Mechanical Muscle Function Research Articles

The psoas major muscle: A three-dimensional geometric study

The purpose of this study was to use anatomical data obtained from cadavers, and geometrical scaling data obtained from MRI scans of living subjects, to assess the line of action and mechanical function of the psoas major muscle in three dimensions about each lumbar spine level. In addition, the line of action of the psoas major was documented as a function of lordosis. A total of seven cadavers were dissected from which fibre/tendon architecture was measured, while MRI scans were performed on 15 males to obtain centroid paths and area scales of the muscle over its length. In this way, the curving path of muscle line of action was accommodated together with force and moment predictions that recognized the presence of a tendon at lower lumbar levels (up to L3 in some subjects) significantly increasing the stress. Results confirm that the mechanics of the psoas cannot be adequately represented with a series of straight line vectors from vertebral origins to insertion. Moreover, the mechanical action of the psoas major does not change as a function of lumbar spine lordosis as the muscle path of action changes in accordance with changes in spine posture. Functionally, contrary to claims, the psoas cannot act as a ‘derotator’ of the spine, does not impose large shear forces on the spine in any posture except at L5-S1, and cannot have major affects to ‘control lordosis’. It has the potential to stabilize the lumbar spine with compressive loading and with bilateral activation, to laterally flex it, and can create large anterior shear forces but only at L5-S1.

Myoglobin facilitated oxygen diffusion maintains mechanical function of mammalian cardiac muscle.

Myoglobin, an intracellular iron containing protein that binds oxygen reversibly, has been shown in model systems to facilitate the diffusion of oxygen and thereby maintain the mechanical function of exercising canine skeletal muscle and of hypoxic benthic fish hearts. Since no such role has yet been established for mammalian cardiac muscle small diameter (less than or equal to 0.70 mm) isolated kitten papillary muscles were stimulated at 24 X min-1 under isometric conditions in a physiological bath maintained at 30 degrees C with an oxygen tension of approximately equal to 450 mm Hg (59.8 kPa) to obtain a level of oxygenation just adequate to meet the metabolic needs of the muscles, as confirmed experimentally. Myoglobin was inactivated by adding 2 X 10(-3) mol X litre-1 sodium nitrite to the bath to abolish the facilitated diffusion of oxygen in the presence or absence of glycolytic blockade by 10(-4) mol X litre-1 sodium iodoacetate. This resulted in a 22(8)% (with blockade) or 10(3)% (without blockade) decrease (p less than 0.05) in the maximal rate of relaxation (-dT/dtmax) of the papillary muscles. Since the depression in mechanical function was reversible by increasing the bath oxygen tension to approximately equal to 600 mm Hg (79.8 kPa) it is concluded that the myoglobin facilitated diffusion of oxygen plays a role in maintaining the mechanical function of mammalian cardiac muscle under normal conditions. Furthermore, the maximal rate of relaxation of cardiac muscle is a sensitive indicator of the presence of hypoxia.

Myosin adenosine triphosphatase activity in the volume-overloaded hypertrophied feline right ventricle.

SUMMARY Chronic pressure overload leads to hypertrophy, depressed mechanical function, and reduced myosin ATPase activity. However, it is not known whether the lowered myosin ATPase activity results from the hypertrophic process per se or whether the elevated afterload is required for the depressed myosin ATPase activity. Further, a causal relationship between lowered myosin ATPase and weakened mechanical function in pressure overload has not been established. Chronic volume overload on the myocardium, leading to hypertrophy equivalent to that in pressure overload, allows the effects of pressure overload to be separated from the effects of hypertrophy and provides insight into the association between myosin ATPase and mechanical function. We produced large atrial septal defects (ASD) with a transvenous biopsy catheter in six adult cats. This resulted in 63% right ventricular hypertrophy, normal (P > 0.05) papillary muscle mechanical function (velocity at 0.5-g/mm 1 load: control - 1.01 ± 0.05 muscle lengths per second; ASD - 1.02 + 0.26 muscle lengths per second), and normal (P > 0.05) myosin ATPase activity in three activating mediums (actin: C - 0.20 ± 0.02, ASD «• 0.21 ± 0.03; Ca 1+ : C - 0.41 ± 0.03, ASD - 0.38 ± 0.02; K-EDTA: C - 1.67 ± 0.05, ASD - 1.69 ± 0.07 pmol