Stretch-shortening cycle (SSC) in human skeletal muscle gives unique possib
ilities to study normal and fatigued muscle function. The in vivo force mea
surement systems, buckle transducer technique and optic fiber technique, ha
ve revealed that, as compared to a pure concentric action, a non-fatiguing
SSC exercise demonstrates considerable performance enhancement with increas
ed 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 p
ronounced 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 a
mplitude of the stretch reflex component - and the subsequent force enhance
ment - may vary according to the increased stretch-load but also to the lev
el of fatigue. While moderate SSC fatigue may result in slight potentiation
, the exhaustive SSC fatigue can dramatically reduce the same reflex contri
bution. 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 cha
nges stiffness regulation through direct influences on muscle spindle (disf
acilitation), and by activating III and IV afferent nerve endings (proprios
eptic inhibition). The resulting reduced stretch reflex sensitivity and mus
cle stiffness deteriorate the force potentiation mechanisms. Recovery of th
ese processes is long lasting and follows the bimodal trend of recovery. Di
rect mechanical disturbances in the sarcomere structural proteins, such as
titin, may also occur as a result of an exhaustive SSC exercise bout. (C) 2
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