Key points are not available for this paper at this time.
Studies were conducted to determine relationships between feed efficiency and mitochondrial function and biochemistry. After feed efficiency (FE; gain:feed) was determined in broiler breeder males between 6 and 7 wk of age, mitochondria were isolated from breast and leg muscle from birds with high FE (0.83+/-0.01, n = 6) and low FE (0.64+/-0.01, n = 7). Respiratory chain coupling, assessed by the respiratory control ratio (RCR), was greater in high FE breast, and leg mitochondria provided NADH-linked, but not FADH-linked, energy substrates. There were no differences, however, in the adenosine diphosphate to oxygen (ADP:O) ratio (an index of oxidative phosphorylation) when mitochondria were provided either energy substrate. Electron leak, as determined by generation of H202, was greater in the low FE than in high FE breast mitochondria. Electron leak increased following inhibition of electron transport at Complex I (with rotenone) and Complex III (with antimycin A) in low FE but not in high FE breast mitochondria. There were no differences in basal electron leak in leg mitochondria between groups, but H202 generation was elevated (P < 0.07) compared to basal values in low FE leg mitochondria after Complex I inhibition. The activities of Complexes I and II were greater in high FE breast and leg muscle mitochondria compared to those in low FE mitochondria. The results indicate that lower respiratory chain coupling in low FE muscle mitochondria may be due to lower activities of Complexes I and II and defects in electron leak and provide insight into cellular mechanisms associated with the phenotypic expression of feed efficiency in broilers.
Bottje et al. (Mon,) studied this question.