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Purpose: To determine whether coracohumeral distance was significantly narrowed in the presence of a torn subscapularis., Type of Study: Retrospective cohort study., Methods: The coracohumeral distance of a consecutive series of patients (n = 35, 36 shoulders) requiring an arthroscopic repair of the subscapularis was compared with a control group (n = 35). The control group consisted of patients who underwent shoulder arthroscopy but who did not have any rotator cuff, subscapularis, or subcoracoid pathology. The coracohumeral distance was measured from the tip of the coracoid to the cortex of the proximal humerus on an axial cut of preoperative magnetic resonance imaging. A Student t test was used to determine the statistical differences between the 2 groups., Results: The average coracohumeral distance in the subscapularis group was 5.0 +/- 1.7 mm and the average coracohumeral distance in the control group was 10.0 +/- 1.3 mm. Statistical analysis, using the Student t test, showed that the coracohumeral distance was significantly narrowed in the group of patients with a torn subscapularis., Conclusions: These results show a significant relationship between a narrowed coracohumeral distance and subscapularis pathology., Level of Evidence: Level III, retrospective cohort study.

Ultrasound is well suited to evaluate a wide variety of abnormalities involving skeletal muscle, including traumatic injuries, inflammatory or infectious myositis, atrophy, and tumors. Ultrasound can accurately localize and characterize a lesion, or grade the severity of injury. The unique ability of ultrasound to assess the dynamic function of muscles on the real-time or perform Doppler evaluation of vascularity provides insights that are not readily obtained with other imaging modalities. With ultrasound, image-guided biopsy can be performed in conjunction with a diagnostic evaluation. This article presents a pictorial review of lesions and abnormalities involving skeletal muscles, and discusses characteristic findings, classifications, and imaging methods.

Fatty acid (FA) translocase (FAT)/CD36 is a key protein involved in regulating the uptake of FA across the plasma membrane in heart and skeletal muscle. A null mutation of FAT/CD36 reduces FA uptake rates and metabolism, while its overexpression increases FA uptake rates and metabolism. FA uptake into the myocyte may be regulated (a) by altering the expression of FAT/CD36, thereby increasing the plasmalemmal content of this protein (i.e. streptozotocin-induced diabetes, chronic muscle stimulation), or (b) by relocating this protein to the plasma membrane, without altering its expression (i.e. obese Zucker rats). By repressing FAT/CD36 expression, and thereby lowering the plasmalemmal FAT/CD36 (i.e. leptin-treated animals), the rate of FA transport is reduced. Within minutes of beginning muscle contraction or being exposed to insulin FA transport is increased. This increase is a result of the contraction- and insulin-induced translocation of FAT/CD36 from an intracellular depot to the cell surface. Neither PPAR alpha nor PPAR gamma activation alter FAT/CD36 expression in muscle, despite the fact that PPAR alpha activation increases FAT/CD36 by 80% in liver. A novel observation is that FAT/CD36 also appears to be involved in mitochondrial FA oxidation, as this protein is located on the mitochondrial membrane and seems to be required to participate in moving FA across the mitochondrial membrane. Clearly, FAT/CD36 has an important role in FA homeostasis in skeletal muscle and the heart.

This study examined the actions of 17beta-estradiol (E(2)) and progesterone on the regulation of the peroxisome proliferator-activated receptors (PPARalpha and PPARgamma) family of nuclear transcription factors and the mRNA abundance of key enzymes involved in fat oxidation, in skeletal muscle. Specifically, carnitine palmitoyltransferase I (CPT I), beta-3-hydroxyacyl CoA dehydrogenase (beta-HAD), and pyruvate dehydrogenase kinase 4 (PDK4) were examined. Sprague-Dawley rats were ovariectomized and treated with placebo (Ovx), E(2), progesterone, or both hormones in combination (E+P). Additionally, sham-operated rats were treated with placebo (Sham) to serve as controls. Hormone (or vehicle only) delivery was via time release pellets inserted at the time of surgery, 15 days prior to analysis. E(2) treatment increased PPARalpha mRNA expression and protein content (P<0.05), compared with Ovx treatment. E(2) also resulted in upregulated mRNA of CPT I and PDK4 (P<0.05). PPARgamma mRNA expression was also increased (P<0.05) by E(2) treatment, although protein content remained unaltered. These data demonstrate the novel regulation of E(2) on PPARalpha and genes encoding key proteins that are pivotal in regulating skeletal muscle lipid oxidative flux.

Growing evidence suggests that the ovarian hormones have major effects on lipid and carbohydrate metabolism, and may also play a major role in up-stream molecular signaling mechanisms for regulating substrate metabolism. It appears that the absence of estrogen can impair glucose uptake during exercise. In contrast, progesterone not only impairs contraction-mediated glucose uptake when solely administered, but impairs glucose uptake when physiological concentrations of both estrogen and progesterone are administered. Likewise, progesterone administered to rodents for 14 days decreases glucose transporter (GLUT) 4 protein content in skeletal muscle and adipose tissue. Furthermore removing the ovaries decreases the activity of key oxidative enzymes while estrogen treatment restores the activity of these enzymes. It appears, therefore, that estrogen increases the metabolic capacity for both carbohydrate and lipid metabolism, perhaps increasing the overall metabolic flexibility of skeletal muscle. Conversely, progesterone negates both these effects, and could therefore result in a state of relative metabolic inflexibility, similar to that observed in the metabolic syndrome.

To examine the roles of 17beta-estradiol (E(2)) and progesterone (Prog) in lipid metabolism, skeletal muscle enzyme activities were studied in female Sprague-Dawley rats. Groups included sham-operated rats (C) and ovariectomized rats treated with placebo (O), E(2) (E), Prog (P), both hormones at physiological doses (P + E), or both hormones with a high dose of E(2) (P + HiE). Hormone (or vehicle only) delivery was via time-release pellets inserted at the time of surgery, 15 days before metabolic testing. Results demonstrated that carnitine palmitoyltransferase maximal activity was 19, 21, and 19% lower (P < 0.01) in O, P, and P + E rats, respectively, compared with C rats. Conversely, activity in E and P + HiE rats was 14 and 19% higher (P < 0.01) than in C. beta-Hydroxyacyl-CoA dehydrogenase (beta-HAD) maximal activity was 20% lower (P < 0.01) in O than in C rats; similarly, P and P + E rats were 18 and 19% lower, respectively (P < 0.01); however, treatment with E(2) returned beta-HAD activity to C levels. These results suggest that E(2) plays a role in lipid metabolism by increasing the maximal activity of key enzymes in the fat oxidative pathway of skeletal muscle.

Eight trained men cycled at 70% peak oxygen uptake for 120 min followed by a 30-min performance cycle after ingesting either a high-glycemic index (HGI), low-glycemic index (LGI), or placebo (Con) meal 30 min before exercise. Ingestion of HGI resulted in an elevated (P<0.01) blood glucose concentration compared with LGI and Con. At the onset of exercise, blood glucose fell (P<0.05) such that it was lower (P<0.05) in HGI compared with LGI and Con at 15 and 30 min during exercise. Plasma insulin concentration was higher (P<0.01) throughout the rest period after ingestion of HGI compared with LGI and Con. Plasma free fatty acid concentrations were lower (P<0.05) throughout exercise in HGI compared with LGI and Con. The rates of [6,6-(2)H]glucose appearance and disappearance were higher (P<0.05) at rest after ingestion and throughout exercise in HGI compared with LGI and Con. Carbohydrate oxidation was higher (P<0.05) throughout exercise, whereas glycogen use tended (P = 0.07) to be higher in HGI compared with LGI and Con. No differences were observed in work output during the performance cycle when comparing the three trials. These results demonstrate that preexercise carbohydrate feeding with a HGI, but not a LGI, meal augments carbohydrate utilization during exercise but does not effect exercise performance.