Conversion to a rearfoot strike pattern during running for prevention of recurrent calf strains: A case report.

Background: Running-related injuries are prevalent musculoskeletal complaints in the United States military. Although, run retraining is an extensively researched method for reducing pain and improving function in runners, its clinical utility remains low.

Case Description: The patient had a seven-year history of recurrent right calf strains.

Factors related to intra-tendinous morphology of Achilles tendon in runners.

The purpose of this study was to determine and explore factors (age, sex, anthropometry, running and injury/pain history, tendon gross morphology, neovascularization, ankle range of motion, and ankle plantarflexor muscle endurance) related to intra-tendinous morphological alterations of the Achilles tendon in runners. An intra-tendinous morphological change was defined as collagen fiber disorganization detected by a low peak spatial frequency radius (PSFR) obtained from spatial frequency analysis (SFA) techniques in sonography. Ninety-one runners (53 males and 38 females; 37.

Mechanism of activation of liver acetyl-CoA carboxylase by cell swelling.

The activation of hepatic glycogen synthase by the amino-acid-induced cell swelling has been attributed to the stimulation of [glycogen-synthase]-phosphatase resulting from an increase in the intracellular content in glutamate and aspartate, and a decrease in intracellular Cl-, which is a compensatory response to cell swelling [Meijer, A. J., Baquet, A.

Cell shrinkage follows, rather than mediates, the short-term effects of glucagon on carbohydrate metabolism.

The initial effects of glucagon on glycogen breakdown in isolated hepatocytes were found to be independent of cell volume and, when it occurred, cell shrinkage followed rather than mediated the glycogenolytic effect of glucagon. Similar conclusions could be drawn for the effect of glucagon on glycolysis/gluconeogenesis and for the antagonistic effect of insulin on glucagon action.

Mechanism of activation of liver glycogen synthase by swelling.

The mechanism linking the stimulation of liver glycogen synthesis to swelling induced either by amino acids or hypotonicity was studied in hepatocytes, in gel-filtered liver extracts, and in purified preparations of particulate glycogen to which glycogen-metabolizing enzymes are bound. High concentrations of KCl, but not of potassium glutamate, were found to inhibit glycogen synthesis in permeabilized hepatocytes. Similarly, physiological concentrations (30-50 mM) of Cl- ions were also found to inhibit synthase phosphatase in vitro, whereas 10-20 mM Cl- ions, a concentration found in swollen hepatocytes, did not inhibit synthase phosphatase.