Abstract

Atlantic salmon (average body weight 2.9 ± 0.1 kg) were subjected to either minimal pre-slaughter crowding stress (NS group), 20 min (short-term stress, SS group) or about 24 h pre-slaughter crowding stress (long-term stress, LS group). Significant negative effects were mostly seen due to long-term stress (LS) at early stages post-mortem, but also short-term stress (SS) had significant negative impacts on muscle quality of pre- and post-rigor fillets. Pre-slaughter long-term stress (LS) significantly lowered muscle pH, softened the fillets and increased muscle cathepsin L gene expression, immediately post-mortem. A tendency of increased cathepsin B gene expression and cathepsin B total activity was also seen. Stress further accelerated the incidence of myofibre–myofibre detachments, increased the percentage of myofibre–myocommata detachments over the storage period and increased the percentage of myofibre breakages and contracted myofibres 96 h post-mortem. Significant correlations were observed between muscle pH and cathepsin B + L activity, muscle texture and muscle degradation parameters. Cathepsin B activity was correlated to muscle degradation and cathepsin L gene expression to muscle degradation and texture. Pre-slaughter stress, especially long-term stress (LS), thus seems to accelerate cathepsin activity, resulting in faster muscle degradation, directly or indirectly connected to the low initial muscle pH. No significant variation was observed between pre-rigor and post-rigor filleting, except that pre-rigor filleting significantly increased the percentage of myofibre breakages.

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