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Engineered Muscle Actuators 253

9.6.2.6 Fatigue (Mechanical and Metabolic)

These failure modes apply to all classes of living muscle actuators. For metabolic fatigue the
preferred countermeasures will include genetic engineering of the muscle to promote fatigue-
resistant fiber types, the provision of adequate perfusion of the tissue actuator, and the development
of protocols for actuator control that optimize total work output, such as the intermittent locomotory
behavior of both terrestrial and aquatic animals. It is in terms of mechanical fatigue that living
actuators have an enormous advantage over fully synthetic actuators. By monitoring the state of
health of the actuator and modifying the mechanical demands accordingly, it is possible to promote
functional adaptation of the living component of the actuator as well as the tissue or synthetic
interface. It will be necessary to identify biomarkers of mechanical fatigue, such as reduced or
altered contractility, to actively detect these markers, and to respond with appropriate modifications
of the embedded excitation and control algorithms to allow tissue functional adaptation. In
principle a properly monitored and controlled living muscle actuator will exhibit improved dy-
namic performance and structural resilience with use over a period of decades, unlike any synthetic
actuator technology currently available.

9.6.2.7 Toxicity

A serious problem for all classes of living muscle actuators, the best countermeasure is barrier
exclusion of exogenous toxic agents, the use of biocompatible materials in the fluid-space of the
hybrid actuator assembly, and the clearance of toxic metabolic byproducts via a perfusion and
filtration system integrated with the living actuator.

9.6.2.8 Electrochemical Tissue Damage

This failure mode affects all classes of living muscle actuators when exposed to chronic electrical
stimulation. The single best countermeasure is to promote and maintain tissue phenotype exhibiting
very high excitability. In addition to vastly improving the excitation efficiency of the tissue, adult
muscle phenotype excitability can yield as much as a 99.9% reduction in electrical pulse energy
requirements for any given level of muscle activation, when compared with chronically denervated
or tissue engineered muscle tissue arrested at early developmental stages. For this reason, the
development of electro-mechanical muscle bioreactor systems and maintenance stimulation proto-
cols form a core component of all current research on muscle tissue engineering. Additional
countermeasures include the selection of appropriate electrode materials, the use of minimally
energetic stimulation protocols, the use of pure bipolar stimulation pulses with careful attention to
charge balancing, and the use of high-impedance outputs to the electrodes when not stimulating.

9.6.2.9 Damage from Incidental Mechanical Interference

The living actuator will require electrodes to be placed in contact with the tissue, the presence of
tubing for perfusion, and other structures required within the hybrid actuator. Lateral mechanical
contact between these synthetic objects and the living muscle tissue can result in a range of
mechanical failures, including abrasion, incision, and chronic pressure atrophy. The appropriate
countermeasure for this is careful mechanical design of the hybrid actuator assembly, with these
considerations explicitly included in the system Design Specification.

9.6.2.10 Retrograde or Arrested Phenotype (Failure to Thrive)

Effective countermeasures for this failure mode have been reported for denervated whole muscles
in vivo, employing a long-term electrical stimulation protocol (Dennis et al., 2003; Dow et al.,