Afterload and Velocity of Shortening:
There is also a relationship between the load (afterload) on a muscle and the velocity of shortening (Figure 10). At high load there is no shortening (isometric contraction) so velocity is zero. At no load, velocity of shortening is maximal, but no work is done since no force is moved (work = force x distance). Power output is maximal at intermediate values of afterload, ie. shortening and velocity.
Preloading a muscle increases the velocity of shortening, but does not change the maximal velocity of shortening (Vmax). Preload and afterload have different effects on velocity of muscle contraction.
Although varying the afterload and preload alters tension generation, extent of shortening, and velocity of shortening, inotropicity (contractility) is not altered by these maneuvers.
Inotropicity (ie. contractility) may be altered by neurotransmitters, hormones, and factors intrinsic to cardiac muscle. This results in changed active state. Increased release of sarcoplasmic of Ca++ facilitates cross-bridge formation and cycling rate, and increases maximal velocity of shortening. This is not seen in skeletal muscle.
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