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Young et al. (1973) reported that changes in 3-methylhistidine:creatinine ratios reflected changes in 24-hour urinary excretion of 3-methylhistidine in fasted humans, and Haverberg et al. (1975) showed that 40% and 45% increases in urinary excretion of 3-methylhistidine per unit body weight and 3-methylhistidine:creatinine ratios, respectively, accompanied a mean 35% decline in body mass of rats during 14 days of protein-energy restriction. Similarly, 3-methylhistidine:creatinine ratios of undernourished patients were more than double those of normal children (Nagabhushan and Narasinga Rao 1978). In contrast, in protein-restricted rats, 24-hour urinary 3-methylhistidine excretion (µmol/day), urinary 3-methylhistidine output per unit body weight, and 3-methylhistidine:creatinine ratios decreased 81%, 71%, and 68%, respectively (Haverberg et al. 1975).

Our analysis of data pooled from the control and treatment deer (Fig. 2) demonstrated that mass loss explained a substantial portion of the variability of 3-methylhistidine:creatinine ratios (R² = 0.82). However, the results were based on a small sample of deer (n = 7) and likely underrepresents the degree of heterogeneity of this relationship in natural populations. Nonetheless, the relationship in our sample is well defined and is consistent with the urinary urea nitrogen:creatinine-cumulative mass loss curve (DelGiudice et al. 1994a).

The marked effect of the short-term (4 days) severe nutritional restriction on the already restricted deer was manifested in their deteriorated physical condition relative to the controls. Mean urea nitrogen:creatinine ratios doubled in both groups following deprivation (DelGiudice et al. 1994a), but whereas 3-methylhistidine:creatinine ratios almost doubled in the treatment deer, they only increased 22-24% in two control deer and decreased in the third. These data suggest that 3-methylhistidine:creatinine ratios may be more indicative of long-term nutritional stress than urea nitrogen:creatinine ratios. Case (1996) reported a greater tendency for urinary urea nitrogen:creatinine ratios, compared to 3-methylhistidine:creatinine ratios, to increase with decreasing kidney fat indices of free-ranging caribou (Rangifer tarandus). He suggested that 3-methylhistidine:creatinine may be more reflective of long-term undernutrition and poor condition.

Our study provides preliminary results indicating a potentially useful relationship among winter nutritional restriction, mass loss, and urinary 3-methylhistidine:creatinine in white-tailed deer; however, our sample (n = 7) was small. To better understand what the urinary 3-methylhistidine:creatinine ratios represent relative to protein degradation, detailed isotopic studies are needed to quantify the kinetics of 3-methylhistidine and the relative contributions from skeletal and non-skeletal muscle protein pools. Approximately 90% of the total body pool of 3-methylhistidine occurs in skeletal muscle, primarily in actin and myosin, which comprise 65% of muscle protein and 30-35% of total body protein in humans (Asatoor and Armstrong 1967; Johnson et al. 1967; Young and Munro 1978). Although skeletal muscle is the largest pool of 3-methylhistidine in the body, protein turnover rate in this pool (and subsequent release of 3-methylhistidine) should be compared to that in the smaller non-skeletal muscle tissues (e.g., gastrointestinal tract, skin) to determine their relative contributions to the urinary 3-methylhistidine excreted by deer. This question should be studied experimentally, randomizing deer to varying feeding regimes (e.g., dietary energy and protein deficiencies, fasting, optimal diets). Research should investigate the effect of nutritional restriction and condition deterioration on urinary creatinine excretion and on actin and myosin content of 3-methylhistidine in the various body pools of deer (Young et al. 1973; Haverberg et al. 1975; Nishizawa et al. 1977; Young and Munro 1978).