Increased partitioning of amino acids (AA) from skeletal muscle to the intestine and immune system during parasitic infection may be the cause of poor growth in parasitised animals. The effect of an established Trichostrongylus colubriformis infection (6000 L3 T. colubriformis larvae for 6 d (n 5) or kept as parasite-free controls (n 6)) on AA fluxes across the mesenteric-drained viscera, portal-drained viscera (PDV), liver, total splanchnic tissues (TSP) and hindquarters were determined in lambs fed fresh Sulla (Hedysarum coronarium; 800 g DM/d) 48 d post-infection. The lambs were infused with ρ-aminohippuric acid (PAH; 723 mg/h) into the mesenteric vein for 8 h to measure TSP plasma flow. Concurrently, indocyanine green (ICG; 14·6 mg/h) was infused into the abdominal aorta to measure plasma flow across the hindquarters. Blood was continuously collected from the mesenteric, portal and hepatic veins, vena cava and the mesenteric artery and plasma harvested. PAH, ICG, AA, metabolite and insulin concentrations were measured. Intestinal worm burdens on day 48 post-infection were higher in the infected lambs (P < 0·05). Plasma flows across the tissue beds were unaffected by parasitic infection (P>0·10). There was a 28 % reduction in the release of AA from the PDV of infected lambs (P < 0·05). The uptakes of most AA were similar in the liver; however, there was increased uptake (P < 0·10) of AA by the TSP of infected lambs. Despite this reduction in AA availability at the liver, there was no effect of parasitic infection on AA uptake across the hindquarters (P < 0·05).

Both plasma and red blood cells contain amino acids (AA), but the relative amount of AA transferred from each vascular compartment to the tissues remains unclear. For splanchnic tissues, the relative transfers between the plasma, the red blood cells and the tissues may vary with nutritional state, but whether the same situation pertains for other tissues is not known. The current study focused on the transfer of lysine from plasma and red blood cells across the hindquarters of sheep offered four levels of intakes (0.5, 1.0, 1.5 and 2.5×maintenance energy). This design, coupled with use of [U-13C]lysine as tracer, also allowed the effect of intake on protein kinetics to be examined. At all intakes, the concentration of lysine in the sheep’ red blood cells exceeded that in plasma by 50 % (P<0.001), while the distribution of labelled lysine between the plasma and the red blood cells was 0.71:0.29. Net lysine uptake by the hindquarters increased in a linear manner (P<0.001) with intake, with more than 90 % extracted from the plasma. Free lysine enrichments in plasma from the posterior vena cava were less than that from the artery (P<0.001), but those in red blood cells were not different between the artery and vein. The red blood cells thus play a minor role in the transfers to and from the hindquarter tissues, regardless of intake. Based on plasma transfers and the enrichment of lysine in arterial plasma, hindquarter protein synthesis increased linearly with intake (P<0.001). In contrast, protein breakdown was unaffected by intake. The contribution of hindquarter protein synthesis to whole-body lysine flux remained unchanged with intake (18–20 %).

Adaptation of energy metabolism to undernutrition and to the duration of undernutrition was studied in adult, non-pregnant, non-lactating ewes at the whole-animal, portal-drained viscera, liver and hindquarters levels. Arterio-venous and indirect calorimetry techniques were used. Animals were successively fed at 1 times (3 weeks) and at 0.5 times (7 weeks) their metabolizable energy requirements for maintenance (MEm). Portal, hepatic and hindquarters blood flows in quietly standing ewes decreased by 22, 19 and 11% respectively within the first week of undernutrition and remained at that level thereafter. Standardizing hindquarters blood flow to that in a given posture (quietly standing) reduced blood flow by 9.8%. In the portal-drained viscera and liver, O2 extraction rates decreased, leading to 34 and 38% drops in O2 consumption with underfeeding respectively. In the hindquarters, O2 extraction rate increased, partly counterbalancing the drop in blood flow. Thus O2 consumption of hindquarters tended to decrease but the effect was not significant. All changes appeared to be completed from day 5 of underfeeding. Consequently, the portal-drained viscera, liver and carcass were responsible for 39, 32 and 5% respectively of the drop in whole-animal O2 consumption with underfeeding. At the end of the 0.5 X MEm period, in vivo metabolic rates averaged 1.65, 4.89 and 0.38 mmol O2 consumed/d per g fresh weight of adipose-tissue-free portal-drained viscera, liver and boneless hindquarters respectively. Undernutrition imposed a much greater nutritional challenge to splanchnic tissues than to hindquarters. The former reduced theirenergy expnditure whereas hindquarters metabolism adapted by counteracting the slight drop in nutrient supply.