The present study aimed to investigate the effects of acute
sepsis on diaphragm contractility and relaxation, via examining the Ca2+‑uptake function of sarco/endoplasmic reticulum Ca2+
adenosine triphosphatase (SERCA), and the
protein levels of SERCA1, SERCA2 and the
ryanodine receptor (RyR) of the sarcoplasmic reticulum (SR). A
sepsis rat model was established through cecal
ligation and
puncture (CLP). A total of 6 and 12 h following CLP, the isometric contractile and relaxation parameters of the diaphragm were measured. In addition, Ca2+ uptake and release from the SR, and the
protein expression levels of SERCA1, SERCA2 and RyR in diaphragm muscle tissue were investigated. At 6 and 12 h post‑CLP, the diaphragm half‑relaxation time was prolonged and the maximum rate of tension decline was decreased and the Ca2+‑uptake function of SERCA was markedly reduced. The maximum rate of twitch force development, the maximal twitch and tetanic tension, and the release function of SR were decreased at 12 h post‑CLP. A total of 12 h following CLP, the
protein expression levels of SERCA1 were significantly downregulated, and its activity was significantly reduced; conversely, the
protein levels of SERCA2 remained unaltered. The present findings indicated that at the acute stage of
sepsis induced by CLP the contractile and relaxation functions of the diaphragm were significantly compromised. The impairments in relaxation may be a result of the impaired uptake function of the SR and the downregulation in SERCA1
protein expression. Conversely, the compromised contractility may be a result of the impaired release function of the SR and the downregulation in RyR
protein levels. This could provide some new insights into the treatment of
sepsis. In acute stages of
sepsis, the improvement of SERCA function could reduce the disequilibrium of
calcium homeostasis to improve the
critical illness myopathy and
respiratory failure.