Effect of a high crude protein content diet during energy restriction and re-alimentation on animal performance, skeletal growth and metabolism of bone tissue in two genotypes of cattle

Abstract

The objective of this study was to investigate the effect of diet crude protein (CP) content and metabolisable energy (ME) intake on skeletal growth and associated parameters of growing steers prior to and during compensatory growth in weight and catch-up growth in skeletal elongation. The experiment was a factorial design with two cattle genotypes [Brahman crossbred (BX, 178 ± 6 kg) and Holstein-Friesian (HF, 230 ± 34 kg)] and three nutritional treatments; high CP content and high ME intake (HCP-HME), high CP content and low ME intake (HCP-LME) and low CP content and low ME intake (LCP-LME) with the ME intake of HCP-LME matched to that of LCP-LME. Nutritional treatments were imposed over a 103 d period (Phase 1), and after this, all steers were offered ad libitum access to the HCP-HME nutritional treatment for 100 d (Phase 2). Steers fed the high CP content treatment with a low ME intake, showed higher hip height gain (P = 0.04), larger terminal hypertrophic chondrocytes (P = 0.02) and a higher concentration of total triiodothyronine in plasma (P = 0.01) than steers with the same ME intake of the low CP content treatment. In addition, the low CP treatment resulted in significant decreases in bone volume (P = 0.03), bone surface area (P = 0.03) and the concentration of bone-specific alkaline phosphatase in plasma (P < 0.001) compared to steers fed the HCP-HME treatment. A significant interaction between genotype and nutritional treatment existed for the concentration of thyroxine (T4) in plasma where HF steers fed LCP-LME had a lower T4 concentration in plasma (P = 0.05) than BX steers. All steers with a restricted ME intake during Phase 1 demonstrated compensatory growth during Phase 2. However, HF steers fed the LCP treatment during Phase 1 showed a tendency (P = 0.07) for a greater LWG during Phase 2 without any increase in dry matter intake. Results observed at the growth plate and hip height growth suggest that catch-up growth in cattle may also be explained by the growth plate senescence hypothesis. Contrary to our initial hypothesis, the results demonstrate that greater CP intake during ME restriction does not increase compensatory gain in cattle during re-alimentation.

Fig 1

Mason trichrome stained sections of cattle’s growth plate and trabecular of tuber coxae bone and photographed at 1X (a) and 4X (b) objectives. Histomorphometric assessments were conducted at the trabecular bone (a) as well as at the proliferative and hypertrophic zones of the growth plate (b).

Fig 2

Dry matter (DM) intake and liveweight gain of Holstein-Friesian (a and b) and Brahman crossbred (c and d) steers fed high crude protein and high metabolizable energy content (HCP-HME), high CP and low ME content (HCP-LME) and low CP and low ME content (LCP-LME) diets throughout the experiment. The different nutritional treatments were imposed from day 1 until day 103 (Phase 1), after that all steers were fed HCP-HME ad libitum until day 203 (Phase 2). Dashed grey line represents the transition from Phase 1 to Phase 2. Error bars represents standard error of the mean.

Fig 3. Effect of metabolizable energy (ME) intake (MEI) on liveweight gain (LWG; a; Y = -0.507 +5.95X, R² = 0.92, RSE = 0.16, P < 0.001) and crude protein (CP) intake (CPI) on hip height gain (HHG; b; Y = 16.41 + 13.75X, R² = 0.82, RSE = 13, P < 0.001) of steers fed high CP content and high ME intake (HCP-HME), high CP content and low ME intake (HCP-LME) and low CP content and low ME intake (LCP-LME).

Each symbol represents the mean for an individual steer from Phase 1 and Phase 2 of the experiment.

Fig 4. Change in trabecular bone volume (Bv/Tv) of tuber coxae samples collected from Holstein-Friesian (HF) and Brahman crossbred (BX) steers fed different nutritional treatments (Phase 1; a) and during re-alimentation (Phase 2; b).

During Phase 1, the interaction between genotype and nutritional factors was not significant so the means of both genotypes were pooled by nutritional treatment. Data are expressed as mean ± SEM. Means with different letters are significantly different (Tukey, P < 0.05).