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M W Repeck

Publications and source records attributed to M W Repeck.

2 recordsLinked to original sources

Control of stiffness by the medium latency electromyographic response to limb perturbation.

It is hypothesized that the medium latency electromyographic (EMG) response (ML) to limb perturbation functions to preset limb stiffness to a constant initial level. Three predictions are derived from this hypothesis: Firstly, in the presence of an instruction calling for opposition to limb perturbation, a control signal, ML, will be observed and will lead to the establishment of a constant level of limb stiffness. Secondly, in the absence of an instruction to oppose, no control signal will be observed and correspondingly a constant stiffness will not be generated. Thirdly, the latency of onset of stiffness control will covary with the latency of onset of ML. These predictions were tested in experiments involving perturbation of the human forearm about the elbow joint, with surface EMG measurements and computation of the limb stiffness function. The results are in accord with these predictions, and support the hypothesis that ML functions in the feedforward control of limb stiffness.

Adult↗

Transmural mitochondrial differences in myocardium.

Two functional mitochondrial populations with different sedimentation rates (S) were obtained from homogenates of canine myocardium by rate zonal centrifugation using an iso-osmotic Ficoll gradient. To ascertain the origin of these populations, the left ventricular wall of normal myocardium was divided into subepicardial (outer one-third), intermediate (middle on-third), and subendocardial (inner one-third) layers. The slow S mitochondria comprised 75% of the mitochondrial population of the subepicardial layer. In contrast, the fast S mitochondria contributed 65% of the subendocardial population. Intermediate layer mitochondria resembled those of the subepicardium. Mitochondria isolated from the three layers had approximately the same density, as shown by isopycnic zonal centrifugation. These studies indicate that mitochondria from subepicardial and subendocardial layers of normal myocardium differ in size and shape but not in density. Electron micrographs (EM) of the subepicardium showed many mitochondria as long as 4 to 8 sarcomeres. Mitochondria from the outer and inner layers of normal myocardium had the same oxidative phosphorylation parameters. Acute myocardial infarction, lasting 1 or 2 hr, resulted in the selective loss of the fast S mitochondria. Because the fast S mitochondria are prevalent in the subendocardium, these results may explain the greater vulnerability of this layer to anoxia.

Animals↗