RESPONSES OF SHEEP TO ANNUAL CYCLES IN NUTRITION .2. EFFECTS OF DIET AND ENDOGENOUS GROWTH-HORMONE DURING REPLENISHMENT

The role of growth hormone (GH) in normal growth is well established, but its role during recovery after live-weight loss in adults is less defined. This study examined the interaction of endogenous GH with ene rgy or protein supplements during re-feeding of ewes in low body condi tion. Control ewes and ewes immunized against growth hormone-releasing hormone were housed in individual pens and given food below maintenan ce for 107 days, before re-feeding was initiated by supplementing half of each group with either fish meal or barley for 28 days (P1), after which the supplements were switched for a further 28 days (P2). Follo wing supplementation, the ewes grazed abundant green pasture for 92 da ys before slaughter. Immunization reduced plasma concentrations of GH, insulin, insulin-like growth factor1 (IGF-1) and prolactin. Productio n responses to the two food supplements were similar in the control an d immunized ewes, but when grazed at pasture immunized ewes gained liv e weight more slowly (P = 0.06), grew less wool (P < 0.01), and had he avier fat depots, but lighter carcass, skin and liver weights at slaug hter. The sequence of re-feeding treatments affected subsequent wool p roduction in both control and immunized ewes. During P2, and for 52 da ys after supplementation ceased, ewes supplemented with fish meal then barley (F/B) produced less wool (P < 0.05) than those supplemented wi th barley followed by fish meal (B/F). At slaughter, the F/B ewes had lighter omental and kidney depots than the B/F ewes (P < 0.05). It is concluded that during live-weight regain, endogenous GH initially affe cted fat deposition, which in turn affected food intake and wool growt h. Furthermore, provision of supplements with a high protein to energy ratio to sleep in low body condition, followed by supplements with a low protein to energy ratio, caused a prolonged suppression of wool gr owth. This effect was not mediated by endogenous GH.