Based on the cross-bridge theory of muscle contraction, the steady-state isometric force of a muscle is uniquely determined by the extent of actin-myosin overlap in a sarcomere, and thus muscle length. However, it has been shown that this prediction is not necessarily correct. Rather, it has been found that the steady-state isometric force at a given length can take many values depending on the contractile history preceding isometric contractions. Specifically, isometric forces following stretch of a muscle are greater and following shortening are smaller than the corresponding forces for purely isometric contractions. These properties of skeletal muscle contraction are referred to as (residual) force enhancement and force depression, respectively. Despite vast study of these history-dependent phenomena, the detailed mechanisms underlying force enhancement and force depression remain largely unknown. In this thesis, experiments with intact single fibres from frog (rana pipiens) are described in an attempt to gain further insight into history-dependent properties and mechanisms of muscle contraction. Single fibres were prepared for mechanical analysis in an experimental chamber so that force and sarcomere length measurements could be made for controlled activation, contractile conditions, and temperature. Specifically, the steady-state isometric forces following a variety of stretch and shortening conditions were compared to the steady-state isometric forces following purely isometric reference contractions at the corresponding length. Force enhancement following stretch of activated fibres was shown to exceed the plateau of the force-length relationship, suggesting that force enhancement is caused by the recruitment of additional force that is not available for isometric contractions. Furthermore, force enhancement for specific conditions was also associated with an increase in passive force, suggesting that passive structural elements might contribute to the observed force enhancement. Finally, when biasing cross-bridges to weakly or strongly bound attachment configurations, we observed that force enhancement was increased in preparations with cross-bridges that were initially biased towards weakly bound states, suggesting that force enhancement might be, in part, caused by a stretch- induced increase in the ratio of strongly to weakly bound cross-bridges. Force depression following shortening in normal fibres and fibres in which cross-bridge states were biased towards weakly bound configurations were associated with a decrease in fibre stiffness. This decrease in stiffness was related to the initial cross-bridge configurations, suggesting that force depression might be caused by a shortening-induced inhibition of the strongly bound cross-bridges.