ABSTRACT
OBJECTIVES: In this study, the hypothesis that tennis players with scapular dyskinesia present a smaller subacromial space than non-athletes was investigated. Additionally, the correlation between the size of the subacromial space and abnormalities in scapular movement during arm abduction was studied. DESIGN: Cross-sectional study. PARTICIPANTS: A total of 53 elite tennis players and 20 control participants were enrolled in the study. Participation was restricted to elite-level, junior tennis players who had no current shoulder pain or history of shoulder injuries. INTERVENTION: Each individual was examined for scapular dyskinesia by a single physician and by ultrasound, with the results analysed in a blind fashion by a single radiologist. RESULTS: 43.4% of the tennis players and 20% of control participants presented with scapular dyskinesia. Of the 106 shoulders evaluated, 39.6% of tennis players and 10% of control participants presented with scapular dyskinesia in the clinical examination (p = 0.005). Ultrasonographic measurements demonstrated that tennis players presented statistically smaller subacromial spaces compared with control participants (p<0.001). A decrease in the subacromial space was observed in tennis players when the shoulder was raised from 0 degrees to 60 degrees of abduction; however, dyskinesia-afflicted athletes demonstrated a significantly greater decrease following this movement (19.3 vs 13.8 mm, p = 0.002). CONCLUSIONS: The results of this study demonstrated that tennis players with scapular dyskinesia present a smaller subacromial space than control participants. Furthermore, when the shoulder was analysed dynamically, moving from neutral abduction to 60 degrees of elevation, the tennis players with scapular dyskinesia presented a greater reduction in the subacromial space compared with unaffected athletes.
Subject(s)
Acromioclavicular Joint/pathology , Dyskinesias/pathology , Joint Diseases/pathology , Scapula/pathology , Tennis , Acromioclavicular Joint/diagnostic imaging , Adolescent , Case-Control Studies , Child , Cross-Sectional Studies , Dyskinesias/diagnostic imaging , Female , Humans , Joint Diseases/diagnostic imaging , Male , Scapula/diagnostic imaging , UltrasonographyABSTRACT
In the present study we have examined the levels and phosphorylation state of the insulin receptor and insulin receptor substrate 1 (IRS-1) as well as the association between IRS-1 and phosphatidylinositol 3-kinase (PI 3-kinase) in the liver and muscle of rats treated with glucagon. There was a decrease in the insulin-stimulated receptor and IRS-1 phosphorylation levels which was paralleled by a reduced association between IRS-1 and PI 3-kinase in vivo in the liver and muscle of glucagon-treated rats. These observations suggest that glucagon, probably acting through cAMP, may impair insulin signaling in the three early steps in insulin action after binding.
Subject(s)
Glucagon/pharmacology , Insulin/pharmacology , Liver/metabolism , Muscle, Skeletal/metabolism , Phosphoproteins/metabolism , Phosphotransferases (Alcohol Group Acceptor)/metabolism , Animals , Insulin Receptor Substrate Proteins , Liver/drug effects , Male , Muscle, Skeletal/drug effects , Phosphatidylinositol 3-Kinases , Phosphoproteins/drug effects , Phosphoproteins/isolation & purification , Phosphorylation , Phosphotransferases (Alcohol Group Acceptor)/drug effects , Phosphotyrosine , Rats , Reference Values , Tyrosine/analogs & derivatives , Tyrosine/metabolismABSTRACT
Epinephrine is known to produce insulin resistance, but the exact molecular mechanism involved is unknown. In the present study we have examined the levels and phosphorylation state of the insulin receptor and of insulin receptor substrate 1 (IRS-1), as well as the association between IRS-1 and phosphatidylinositol 3-kinase (PI 3-kinase) in the liver and muscle of rats treated with epinephrine. The results demonstrate a decrease in insulin-stimulated receptor and IRS-1 phosphorylation levels which was accompanied by a reduction in the association of IRS-1 with PI 3-kinasein vivo in liver and muscle of epinephrine treated rats. These data suggest that molecular post-receptor defects may explain some aspects of the insulin resistance induced by catecholamines.
