Differences in scapular orientation, subacromial space and shoulder pain between the full can and empty can tests.

BACKGROUND: The empty and full can arm positions are used as diagnostic tests and in therapeutic exercise programs for patients with subacromial impingement syndrome. The adverse effects of these arm positions on the rotator cuff have not been fully described. The purpose of this investigation was to compare the acromio-humeral distance, three-dimensional scapular position, and shoulder pain during maximum isometric contractions in the empty and full can arm positions. METHODS: Subjects with subacromial impingement syndrome (n=28) and a matched control group without shoulder pain (n=28) participated. Acromio-humeral distance, scapular/clavicular positions and shoulder pain were measured during maximal isometric contractions in each position. FINDINGS: No difference was found in acromio-humeral distance (P=0.314) between the arm positions or between the groups (P=0.598). The empty can position resulted in greater scapular upward rotation (P<0.001, difference=4.9°), clavicular elevation (P<0.001, difference=2.7°), clavicular protraction (P=0.001, difference=2.5°) and less posterior tilt (P<0.001, difference=3.8°) than the full can position. No differences in the scapular positions were found between the groups. Positive correlations were seen between the scapular positions in the control and not in the subacromial impingement group. INTERPRETATION: Our results did not show a difference in acromio-humeral distance between the arm positions or groups, indicating that the kinematic differences between the positions are not associated with altered acromio-humeral distance. The increased pain in the EC position might be due to the lack of an association amongst the scapular positions rather than the deficiency of a single scapular motion.

Adjustable passive length-tension curve in rabbit detrusor smooth muscle.

Until the 1990s, the passive and active length-tension (L-T) relationships of smooth muscle were believed to be static, with a single passive force value and a single maximum active force value for each muscle length. However, recent studies have demonstrated that the active L-T relationship in airway smooth muscle is dynamic and adapts to length changes over a period of time. Furthermore, our prior work showed that the passive L-T relationship in rabbit detrusor smooth muscle (DSM) is also dynamic and that in addition to viscoelastic behavior, DSM displays strain-softening behavior characterized by a loss of passive stiffness at shorter lengths following a stretch to a new longer length. This loss of passive stiffness appears to be irreversible when the muscle is not producing active force and during submaximal activation but is reversible on full muscle activation, which indicates that the stiffness component of passive force lost to strain softening is adjustable in DSM. The present study demonstrates that the passive L-T curve for DSM is not static and can shift along the length axis as a function of strain history and activation history. This study also demonstrates that adjustable passive stiffness (APS) can modulate total force (35% increase) for a given muscle length, while active force remains relatively unchanged (4% increase). This finding suggests that the structures responsible for APS act in parallel with the contractile apparatus, and the results are used to further justify the configuration of modeling elements within our previously proposed mechanical model for APS.

A mechanical model for adjustable passive stiffness in rabbit detrusor.

Strips of rabbit detrusor smooth muscle (DSM) exhibit adjustable passive stiffness characterized by strain softening: a loss of stiffness on stretch to a new length distinct from viscoelastic behavior. At the molecular level, strain softening appears to be caused by cross-link breakage and is essentially irreversible when DSM is maintained under passive conditions (i.e., when cross bridges are not cycling to produce active force). However, on DSM activation, strain softening is reversible and likely due to cross-link reformation. Thus DSM displays adjustable passive stiffness that is dependent on the history of both muscle strain and activation. The present study provides empirical data showing that, in DSM, 1) passive isometric force relaxation includes a very slow component requiring hours to approach steady state, 2) the level of passive force maintained at steady state is less if the tissue has previously been strain softened, and 3) tissues subjected to a quick-release protocol exhibit a biphasic response consisting of passive force redevelopment followed by force relaxation. To explain these and previously identified characteristics, a mechanical model for adjustable passive stiffness is proposed based on the addition of a novel cross-linking element to a hybrid Kelvin/Voigt viscoelastic model.

ROK-induced cross-link formation stiffens passive muscle: reversible strain-induced stress softening in rabbit detrusor.

Passive mechanical properties of strips of rabbit detrusor smooth muscle were examined and found by cyclic loading in a calcium-free solution to display viscoelastic softening and strain-induced stress softening (strain softening). Strain softening, or the Mullins effect, is a loss of stiffness attributed to the breakage of cross-links, and appeared irreversible in detrusor even after the return of spontaneous rhythmic tone during 120 min of incubation in a calcium-containing solution. However, 3 min of KCl or carbachol (CCh)-induced contraction permitted rapid regeneration of the passive stiffness lost to strain softening, and 3 microM of the RhoA kinase (ROK) inhibitor Y-27632 prevented this regeneration. The degree of ROK-induced passive stiffness was inversely dependent on muscle length over a length range where peak CCh-induced force was length independent. Thus rabbit detrusor displayed variable passive stiffness both strain- and activation-history dependent. In conclusion, activation of ROK by KCl or CCh increased passive stiffness softened by muscle strain and thereby attributed to cross-links that remained stable during tissue incubation in a calcium-free solution. Degradation of this signaling system could potentially contribute to urinary incontinence.