Poult. Sci.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Poult Sci 2007. 86:545-554
© 2007 Poultry Science Association
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lin, H.
Right arrow Articles by Dong, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, H.
Right arrow Articles by Dong, H.

PHYSIOLOGY, ENDOCRINOLOGY, AND REPRODUCTION

Effects of Diet and Stress Mimicked by Corticosterone Administration on Early Postmortem Muscle Metabolism of Broiler Chickens

H. Lin1, S. J. Sui, H. C. Jiao, K. J. Jiang, J. P. Zhao and H. Dong

Department of Animal Science, Shandong Agricultural University, Taian, 271018, P. R. China

1 Corresponding author: hailin{at}sdau.edu.cn


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Three experiments were conducted to evaluate the effects of preslaughter physiological states mimicked by long- or short-term administration of corticosterone (CORT) and dietary energy sources on muscle glycogen contents and meat quality of broiler chickens. In experiment 1, the broilers were fed a high lipid diet (LD) or a normal diet (ND) that differed in carbohydrate (3.8%) and lipid (2.5%) contents from 21 d of age. From 28 d of age onwards, 50% of the chickens in each dietary treatment were subjected to CORT treatment (30 mg/kg of diet). At 7 and 11 d after CORT supplementation, musculus pectoralis major was sampled before and immediately after slaughter and analyzed for glycogen, pH, and R-value. In experiment 2, broilers, fed with the LD or ND diet from 21 d of age were subjected to 1 single s.c. injection of CORT (4 mg/kg of BW) for 3 h to mimicked acute stress at 46 d of age. In experiment 3, broiler chickens were supplied with water supplemented with glucose (30 g/L) for 1 wk before slaughter and were then subjected to the same CORT treatment as experiment 2. Blood and muscle samples were respectively obtained before and immediately after slaughter and analyzed for plasma glucose, urate and lactic acid, and muscle variables. Plasma concentrations of glucose and urate were significantly increased by acute CORT administration, whereas the lactic acid was not changed. Neither dietary energy source nor water glucose supplementation had any influence on the plasma variables. Dietary energy source or water glucose supplementation could not alter glycogen stores in musculus pectoralis major. Breast muscle glycogen stores were increased by stress mimicked by long-term CORT administration rather than by acute treatment. Preslaughter stress reactions had no relation to the depletion of breast muscle glycogen during the initial postmortem period. The initial breast muscle pH was significantly decreased by long-term CORT administration. The result suggests that short-term upregulation of circulating CORT is not involved in the elevated drip loss induced by preslaughter stress.

Key Words: stress • corticosterone • glycogen • drip loss • broiler chicken


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In postmortem muscle cells, the generation of ATP relies on the anaerobic pathway and results in the accumulation of lactic acid as a waste product and, in turn, the decline of muscle pH. A rapid pH drop occurring at higher muscle temperature results in decreased meat quality (e.g., water-holding capacity). The energy stores in muscle seem to associate with the quantity of accumulated lactate and the magnitude of pH decline. The higher glycolytic potential results in lower ultimate pH and higher drip loss (Berri et al., 2005). A combined glucose and creatine supplementation increases the lightness and drip loss of breast meat (Young et al., 2004).

Broiler chickens may face many stressors at market age, including feed withdrawal, catching, crating, transport, high environmental temperature, and stunning (Sams, 1999; Ali et al., 1999). Warriss et al. (1993) found that stressful environment in transportation had an inconsistent effect on postmortem glycogen concentration of breast meat but reduced its ultimate pH. Shackling could stimulate the antemortem glycolysis activity in breast muscle (Debut et al., 2005). Stunning may change the development of rigor mortis (Papinaho and Fletcher, 1995) and alter the metabolic rate of breast muscle (Savenije et al., 2002a,b). Preslaughter heat stress causes a reduction in initial breast muscle pH in broiler chickens (Sandercock et al., 2001), accelerates rigor mortis development, and reduces meat quality (Northcutt et al., 1994; McKee and Sams, 1997). The results indicate that preslaughter stress may play a role in the meat quality via the influence on the pre- or postslaughter muscle metabolism or both.

Glucocorticoids, as the final effectors of the hypothalamic-pituitary-adrenal axis, participate in the control of whole body homeostasis and the response of the organism to stress by stimulating the release of energy stores via promoting glucose mobilization and lipolysis (Harvey et al., 1986). In broiler chickens subjected to preslaughter stress such as transport, the circulating level of corticosterone (CORT) was observed to be increased (Kannan et al., 1997a,b). Hence, we hypothesized that the stress reactions induced by high circulating CORT could change the metabolic status in antemortem muscles, followed by the initial postmortem muscles and thereafter the decreased meat quality.

In broiler chickens, muscle glycogen reserves are not significantly changed by feeding status (feed withdrawal and refeeding; Warriss et al., 1988, 1993; Edwards et al., 1999). In contrast, a recent study by Rosenvold et al. (2001) proved that the muscle glycogen stores of slaughter pigs could be altered through strategic finishing feeding.

The objective of the present study was to determine the effect of preslaughter stress mimicked by long- or short-term administration of CORT on glycogen depletion and meat quality characteristics in musculus pectoralis major (PM) of broiler chickens. Meanwhile, the influence of different dietary energy sources was investigated as well. In the present study, the effect of CORT and dietary energy sources on the metabolic variables during the exsanguination process were estimated by the difference between the muscle biopsies and corresponding muscle samples obtained immediately after slaughter. Dietary supplementation or 1 single injection of CORT was used to mimic long or acute stress responses, which have been successfully used in previous studies (Malheiros et al., 2003; Lin et al., 2004a,b).


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Experimental Chickens and Diets
The broiler chickens (Arbor Acres) of both sexes were obtained from a local hatchery at 1 d of age and reared in an environmentally controlled room. The brooding temperature was maintained at 35°C for the first 2 d, decreased gradually to 21°C (45% RH) until 28 d, and thereafter maintained as such to 39 d of age. The light regimen was 23L:1D. The birds had free access to feed and water during the entire rearing period.

Experiment 1.
Two hundred forty broiler chicks were assigned randomly to 12 pens of 20 chicks at 1 d old. From d 1 to 21, all the chicks received a starter diet with 21.5% CP and 3,000 kcal of ME/kg. From d 21 onward, the chickens were provided with 2 experimental diets, which were isocaloric and isonitrogenic but differed in lipid and carbohydrate contents (Table 1Go). One half of the chickens (6 pens of 20 chickens) were fed a diet with the high lipid content (crude fat: 9.9%, LD), and the other half of chickens were fed the normal diet (crude fat: 7.5%, ND). From 28 d of age onwards, 3 pens of chickens in each dietary treatment were randomly selected for CORT treatment, as a dose of 30 mg of CORT/kg of diet, whereas the other 3 pens of chickens continued to consume the normal diets. Feed intake and BW gain were recorded at 28, 35, and 39 d of age, and feed efficiency (feed:gain) was calculated and reported elsewhere (Lin et al., 2006).


View this table:
[in this window]
[in a new window]

  		Table 1. Ingredients and calculated analysis of experimental diets1
 
At 39 d of age, 10 chickens of both sexes with similar BW were selected from each treatment. A biopsy of breast muscle was sampled according to the description of Quentin et al. (2003). Immediately after the muscle biopsies were obtained from the left PM, the broiler chickens were killed by exsanguination. The right PM was sampled immediately after slaughter. Immediately after sampling, the muscle samples were frozen and stored in liquid N until the analysis of glycogen, R-value, and pH. The eviscerated carcasses were chilled overnight (24 h) in a cooling cell at 4°C. At 4 h postmortem, a muscle sample was cut from the right PM using a 20 x 20 mm cork borer (10 mm in depth, 20 mm apart from the previous sampling area) at a right angle to the muscle fiber direction and used for the measurement of drip loss as described by Young et al. (2004).

Experiment 2.
Two groups of 40 broiler chickens (4 pens of 20 chickens) with both sexes were used in this experiment. The experimental chickens were randomly subjected to 1 of the 2 dietary treatments, ND or LD, as described in experiment 1 from 21 to 45 d of age. At 46 d of age, 10 chickens of both sexes with similar BW were selected from each pen and subjected to 1 of the 2 treatments: 1 single s.c. injection of CORT (4 mg/kg of BW in corn oil) or corn oil (sham control). During the 3-h exposure, feed was withdrawn, and the broiler chickens had free access to water. The BW loss during the 3-h CORT exposure was recorded.

Before and at 3 h after CORT treatment, blood was drawn from a wing vein of all the 10 chickens using a heparinized syringe within 30 s and collected in iced tubes. Plasma was obtained after centrifugation at 400 x g for 10 min at 4°C and stored at –20°C for further analysis of glucose, urate, and lactic acid. Immediately after the blood was sampled, the muscle biopsy was obtained from the left PM, and then the broiler chickens were killed by exsanguination. The right PM was sampled immediately after slaughter. All the muscle samples were frozen and stored in liquid N until further analysis of glycogen, pH, and R-value. The eviscerated carcasses were chilled overnight (24 h) in a cooling cell at 4°C. At 4 h after slaughter, the muscle samples were cut from the right breast as described in experiment 1 and used for the measurement of drip loss. At 24 h postmortem, the muscle samples were cut again at 30 mm apart from the previous sample area and stored in liquid N for pH analysis.

Experiment 3.
Four pens of 10 broiler chickens with both sexes were used in this experiment. At 42 d of age, 2 pens of chickens were assigned to drink water supplemented with glucose (30 g/L; GLU), and the other 2 pens of chicken were supplied with tap water serving as control group (TAP). All the experiment chickens were fed ad libitum with a commercial broiler finisher diet (14.0 MJ of ME/kg of diet, 19.5% CP). Feed intake and water consumption were recorded daily, whereas BW gain was recorded at the end of the 7-d experimental period.

At 49 d of age, the experimental chickens in each water treatment were randomly subjected to 1 of the following treatments: 1 single s.c. administration of CORT (4 mg/kg of BW) or injection of corn oil (sham control) at 3 h before slaughter. During the 3-h exposure, feed was withdrawn, and all the broiler chickens had free access to tap water. Body weight loss during the 3-h CORT exposure was recorded.

Before and at 3 h after CORT treatment, the plasma was obtained from all 10 chickens of each treatment in the same way as experiment 2 and stored at –20°C for further analysis of glucose, urate, and lactic acid. The slaughtering and muscle sampling procedures were the same as that of experiment 2. Immediately after sampling, muscle samples were frozen and stored in liquid N. The samples obtained before and immediately after slaughter were used for the analysis of glycogen, pH, and R-value, whereas the samples obtained at 24 h postmortem were only used for the analysis of pH. A muscle sample was also obtained for the measurement of drip loss as described in experiment 2.

Measurement
Plasma concentrations of glucose, urate, and lactic acid were measured with commercial colorimetric diagnostic kits in experiments 2 and 3.

Glycogen contents were determined with commercial kits (Nanjing Jiancheng Bioengineering Institute, Nanjing City, P. R. China). Muscle pH was determined by using a modified iodoacetate method (Jeacocke, 1977). In brief, approximately 2.0 g of breast muscle tissue was homogenized in 20 mL of a 5 mM iodoacetate solution with 150 mM KCl for 10 s, and the pH of the homogenate was determined using a pH meter calibrated at pH 4.0 and 7.0.

The R-value is an estimation of the status of rigor as measured by conversion of ATP to ADP and AMP. The R-value was analyzed according to the method described by Savenije et al. (2002a). In brief, 1.0 g of tissue was homogenized in 12.5 mL of perchloric acid (0.85 M) in slushy ice. The homogenate was centrifuged at 400 x g for 10 min, and 100 µL of supernatant was pipetted into 2.5 mL of 100 mM sodium phosphate buffer (pH 7.0). The absorbance at 250 nm (A250) and 260 nm (A260) was read, and the R-value was calculated as A250/A260.

Drip loss was measured essentially as described by Young et al. (2004). Samples were placed in a container covered with polyethylene film to avoid evaporation at 4 to 6°C for 48 h. The samples were kept without contact with the inside of the container and with the fiber direction of muscle samples horizontal to gravity, and drip loss was determined by weighing.

Statistical Analysis
In experiment 1, the statistical analyses of the variables glycogen content, R-value, and pH were respectively conducted for the data of each day of age. The data were analyzed by the method of repeated measurement analysis (version 8e, SAS Institute, 1998) by using each chicken as replicate, and the main effects of diet, CORT, and time were estimated. The interactions between CORT and diet and time were analyzed as well. The time effect within treatment was further estimated by the method of paired t-test.

A 1-way ANOVA model was used to analyze the growth performance and drip loss in experiments 2 and 3, and the main effects of CORT were estimated. For the statistical analyses of variables plasma glucose, uric acid and lactic acid, and muscle glycogen, R-value and pH, the repeated measurement analysis was conducted to evaluate the main effects of CORT, diet or water treatment, and time, as well as their interaction. Paired t-test was used to evaluate the time effect within treatment. Means were considered significantly different at P < 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Experiment 1
Neither the preslaughter nor the initial postmortem glycogen contents in PM were significantly affected (P > 0.05) by dietary energy sources during the 17-d experimental period (Figure 1Go). Chronic CORT administration, however, significantly increased the pre- and postslaughter glycogen level of PM at 7- and 11-d time points after treatment. The obvious interaction (P < 0.05) between diet and CORT treatment was only observed at 39 d of age (11 d after CORT treatment), and the CORT chickens consuming the ND diet had higher (P < 0.05) glycogen stores in PM (Figure 1Go, panel D). Compared with preslaughter level, the initial postmortem glycogen contents in PM were not obviously changed at 21 and 39 d of age regardless of diet or CORT treatment. At 28 d of age, however, the glycogen content significantly declined after slaughter in both diet treatments (LD, 2.52 vs. 2.05; ND, 2.81 vs. 2.14). At 35 d of age, the significant decline in glycogen stores after slaughter was only detected in CORT-LD chickens, whereas there was a decreasing trend in control chickens fed the LD diet (P = 0.0536) and CORT chickens consuming the ND diet (P = 0.0640), respectively. There was no significant change in control chickens fed the ND diet (P > 0.05).


Figure 1
View larger version (34K):
[in this window]
[in a new window]

  		Figure 1. Effects of dietary energy sources and corticosterone (CORT) administration (30 mg/kg of diet) on glycogen contents in musculus pectoralis major muscle before and immediately after slaughter (n = 10). LD-NR = high lipid diet-control treatment; ND-NR = normal diet-control treatment; LD-CORT = high lipid diet-corticosterone treatment; ND-CORT = normal diet-corticosterone treatment. a–cMeans with different letters within the same time point differ significantly (P < 0.05). x,yMeans with different letters (x,y) within the same treatment differ significantly (P < 0.05).

 
The preslaughter pH in PM (muscle biopsy) was not significantly (P > 0.05) affected by either dietary energy source or CORT treatment at any day of age (Figure 2Go). The initial postmortem pH in PM, however, was significantly decreased by chronic CORT treatment compared with control group at both 35 and 39 d of age. There was no obvious effect of diet at any day of age. Compared with the antemortem level, the initial postmortem pH of PM was not obviously changed in 21- and 28-d-old chickens. At 35 and 39 d of age, however, initial postmortem pH was significantly (P < 0.05) decreased in all the treatment, except CORT chickens fed the LD diet at 39 d of age (P = 0.0902). Neither diet nor chronic CORT treatment had an obvious effect (P > 0.05) on the antemortem or postmortem R-value of PM (Table 2Go). Regardless of diet or CORT treatment, the R-value was significantly (P < 0.01) increased after slaughter compared with the preslaughter value at any day of age. The drip loss was not obviously altered (P > 0.05) by either diet or CORT treatment (Table 2Go).


Figure 2
View larger version (28K):
[in this window]
[in a new window]

  		Figure 2. Effects of dietary energy sources and corticosterone (CORT) administration (30 mg/kg of diet) on pH in musculus pectoralis major before and immediately after slaughter (n = 10). LD-NR = high lipid diet-control treatment; ND-NR = normal diet-control treatment; LD-CORT = high lipid diet-corticosterone treatment; ND-CORT = normal diet-corticosterone treatment. a–cMeans with different letters within the same time point differ significantly (P < 0.05). x,yMeans with different letters (x,y) within the same group differ significantly (P < 0.05).

 

View this table:
[in this window]
[in a new window]

  		Table 2. Effect of dietary energy sources and corticosterone (CORT, 30 mg/kg of diet) treatments on R-value and drip loss of musculus pectoralis major of broiler chickens in experiment 11
 
Experiment 2
At 3 h after treatment, BW loss of CORT chickens was significantly (P < 0.01) higher compared with control chickens, and dietary energy sources had no obvious (P > 0.05) effect (Table 3Go). Compared with control chickens, the levels of plasma glucose and urate were significantly (P < 0.05) increased by acute CORT treatment, except that the lactic acid was not obviously changed (P > 0.05; Table 3Go). Dietary energy sources had no detectable effect on plasma glucose, urate, and lactic acid during the 3-h experiment. Within the CORT treatment, however, chickens consuming the LD diet had a higher (P < 0.05) level of glucose compared with that of chickens fed the ND diet. Compared with the basal levels before treatment, the concentrations of plasma urate and lactic acid in control chickens were significantly (P < 0.05) decreased at 3 h after treatment, whereas the glucose concentration was not obviously altered. In CORT chickens, however, the concentrations of glucose and urate were significantly (P < 0.05) increased after treatment compared with the basal levels, whereas lactic acid remained the same.


View this table:
[in this window]
[in a new window]

  		Table 3. Effect of s.c. corticosterone administration (CORT, 4 mg/kg of BW) and dietary energy sources on BW loss and concentrations of plasma glucose, lactic acid, and urate of broiler chickens in experiment 21
 
The ante- or postmortem glycogen contents in PM were not obviously affected by diet or acute CORT treatments (Table 4Go). Compared with antemortem levels, the postmortem glycogen stores were significantly (P < 0.05) decreased in all the groups regardless of diet or acute CORT administration. There was no significant effect of diet, CORT, and their interaction on ante- or postmortem pH and R-value (Table 4Go). Regardless of diet or CORT treatment, pH in PM increased (P < 0.05) immediately after slaughter and then declined at 24 h postmortem. The final pH at 24 h postmortem, however, remained at higher levels compared with the preslaughter values, except in CORT-ND chickens. The R-value of PM had no significant change immediately after slaughter. Drip loss of breast meat was significantly (P < 0.05) decreased by CORT treatment (control, 2.10% vs. CORT, 1.77%), and the lowest value was detected in the CORT-LD group (Table 4Go).


View this table:
[in this window]
[in a new window]

  		Table 4. Effect of s.c. corticosterone treatment (CORT, 4 mg/kg of BW) and dietary energy sources on glycogen contents, pH, R-value, and drip loss in musculus pectoralis major of broiler chickens in experiment 21
 
Experiment 3
During the 1-wk period of water glucose supplementation (30 g/L, GLU), there was no difference in BW gain between the GLU and control chickens (GLU, 90.1 g vs. TAP, 89.4 g). The feed intake of GLU chickens was lower than that of control chickens (GLU, 153.1 g vs. TAP, 169.2 g), whereas the total ME intake was almost the same in the 2 groups (GLU, 2.36 MJ/d vs. TAP, 2.36 MJ/d).

During the 3-h period of CORT administration, BW loss of CORT chickens was significantly (P < 0.0001) increased by acute CORT administration compared with control chickens regardless of water treatment (Table 5Go). In control groups, however, GLU chickens had less (P < 0.05) BW loss than that of TAP chickens. Glucose supplementation had no obvious effect on the concentrations of plasma glucose, lactic acid, and urate at any time point. Plasma concentrations of glucose and urate were significantly (P < 0.05) increased by CORT treatment when compared with control chickens or their basal levels, whereas the lactic acid remained the same. In control chickens, the plasma level of urate was decreased after the 3-h treatment compared with the basal level, whereas the levels of glucose and lactic acid stayed unchanged (Table 5Go). No significant interaction of GLU and CORT treatments was observed on any plasma parameter.


View this table:
[in this window]
[in a new window]

  		Table 5. Effect of s.c. corticosterone administration (CORT, 4 mg/kg of BW) and water glucose supplementation (GLU, 30 g/L) on BW loss and plasma parameters of broiler chickens in experiment 31
 
The pre- or postslaughter glycogen contents in PM were not affected by either GLU treatment or acute CORT administration (Table 6Go). Compared with the preslaughter levels, the initial postmortem glycogen contents were reduced in all the treatments regardless of GLU or CORT treatment. Muscle pH in PM was not obviously influenced by GLU or acute CORT treatment at any time point. Immediately after slaughter, muscle pH of PM showed a rising trend (P < 0.1) and thereafter remained unchanged at 24 h postmortem in all the treatments except in CORT-GLU chickens that pH first increased (P < 0.05) and then significantly (P < 0.05) decreased. Compared with the antemortem pH of PM, the ultimate pH at 24 h postmortem was significantly higher in control-GLU chickens and in CORT-TAP chickens, whereas there was no obvious change in the other 2 groups. The ante- or postmortem R-value of PM was not obviously influenced (P > 0.05) by either GLU or acute CORT treatment. Meanwhile, there was no significant (P > 0.05) change immediately postslaughter as well. The drip loss of PM tended to be decreased by CORT administration (P = 0.060), whereas no significant effect was found in water glucose treatment.


View this table:
[in this window]
[in a new window]

  		Table 6. Effect of s.c. corticosterone administration (CORT, 4 mg/kg of BW) and water glucose supplementation (GLU, 30 g/L) on glycogen content, pH, R-value, and drip loss in musculus pectoralis major of broiler chickens in experiment 31
 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Effect of Dietary Energy Source
Growth rate may cause difference in muscle metabolism. The broiler chickens selected for higher growth rate of BW and breast muscles had decreased glycolytic potential of PM (Berri et al., 2001). In the present experiment, neither the BW nor the breast proportion was affected by dietary treatment (Lin et al., 2006), suggesting the role of growth rate could be excluded. In previous studies, the glycogen reserves in breast muscles were not obviously changed by feeding status (Warriss et al., 1988, 1993; Edwards et al., 1999). A recent study by Rosenvold et al. (2001) showed that the muscle glycogen stores of slaughter pigs could be altered through strategic finishing feeding. In chickens, however, the glycogen contents of the "red muscle," rather than the "white muscle," seem to be more susceptible to dietary treatment (Rosebrough and Begin, 1975; Warriss et al., 1988). In line with the previous studies, the present result indicated that dietary energy source had no obvious influence on glycogen stores of PM. The differences in dietary carbohydrate and lipid contents in experiment 1 were not very pronounced and, hence, the effect of dietary strategy could not be excluded completely.

On the other hand, muscle glycogen stores in slaughter pigs may be decreased when there is a reduction in the consumption of readily digestible carbohydrates (Rosenvold et al., 2001). To further investigate the possible effect of oral energy source on glycogen stores in breast muscles, the experimental chickens were provided with glucose water for 1 wk before market age in experiment 3. In contrast to the study in pig (Rosenvold et al., 2001), the present result indicated that the glycogen stores in PM of broiler chickens were not affected by glucose supplementation. In this experiment, the chickens drinking glucose water ate less feed to compensate the extra energy intake from glucose and had the same amount of ME intake (GLU vs. TAP, 2.36 vs. 2.36 MJ/d per bird). Although there was similar ME intake, the GLU chickens consumed more carbohydrate (GLU, 87.1 g vs. TAP, 80.7 g), especially more absorbable carbohydrate than TAP chickens, indicating that the glycogen contents in PM of broiler chickens are hardly to be altered by dietary strategy within a short period.

In the 3 experiments, dietary energy source or oral glucose supplementation had no obvious influence on the pre- or postslaughter level of R-value, suggesting the cellular energy status is not altered by dietary treatment. Moreover, the initial pH and pH at 24 h postmortem were not affected by dietary treatments as well. The results may indicate that the postmortem glycolytic process is not affected by dietary treatment, in line with the result of Rosenvold et al. (2001).

Effect of CORT Treatment
In the 3 experiments of the present study, the growth performance of broiler chickens was decreased by either chronic (11 d) or acute (3 h) CORT administration, suggesting the disadvantage influence of stress mimicked by CORT administration. The simultaneously elevated concentrations of plasma glucose and uric acid in the 2 experiments indicated the augmented glycogenesis and enhanced protein oxidation.

The significantly increased antemortem muscle glycogen concentration by chronic CORT treatment indicated the augmented glycogenesis in PM. Because the phenomena were not observed in acute CORT treatment (experiment 2 and 3), the result indicates that muscle glycogen stores are increased by chronic stress rather than by acute stress. The higher glycogen stores in PM of CORT-ND chickens at 39 d of age (experiment 1) indicated that there is a significant interaction between dietary energy source and stress, and the diet rich in carbohydrate is favorable for the glycogen accumulation in PM. Because the phenomena were not observed in chickens of 35 d of age, if there was a time effect, it needs to be investigated further.

The depletion of muscle glycogen immediately after slaughter was observed in all 3 experiments conducted in the present study. Because there was a similar trend in different treatments, the depletion of muscle glycogen in the initial postslaughter period seemed to have no relation to either CORT or dietary energy sources. In other words, neither the antemortem stress reactions induced by chronic or acute glucocorticoid administration nor the dietary treatment could influence the early postmortem glycogen metabolism immediately after slaughter. Moreover, the results also indicate that the initial postmortem glycogen contents in PM are dependent on their preslaughter stores.

In the present study, the preslaughter pH of PM was changed neither by long-term nor by short-term CORT administration, suggesting that antemortem pH in PM can be well-controlled and is not altered by preslaughter stress reactions. Immediately after slaughter, however, the initial postmortem pH was significantly lowered by long-term CORT treatment at both 35 and 39 d of age (7 and 11 d after CORT administration). It means that the initial postmortem pH could be affected by antemortem stress. This result was consistent with the previous study of Sandercock et al. (2001), who reported a significant fall in initial muscle pH in heat-stressed broiler chickens. The lower postmortem pH in PM of CORT chickens indicated the fast acidification after slaughter. The decreased initial pH seems not to be the consequence of the fast glycolytic metabolism immediately after slaughter, because the obvious decline of glycogen contents was observed in 35-d but not in 39-d-old chickens. Moreover, the similar pre-or postslaughter R-value in CORT and control chickens also implies that the depletion of ATP is out of relation to the decreased pH by stress. On the other hand, Kannan et al. (1998) reported that CORT administration for 48 h had no significant influence on the initial postmortem pH of PM. In line with this result, acute CORT treatment (3 h) had no obvious effect on the ante- or postmortem pH of PM in the present study (experiments 2 and 3). The result means that the effect of antemortem physiological status elicited by long-term CORT administration could influence the initial postmortem muscle pH, whereas the short-term upregulation of CORT is not involved in the early postmortem event.

In experiment 1, muscle pH decreased immediately after slaughter in broiler chickens at 35 and 39 d of age, indicating the rapid accumulation of acidic substances. However, the decline of initial pH was not observed at 21 and 28 d of age of experiment 1 and 3, and, moreover, there was even a significant increase in experiment 2. It showed that the decreasing of muscle pH was not the necessary result at the beginning of postslaughter. The changes in glycogen stores and R-value after exsanguination were inconsistent with pH in all 3 experiments, implying that the initial muscle pH is a result of comprehensive metabolic processes but not solely dependent on accumulation of acidic substance. Moreover, the glycogen breakdown is not necessary to induce a reduction of pH.

In experiment 2, the decline of pH at 24 h postmortem compared with the initial postmortem value was in accordance with the previous works (McKee and Sams, 1997), suggesting the accumulation of lactic acid during the process of rigor mortis. On the other hand, the ultimate pH at 24 h postmortem was still higher than the preslaughter value. It may imply the loss or depletion of acidic substances after slaughter. Because this change was not obvious in experiment 3, the underlying mechanism needed to be further investigated.

The R-value is an indirect indicator of ATP depletion in muscle. The unaltered R-value by either long- or short-term CORT treatment indicated the depletion of ATP is not affected by chronic or acute antemortem stress mimicked by CORT administration. In experiment 1, R-value increased after slaughter in all the treatments at each day of age, whereas the glycogen stores differently depleted. In experiments 2 and 3, however, the exhaustion of ATP was not observed at the initial period of postslaughter, but there was a significant reduction in glycogen contents. The result showed that the depletion of ATP seemed to have no direct relation to the breakdown of glycogen stores.

In the present study, the drip loss of breast meat tended to be increased by chronic CORT treatment (P = 0.13), coinciding with the lower initial postmortem breast muscle pH. This result is consistent with the findings of Sandercock et al. (2001), who reported that the higher drip loss in heat-stressed chickens was more closely associated with the initial postmortem pH. In the acute stress model (CORT administration for 3 h), however, the drip loss of breast meat tended to decline compared with control chickens in both experiment 2 (P < 0.05) and experiment 3 (P = 0.06), indicating the increased water-holding capacity. Because the preslaughter stress could decrease the water-holding capacity (Northcutt et al., 1994; McKee and Sams, 1997), the present result may indicate the short-term upregulation of circulating CORT is not involved in this disadvantage effect of preslaughter stress on meat quality.

It is possible that the commercial slaughter conditions different from that used in the present study, such as food withdrawal, stunning, and cooling, could differentially influence the stress responses and muscle metabolism. Nevertheless, under the current experimental conditions, it could be concluded that dietary treatment could not alter glycogen stores in PM. The glycogen stores of PM can be increased by stress mimicked by long-term CORT administration rather than by acute treatment. Preslaughter stress reactions had no relation to the depletion of breast muscle glycogen during the initial postmortem period. The initial breast muscle pH was significantly decreased by long-term CORT administration. The result suggests that short-term upregulation of circulating CORT is not involved in the elevated drip loss induced by preslaughter stress.


   ACKNOWLEDGMENTS
 
This work was supported by grants from the National Basic Research Program of China (2004CB117507). The project was supported by the Program for New Century Excellent Talents in University and sponsored by the Foundation for the Returned Overseas Chinese Scholars, State Education Ministry.

Received for publication July 27, 2006. Accepted for publication November 22, 2006.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Ali, A. S., A. P. Harrison, and J. F. Jensen. 1999. Effects of some ante-mortem stressors on peri-mortem and postmortem biochemical changes and tenderness in broiler breast muscle: A review. World’s Poult. Sci. J. 55:403–414.[ISI]

Berri, C., M. Debut, V. Sante-Lhoutellier, C. Arnould, B. Boutten, N. Sellier, E. Baeza, N. Jehl, Y. Jego, M. J. Duclos, and E. Le Bihan-Duval. 2005. Variations in chicken breast meat quality: Implications of struggle and muscle glycogen content at death. Br. Poult. Sci. 46:572–579.[ISI][Medline]

Berri, C., N. Wacrenier, N. Millet, and E. Le Bihan-Duval. 2001. Effect of selection for improved body composition on muscle and meat characteristics of broilers from experimental and commercial lines. Poult. Sci. 80:833–838.[Abstract/Free Full Text]

Debut, M., C. Berri, C. Arnould, D. Guemene, V. Sante-Lhoutellier, N. Sellier, E. Baeza, N. Jenl, Y. Jego, C. Beaumont, and E. Le Bihan-Duval. 2005. Behavioural and physiological responses of three chicken breeds to pre-slaughter shackling and acute heat stress. Br. Poult. Sci. 46:527–535.[ISI][Medline]

Edwards, M. R., J. P. McMurtry, and R. Vasilatos-Younken. 1999. Relative insensitivity of avian skeletal muscle glycogen to nutritive status. Domest. Anim. Endocrinol. 16:239–247.[ISI][Medline]

Harvey, S., C. G. Scanes, and K. I. Brown. 1986. Adrenals. Page 479–493 in Avian Physiology. 4th ed. P. D. Sturkie, ed. Springer-Verlag, New York, NY.

Jeacocke, R. E. 1977. Continuous measurement of the pH of beef muscle in intact beef carcasses. J. Food Technol. 12:375–386.

Kannan, G., J. L. Heath, C. J. Wabeck, and J. A. Mench. 1997a. Shackling of broilers: Effects on stress responses and breast meat quality. Br. Poult. Sci. 38:323–332.[ISI][Medline]

Kannan, G., J. L. Heath, C. J. Wabeck, S. L. Owens, and J. A. Mench. 1998. Elevated plasma corticosterone concentrations influence the onset of rigor mortis and meat color in broilers. Poult. Sci. 77:322–328.[Abstract/Free Full Text]

Kannan, G., J. L. Heath, C. J. Wabeck, M. C. Souza, J. C. Howe, and J. A. Mench. 1997b. Effects of crating and transport on stress and meat quality characteristics in broilers. Poult. Sci. 76:523–529.[Abstract/Free Full Text]

Lin, H., E. Decuypere, and J. Buyse. 2004a. Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus). 1. Chronic exposure. Comp. Biochem. Physiol. B Biochem. Mol. Biol. 139:737–744.[Medline]

Lin, H., E. Decuypere, and J. Buyse. 2004b. Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus). 2. Short-term effect. Comp. Biochem. Physiol. B Biochem. Mol. Biol. 139:745–751.[Medline]

Lin, H., S. J. Sui, H. C. Jiao, J. Buyse, and E. Decuypere. 2006. Impaired development of broiler chickens by stress mimicked by corticosterone exposure. Comp. Biochem. Physiol. A Mol. Integr. Physiol. 143:400–405.[Medline]

Malheiros, R. D., V. M. Moraes, A. Collin, E. Decuypere, and J. Buyse. 2003. Free diet selection by broilers as influenced by dietary macronutrient ratio and corticosterone supplementation. 1. Diet selection, organ weights, and plasma metabolites. Poult. Sci. 82:123–131.[Abstract/Free Full Text]

McKee, S. R., and A. R. Sams. 1997. The effect of seasonal heat stress on rigor development and the incidence of pale, exudative turkey meat. Poult. Sci. 76:1616–1620.[Abstract/Free Full Text]

Northcutt, J. K., E. A. Foegeding, and F. W. Edens. 1994. Water-holding properties of thermally preconditioned chicken breast and leg meat. Poult. Sci. 73:308–316.[ISI][Medline]

Papinaho, P. A., and D. L. Fletcher. 1995. Effect of stunning amperage on broiler breast muscle rigor development and meat quality. Poult. Sci. 74:11527–11534.

Quentin, M., K. Bigot, S. Tesseraud, Y. Boirie, I. Bouvarel, and M. Picard. 2003. Is ribosomal capacity a potential metabolic marker of muscle development? Measurement by muscular biopsy. Poult. Sci. 82:1530–1535.[Abstract/Free Full Text]

Rosebrough, R. W., and J. J. Begin. 1975. The effect of non-protein energy source and age on the blood glucose level and the muscle glycogen content of young chicks. Poult. Sci. 54:1327–1329.[ISI][Medline]

Rosenvold, K., J. S. Petersen, H. N. Lærke, S. K. Jensen, M. Therkildsen, A. H. Karlsson, H. S. Møller, and H. J. Andersen. 2001. Muscle glycogen stores and meat quality as affected by strategic finishing feeding of slaughter pigs. J. Anim. Sci. 79:382–391.[Abstract/Free Full Text]

Sams, A. R. 1999. Meat quality during processing. Poult. Sci. 78:798–803.[Abstract/Free Full Text]

Sandercock, D. A., R. R. Hunter, G. R. Nute, M. A. Mitchell, and P. M. Hocking. 2001. Acute heat stress-induced alterations in blood acid-base status and skeletal muscle membrane integrity in broiler chickens at two ages: Implications for meat quality. Poult. Sci. 80:418–425.[Abstract/Free Full Text]

SAS Institute. 1998. User’s Guide: Statistics. SAS Inst. Inc., Cary, NC.

Savenije, B., E. Lambooij, M. A. Gerritzen, K. Venema, and J. Korf. 2002a. Effects of feed deprivation and transport on preslaughter blood metabolites, early postmortem muscle metabolites, and meat quality. Poult. Sci. 81:699–708.[Abstract/Free Full Text]

Savenije, B., F. J. Schreurs, H. A. Winkelman-Goedhart, M. A. Gerritzen, J. Korf, and E. Lambooij. 2002b. Effects of feed deprivation and electrical, gas, and captive needle stunning on early postmortem muscle metabolism and subsequent meat quality. Poult. Sci. 81:561–571.[Abstract/Free Full Text]

Warriss, P. D., S. C. Kestin, S. N. Brown, and E. A. Bevis. 1988. Depletion of glycogen reserves in fasting broiler chickens. Br. Poult. Sci. 29:149–154.[ISI][Medline]

Warriss, P. D., S. C. Kestin, S. N. Brown, T. G. Knowles, L. J. Wilkins, J. E. Edwards, S. D. Austin, and C. J. Nicol. 1993. The depletion of glycogen stores and indices of dehydration in transported broilers. Br. Vet. J. 149:391–398.[ISI][Medline]

Young, J. F., A. H. Karlsson, and P. Henckel. 2004. Water-holding capacity in chicken breast muscle is enhanced by pyruvate and reduced by creatine supplementation. Poult. Sci. 83:400–405.[Abstract/Free Full Text]




This article has been cited by other articles:


Home page
 Poult. Sci.Home page
C. G. Scanes
Perspectives on Analytical Techniques and Standardization
Poult. Sci., November 1, 2008; 87(11): 2175 - 2177.
[Full Text] [PDF]

Home page
 Poult. Sci.Home page
J. Gao, H. Lin, Z. G. Song, and H. C. Jiao
Corticosterone Alters Meat Quality by Changing Pre-and Postslaughter Muscle Metabolism
Poult. Sci., August 1, 2008; 87(8): 1609 - 1617.
[Abstract] [Full Text] [PDF]

Home page
 Poult. Sci.Home page
H. A. Olanrewaju, J. P. Thaxton, W. A. Dozier III, and S. L. Branton
Electrolyte Diets, Stress, and Acid-Base Balance in Broiler Chickens
Poult. Sci., July 1, 2007; 86(7): 1363 - 1371.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lin, H.
Right arrow Articles by Dong, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, H.
Right arrow Articles by Dong, H.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS