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PubMed2004

Roles of motor-unit recruitment in producing force variability of simulated muscle contractions.

The purpose of this study was to examine the effect of motor-unit recruitment on force variability by using computer simulated isometric contractions of a hand muscle (i.e., first dorsal interosseus). The force was simulated at 10 levels of excitation, ranging from 10 to 100% of maximum. Two recruitment conditions were simulated to compare the relative effect of motor-unit recruitment (MUR) on the relationship of force variability and level of force. One condition (40%MUR) recruited all motor units at 40% of the maximum excitation level, and the other (50%MUR) recruited all motor units at 50% of the maximum. The 40%MUR condition had a greater number of motor units than the 50%MUR group before the excitation level reached 50% of the maximum. The results showed that force variability increased at a faster rate before the completion of motor-unit recruitment and, thereafter, increased at a slower rate. In addition, the 40%MUR group showed greater force variability than the 50%MUR group. These data suggest that motor-unit recruitment is an important factor in causing force variability.

Biomechanical Phenomena↗
PubMedDate not supplied

Vibrations and sounds produced during sustained voluntary muscle contraction.

In 20 normal subjects, sounds or vibrational signals were recorded from the biceps brachii muscle during voluntary isometric contraction. Fourier analysis showed presence of predominantly low frequency components with little contributions beyond 60 or 70 Hz. Relatively high amplitude peaks occurring below 20 Hz were seen in the frequency spectrum with the most prominent of these peaks occurring at a mean frequency of 11.3 Hz. A majority of subjects had one or two additional peaks, each appearing on either side of the major peak with mean frequencies of 7.3 and 16.2 Hz. In general, subjects who could not sustain a very steady contraction had more peaks compared to those who were able to maintain a smoother contraction. Between 20 and 50 Hz, several well-defined but much smaller peaks were also seen. The frequencies of some of these small peaks can be expressed as exact harmonics of the previously described larger peaks in 85% of subjects.

Adult↗
PubMed2004

Biochemical properties of V91G calmodulin: A calmodulin point mutation that deregulates muscle contraction in Drosophila.

A mutation (Cam7) to the single endogenous calmodulin gene of Drosophila generates a mutant protein with valine 91 changed to glycine (V91G D-CaM). This mutation produces a unique pupal lethal phenotype distinct from that of a null mutation. Genetic studies indicate that the phenotype reflects deregulation of calcium fluxes within the larval muscles, leading to hypercontraction followed by muscle failure. We investigated the biochemical properties of V91G D-CaM. The effects of the mutation on free CaM are minor: Calcium binding, and overall secondary and tertiary structure are indistinguishable from those of wild type. A slight destabilization of the C-terminal domain is detectable in the calcium-free (apo-) form, and the calcium-bound (holo-) form has a somewhat lower surface hydrophobicity. These findings reinforce the indications from the in vivo work that interaction with a specific CaM target(s) underlies the mutant defects. In particular, defective regulation of ryanodine receptor (RyR) channels was indicated by genetic interaction analysis. Studies described here establish that the putative CaM binding region of the Drosophila RyR (D-RyR) binds wild-type D-CaM comparably to the equivalent CaM-RyR interactions seen for the mammalian skeletal muscle RyR channel isoform (RYR1). The V91G mutation weakens the interaction of both apo- and holo-D-CaM with this binding region, and decreases the enhancement of the calcium-binding affinity of CaM that is detectable in the presence of the RyR target peptide. The predicted functional consequences of these changes are consonant with the in vivo phenotype, and indicate that D-RyR is one, if not the major, target affected by the V91G mutation in CaM.

Animals↗
PubMed2003

Do inflammatory mediators influence the contribution of airway smooth muscle contraction to airway hyperresponsiveness in asthma?

It is now accepted that a host of cytokines, chemokines, growth factors, and other inflammatory mediators contributes to the development of nonspecific airway hyperresponsiveness in asthma. Yet, relatively little is known about how inflammatory mediators might promote airway structural remodeling or about the molecular mechanisms by which they might exaggerate smooth muscle shortening as observed in asthmatic airways. Taking a deep inspiration, which provides relief of bronchodilation in normal subjects, is less effective in asthmatic subjects, and some have speculated that this deficiency stems directly from an abnormality of airway smooth muscle and results in airway hyperresponsiveness to constrictor agonists. Here, we consider some of the mechanisms by which inflammatory mediators might acutely or chronically induce changes in the contractile apparatus that in turn might contribute to hyperresponsive airways in asthma.

Animals↗