The nutritional requirements of rainbow trout (Table 2) are better described than those of most farmed fish species, although nearly all studies on nutritional requirements of trout have been conducted using fingerling or juvenile fish. However, given the similarity in digestive capacity between fry and post-juvenile rainbow trout, dietary requirements for most nutrients are likely similar for larger fish. Exceptions are likely to revolve around optimum protein:energy ratio and perhaps requirements for dietary minerals associated with skeletal development in young fish. Reviews on rainbow trout nutrition include Cho and Cowey (1991), NRC (1993) and Hardy (2002).
All fish examined to date require ten essential amino acids; rainbow trout are no exception. For the most part, the quantitative dietary requirements for essential amino acids are established, although there is some evidence that the reported requirement for lysine slightly underestimates the true requirement by about 15 percent. Lysine, methionine and arginine (or threonine) are the first, second and third most limiting amino acids in rainbow trout feeds when fishmeal level is reduced and plant protein sources are increased. Although fish require amino acids, not protein per se, there are apparent minimum dietary protein levels for maximum trout performance (Table 2). As is the case with most fish, the optimum protein level in feeds depends upon dietary energy content, and the ratio of essential to non-essential (or indispensible to dispensable) amino acids. A ratio of 55:45 appears optimal (Green, Hardy and Brannon, 2004).
Rainbow trout efficiently use dietary lipids and require dietary sources of n-3 fatty acids (Table 2). The n-3 fatty acid requirements of rainbow trout are most effectively met by eicosapentaenoic acid (EPA) (20:5n-3) and docosahemaenoic acid (DHA) (22:6n-3). Trout have a limited capacity to convert linolenic acid (18:3n-3) or stearidonic acid (C18:4n-3) to EPA or DHA. The dietary requirement of trout for n-3 fatty acids is 1.0 percent of the diet to 20 percent of dietary lipid (NRC, 1993). Signs of n-3 deficiency include poor growth, high feed conversion ratio and a shock syndrome resembling fainting. Accumulation of C20:3n-6 in polar lipids is a sign of essential fatty acid deficiency in rainbow trout.
Rainbow trout do not have a dietary requirement for carbohydrates and can, in fact, thrive when fed diets lacking carbohydrate. However, some carbohydrate in practical feed is unavoidable when conventional feed ingredients are used and also beneficial to trout, as evidenced by improved feed conversion ratios when some carbohydrate is present in the diet. However, there is a limit to the capacity of rainbow trout to tolerate high dietary carbohydrate levels when fed over an extended period. Over 30 percent of available carbohydrate in the diet is sufficient to cause liver and muscle glycogen stores to reach maximum saturation and for metabolic shifts indicating metabolic stress to become evident when fish are fed over a long period. Based on a number of perspectives and studies, the optimum available carbohydrate level for rainbow trout is 15–17 percent. As is the case for most carnivorous fish species, simple carbohydrates, e.g. glucose and dextrose, are more available than are complex carbohydrates. Raw starch is essentially unavailable, whereas cooked starch is highly available to trout. Non-soluble polysaccharides (NSP) are also completely unavailable to rainbow trout. For a review of carbohydrate utilization in fish, see Stone (2003).
Rainbow trout farming is, for the most part, intensive; no natural food is available in flow-through trout farming systems. Therefore all essential nutrients, including vitamins, must be provided by the feed. Rainbow trout require 15 vitamins (Table 2), although the quantitative dietary requirements are not necessarily exact for some. For example, the requirements for the fat-soluble vitamins A and D were determined using fish performance criteria, e.g. growth and survival rates, in only a few research studies. In contrast, the requirements for ascorbic acid, thiamine, riboflavin, pyridoxine and pantothenic acid are considered very accurate. The key difference between these two groups of vitamins is that for the latter group, sensitive clinical or enzymatic response variables have been developed that permit researchers to detect differences in the responses of fish associated with very small differences in dietary vitamin level. As is the case in terrestrial animals and poultry, the dietary requirements for some vitamins are affected by other factors, both dietary and environmental. For example, the dietary requirement for pyridoxine varies with dietary protein level (Hardy, Halver and Brannon, 1979). Similarly, the requirement for vitamin E varies with dietary lipid level and oxidation status of dietary lipid (Bell and Cowey, 1985). Ascorbic acid has the distinction of having several apparent requirements; one for maximum growth, another for maximum tissue storage and a third for maximum disease resistance (Halver, 2002). The foregoing illustrates an important point – absolute dietary requirements for vitamins in fish are difficult to establish without precise clinical response variables that accurately measure the effects of vitamins on metabolism and organism health. For the better part of a decade, animal and human nutritionists were influenced by the connection between individual vitamin deficiencies and specific clinical signs of deficiency (Heaney, 2008), such as deficiency of pantothenic acid and the occurrence of clubbed gills in fish. However, all cells in the body require all vitamins. A dietary level sufficient to prevent the appearance of clinical signs of deficiency may not necessarily be optimal for all cells or tissues (Heaney, 2008). Hence, it is prudent to slightly over fortify diets with vitamins, not only to allow for loss of vitamin activity associated with feed manufacture and storage (Gabaudan and Hardy, 2000), but also to account for cellular needs that may not yet be known.
The dietary mineral requirements of rainbow trout are somewhat well quantified, although as is the case with other species of fish, trout can obtain some of their mineral requirements directly from rearing water. Phosphorus is a notable exception. Whereas fish can obtain phosphorus from rearing water, free phosphorus levels in freshwater are too low to contribute to the needs of fish. Most mineral requirements for trout were identified by specific clinical signs of deficiency that resulted from inadequate dietary levels or from antagonistic interactions in feeds that reduced the bioavailability of minerals such that deficiency occurred. For example, a widespread outbreak of cataracts in the early 1980s in salmon hatcheries in the Pacific Northwest of the United States of America and in the Province of British Columbia, Canada was traced to suboptimal levels of zinc in feeds containing high-ash fishmeal and relatively high levels of phytic acid (Richardson et al., 1985). This resulted in a conditioned deficiency, defined as one occurring in the presence of seemingly adequate dietary levels but caused by reduced availability due to interactions among feed constituents. Although the salmon feed contained a trace mineral premix supplying zinc in adequate amounts, further supplementation was required to overcome the interactions that lowered the availability of zinc. The first trace element for which a clinical disease condition was identified was iodine, the lack of which causes goiter (enlarged thyroid gland) in trout (Marine, 1914, cited in NRC, 1973).
Reducing the percentage of fishmeal in rainbow trout feeds is a focus of feed producers, who use plant-derived proteins such as soybean meal or corn gluten meal to supply dietary protein in low-fishmeal feeds. Lowering fishmeal levels in trout feeds, however, has risks. Fishmeal is an excellent source of minerals coming from fish bone, whereas plant proteins are relatively poor sources of essential minerals. Furthermore, plant proteins contain phytic acid, the storage form of phosphorus in grains and oilseeds. Phytic acid, especially in the presence of calcium phosphate, binds with divalent cations, e.g. zinc, manganese and iron, making them unavailable for absorption in the gut. Supplementing trout feeds with microbial phytase, the enzyme that hydrolyzes phosphorus from phytate, increased the available phosphorus in trout feeds. Microbial phytase is commercial available. Approximately 1 000 FTU of activity per kg feed is sufficient to increase phosphorus availability (Sugiura et al., 2001). One FTU (phytase unit) is the amount of enzyme that liberates 1 µmole of phosphate/min from 0.0051 mol/l of Na phosphate at 37 °C and pH 5.5.
