Postharvest treatment of strawberry fruit with an elevated $pCO_2$ induces transient increases in the fruit firmness. The mechanism responsible for this firmness increase is not clearly understood. This study addressed the physiological responses of strawberry fruit to $CO_2$ treatment to understand the factors to induce firmness increase. High $CO_2$ treatment induced modification of pectic polymers, the decrease of water-soluble pectins (WSP) and increase of chelator-soluble pectins (CSP), which are the major factors for firmness increase. The shift of WSP to CSP is related with calcium binding to WSP. The calcium binding to wall polymers was induced without changes of PME activity and methoxy content of WSP and CSP. Our results suggested that fruit firmness increase of strawberry by postharvest $CO_2$ treatment occurred primarily through pectin polymerization mediated by calcium.