Soft-Tissue Pathomechanics - Fundamentals and Assessment Tools for Occupational Ergonomics - page 355

contractions were maximal. The results of their study showed that the loss of force was due to changes in
contractile elements, not the level of muscle activation. This was the first study to suggest that the
force decrement resulting from eccentric muscle actions is not the result of less muscle activation, but
instead may have a mechanical etiology. Thus, the force deficit seen after eccentric contraction-
induced injury in both humans and animals is due to damage of the contractile proteins and supporting
structures, not central nervous system activation level.
Once eccentric contractions were identified as causing muscle injury, it was important to investigate
how the injurious response could be modified by mechanical exposure factors (e.g., force, strain,
strain rate, number of repetitions, and velocity). The primary factors that have been studied have
some generalizability to occupational physical exposures.

15.4.3 Factors Affecting Acute Muscle Injury
15.4.3.1 The Effect of Muscle Force on Myofiber Injury
The in situ results of eccentric contraction-induced injury have been supported in general by in vitro
animal models. Warren 285 used isolated rat soleus muscles to investigate mechanical factors associated
with the initiation of eccentric contraction-induced muscle injury. The results indicated that a reduction
in contractile force was most related to high forces during lengthening. This finding was also supported
by other work. 110,178,253 In Warren's model, the primary criterion used to quantify injury was a reduction
in twitch tension (P t ), which has previously been shown in muscles injured by eccentric contractions.
The eccentric contraction group was compared against muscles performing isometrically using the
same stimulation protocol. This study clearly demonstrated that eccentric contraction-induced muscle
injury has a mechanical etiology. The predominant factor was mechanical force during lengthening
with failure occurring above 113% P o (“P o ” denotes maximum isometric force of the target muscle).
In a follow-up study by Warren, 284 the focus was to investigate whether injury is the result of high
tensile force after one contraction or the result of multiple contractions. The protocol consisted of
0.25 L o excursions with a velocity of 1.5 l o

sec at a force of 180% P o . Muscles performing more than
eight eccentric contractions resulted in injury since marked force decrements were observed after the
eighth contraction. This suggests that it requires more than one repetition to result in myofiber injury
within the physiological range.

/

15.4.3.2 The Effect of Muscle Length Changes on Myofiber Injury
To determine if muscle strain was important in susceptibility to injury, Zerba and Faulkner 314 studied
mouse EDL muscles in situ. Isometric force was checked immediately post-test and 3 days after the pro-
tocol. Only muscles stretched to 75% L f (length of the muscle fiber) at L f / sec produced injury 3 days later.

Muscles stretched at lower velocities and fiber strain did not exhibit any signs of injury. They hypothesized
that strain and strain rate were synergistic in the etiology of muscle injury. Lieber and Frid ´ n 162,165 also
investigated whether muscle damage was a function of muscle force or muscle strain. Rabbit TA muscle
was used in situ via securing the distal tendon to a servomotor. The TA muscle was selected due to a
30 pennation angle and negligible angular rotation during stretch. Final results indicated that muscle

strain (change in length of the muscle) produced the most profound changes in muscle performance
(via a force decrement) and that muscle strain was more responsible than force during lengthening in pro-
ducing contraction-induced injury. Warren et al. 284 found no observed difference in force deficit when
stretches were initiated from either 85% L or 90% L o . In contrast, Hunter and Faulkner, 129 MacPherson
et al., 172 and Brooks and Faulkner 39 found that 30% strain was necessary to produce a force deficit after
a single stretch and larger force deficits resulted when stretches were initiated from a longer initial
length, or terminated at a longer final length. This finding was also supported in multiple repetition
models. 110,305 Thus, it appears from both single- and multiple repetition models that muscle length
during stretch has an impact on the resultant force deficit and myofiber injury. However, the effect of
muscle length repetitive exposures of eccentric muscle actions has not been investigated to date.

8