REDUCING OF STRESS IN THE HIP JOINT ARTICULAR SURFACE IN SKIING

INTRODUCTION - It was recently shown that too high contact stress in the articular surface of the hip joint can accelerate the arthrosis development in the hip joint ( Hadley et al., 1990). Increased contact stress in the hip joint articular surface can result from too small hip joint articular surface andlor from too high resultant hip joint force. Since the resultant hip joint force. Since the resultant hip -joint force is permanently increased during sport activities it is understandable that the incidence of the hip arthrosis among people with high exposure to sport is significantly higher compared to those with low exposure (Vingard et al., 1993). The acetabular dysplasia in sportsmen, i.e, small femoral head coverage, additionally increase the probability of hip arthorsis development. During skiing changes in the position of the upper body occur. They are associated with varying degrees of pelvic tilting, which influence the hip joint contact stress distribution (Iglic et al., 1994). The aim of this work was to determine how acetabular dysplasia and pelvic tilt affect the hip joint contact stress distribution after shifting of the upper part of the body towards the weight-bearing leg in slow skiing. METHODS - A three-dimensional model of the hip joint articular surface is used in order to calculate hip joint contact stress distribution (Iglic et al., 1993a). the resultant hip joint force for various body positions is calculated separately by using a static three-dimensional model of the adult hip in the one-legged stance (Iglic et at., 1993b, lglic et al., 1994). RESULTS - It is shown that the decrease of the hip joint contact stress after the shifting of the upper part of the body towards the supporting leg is more effective in the case of large inclination of the pelvis during the shifting og the of the upper part of the body towards the supporting leg hip the stress can be in the case of severe acetabular dysplasia and small inclination of the pelvis even increased in spite of the fact that the resultant hip joint force is considerably reduced. CONCLUSIONS - In accordance with the results of this study it can be concluded that the subjects with borderline acetabular dysplasia should be encouraged to turn during skiing with increased pelvic tilt on the side of the non-weight-bearing leg with simultaneously shifting of the upper part of the body towards the weight-bearing leg. In this way the dysplastic hip is unloaded to an optimum degree. consequently, the risk for arthrosis development is decreased. REFERENCES - Hadley N.A., Brown T.D., Weinstein S.L. (1990) J. Orthop. Res. 8:504-513. lglic A,, Kralj-lglic V., Antolic V., Srakar F., Stanic U. (1993a) IEEE Trans. Rehab. Engr. 1 :207-212. lglic A,, Srakar F., Antolic V. (1993b) Clin. Biomech. 8:223-224. lglic A,, Kralj- lglic V., Antolic V. (1994) Acta Chir. Orthop. Traum. Cech. 61.268- 270. Vingard E., Alfredsson L.. Goldie I., Hoghstedt C. (1 993) Am.J.Sports Med. 21.195-200

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated β adrenergic receptor (ADRβ) desensitization. Our objectives were to measure insulin-sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRβ2 agonist and ADRβ1/β3 antagonists for 1 month normalizes their glucose metabolism. Growth, glucose-stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR-AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole-bodyGUR were not different from controls.Of importance, ADRβ2 stimulation with β1/β3 inhibition increases both insulin sensitivity and whole-body glucose utilization in IUGR lambs. In IUGR and IUGR-AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and ex vivo skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle than in controls but GLUT1 was greater in IUGR-AR. ADRβ2, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR-AR lambs heart rates were greater, which was independent of cardiac ADRβ1 activation. We conclude that targeted ADRβ2 stimulation improved whole-body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch-up growth in IUGR lambs as early as 1 month of age and are inherent to the islets and myocytes

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated β adrenergic receptor (ADRβ) desensitization. Our objectives were to measure insulin-sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRβ2 agonist and ADRβ1/β3 antagonists for 1 month normalizes their glucose metabolism. Growth, glucose-stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR-AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole-bodyGUR were not different from controls.Of importance, ADRβ2 stimulation with β1/β3 inhibition increases both insulin sensitivity and whole-body glucose utilization in IUGR lambs. In IUGR and IUGR-AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and ex vivo skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle than in controls but GLUT1 was greater in IUGR-AR. ADRβ2, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR-AR lambs heart rates were greater, which was independent of cardiac ADRβ1 activation. We conclude that targeted ADRβ2 stimulation improved whole-body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch-up growth in IUGR lambs as early as 1 month of age and are inherent to the islets and myocytes

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated β adrenergic receptor (ADRβ) desensitization. Our objectives were to measure insulin‐sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRβ2 agonist and ADRβ1/β3 antagonists for 1 month normalizes their glucose metabolism. Growth, glucose‐stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR‐AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole‐body GUR were not different from controls. Of importance, ADRβ2 stimulation with β1/β3 inhibition increases both insulin sensitivity and whole‐body glucose utilization in IUGR lambs. In IUGR and IUGR‐AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and ex vivo skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR‐AR skeletal muscle than in controls but GLUT1 was greater in IUGR‐AR. ADRβ2, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR‐AR lambs heart rates were greater, which was independent of cardiac ADRβ1 activation. We conclude that targeted ADRβ2 stimulation improved whole‐body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch‐up growth in IUGR lambs as early as 1 month of age and are inherent to the islets and myocytes.Bill and Melinda Gates Foundation Global Health, Gates Foundation [OPP1066912]; United States Department of Health & Human Services, National Institutes of Health (NIH) - USA [R01DK-084842]; United States Department of Agriculture (USDA), National Institute of Food and Agriculture [2012-67012-19855, T32 HL007249, 2015-03545]; United States Department of Health & Human Services, National Institutes of Health (NIH) - USA [T32 HD007186, K12 HD068372, UL1TR001082]Open access articleThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]