The role of sodium ions in the pathogenesis of skeletal muscle damage in broiler chickens

The effect of sodium ions (Na⁺) on calcium (Ca²⁺)-mediated muscle damage in broiler chickens was investigated using an in vitro muscle preparation. Muscle Ca²⁺ accumulation was determined by ⁴⁵Ca²⁺ uptake. Muscle damage was assessed by measurement of the efflux of the intracellular enzyme creatine kinase (CK) into the incubation medium. Loading muscle cells with Na⁺ by means of the sodium ionophore monensin led to concentration-dependent (25 to 200 μM) increases in ⁴⁵Ca²⁺ uptakes and corresponding and proportional CK losses. The greatest responses occurred at 100 μM ionophore or greater, reflected in a 49% increase (P <0.05) in 45Ca2+ uptake and an associated 140%-fold increase (P <0.001) in CK efflux. Inhibition of muscle Na⁺/K⁺-ATPase activity with ouabain (2 mM) induced a 56% increase in 45Ca2+ uptake and a 60%-fold increase (P <0.001) in total CK loss. The combined use of ionophore and ouabain resulted in 90 and 130%-fold elevations in ⁴⁵Ca²⁺ uptake and CK loss, respectively. In monensin-treated muscles, inhibition of external Ca²⁺ influx from the incubation medium by chelation with 1,2 bis(2-aminophenoxy)ethane-N,N,N′,N′ tetracetic acid (5mM) markedly reduced ⁴⁵Ca²⁺ uptake (38%: P <0.05) but increased CK release by 85% (P <0.001). The results demonstrate that initial elevations in muscle Na⁺ can facilitate increases in muscle Ca²⁺ and lead to alterations in muscle cell membrane integrity and CK loss. The Na⁺-induced increases in myocellular Ca²⁺ may be mediated via direct extracellular Ca²⁺ entry or redistribution from internal Ca²⁺ stores. It is proposed that in order to reduce or prevent myopathies in poultry, exposure to conditions that may lead to elevations in muscle Na⁺ (e.g., increased muscle activity and stress or accidental ionophore toxicosis) should be avoided. The findings of this study have implications for management strategies of bird welfare, muscle pathology, and product quality.