Fallback pigs are those that fail to achieve performance in the barn equal to that of their contemporaries. The objective of this dissertation was to characterize fallback pigs in order to implement preemptive strategies to minimize the negative effects of fallback pigs within the larger barn or system population. To complete this objective, a total of 1,174 pigs were utilized in two experiments. In Experiment 1, 120 weanling pigs (PIC C22/C29 × 337) were utilized in growth, metabolism, and comparative slaughter experiments. Forty barrows from each of the lightest, median, and heaviest 10% of pigs at weaning were placed in individual metabolism crates. Eight pigs from each weaning weight category were harvested on d 5 post-weaning as the initial slaughter group. The remaining 32 pigs in each category were part of the metabolism group, and were utilized in a 27-d growth and metabolism experiment and harvested on d 32 and 33 post-weaning. After the completion of the live animal component of the experiment, pigs within each initial BW category were further stratified into the slowest, median, or fastest 33% ADG categories. This resulted in a total of nine treatments. Fallback pigs were designated as those belonging to the slowest ADG category from either the lightest or median BW categories. Data were analyzed using the GLIMMIX procedure of SAS. There was no effect (P = 0.30) of BW(ADG) category on feed efficiency, which suggests that ADG improvements were primarily driven by, or at least associated with, ADFI. All tissue deposition rates, which were calculated as the difference between tissue nutrient concentrations of the metabolism and initial slaughter groups, were maximized (P < 0.0002) by BW(ADG) category, even when equalized per unit of body weight. The apparent total tract digestibility of dry matter, gross energy, nitrogen, and ash, as well as the related dietary energy content, were maximized (PP > 0.87) by BW(ADG) category. There was no effect (P > 0.16) of BW(ADG) category on active ileal glucose, lysine, or glutamine transport. Meanwhile, measures of ileal morphology were greatly affected (P < 0.0001) by BW(ADG) category, but not in a consistent manner. Among the measures in a standard blood chemistry panel, creatinine, and albumin concentrations were significantly decreased (P < 0.03) by BW(ADG) category, which may indicate dehydration or poor physiological regulation among fallback pigs, and is an area that warrants further exploration. Pigs from the slowest ADG, heaviest BW category had lower (P < 0.05) hemoglobin concentration compared to pigs from the fastest ADG categories, which may indicate anemia. No other measures, including white blood cell or lymphocyte concentrations, were affected (P > 0.10), suggesting that pigs had similar health status. Thus, Exp. 1 suggested that the underlying cause for fallback from performance lies jointly with poor feed intake and poor utilization of absorbed nutrients. In Experiment 2, 1,054 pigs (Danbred 600 × Newsham NC32) were farrowed at a commercial sow farm, weighed at birth (BRW), and tagged individually. At 16 or 17 days of age, 1,054 pigs were weaned and moved to a commercial wean-to-finish barn. Mortalities were recorded on a daily basis. Pigs originated from a PRRSV negative herd, but broke with the disease in week 2 post-weaning. Pigs were weighed individually at weeks 0, 3, 6, and 22 post-weaning. Average daily gain from weeks 0 to 3 post weaning was termed transition ADG (tADG). One pig from each of the 10th, 30th, and 70th percentiles was used to create a `set' of three pigs with the same gender, litter size and parity. Forty such sets were created, for a total of 120 pigs. On each of weeks 3 and 22 post-weaning, 20 sets of pigs were harvested to determine nutrient digestibility, carcass composition, and organ system tissue evaluation. Lung, lymph node, and digesta were analyzed for presence of various pathogens by PCR and culture methods. Data were analyzed using the GENMOD, GLIMMIX, and REG procedures of SAS. Birth weight was a good predictor (P < 0.02; R² > 0.97) of overall post-weaning growth performance and final weight, except for the period immediately after weaning (P = 0.99). Transition ADG was an excellent predictor of subsequent post-weaning growth (P < 0.0001; R² > 0.98) and a good predictor of post-weaning mortality (P < 0.0001; R² = 0.82). There was a significant BRW × tADG interaction for mortality, where pigs from the 10th percentile of transition ADG and BRW heavier than 1.51 kg had greater mortality than those with birth weights from 1.26 to 1.50 kg (P < 0.05). Neither birth weight nor transition ADG affected apparent total tract digestibility of nutrients or energy (P > 0.15), but these values were substantially lower than other values in the literature. Transition ADG did not affect carcass composition (P > 0.11), but pigs with BRW heavier than 1.76 had more backfat than all other pigs and larger longissimus muscle area at 22 weeks post-weaning than pigs with BRW lighter than 1.25 kg (P < 0.05). There was no correlation (P > 0.12) between tADG and pathogen presence at either 3- or 22-weeks post-weaning. Incidence and severity of microscopic lesions in the large intestine decreased linearly with increasing tADG (incidence: P = 0.01; 65, 55, 25% for 10th, 30th, and 70th percentiles, respectively; severity: P = 0.01; 1.15, 0.75, 0.16 for 10th, 30th, and 70th percentiles, respectively) at 3-weeks post-weaning. Lesion incidence and severity were also affected (P < 0.04) by tADG at 22-weeks post-weaning. Birth weight affected (P = 0.02) Haemolytic E. coli and Salmonella spp. B isolation at 3-weeks post-weaning, as well as Brachyspira spp. isolation at 22-weeks post-weaning (P = 0.05). There were no effects (P > 0.21) of BRW or tADG on serum or ileum mucosa scraping immune markers. Thus, Exp. 2 suggested that tADG, but not BRW is related to post-weaning mortality. Both BRW and tADG are indicative of subsequent growth performance, but not due to differences in nutrient digestibility. Finally, poor tADG is not correlated with pathological or immunological markers of enteric disease. In all, the primary cause of fallback pigs appears to be poor feed intake. Our experiments yielded conflicting results if total tract nutrient digestibility varies by pig weight or growth rate, but fallback in pigs does not seem to be associated with differences in birth weight or disease incidence.