Biomedical Engineering Reference
In-Depth Information
9.5.1.3
Excitatory (Excitation-Contraction Coupling)
This aspect of efficiency is often overlooked in muscle research, but it can easily be the dominant
form of energy loss in engineered muscle actuators. This is because muscle rapidly degenerates
when maintained in an inactive state. In addition to loss of mass (atrophy), muscle tissue also
experiences a loss of excitability. In order to elicit a contraction, muscle is subjected to electrical
pulses characterized by a specified pulse width and pulse amplitude at a specified duty cycle and
duration. For any given level of contractile activation, reduced excitability manifests as either
increased pulse width, pulse amplitude, or both that are required to elicit the desired force or power
output. Based upon our extensive preliminary data with engineered muscle, developing muscle,
injured and aging muscle, denervated muscle in vivo , and denervated-stimulated muscle both
in vivo and in vitro , we calculate that unless care is taken, muscle tissue can degenerate to the
point, where the excitability is reduced by three orders of magnitude, thus requiring approximately
1000 times the electrical energy to elicit any given level of contraction. We have also reported that
the excitability of denervated muscle can be maintained at control levels by applying the correct
form of electrical stimulation.
9.5.2
Static Contractility
Static measures of contractility are readily made, and allow repeatable quantitative evaluation of
living muscle function and normalized comparisons between muscle preparations of vastly differ-
ing size and architecture. These metrics include: peak twitch force ( P t ), peak tetanic force ( P o ), the
force-frequency relationship, specific force (s P o ), baseline force ( P b ), excitability (rheobase, R 50
and chronaxie, C 50 ), and the length-tension relationship.
Principal FoM (physical units follow definition):
peak normalized twitch force: P t ¼ maximum force, single pulse input (kPa);
specific force: sP o ¼ peak tetanic contractile force or physiologic CSA (kPa);
specific baseline force: s P b ¼ baseline tensile force or physiologic CSA (kPa);
rheobase: R 50 ¼ pulse field amplitude to elicit 0.5 P t at wide pulse width (V/m);
chronaxie: C 50 ¼ pulse width to elicit 0.5P t at field amplitudes ¼ 2 R 50 (s).
9.5.3
Dynamic Contractility
Measures of dynamic contractility are considerably more experimentally challenging than meas-
ures of static contractility; however, they provide considerably more insight into the function of
living muscle as a practical actuator. For this purpose, it will in general be necessary to develop
bioreactors specifically to monitor these values during the extended ex vivo maintenance of each
class of living muscle actuator (whole explanted or engineered). Dynamic contractility is generally
evaluated using one or more the following metrics: peak power, sustained power, power density
(W/kg), maximum velocity ( L f / s , where L f ¼ muscle fiber length), rate of force development
(d p /d t ), fatigue resistance (metabolic), and work loop performance (net power output during cyclic
loading).
Principal FoM (physical units follow definition):
peak normalized power density: i.e., peak power output/tissue mass (W/kg);
sustained power: i.e., power output at 20% duty cycle continuous (W/kg);
maximum contractile velocity: V max ¼ maximum contractile velocity, unloaded ( L f / s );
rate of force development: d p /d t (where p is relative force, P / P max )(s -1 )
In general it is necessary to assemble the instrumentation systems that are necessary for quantitative
evaluation of muscle actuator function. For larger muscles that generate at least 10 mN of force
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