1,679 ± 127* 74 ± 9 28 ± 15* 157 ± 10 158 ± 20 0.48 ± 0.06 0.14 ± 0.11* 284 ± 30 486 ± 76* 1.83 ± 0.20 3.54 ± 1.10* 7 8 2,124 ± 100 1,813 ± 128* 75 ± 7 67 ± 9 149 ± 13 161 ± 21 0.51 ± 0.05 0.45 ± 0.09 287 ± 31 470 ± 77* 1.92 ± 0.09 3.28 ± 0.94* 9 10 2,268 ± 115 1,936 ± 139* 72 ± 9 61 ± 13 126 ± 7 132 ± 21 0.56 ± 0.04 0.47 ± 0.10 269 ± 22 412 ± 75* 2.13 ± 0.14 3.50 ± 1.05* Experiment 2 1 2 1,440 ± 62 1,385 ± 78 103 ± 15 73 ± 21* 144 ± 9 155 ± 12 0.70 ± 0.07 0.45 ± 0.11* 273 ± 15 440 ± 74* 1.90 ± 0.07 2.94 ± 0.59* 3 4 1,598 ± 64 1,416 ± 84* 79 ± 5 16 ± 10* 154 ± 5 171 ± 9 0.51 ± 0.02 0.11 ± 0.06* 307 ± 21 622 ± 85* 1.98 ± 0.08 3.70 ± 0.55* 5 8 1,993 ± 70 1,569 ± 108* 84 ± 2 38 ± 6* 153 ± 6 191 ± 11* 0.55 ± 0.01 0.20 ± 0.03* 289 ± 14 577 ± 60* 1.88 ± 0.06 3.07 ± 0.40* 9 12 2,301 ± 81 1,822 ± 112* 92 ± 5 63 ± 7* 177 ± 5 160 ± 7 0.55 ± 0.03 0.34 ± 0.04* 348 ± 17 360 ± 62 1.88 ± 0.08 2.64 ± 0.32* 13 16 2,615 ± 72 2,093 ± 117* 78 ± 3 68 ± 3 178 ± 6 129 ± 9* 0.45 ± 0.03 0.43 ± 0.03 364 ± 25 237 ± 38* 1.96 ± 0.09 2.28 ± 0.24 1 CON = control, G/F = gain to feed intake, and W/F = water to feed intake. *ACTH mean ± SEM differ significantly from their corresponding CON mean (P 0.05). Reduction in gain caused by ACTH was approximately 30% during the early part of the stress period, and it peaked at 80% during the middle of the stress period. This reduction in gain persisted throughout the experimental period; at 1 wk poststress, this reduction in gain was still 23% (Table 2). Feed intake in chicks of Experiment 1 was increased during Days 1 to 2 (Table 1). The ACTH-treated chicks also ate more feed than did CON during Days 5 to 8 in Experiment 2. As summarized in Table 2, during ACTH treatment, there was a consistent and progressive increase in feed intake, at least on a percentage basis, by the ACTH-treated chicks. However, at 1 wk poststress, this effect was reversed. At this time, ACTH-treated chicks exhibited a decrease in feed intake compared with CON chicks. The gain/feed (G/F) intake ratio results were similar to those of daily gain (Table 1). Specifically, reductions in G/F in ACTH-treated chicks were noted at Days 1 to 2, 3 to 4, and 5 to 6 during Experiment 1 and at Days 1 to 2, 3 to 4, 5 to 8, and 9 to 12 during Experiment 2. Overall, there was a consistent decrease in G/F ratio, on a percentage basis, as shown in Table 2. Water intake was elevated throughout the stress period in ACTH-treated chicks in both experiments (Table 1). In fact, this increase averaged 88% in ACTH-treated chicks during stress (Table 2). As with feed intake, this effect was reversed at 1 wk poststress in Experiment 2. At this time, the ACTH-treated chicks drank less water than did CON chicks. Water/feed intake (W/F) ratio results paralleled those of water intake during the stress period (Table 1). In both experiments, there were increases in water intake by ACTH-treated chicks at all times during stress (Table 2). However, at 1 wk poststress in Experiment 2, the W/ F ratio differed from that of water intake. At this time, the W/F ratio did not differ in ACTH-treated and CON chicks. Total excreta output by ACTH-treated chicks were increased in both experiments, except on Days 7 to 8 and 9 to 10 in Experiment 1 (Table 3). The magnitude of increased output of excreta by ACTH-treated chicks is shown in Table 2. Average increase during stress was 234%, and at 1 wk poststress, this increase remained at approximately 100%. As indicated by results concerning total dry excreta and total water in excreta in Table 3, dry matter and water contents were increased in ACTHtreated chicks, with the exception that dry matter and water outputs were not different from CON on Days 7 to 8 and 9 to 10 in Experiment 1 (Table 3). When results of both experiments are combined, average outputs of dry matter and water in excreta of ACTH-treated chicks during stress are 55 and 187% more than that of CON chicks, respectively (Table 2). Furthermore, average increases in outputs of dry matter and water in ACTHtreated chicks at 1 wk poststress were 44 and 123%, respectively. Chemical compositions of excreta of chicks in Experiment 2 are presented in Table 4. Percentage dry matter

386 PUVADOLPIROD AND THAXTON TABLE 2. Changes in performance, digestion, and nutrient utilization in broilers by adrenocorticotropin (ACTH) treatment 1 1-wk Early stress Midstress Late stress Poststress Parameter 2 (Day 1 2) (Day 3 4) (Day 5 8) (Day 9 16) BW 3.82 11.39 18.83 20.31 Gain 29.13 79.75 54.76 22.94 Feed intake 7.64 11.04 24.84 18.59 G/F ratio 35.71 78.43 63.64 23.00 Water intake 61.17 102.61 99.65 16.15 W/F ratio 54.74 86.87 63.30 28.12 Total excreta 181.05 248.65 273.53 100.80 Total dry excreta 51.85 92.59 111.11 43.94 Total water in excreta 232.35 298.81 333.33 122.95 Digestion profile Dry matter 11.62 18.08 16.74 11.18 Gross energy 8.48 13.08 7.88 0.81 Carbohydrate 11.65 17.93 11.66 0.77 Fat 0.80 0.77 0.50 1.92 Nitrogen compounds 55.48 70.01 39.83 9.98 Absorption profile Gross energy 1.45 3.28 10.22 21.58 Carbohydrate 4.21 8.58 16.79 20.90 Fat 6.45 9.99 33.49 18.18 Nitrogen compounds 49.83 65.33 20.61 28.33 Ash 110.11 131.01 25.44 48.92 1 Percentage of each parameter is calculated as (ACTH control) 100/control. 2 G/F = gain/feed intake; W/F = water/feed intake. was decreased in ACTH-treated chicks at all times, except at Days 13 to 16. Gross energy content of excreta was not consistently altered by ACTH treatment but was reduced on Days 9 to 12 in ACTH-treated chicks. Percentage carbohydrate in excreta was increased during the stress period; thereafter, it was not different from that of the CON chicks. Percentage fat in excreta was decreased in ACTH-treated chicks on Days 3 to 4, 5 to 8, and 13 to 16. Percentage nitrogen in excreta was increased in ACTH-treated chicks at all times except at Days 13 to 16. Percentage ash content was reduced on Days 1 to 2 and 3 to 4 in ACTH-treated chicks. Results in Table 5 represent digestion of various nutrients of chicks in Experiment 2. These results are expressed as percentages. Digestion of dry matter was lower in ACTH-treated chicks than in CON chicks at all times of measurement. As shown in Table 2, this reduction in digestion of dry matter was lower at the midstress and late stress periods compared with the early stress period. Total energy released by digestion in ACTH-treated chicks, as well as digestion of carbohydrates, was reduced throughout the stress period. However, during recovery, both energy and carbohydrate digestibilities did not differ from that of the CON chicks. TABLE 3. The effect of adrenocorticotropin (ACTH) on the excretory data of broiler chicks Excretory dry Excretory Total excreta matter content water content (g/d) (g/d) (g/d) Days Control (CON) ACTH CON ACTH CON ACTH Experiment 1 1 2 132 ± 23 295 ± 43* 31 ± 2 47 ± 4* 101 ± 21 248 ± 39* 3 4 138 ± 24 292 ± 56* 35 ± 4 47 ± 5* 103 ± 21 245 ± 52* 5 6 145 ± 24 279 ± 53* 38 ± 4 48 ± 2* 107 ± 20 230 ± 49* 7 8 130 ± 20 258 ± 52 33 ± 3 46 ± 4 97 ± 17 212 ± 48 9 10 129 ± 18 244 ± 57 31 ± 3 41 ± 6 98 ± 15 203 ± 51 Experiment 2 1 2 95 ± 9 267 ± 66* 27 ± 2 41 ± 4* 68 ± 7 226 ± 62* 3 4 111 ± 6 387 ± 74* 27 ± 2 52 ± 2* 84 ± 6 335 ± 72* 5 8 102 ± 9 381 ± 65* 27 ± 1 57 ± 3* 75 ± 9 325 ± 63* 9 12 116 ± 8 307 ± 62* 32 ± 1 53 ± 4* 84 ± 8 254 ± 58* 13 16 134 ± 14 195 ± 36* 34 ± 1 42 ± 4* 99 ± 12 154 ± 33* *ACTH mean ± SEM differ significantly from their corresponding CON mean (P 0.05).

STRESS, DIGESTION AND METABOLISM 387 TABLE 4. The effect of adrenocorticotropin (ACTH) on the excretory chemical composition of broiler chicks resulting from Experiment 2 Days Control (CON) ACTH CON ACTH CON ACTH Dry matter (%) Gross energy (kcal/g) Carbohydrate (%) 1 2 28.30 ± 0.96 17.95 ± 2.89* 3.71 ± 0.02 3.67 ± 0.05 19.95 ± 2.41 30.60 ± 4.32* 3 4 24.86 ± 1.98 14.68 ± 1.69* 3.77 ± 0.02 3.63 ± 0.11 20.59 ± 1.69 39.54 ± 3.29* 5 8 27.35 ± 2.14 16.31 ± 1.88* 3.62 ± 0.03 3.56 ± 0.08 20.90 ± 1.71 42.19 ± 6.11* 9 12 28.35 ± 1.92 19.80 ± 3.09* 3.69 ± 0.04 3.51 ± 0.02* 26.12 ± 1.41 23.30 ± 2.65 13 16 26.59 ± 2.06 23.63 ± 2.90 3.68 ± 0.03 3.65 ± 0.03 26.94 ± 1.76 20.15 ± 1.33 Fat (%) Nitrogen (%) Ash (%) 1 2 3.00 ± 0.20 2.34 ± 0.25 5.49 ± 0.08 7.96 ± 0.30* 15.66 ± 0.45 12.94 ± 1.21* 3 4 3.78 ± 0.25 2.33 ± 0.15* 5.70 ± 0.16 8.10 ± 0.40* 15.30 ± 0.14 12.40 ± 1.65* 5 8 4.08 ± 0.26 2.74 ± 0.33* 5.76 ± 0.14 7.29 ± 0.40* 14.97 ± 0.20 13.76 ± 1.53 9 12 1.98 ± 0.11 1.48 ± 0.23 6.07 ± 0.17 7.34 ± 0.16* 14.87 ± 0.24 15.72 ± 0.58 13 16 3.44 ± 0.15 2.49 ± 0.54* 6.10 ± 0.23 6.13 ± 0.21 12.86 ± 0.13 13.39 ± 0.29 *ACTH mean ± SEM with this symbol differ significantly from their corresponding CON mean (P 0.05). Digestion of nitrogen-containing compounds (i.e., protein) was reduced during the stress period by ACTH treatment, and was similar in both groups during the recovery period. As shown in Table 2, average reduction of digestion of proteins was 55% during the stress period. Digestion of fats was not affected by ACTH treatment at any time during the experiment. Effects of stress on nutrient absorption profiles of chicks of Experiment 2 are presented in Table 6. Energy absorption (i.e., ME) was not different between CON and ACTH-treated chicks during stress. However, during recovery, ME was reduced in ACTH-treated chicks. Absorption of carbohydrates in ACTH-treated and CON chicks was not different during the early and middle parts of stress (i.e., Days 1 to 2 and 3 to 4). However, during the last part of the stress period (i.e., Days 5 to 8), carbohydrate absorption was increased in ACTHtreated chicks. Conversely, during the recovery period (i.e., Days 9 to 12 and 13 to 16), carbohydrate absorption was lower in ACTH-treated chicks. Nitrogen absorption was decreased in ACTH-treated chicks at all times of measurement, except at Days 5 to 8. Fat absorption in ACTH-treated chicks was increased on Days 5 to 8. Fat absorption was lower in ACTH-treated chicks on Days 13 to 16. Only one significant effect was noted for ash absorption. On Days 3 to 4, ACTH-treated chicks exhibited a lower ash absorption value than the CON chicks. DISCUSSION In the present report, as well as in previous reports (Puvadolpirod and Thaxton, 2000a,b,c), a stress model in broilers based on continuous infusion of ACTH has been described. In this model, reductions in BW, gain, and carcass weight, along with sustained elevated levels of CS and a wide array of physiological adaptive responses, collectively, constitute stress in chicks. The unifying explanation of these stress changes is adrenolcortical-mediated gluconeogenesis. There is a considerable body of research which describes the physiology of stress in chickens (Siegel, 1995). However, descriptions of digestion and metabolism inherent to stress in chickens are limited. Siegel and Van Kampen (1984) presented results concerning energy efficiency following injections of pharmacological doses of CS in chicks. Energy absorption efficiency was decreased; whereas, energy retention efficiency was increased, and this energy was stored as fat. In the present study, the overall profile of digestion and feed utilization indicated that, during stress, there was a slight increase in feed intake concomitant with significant decreases in digestion of proteins and carbohydrates, whereas fat digestibility was unaffected. Several reports suggest that feed intake increases during periods of stress in chicks (Brown et al., 1958; Nagra and Meyer, 1963; Siegel and Van Kampen, 1984). A definitive physiological explanation for increased feed intake in stressed birds is lacking. Zachariasen and Newcomer (1974) injected ACTH intracerebally in chicks and found that feed intake regulation was altered. Furthermore, intracerebral injections of various catecholamines also influenced feed intake profiles in chicks (Denbow et al., 1981; Kuenzel et al., 1987). In a review of peripheral and central control of food intake, Denbow et al. (1989) detailed the effects that catecholamines and pancreatic polypeptides exert on feed intake regulation, especially in appetite control centers of the brain. Edens and Siegel (1972) and Brown-Borg (1990) have shown that adrenocortical responsiveness is directly related to secretion of epinephrine and norepinephrine and possibly other catecholamines. Therefore, stress modulation of higher brain centers may be a plausible explanation for increased feed intake during stress followed by decreased feed intake during recovery. The ACTH-treated chicks exhibited significant polydipsia and polyuria throughout the stress and recovery periods. These findings agree with the conclusion of Siegel and Van Kampen (1984) that there has to be excess water consumption to clear metabolic uric acid and excess electrolytes, especially the NH 3 -ion. Litwack and Singer (1972) showed that CS altered metabolic levels of various digestive enzymes, especially enzymes involved with lipolytic, glycolytic, and gluconeogenic reactions. Therefore, it is possible that reduction in digestive release of gross energy and digestion

TABLE 5. The effect of adrenocorticotropin (ACTH) on nutrient digestibility of broiler chicks in Experiment 2 1 Dry matter (%) Energy (%) Carbohydrate (%) Nitrogen (%) Fat (%) Days Control (CON) ACTH CON ACTH CON ACTH CON ACTH CON ACTH 1 2 78.93 ± 2.50 69.76 ± 4.11* 83.22 ± 0.02 76.16 ± 0.03* 79.97 ± 2.73 70.65 ± 5.39* 66.64 ± 4.00 29.67 ± 11.59* 90.94 ± 1.24 90.21 ± 1.21 3 4 80.15 ± 0.91 65.66 ± 2.33* 84.26 ± 0.01 73.24 ± 0.02* 80.99 ± 1.18 66.47 ± 3.41* 67.52 ± 0.92 20.25 ± 5.35* 89.28 ± 0.88 88.59 ± 0.97 5 8 80.11 ± 0.92 66.70 ± 2.87* 84.79 ± 0.01 78.11 ± 0.03* 81.20 ± 1.03 71.73 ± 3.26* 67.36 ± 1.37 40.53 ± 2.41* 88.60 ± 0.52 89.04 ± 1.03 9 12 78.52 ± 0.33 68.25 ± 2.10* 83.79 ± 0.00 83.44 ± 0.02 78.90 ± 0.67 78.69 ± 1.46 63.86 ± 1.78 53.37 ± 1.45 94.19 ± 0.23 95.35 ± 0.74 13 16 78.22 ± 0.18 70.97 ± 1.67* 83.20 ± 0.00 82.20 ± 0.01 78.76 ± 1.25 77.75 ± 2.04 62.31 ± 2.67 60.21 ± 4.63 89.56 ± 0.31 91.93 ± 1.98 1 Calculated by nutrient intake per day nutrient excreted per day 100/nutrient intake per day. *ACTH mean ± SEM with this symbol differ significantly from their corresponding CON mean (P 0.05). TABLE 6. The effect of adrenocorticotropin (ACTH) on the nutrient absorption of broiler chicks in Experiment 2 1 Energy (ME, kcal/d) Carbohydrate (g/d) Nitrogen (g/d) Fat (g/d) Ash (g/d) Days Control (CON) ACTH CON ACTH CON ACTH CON ACTH CON ACTH 388 PUVADOLPIROD AND THAXTON 1 2 504.84 ± 35.99 497.50 ± 54.54 81.09 ± 6.13 76.68 ± 10.36 3.01 ± 0.29 1.51 ± 0.57* 8.22 ± 0.50 8.75 ± 0.74 0.89 ± 0.69 0.09 ± 0.75 3 4 543.73 ± 18.61 525.87 ± 40.36 87.38 ± 2.80 79.88 ± 7.39 3.23 ± 0.13 1.12 ± 0.32* 8.61 ± 0.24 9.47 ± 0.55 1.58 ± 0.46 0.49 ± 1.18* 5 8 543.54 ± 22.66 599.10 ± 53.72 89.87 ± 3.45 104.96 ± 3.01* 3.30 ± 0.12 2.62 ± 0.11 8.78 ± 0.42 11.72 ± 0.51* 1.69 ± 0.49 1.26 ± 1.56 9 12 611.73 ± 17.51 520.91 ± 27.45* 97.54 ± 3.69 84.67 ± 4.37 3.50 ± 0.17 2.55 ± 0.16* 10.42 ± 0.42 9.21 ± 0.58 2.81 ± 0.98 1.21 ± 0.74 13 16 617.61 ± 19.30 443.19 ± 31.16* 99.63 ± 1.86 71.30 ± 4.30* 3.49 ± 0.17 2.46 ± 0.26* 10.14 ± 0.16 7.51 ±.32* 2.30 ± 0.29 1.40 ± 0.41 1 Calculated by nutrient intake per day nutrient excreted per day. *ACTH mean ± SEM with this symbol differ significantly from their corresponding CON mean (P 0.05).

STRESS, DIGESTION AND METABOLISM 389 of dry matter and nitrogenous compounds in ACTHtreated chicks during stress (Table 5) may be caused by incomplete digestion due to increased feed passage time rather than by inadequate levels of digestive enzymes. Moreover, increased water intake of ACTH-treated chicks would probably cause a dilution effect and result in changes in ph and osmolarity. These changes in the environment of the digestive tract would undoubtedly cause digestive inefficiency. Therefore, the putative reduction in digestibility could have been caused by altered enzymatic reactions and changes in the gut environment, coupled with an insufficient time for digestion to be completed. It is noteworthy that reductions in digestibilities of the various nutrients paralleled changes in circulating levels of CS. Specifically, initial reduction in digestion occurred by the end of the first day of ACTH treatment, and CS levels were elevated significantly by 6 h postinitiation of ACTH delivery (Puvadolpirod and Thaxton, 2000c). Also, the peak period for reductions in digestion of all nutrients was at Days 3 to 4 of ACTH treatment, which was when maximum circulating levels of CS occurred. During the 1-wk recovery period, the only effect attributed to ACTH treatment was that digestion of dry matter remained reduced. Reduction in absorption of nitrogenous compounds was not unexpected. This model supports previous findings of Odedra et al. (1983) and Siegel and Van Kampen (1984) that proteins derived from skeletal muscle are the major sources of noncarbohydrate compounds, which are preferentially metabolized to provide energy to resist stress. Administration of ACTH (Adams, 1968) or CS (Davison et al., 1985) is reported to cause a dramatic increase in uric acid excretion because of exacerbated gluconeogenesis. Basically, besides ash absorption, the only nutrient that exhibited reduced absorption during stress was nitrogenous compounds. However, during the recovery period, nitrogenous compounds, carbohydrates, and fats all exhibited reductions in absorption. Results of the present study suggest that digestion of gross energy, carbohydrates, proteins, and fats was affected more during the stress period than was absorption of these nutrients. Detailed studies concerned with specific digestive functions in stressed chicks certainly are warranted. Energy and fat absorption profiles during stress differed from that of nitrogenous compounds. Specifically during recovery, absorption of energy and fat were severely limited. This may be explained by decreased feed intake during recovery. Bell (1984) described a glucocorticoid withdrawal syndrome in humans. This phenomenon occurred 1 to 5 d following cessation of prolonged administration of glucocorticoids. Bell (1984) postulated that homeostasis of hypothalamic-hypophyseal-adrenocortical functions requires a period of adjustment. If chicks of this study were simply experiencing glucocorticoid withdrawal, then possibly 1 wk was insufficient time to establish homeostasis. In summary, during stress, there is a slight increase in feed intake concomitant with significant decreases in digestion of gross energy, carbohydrates, and proteins, and digestion of fat is unaffected. Reduction in digestion of these nutrients was affected more during the stress period than was absorption. Conversely, after cessation of ACTH infusion, reduction of all nutrient absorption occurred, whereas digestion of these nutrients appeared to return to the range of CON values. Present findings can now be incorporated into the evolving stress model, which has been proposed (Puvadolpirod and Thaxton, 2000a,b,c,). This model indicates that all physiological parameters, with the exception of thymic atrophy, reduced BW and carcass weight return to the range of CON values within 1 wk after cessation of ACTH infusion. Additionally, present results indicate clearly that feed intake and absorption of energy, dry matter, and nitrogenous compounds do not return to the range of CON within 1 wk after cessation of ACTH infusion. Present results indicate that following a severe stress episode, broilers may establish a new setpoint for feed intake that persists until the birds are slaughtered. Whether this new setpoint for feed intake remains throughout the life of the bird is unknown. Also, losses in skeletal muscle because of prolonged gluconeogenesis may require extended periods for complete recovery. REFERENCES Adams, B. M., 1968. 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