In heart pathological conditions, fibroblasts proliferate and differentiate into myofibroblasts (Mfbs). This study aimed to investigate the role of Mfbs on the mechanical contraction of cardiac fiber. Mathematical modeling was done using a combination of (1) the Maleckar et al. model of the human atrial myocyte, (2) the MacCannell et al. active model of the human cardiac Mfb, (3) our formulation of I Na_myofb based upon experimental findings from Chatelier et al., and (4) the Hill three-element rheological scheme of a single segment of cardiac fiber. For Mfb-myocyte coupling, different ratios of myocytes to Mfbs and gap-junctional conductances were set based on available physiological data. Both isometric contraction and isotonic contraction were considered to illustrate the effect of Mfbs on cardiac fiber's tension and strain. The results showed that (1) Mfbs decreased APD 50 and increased V rest depolarization, (2) Mfbs regulated myocyte peak force and (3) Mfbs reduced the fiber peak force in isometric contraction and the fiber peak strain in isotonic contraction. The identified effects demonstrated that Mfbs play an important role of modulating cardiac mechanical behavior. It should be considered in future pathological cardiac mathematical modeling, such as atrial fibrillation and cardiac fibrosis.