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Two experiments, one using 0+ the other 1 + rainbow trout, were conducted to investigate the effect of prolonged starvation on plasma growth hormone levels. The results from both experiments were essentially the same. As expected, starvation resulted in cessation of growth and in a lower coefficient of condition, whereas fed fish continued to grow and remained in good condition. Starvation had relatively little effect on the plasma cortisol level; in one experiment levels were elevated temporarily in starved fish, although by the end of the experiment there was no longer any difference between starved and fed fish, and in the other experiment plasma cortisol levels remained very low throughout the course of the experiment in both starved and fed fish. In contrast, in both experiments starvation had a pronounced effect on the plasma growth hormone level, which rose steadily during both experiments, such that it was six times higher after 1 month of starvation in 0+ fish. and five times higher after 6 weeks of starvation in 1 + fish. Thus, paradoxically, fed fish had very low plasma growth hormone levels and grew rapidly, whereas starved fish had elevated plasma growth hormone levels but did not grow. In both experiments a strong negative correlation was observed between the plasma growth hormone level and the coefficient of condition of the fish. The results are discussed with regard to the well-established metabolic changes that occur during starvation, and it is suggested that a major role of growth hormone during starvation is to aid in the mobilisation of fatty acids and glycerol from adipose stores.

The distributions of the diameters of skeletal muscle fibres and adipocytes were studied in rainbow trout. The cellularity of perivisceral adipose tissues and subcutaneous ventral and dorsal adipose tissues were characterized more specifically. In these tissues, a population of small adipocytes was distinguishable from larger adipocytes. The same was observed in white muscle. The effects of extrinsic factors (dietary lipid in two different thermal conditions) and intrinsic factors (strains in two different saline conditions, growth hormone) on the long-term response of the cellularity of both muscle and adipose tissues were studied. The effects of thermal environment were tested on fish fed the same ration and the effects of saline environment on fish fed ad libitum. The mean size of white muscle fibres was relatively unaffected by the different treatments tested: genetic origin and dietary lipid in different environmental conditions. There were significant differences in growth rate due to genetic origin and saline environment. The possible involvement of hyperplasia in response to these different factors is discussed. Growth hormone supplementation enhanced the percentage of small diameter fibres indicating a role of this hormone in the control of muscle hyperplastic growth. The mean size of adipose cells was affected only slightly by the different treatments tested. An increase in adipose cell size with aging and lipid content was observed. The percentage of small adipocytes also increased with aging. Thus, it is proposed that the development of adipose tissues, and thus fat retention, both result from the recruitment of new adipocytes and from the increase in size of existing adipocytes. The hyperplastic process contributed significantly to the differences in fat retention due to different treatments tested (strains, thermal and saline environments). When partially substituting fish oils for corn oils in the diet, a large increase in the ventral adipose cell size was seen indicating a potential negative effect of n-6 fatty acids on cell proliferation. Growth hormone treatment, on the contrary, induced a decrease in the size of perivisceral adipocytes. Thus, diet and hormonal status affect adipose cells size through two different metabolic pathways: lipogenesis and lipolysis respectively. 1997 The Fisheries Society of the British Isles

A study utilizing casein-corn gluten meal based diets supplemented with crystalline amino acids was conducted to determine the quantitative arginine requirement of Atlantic salmon smolts. Fish were gradually acclimated to sea water (32 ppt ) and maintained for 8 weeks prior to commencement of the study. Triplicate groups of Atlantic salmon were fed to satiation diets (CP: 40% DM) containing 1.1-3.2 g Arg/lOO g diet (2.7-8% of protein)for a period of 8 weeks. Growth, feed utilization and nitrogen retention data showed the requirement for arginine of Atlantic salmon to be 1.6% of dry matter (4.1% of dietary protein). An arginine requirement of 1.6% of dry matter (4.1% of dietary protein) was also obtained from broken-line regression of expired 14C02 (following an intraperitoneal injection of L-[ U-'4C]arginine versus dietary concentration. Except for the loss of appetite resulting in a low feed intake and depressed growth, no nutritional deficiency signs were observed in fish fed an arginine deficient diet for 98 days. The significance of several biochemical indices measured including liver arginase activity and plasma arginine, insulin and growth hormone levels of fish fed graded levels of arginine supplement is also discussed.