Compensatory and catch-up growth in cattle

Abstract

Variation in nutrition leads to periods of restricted and accelerated changes in the liveweight of cattle, but less is known about the effect of level of nutrition and/or specific nutrients on skeletal growth. The endochondral ossification process at the epiphyseal growth plate drives longitudinal bone growth and by inference sets growth in skeletal muscle via a passive stretch mechanism. The physiological and morphological mechanism behind animal growth that drives adaptation of mammals during the transition from a low to high plane of nutrition remains a major biological question. Two experiments examined the effect of protein and energy on skeletal growth the perspective of the dimensional changes, trabecular bone remodelling (histology and bone biomarkers) and hormone. Data was then collated from these and other experiments conducted within this laboratory to develop a growth curve in liveweight-for-hip height of well-fed cattle and to identify deviations from this “normal” growth relationship. In the first experiment (Chapter 4), the effects of low and high crude protein (CP) content diets during metabolizable energy (ME) restriction on subsequent re-alimentation in Bos indicus and Bos taurus cattle were evaluated. Three treatment diets were applied; a control diet (High CP-High ME) and two restricted pair-fed ME intake diets differing in CP content (Low CP–Low ME and High CP-Low ME) for 93 days followed by re-alimentation of all treatment groups offered ad libitum access to the High CP-High ME diet for 103 days. In the second experiment (Chapter 5), a 2 x 5 factorial design was used to determine the effect of supplementation (0, 1, 2.5, 5, 10 g protein meal/kg LW.day) of a low CP hay during the first dry season (169 days) and weaning weight [Early (118 kg) vs. Normal (183 kg)] on long-term (~2 years) growth in liveweight and the skeleton and reproduction of replacement heifers in northern Australia. After the first dry season all treatment groups were subjected to the same level of nutrition by grazing the same pasture together. Across both experiments, higher plane of nutrition increased liveweight gain and skeletal elongation growth. Increases in ME and CP intake in cattle were positively associated with the height of proliferative and hypertrophic zones as well as with the diameter of terminal hypertrophic chondrocytes measured in growth plate biopsies of the tuber coxae. In addition, the diameter of terminal hypertrophic chondrocytes showed significant correlation with the broader measure of hip height gain in both experiments. Plasma bone-specific alkaline phosphatase and pyridinoline appeared to be effective bone biomarkers of formation and resorption in growing cattle respectively. Low ME intake severely reduced the plasma insulin and insulin-like growth factor 1 concentration in cattle, independent of CP intake. Cattle with the higher CP intake during ME restriction had higher concentration of triiodothyronine in the plasma and this was correlated with larger terminal hypertrophic chondrocytes at the tuber coxae growth plate as well as increased hip height gain. After nutritional restriction, cattle showed an increase in dry matter intake and liveweight gain for approximately 40 to 60 days after commencement of the re-alimentation phase followed by a subsequent decrease to values similar to unrestricted counterparts. Skeletal growth of previously restricted cattle was greater than unrestricted counterparts at the same age and was associated with increased proliferative and hypertrophic zones heights without differences in any measured plasma hormone concentration. Nutritional restriction at the early weaning weight did not cause permanent stunting, however it increased the time frame necessary to achieve reproductive target liveweights for satisfactory pregnancy rates (>80%) of replacement heifers in northern Australia. In Chapter 7, a “normal” liveweight-for-hip height relationship model was generated for well-fed Bos indicus cattle using data from the two experiments in this thesis as well as results from 4 other studies by our reseach group and a groups of mature fistulated steers. A decrease from the normal liveweight-for-hip height relationship was observed during nutritional restriction. The difference between the actual liveweight of an animal and the expected liveweight based on its hip height was identified as the “Liveweight gap”. A significant relationship was found between liveweight gain during compensatory growth and the Liveweight gap. The return to the normal liveweight-for-hip height relationship was associated with the decrease in dry matter intake during compensatory growth. It is concluded that cattle can exhibit catch-up growth in skeletal growth and compensatory growth in liveweight after a period of nutritional restriction. The results support the concept that catch-up growth in the skeleton is caused by a delay in growth plate senescence during nutritional restriction and that compensatory growth in weight is caused by a deviation from the liveweight-for-hip height relationship probably related to the passive stretch mechanism of bone length on skeletal muscle.