Stretch-shortening cycle (SSC) in human skeletal muscle gives unique possibilities to study normal and fatigued muscle function. The in vivo force measurement systems, buckle transducer technique and optic fiber technique, have revealed that, as compared to a pure concentric action, a non-fatiguing SSC exercise demonstrates considerable performance enhancement with increased force at a given shortening velocity. Characteristic to this phenomenon is very low EMG-activity in the concentric phase of the cycle, but a very pronounced contribution of the short-latency stretch-reflex component. This reflex contributes significantly to force generation during the transition (stretch-shortening) phase in SSC action such as hopping and running. The amplitude of the stretch reflex component - and the subsequent force enhancement - may vary according to the increased stretch-load but also to the level of fatigue. While moderate SSC fatigue may result in slight potentiation, the exhaustive SSC fatigue can dramatically reduce the same reflex contribution. SSC fatigue is a useful model to study the processes of reversible muscle damage and how they interact with muscle mechanics, joint and muscle stiffness. All these parameters and their reduction during SSC fatigue changes stiffness regulation through direct influences on muscle spindle (disfacilitation), and by activating III and IV afferent nerve endings (proprioseptic inhibition). The resulting reduced stretch reflex sensitivity and muscle stiffness deteriorate the force potentiation mechanisms. Recovery of these processes is long lasting and follows the bimodal trend of recovery. Direct mechanical disturbances in the sarcomere structural proteins, such as titin, may also occur as a result of an exhaustive SSC exercise bout.