Northern Prairie Wildlife Research Center
Nutritional restriction of deer (Odocoileus spp.) and other mammals is associated with fat mobilization and degradation of endogenous protein, but there is far less physiological tolerance of the latter (Cahill 1970; Torbit et al. 1985; Heymsfield and Williams 1988; DelGiudice et al. 1990). Because skeletal muscle protein accounts for most of total body protein, it is of primary importance to whole-body protein metabolism (Daniel et al. 1977; Harris and Milne 1978). Thus, physiological indicators of muscle catabolism may aid assessment of winter nutritional restriction of deer.
Assessment of nutritional restriction and changes in body composition through urinalysis have been studied extensively (Tallen et al. 1955; Cowgill and Freeberg 1957; Young et al. 1972; Long et al. 1975; Harris and Milne 1978; Ballard and Tomas 1983; Hovell et al. 1987; Forbes 1988; Hoffer 1988), but only recently has this knowledge been applied to cervids. Studies of captive and free-ranging cervids have examined the effects of winter nutritional restriction, and in some cases, refeeding, on urinary urea nitrogen, electrolytes, hydroxyproline, and allantoin (Eriksson and Valtonen 1974; Warren et al. 1982; DelGiudice et al. 1987, 1988, 1990, 1991a,b, 1994a,b, 1997; Parker et al. 1993; Garrott et al. 1996; Vagnoni et al. 1996). Urinary urea nitrogen has been studied most thoroughly and has exhibited potential for evaluating nutritional or dietary restriction and indicating changes in endogenous protein degradation and fat loss (Warren et al. 1982; DelGiudice et al. 1987, 1991a, 1994a,b, 1997; Case 1996; Moen and DelGiudice 1997).
Urinary NT-methylhistidine or 3-methylhistidine, a methylated amino acid, was first identified in urine by Tallen et al. (1955). It occurs primarily (≥ 90%) in actin and myosin of skeletal muscle, and there is no exogenous source of this chemical for herbivores (Asatoor and Armstrong 1967; Johnson et al. 1967). Studies employing radio-labelled 3-methylhistidine have reported urinary 3-methylhistidine to be a reliable indicator of muscle protein degradation in humans, rats, cattle, rabbits, chicks, and frogs (Cowgill and Freeberg 1957; Young et al. 1972; Long et al. 1975; Harris and Milne 1978; Ballard and Tomas 1983), but not in sheep or pigs (Harris and Milne 1980; 1981). In species where 3-methylhistidine has shown potential, it was not re-utilized for protein synthesis after release during protein breakdown, only a small proportion was converted into a N-acetyl derivative, and most was excreted quickly and quantitatively in the urine (Young et al. 1972; Long et al. 1975; Harris and Milne 1978).
Although changes in urinary excretion of 3-methylhistidine and 3-methylhistidine: creatinine ratios have been associated with alterations in nutrition and body mass, the reliability of these characteristics for indexing muscle protein breakdown has been debated (Young et al. 1973; Haverberg et al. 1975; Nagabhushan and Narasinga Rao 1978; Young and Munro 1978; Ballard and Tomas 1983; Rennie and Millward 1983). At the center of this debate are questions concerning quantities of 3-methylhistidine in urine contributed by skeletal muscle versus non-skeletal muscle sources at various nutritional states, and this is related not just to respective pool sizes and relative contents of 3-methylhistidine, but to turnover rates of protein as well (Nishizawa et al. 1977; Ballard and Tomas 1983; Rennie and Millward 1983).
To our knowledge, there are no published studies addressing the relation between nutrition and urinary 3-methylhistidine of deer. Our objective in this initial effort was to assess the effect of chronic moderate and severe nutritional restriction during winter on urinary 3-methylhistidine:creatinine ratios of white-tailed deer (O. virginianus) and to relate these ratios to mass loss and urea nitrogen:creatinine ratios reported previously (DelGiudice et al. 1994a).