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Effect of the live weight gain of steers during winter grazing on digestibility, acid-base balance, blood flow, and oxygen consumption by splanchnic tissues during adaptation and subsequent feeding of a high-grain diet^1,2

M. J. Hersom^*, C. R. Krehbiel^*,3, G. W. Horn^* and J. G. Kirkpatrick

^* Department of Animal Science and and Veterinary Teaching Hospital and Department of VeterinaryClinical Sciences, Oklahoma State University, Stillwater 74078

	Abstract

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Ten multicatherized steers were used in a completely random design to determine the effect of previous BW gain on blood flow, acid-base balance, and oxygen consumption across portal-drained viscera and liver of growing beef steers fed a high-grain diet. Treatments were high (1.31 ± 0.09 kg/d) or low (0.68 ± 0.07 kg/d) daily BW gain during an 82-d winter wheat pasture grazing period and a subsequent 37-d transition period. Blood flow, blood gas measurements, and oxygen consumption were determined on d 0, 14, 28, 42, and 64 of a high-grain finishing period. Compensatory growth was evident in low-gain steers; ADG (1.50 vs. 1.11 kg/d, P < 0.05) and gain efficiency (0.221 vs. 0.109 kg/kg, P < 0.01) were greater from d 14 through 28 than for high-gain steers. Arterial base tended (P < 0.12) to be greater in low-gain than in high-gain steers, whereas calculated HCO₃^- (mmol/L; P < 0.20) did not differ between treatments. Arterial O₂ concentration was not different (P < 0.97) between treatments but increased (P < 0.001) with increasing days on feed. Portal blood flow increased with days on feed (P < 0.001) but did not differ (P < 0.34) between treatments. Hepatic blood flow scaled to metabolic BW was 19.7% greater (P < 0.02) in low-gain than in high-gain steers. Across the feeding period, O₂ consumption and CO₂ flux by PDV, liver, and total splanchnic tissue (TST) did not differ (P < 0.33) between treatments. However, TST O₂ consumption (mmol/[h•kg BW^0.75]) tended (P < 0.12) to be greater in low- than in high-gain steers. Compensating steers’ arterial blood acid-base measurements did not change with days on feed, indicating that they were not more susceptible to metabolic acidosis than high-gain steers. However, steers that had lower BW gain before high-grain feeding exhibited increased hepatic blood flow and TST O₂ consumption (metabolic BW basis) during the finishing period compared with high-gain steers. Greater hepatic blood flow and energy expenditure by TST of previously restricted steers might have facilitated compensatory growth.

Key Words: Acid-Base Equilibrium • Blood Flow • Cattle • Compensatory Growth

	Introduction

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Little information is available regarding the effect of previous live BW gain and compensatory growth on total splanchnic tissue (TST) metabolism in beef steers. Compensatory growth has been observed as increased BW gain, increased DMI, and lower ME requirements (Fox et al., 1972; Carstens et al., 1991). However, these characteristics must have metabolic controls that have not been fully elucidated. Integration of nutrient metabolism into growth characteristics implicates the importance of the gastrointestinal tract and liver in animal production (Eisemann et al., 1996). Burrin et al. (1989) showed that blood flow and energy expenditure change in response to changes in DMI and splanchnic tissue mass. Conceivably, compensatory growth in cattle might occur because of changes in blood flow and associated oxygen consumption across TST.

The incidence of subacute acidosis is an important consideration in feeding high-grain diets (Elam, 1976). Acidosis occurs in conjunction with excessive consumption of fermentable carbohydrates (Slyter, 1976) that increase the acid load absorbed from the gastrointestinal tract. Successful adaptation allows the cattle to consume large amounts of high-energy diets, resulting in greater BW gains and gain efficiency. However, Klopfenstein et al. (1999) suggested that compensating steers are aggressive eaters, and acidosis might limit their ability to make compensatory gain. Our hypotheses were that 1) improved growth performance by compensating steers might result from differences in blood flow and energy expenditure by TST and 2) acid-base balance by compensating steers might be compromised during adaptation to and subsequent feeding of a high-grain diet. Therefore, the objectives of this experiment were to determine the effect of previous BW gain of steers on total-tract nutrient digestion, blood acid-base balance, blood flow, and oxygen consumption across TST during adaptation to and finishing on a high-grain diet.

	Materials and Methods

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Animal Management
Ten Angus x Angus-Hereford steers (average initial BW = 205 ± 14 kg, age = 286 ± 11 d) were randomly assigned to one of two treatments. Treatments were high (HG; 1.31 ± 0.09 kg/d) or low (LG; 0.68 ± 0.07 kg/d) daily BW gain while grazing winter wheat pasture (82 d) and during a subsequent transition period (37 d). Stocking density was altered in the LG treatment to maintain the desired BW gain (Hersom et al., 2003a). Following the grazing period, steers were housed in individual, indoor pens (3.5 x 3.5 m) and fed a transition diet (Table 1) to maintain their respective BW gains during surgery for placement of chronic indwelling catheters. During the transition period, the average BW of LG or HG steers was used to determine DMI that resulted in ME-allowable ADG similar to daily BW gain during grazing using the Level 1 Model of NRC (1996). Catheters were surgically placed in the portal vein, a hepatic vein, a mesenteric vein, and an adjacent mesenteric artery as described by Ferrell et al. (1991). Catheter patency was maintained by filling catheters with a heparinized-saline solution (1,000 U/mL) between sampling periods. Steers were allowed a minimum of 21 d to recover from surgery before beginning the initial collection period. The Oklahoma State University Institutional Animal Care and Use Committee approved all experimental procedures.

Sample Collection
Steers were placed in stanchions in a climate-controlled room (23 to 27°C, 15% humidity) 6 d before the initiation of each blood collection. Total fecal collections were weighed daily for 3 d before blood collection. A subsample (10%) of the daily fecal collection was composited for the 72-h fecal collection period. Simultaneous diet samples were also collected. Blood was collected on d -1, 0, 13, 14, 27, 28, 41, 42, 63, and 64 of the experiment. Five steers were sampled during each day of sampling (e.g., three HG and two LG steers were sampled on d -1, and two HG and three LG steers were sampled on d 0).

On the morning of sampling, a priming dose of 20 mL of 7% (wt/vol; d -1, 0, 13, 14, 27, 28) or 10% (wt/vol; d 41, 42, 63, 64) para-aminohippurate (PAH, pH = 7.4) were administered through a 0.45 µm sterile filter (Millipore, Bedford, MA) into the mesenteric vein catheter at 0700. Para-aminohippurate was continuously infused (PHD 2000 Syringe pump; Harvard Apparatus Inc., Holliston, MA) at 0.8 mL/min for 8 h following the priming dose. Blood was collected at hourly intervals from 0800 until 1600. Thirty milliliters of blood was drawn simultaneously from the portal vein, hepatic vein, and mesenteric artery catheters into syringes, and blood was placed into tubes (BD Vacutainer) treated with sodium heparin or potassium oxalate and sodium fluoride. Hourly blood samples were immediately capped and placed on ice for transport to the laboratory. In the laboratory, 90 µL of whole blood was immediately taken for each steer and site for blood gas analysis (1304 pH/Blood Gas Analyzer, Instrumentation Laboratory, Lexington, MA). Calibration of the blood gas analyzer occurred daily using standardized samples (ContrIL Blood gas control #93630, Instrumentation Laboratory) and automated two-point calibration. An additional 40 µL of whole blood was used to determine packed cell volume. Two milliliters of whole blood from each hour within steer and site was used to form a daily whole blood composite. The remaining blood was centrifuged (3,000 x g, 4°C, 20 min) and plasma harvested and frozen (-40°C) for further analysis.

Sample Analysis
Feed and fecal samples were dried in a forced-air oven at 55°C and ground in a Wiley mill to pass a 2-mm screen. Dry matter, ash (AOAC, 1990), and N concentration (LECO, St. Joseph, MI) were determined on feed and fecal samples from each sampling period. Hourly plasma samples from each site were used to determine the concentration of PAH (Harvey and Brothers, 1962) with standards prepared from the infusion solution from each sampling day. Hemoglobin (Hb) concentration in arterial, portal, and hepatic whole blood samples were determined colorimetrically (Procedure #525, Sigma Diagnostics, St. Louis, MO).

Calculations and Statistical Analysis
Digestible OM intake (DOMI) was calculated by multiplying daily OM intake by OM digestibility and was expressed per unit of metabolic BW. Plasma flows through the hepatic portal vein and hepatic vein were calculated using the Fick principle as outlined by Katz and Bergman (1969): blood flow (BF) = IR^PAH/(C_V^PAH - C_A^PAH), in which BF represents plasma flow through the portal-drained viscera (PDV) or liver (mL/min), IR^PAH is the infusion rate (mg/min) of PAH, and C_V^PAH and C_A^PAH are the PAH concentrations (mg/mL) in venous and arterial plasma, respectively. Portal and hepatic plasma flow were calculated directly, whereas hepatic arterial plasma flow was calculated as hepatic BF minus portal BF. Individual plasma flows from any site deviating more than two SD from the mean were deleted and means recalculated (Bohnert et al., 1999). Blood oxygen concentration was calculated as the sum of Hb-bound O₂ (O₂ saturation, % x 1.34 mL O₂/g Hb x g Hb/mL blood) and dissolved O₂ (0.023 mL/mL blood x pO₂ mm Hg/daily mean barometric pressure, mm Hg). Milliliters of O₂ per liter of blood were converted to millimoles per liter by assuming 22.2 mL/mmol O₂ (Huntington and Tyrrell, 1985). Oxygen consumptions were calculated (Burrin et al., 1989) across the PDV, liver, and total splanchnic tissues (TST) using the following equations: PDV consumption = portal BF x (portal_[O2] - arterial_[O2]); hepatic consumption = portal BF x (hepatic_[O2] - portal_[O2]) + arterial BF x (hepatic_[O2] - arterial_[O2]); and TST consumption = PDV consumption + hepatic consumption. Carbon dioxide concentration was calculated using the Henderson-Hasselbach equation (Oddy et al., 1988): CO₂ (mM) = (10^{(pH - 6.12)} x 0.0314 x pCO₂) + (0.0314 x pCO₂). Carbon dioxide flux was calculated for the PDV, liver, and TST similar to O₂ consumption. Respiratory quotient (RQ) for PDV, liver, and TST were calculated as RQ = CO₂ flux/O₂ consumption.

All data were analyzed as a completely random design using the Mixed procedure of SAS (SAS Inst. Inc., Cary, NC). The statistical model included treatment, sampling day, and the interaction as fixed effects. The experimental unit was steer, and the random term was steer within treatment. Data was collected repeatedly across experimental days. The spatial power law covariance structure was used (Littell et al., 1996) because of unequal spacing of collection days. Because of missing observations, least squares means were calculated. Results were considered significant if P < 0.05. Regression analysis was performed using the Proc REG procedure of SAS to examine the relationship of blood base measurements to DOMI, and the relationship of blood flow to BW, DMI, and DOMI.

	Results

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Animal Performance and Total Tract Digestibility
The number of steers sampled during each period and number of catheters patent at each site are listed in Table 2. During transition from grazing to the initiation of the first blood collection (37 d), HG steers had greater (P < 0.002) ADG (1.15 kg/d) compared with LG steers (0.004 kg/d). Average daily gain from the initiation of grazing to the first blood sampling day (d -1) was greater (P < 0.001) for HG than for LG steers (1.31 vs. 0.68 kg/d, respectively).

Blood Gases
Arterial blood pH was not different between treatments (P < 0.56) but tended (P < 0.10) to differ across sampling days; mean arterial pH was 7.43 during the 64-d experiment (Table 4). Arterial partial pressure of carbon dioxide (pCO₂) was not different (P < 0.30) between treatments, but exhibited a sampling day effect (P < 0.01). Arterial pCO₂ generally decreased as days on feed increased. Calculated bicarbonate levels in arterial blood were not different (average = 28.0 mM, P < 0.20) between treatments. Oxygen saturation of arterial, portal, and hepatic blood averaged = 98.4, 78.9, and 66.8%, respectively, and was not different (P < 0.62) between treatments. Similarly, hemoglobin concentration in arterial blood was not different (P < 0.96) between treatments (average = 9.69 g/100 mL); however, hemoglobin concentrations in arterial blood increased (P < 0.001) by 21% from d 0 to 64. Packed cell volume (PCV) did not differ (P < 0.43) between treatments or with increasing days on feed (P < 0.20). Arterial blood base tended (P < 0.12) to be greater in LG than HG steers, and tended (P < 0.12) to decrease across sampling days until d 42. Similarly, portal blood base exhibited a sharp decrease (sampling day effect, P < 0.004) in HG and LG steers until d 28 and then increased. Hepatic base followed a similar pattern, decreasing until d 28 and then increasing (sampling day effect, P < 0.02).

Carbon dioxide flux across the PDV (P < 0.33), liver (P < 0.80), and TST (P < 0.49) did not differ between treatments. Portal-drained visceral CO₂ flux did exhibit a day effect (P < 0.02), generally increasing with increasing days on feed. Hepatic (P < 0.80) and TST (P < 0.49) CO₂ flux did not differ (P < 0.80 and 0.49) across sampling days. Similarly, RQ of the PDV (2.32; P < 0.76), liver (1.86; P < 0.35), and TST (2.08; P < 0.33) were not different between treatments or across days on feed.

	Discussion

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Compensatory growth has been defined as a period of faster or more-efficient rate of growth following a period of nutritional restriction (NRC, 1996). Generally, compensatory growth is characterized by increased rate of BW gain (Fox et al., 1972; Carstens et al., 1991; Sainz et al., 1995), increased feed intake (Fox et al., 1972; Drouillard et al., 1991; Sainz et al., 1995), and increased efficiency of metabolizable energy used for gain (Fox et al., 1972; Carstens et al., 1991). In our experiment, LG steers had greater ADG and increased gain efficiency, characteristic of compensatory growth. Unfortunately, DMI by steers in the present experiment was uncharacteristically low for cattle consuming high-energy diets, and most likely influenced our results. Diet evaluations for growing and finishing cattle (NRC, 1996) suggest that 325-kg animals consuming diets with 1.1 to 1.6 Mcal/kg of NE_g (DM basis) and gaining 1.36 to 1.90 kg/d should consume approximately 2.3 to 2.7% of their BW as DM. Low intakes in the present experiment (1.90% of BW) most likely resulted from problems associated with maintaining intakes by cattle in metabolism stalls, and not a result of ruminal acidosis. Although intakes were low, DMI (% of BW) from d 14 to 28 of the present experiment was 15.7% greater for LG than for HG steers.

Lower diet DM digestibility has been reported (Thomson et al., 1982; Hayden et al., 1993) in realimented cattle after energy restriction for 154 or 92 d, respectively. Thomson et al. (1982) proposed that decreased DM digestibility might result from an increased rate of passage caused by increased DMI by compensating steers. In contrast, mean OM digestibility and DOMI expressed per BW^0.75 were similar between treatments in our experiment. The observed treatment x day interaction for DOMI was primarily due to differences on d 0, when LG steers were being restricted in intake.

Because we expected LG steers to undergo compensatory growth and the associated increase in DMI, we hypothesized that LG cattle might have been more susceptible to metabolic acidosis during adaptation to the high-grain diet (Klopfenstein et al., 1999). Therefore, measures of blood acid-base balance were of interest. Mean blood pH was 7.43, 7.32, and 7.33 for arterial, portal, and hepatic blood, respectively. Leedle et al. (1995) reported mean venous blood pH levels that were similar to those in the present study; however, venous blood pH in their study decreased with increasing days on feed as cows were adapted from 25 to 90% concentrate diets fed at 2% of BW. Partial pressure of CO₂ was not different between treatments, but in both treatments pCO₂ generally decreased as days on feed increased. In addition, arterial blood base was numerically lower in HG steers than in LG steers. This might suggest that LG steers were supplying the PDV with blood that had a greater buffering capacity compared with HG steers. Differences in the ability of PDV tissues to disperse the metabolic acid load into blood could also be important in controlling cellular metabolism and absorption of nutrients. Simple linear regression analysis indicated that portal blood base was negatively related to DOMI (portal base = -0.65 x DOMI + 4.74, r² = 0.24, P < 0.001). The lowest portal blood base in HG steers coincided with the greatest DOMI. Similar simple linear regression analysis showed that hepatic blood base was also negatively related to DOMI (hepatic base = -0.49 x DOMI + 4.69, r² = 0.19, P < 0.005). Decreases in blood base coincided with the adaptation of both HG and LG steers to a finishing diet with greater concentrate levels. The increased concentrate levels would have increased the absorbed acid load from the rumen, which most likely required more buffering. In addition, a shift in the dietary cation-anion difference (DCAD; NRC, 2001) could have been a driving force behind changes in blood acid-base parameters associated with increasing concentrate in the present experiment. Dietary cation-anion difference decreased from -36.6 mEq/kg of DM for the transition diet to -94.4 mEq/kg of DM for the finishing diet. Decreasing the DCAD from 203 to -40 to -63 (Vagnoni and Oetzel, 1998) or from 150 to -150 (Moore et al., 2000) mEq/kg of DM has resulted in decreases in blood bicarbonate and blood base in dry cows, but no difference in blood pH or pCO₂.

Hemoconcentration resulting from dehydration has also been identified as an indication of acidotic conditions in cattle (Huntington and Britton, 1979; Owens et al., 1998; Brown et al., 2000). Cattle in acidotic states have been reported to increase PCV (Huntington and Britton, 1979; Leedle et al., 1995; Brown et al., 2000). In the present study, PCV was not affected by treatment. Under the conditions of the present experiment, we conclude that compensating steers are not at any greater risk of experiencing metabolic acidosis than noncompensating steers. However, it should be emphasized that, due to low intakes, steers were most likely not experiencing subacute acidosis in our experiment.

Blood flow is key to the dispersion and metabolism of absorbed nutrients through splanchnic tissues. Arterial and portal plasma flow were not different between treatments in our experiment, and blood flows were similar to those previously reported (Reynolds and Huntington, 1988; Krehbiel et al., 1992; Eisemann et al., 1996) for growing steers of similar BW, age, and diets. Under steady-state conditions, Huntington et al. (1996) predicted decreased PDV and liver blood flow with increasing levels of dietary concentrate. Reynolds et al. (1991) also observed decreased PDV and liver blood flow in heifers fed 75% concentrate diets compared with 75% alfalfa diets. In contrast, PDV and liver plasma flow increased with increasing concentrate in the diet in the present experiment. Discrepancies among data might be due to differences in BW, age, and DMI of steers used by Huntington et al. (1996) compared with steers used for the present experiment. Our data with growing steers consuming increasing concentrate are confounded with increases in BW and DMI, especially for LG steers.

Variation in blood flow has been shown to occur throughout the day. Whitt et al. (1996) reported portal and hepatic plasma flows increased after feeding and varied by as much as 8 to 9% across the day. Many experiments examining blood flow utilize equally spaced feed delivery during the day (Krehbiel et al., 1992; Huntington et al., 1996; Lapierre et al., 2000). Evenly spaced feeding may decrease variation in blood flow because adherence to the Fick principle is more likely (Huntington, 1999). Our objective in the feeding management of our steers was to more closely replicate our larger feedlot experiments (Hersom et al., 2004a), and more practical feed delivery patterns (i.e., twice daily). As greater variation in blood flow across the day was expected due to the potential lack of steady-state conditions, steers were sampled every hour between the morning and afternoon feedings, and means were computed. Additionally, Huntington (1999) reported that the greatest variation in blood flow is attributable to steer. The point of variation in blood flow is important because subtle differences between treatments in concentrations of such things like oxygen can be magnified or diluted depending on blood flow differences between treatments.

In previous experiments, portal and hepatic blood flow has been shown to increase concomitant with increased DMI (Reynolds et al., 1992; Eisemann et al., 1996) and BW (Eisemann et al., 1996). In the present experiment, the relationship of portal plasma flow (L/[h•kg BW^0.75]) to BW^0.75 (r² = 0.07), DMI (% of BW^0.75; r² = 0.02), and DOMI (kg/[d•BW^0.75]; r² = 0.005) was generally low, and was similar in HG and LG steers. Figure 1 shows the relationship of hepatic plasma flow (L/[h•kg BW^0.75]) to BW^0.75, DMI (% of BW^0.75), and DOMI (kg/[d•BW^0.75]) for HG and LG steers. Hepatic plasma flow increased as DMI (% of BW^0.75; r² = 0.33, P < 0.06) and DOMI (kg/[d•BW^0.75]; r² = 0.32, P < 0.07) increased in LG steers. As described by the first derivative of the cubic equations, hepatic plasma flow scaled to metabolic body size reached an asymptote when DMI was 7.89% of BW^0.75, and when DOMI was 0.070 kg/(d•BW^0.75]. In contrast, hepatic plasma flow decreased quadratically (r² = 0.39; P < 0.03) as DMI (% of BW^0.75) increased in HG steers. The differential response in hepatic plasma flow between LG vs. HG steers most likely occurred because HG steers started the experiment with greater DM and DOMI intake compared with LG steers, which had a greater increase in DMI and DOMI during the first 28 d of the experiment. Across the feeding period, hepatic plasma flow was 6.3% (L/h) or 19.7% (L/[h•kg BW^0.75]) greater in LG than in HG steers.

View larger version (24K): [in this window] [in a new window]   Figure 1. The relationship of hepatic blood flow (L/[h•kg BW0.75]) to a) high-gain (HG) steers metabolic BW (BF = 0.08 BW0.75 + 1.02, r2 = 0.04, P < 0.45); b) low-gain (LG) steers metabolic BW (BF = 0.13 BW0.75 -0.51, r2 = 0.10, P < 0.15); c) HG steers DMI as a percentage of metabolic BW (BF = 0.88 [DMI, % BW0.75]2 x -15.4 DMI, % BW0.75 + 73.2; r2 = 0.39, P < 0.03); d) LG steers DMI as a percentage of metabolic BW (BF = 0.33 [DMI, % BW0.75]3 x -9.4 [DMI, % BW0.75]2 x 86.7 DMI, % BW0.75 - 253.7; r2 = 0.33, P < 0.06); e) HG steers digestible OM intake, kg/(d•BW0.75) (BF = 7,214 [DOMI, kg/(d•BW0.75)]2 x -1,058 DOMI, kg/(d•BW0.75) + 45.6, r2 = 0.14, P < 0.34); f) LG steers digestible OM intake, kg/(d•BW0.75) (BF = 205,674 [DOMI, kg/(d•BW0.75)]3 x -50,670 [DOMI, kg/(d•BW0.75)]2 x 4,071 DOMI, kg/(d•BW0.75) - 96.7; r2 = 0.32, P < 0.07).

Hepatic O₂ consumption increased linearly (r² = 0.26, P < 0.001) with increasing hepatic plasma flow across all observations (Figure 2), but was not different between LG and HG steers across the feeding period. Similar to our results, Freetly et al. (1995) reported a positive linear relationship (r² = 0.52) between liver blood flow and O₂ consumption. Reynolds et al. (1991) reported a 64% increase in hepatic blood flow and a 92% increase in liver O₂ consumption in heifers fed a 75% concentrate diet at 2 vs. 1 x ME intake, respectively. In addition, Freetly et al. (1995) reported decreased hepatic O₂ consumption in lambs restricted to 70% of their ad libitum intake, and predicted that liver O₂ consumption in restricted lambs would be similar to ad libitum-fed lambs by d 38 of realimentation. Freetly et al. (1995) suggested that the rate of decrease in hepatic O₂ consumption in vivo was most likely similar to the rate of decrease in liver organ mass. In our companion experiment (Hersom et al., 2004b), steers that had grazed winter wheat for a low rate of gain had lower absolute liver mass (4.8 vs. 5.6 kg), similar relative liver mass (17.7 vs. 16.6 g/kg of EBW, respectively), and similar in vitro O₂ consumption (7.0 vs. 6.2 µL•min^-1•g^-1) compared with steers that had grazed winter wheat for a high rate of live BW gain. Similar in vivo hepatic O₂ consumption in the present experiment compares favorably with our other results.

View larger version (10K): [in this window] [in a new window]   Figure 2. The relationship of hepatic oxygen consumption (mmol/[h•kg BW0.75]) to hepatic venous blood flow (L/[h•kg BW0.75]; hepatic O2 consumption = -0.724 L/[h•kg BW0.75] + 2.02; r2 = 0.26, P < 0.001).

Mean PDV CO₂ flux of the growing steers in the present experiment was 920 mmol/h, which is lower than values reported by Benson et al. (2002), Reynolds et al. (1988), and Baird et al. (1975) for lactating dairy cows. The increase in PDV CO₂ flux with increasing days on feed might indicate that increased metabolism occurred by the PDV. However, CO₂ flux across the PDV can be influenced by several factors, including gut fermentation, respiratory metabolism in gut tissues, salivary bicarbonate, and VFA absorption (Benson et al., 2002). Respiratory quotient for the PDV (2.32) in the current experiment was greater than that observed for lactating dairy cows (Benson et al., 2002 [0.39] and Reynolds et al., 1988 [0.56]), but similar to the value of 2.37 calculated from Baird et al. (1975). Liver and TST release of CO₂ did not differ between treatments or with increasing days on feed. Hepatic and TST CO₂ flux were lower and RQ greater for finishing steers in the present experiment compared with lactating dairy cows (Benson et al., 2002; Reynolds et al., 1988; Baird et al., 1975). Differences in CO₂ flux and RQ between the present experiment and limited literature values may underscore the dynamics of different physiological states observed between dairy and feedlot cattle.

The TST are key for converting feed to substrates for animal growth; however, digestion, absorption, and metabolism of nutrients by the TST result in an energetic cost (Reynolds, 2002). Whereas one might hypothesize that previously restricted steers must have energy use (i.e., O₂ consumption) that is less than unrestricted steers to exhibit compensatory growth, our results suggest that TST O₂ consumption scaled to metabolic body size was similar or greater for compensating steers. A rapid increase in energy expenditure by TST early in the feeding period might support an increased rate of growth.

	Implications

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Steers restricted in live body weight gain before placement on a high-grain diet can compensate compared with unrestricted steers. Characteristics of compensating steers include greater daily gain and gain efficiency during the finishing period. In addition, when scaled to metabolic body weight, the present data suggest that compensating steers have greater liver blood flow and oxygen consumption by total splanchnic tissues compared with noncompensating steers. Greater energy expenditure by total splanchnic tissues in compensating steers may support an accelerated rate of growth. Under the conditions of the present experiment, compensating steers were not at any greater risk for metabolic acidosis than noncompensating steers; however, a more readily fermentable source of starch, greater intakes, or more aggressive adaptation to a high-grain diet might have altered our results.

	Footnotes

 
¹ Approved for publication by the director of the Oklahoma Agric. Exp. Stn. This research was supported by the Oklahoma Agric. Exp. Stn. under project H-2438 and the Cooperative State Research, Education, and Extension Service, U.S. Department of Agriculture, under Agreement Nos. 99-34198-7481 and 2001-34198-10403.

² The authors thank C. Lunsford, D. Perry, and J. Summers for their help with sample analyses; S. Welty and K. Poling for animal care and sample collection; and C. Gibson, C. James, A. Shannon, T. Smith, and J. Reeves for assistance with sample collection.

³ Correspondence: 208 Anim. Sci. Bldg. (phone: 405-744-8857; fax: 405-744-7390; E-mail: kclinto{at}okstate.edu).

Received for publication April 2, 2003. Accepted for publication August 26, 2003.

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