Non‐technical summary  Muscle function depends on tightly regulated Ca2+ movement between the intracellular sarcoplasmic reticulum (SR) Ca2+ store and cytoplasm in muscle cells. Disturbances in these processes have been linked to impaired muscle function and muscle disease. We disrupted the gene for the SERCA2 SR Ca2+ pump in mouse skeletal muscle to study how decreased transport of Ca2+ into the SR would affect soleus muscle function. We found that the SERCA2 content was strongly reduced in the 40% fraction of soleus muscle fibres normally expressing SERCA2. Muscle relaxation was slowed, supporting the hypothesis that reduced SERCA2 would reduce Ca2+ transport into the SR and prolong muscle relaxation time. Surprisingly, the muscles maintained maximal force, despite the fact that less SERCA2 in these fibres would be expected to lower the amount of Ca2+ released during contraction, and thereby lower the maximal force. Our findings raise important questions regarding the roles of SERCA2 and SR in muscle function.