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Not only does the heart generally beat stronger when it is stimulated to contract faster, the kinetic of contraction is also accelerated, that is, the frequency-dependent acceleration of relaxation (FDAR) [ 1, 2].
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Ventricular myocytes from adult rat hearts were stimulated to contract at 0.5 Hz, and mechanical and intracellular Ca2+ properties were evaluated using an IonOptix Myocam system.
Interventions: The left quadriceps were stimulated to contract against an isokinetic load (resisted) while the right quadriceps contracted against gravity (unresisted) for 1 hour a day, 5 days a week, for 24 weeks.
This is achieved by the muscle being stimulated to contract again by a release in tension in the muscle, which can happen more rapidly than through simple nerve stimulation alone.
Isolated fibres were stimulated to contract, as previously described (Pye et al., 2007; Palomero et al., 2008).
During priming with repeated cycles of angiotensin II-hypoxia, the myocytes are stimulated to contract and raise pulmonary artery pressure.
Cells were exposed to light emitted by a 75W lamp, while being stimulated to contract at a frequency of 0.5 Hz.
Myocytes are exposed to light emitted by a 75 W halogen lamp through either a 360 or 380 nm filter while being stimulated to contract at 0.5 Hz.
Highly aligned collagen fibers would theoretically be associated with a greater force of contracture when myofibroblasts are stimulated to contract along uninterrupted parallel fibers [ 5].
After incubation muscles were stimulated to contract at 1 Hz for an additional 5 minutes in Rhod-2 solution to ensure dye uptake into the muscle.
However, if the neighboring extrafusal fibers were stimulated to contract, they unload the tendon organ, thus bringing it to a subthreshold level.
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