A11 Force Generation Failure

Topic

In general, a muscle experiences a failure in force production precisely when the resulting tension falls below the level predicted by the Hill curve for a given level of neural activation. The cause of this failure may be structural (e.g., a fiber rupture or tear), physiological (e.g., depletion of energy substrates or metabolite accumulation), or neuromuscular (e.g., reflex inhibition or a block at the neuromuscular junction interrupting the neural signal before it reaches the muscle). Since the level of neural activation remains constant across these scenarios, the Hill curve serves as a common reference point against which each of these three causes of failure can be measured.

In the case of a muscle tear, the muscle's functional cross-sectional area is reduced—specifically at the site of the injury—leading to a proportional decrease in the maximum force the muscle can generate during maximal activation. A more extensive injury results in a further reduction of the remaining functional cross-sectional area, thereby further diminishing the muscle's ultimate maximum force output.

Conversely, a muscle contusion affects the muscle's maximum shortening velocity more than its functional cross-sectional area, thereby altering the internal contractile properties of the injured muscle. A more severe contusion causes a greater alteration of these internal contractile properties, leading to a further reduction in the muscle's maximum shortening velocity, even while its maximum isometric force remains relatively intact. Conversely, a paired limb of the same organism may exhibit a bilateral force deficit—specifically when the combined force produced by both limbs together is less than the sum of the individual forces produced by each limb separately. This difference reflects a neural inhibition of inter-limb coordination rather than an intrinsic failure within the muscle tissue of either limb. Consequently, a more intense neural inhibition of inter-limb coordination results in a greater bilateral force deficit for that paired limb.

Thus, using the Hill curve introduced earlier, the final force loss in any of these three injured muscles is quantified as the ratio between the force actually produced by the injured muscle and the force predicted by the Hill curve for a given level of neural activation—regardless of whether the deficit stems from a reduced functional cross-sectional area, altered shortening velocity, or neural inhibition of coordination. A lower ratio between the produced force and the force predicted by the Hill curve results in a more severe final force loss for the injured muscle.

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