The proposed explanatory physiological mechanism
is complex and incompletely understood, with the
majority of studies theorizing four main mechanisms
to that lead to the decrease in muscle tension
and increased ROM; autogenic inhibition, reciprocal
inhibition, stress relaxation, and pain gate control
theory.25 The current findings suggest that the immediate
change in muscle extensibility is likely to be
through either increased stretch tolerance, pain gate
theory, reciprocal or autogenic inhibition. The greatest
initial gains attributed to PNF advocate increased
co-contraction theory, with beneficial effects on surrounding
anatomical structures in addition to the
muscle isolated for contraction. Stress relaxation with
viscoelastic deformation of tissue or reciprocal inhibition
with contraction of the agonist and antagonist
may be plausible theories.26 However the pain gate
control theory may be the most plausible, with the
muscle stretched forcefully into a new end of range
the golgi tendon organs are activated in an attempt
to reduce injury. 27 As the tendons are stretched the
muscle is contracted in a lengthened position, inhibiting
pain, and potentially enabling the golgi tendon
organs to adapt to the new force threshold and
achieve an increase in length. The current results
demonstrating a negative correlation with time for
SS and PNF suggest that if viscoelastic change has
occurred this is short term and is unable to be maintained.
This supports previous observations that post
PNF intervention, muscle activity returned to 50%
within one second and 90% in 10 seconds.
The proposed explanatory physiological mechanism
is complex and incompletely understood, with the
majority of studies theorizing four main mechanisms
to that lead to the decrease in muscle tension
and increased ROM; autogenic inhibition, reciprocal
inhibition, stress relaxation, and pain gate control
theory.25 The current findings suggest that the immediate
change in muscle extensibility is likely to be
through either increased stretch tolerance, pain gate
theory, reciprocal or autogenic inhibition. The greatest
initial gains attributed to PNF advocate increased
co-contraction theory, with beneficial effects on surrounding
anatomical structures in addition to the
muscle isolated for contraction. Stress relaxation with
viscoelastic deformation of tissue or reciprocal inhibition
with contraction of the agonist and antagonist
may be plausible theories.26 However the pain gate
control theory may be the most plausible, with the
muscle stretched forcefully into a new end of range
the golgi tendon organs are activated in an attempt
to reduce injury. 27 As the tendons are stretched the
muscle is contracted in a lengthened position, inhibiting
pain, and potentially enabling the golgi tendon
organs to adapt to the new force threshold and
achieve an increase in length. The current results
demonstrating a negative correlation with time for
SS and PNF suggest that if viscoelastic change has
occurred this is short term and is unable to be maintained.
This supports previous observations that post
PNF intervention, muscle activity returned to 50%
within one second and 90% in 10 seconds.
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