Age- and gender-stratified adult myometric reference values of isometric intrinsic hand strength.

STUDY DESIGN: Descriptive normative. INTRODUCTION: Intrinsic hand strength can be impacted by hand arthritis, peripheral nerve injuries, and spinal cord injuries. Grip dynamometry does not isolate intrinsic strength, and manual muscle testing is not sensitive to change in grades 4 and 5. The Rotterdam Intrinsic Hand Myometer is a reliable and valid test of intrinsic hand strength; however, no adult normative data are available. PURPOSE OF THE STUDY: To describe age- and gender-stratified intrinsic hand strength norms in subjects aged 21 years and above and to determine if factors known to predict grip dynamometry also predict measures of intrinsic hand strength. METHODS: Three trials of 5 measures of maximal isometric intrinsic strength were performed bilaterally by 607 "healthy-handed" adult males and females. Average strength values were stratified by age and gender. Data were analyzed to determine the influence of demographic and anthropometric variables on intrinsic strength. RESULTS: Intrinsic strength generally followed age and gender trends similar to grip dynamometry. Age, gender, body mass index, and the interaction between gender and body mass index were predictors of intrinsic strength, whereas in most cases, the hand being tested did not predict the intrinsic strength. DISCUSSION: With the addition of these findings, age- and gender-stratified hand intrinsic strength norms now span from age 4 through late adulthood. Many factors known to predict grip dynamometry also predict intrinsic myometry. Additional research is needed to evaluate the impact of vocational and avocational demands on intrinsic strength. CONCLUSIONS: These norms can be referenced to evaluate and plan hand therapy and surgical interventions for intrinsic weakness.

Actual Versus Predicted Cardiovascular Demands in Submaximal Cycle Ergometer Testing.

The Astrand-Rhyming cycle ergometer test (ARCET) is a commonly administered submaximal test for estimating aerobic capacity. Whereas typically utilized in clinical populations, the validity of the ARCET to predict VO2max in a non-clinical population, especially female, is less clear. Therefore, the purpose of this study was to determine the accuracy of the ARCET in a sample of healthy and physically active college students. Subjects (13 females, 10 males) performed a maximal cycle ergometer test to volitional exhaustion to determine VO2max. At least 48 hours later, subjects performed the ARCET protocol. Predicted VO2max was calculated following the ARCET format using the age corrected factor. There was no significant difference (p=.045) between actual (41.0±7.97 ml/kg/min) and predicted VO2max (40.3±7.58 ml/kg/min). When split for gender there was a significant difference between actual and predicted VO2 for males, (45.1±7.74 vs. 42.7±8.26 ml/kg/min, p=0.029) but no significant difference observed for females, (37.9±6.9 vs. 38.5±6.77 ml/kg/min, p=0.675). The correlation between actual and predicted VO2 was r=0.84, p<0.001 with an SEE= 4.3 ml/kg/min. When split for gender, the correlation for males was r=0.94, p<0.001, SEE=2.72 ml/kg/min; for females, r=0.74, p=0.004, SEE=4.67 ml/kg/min. The results of this study indicate that the ARCET accurately estimated VO2max in a healthy college population of both male and female subjects. Implications of this study suggest the ARCET can be used to assess aerobic capacity in both fitness and clinical settings where measurement via open-circuit spirometry is either unavailable or impractical.

Metabolic changes in the glucose-induced apoptotic blastocyst suggest alterations in mitochondrial physiology.

Mammalian preimplantation embryos experience a critical switch from an oxidative to a predominantly glycolytic metabolism. In this study, the change in nutrient metabolism between the 2-cell and blastocyst stages was followed by measuring single embryo concentrations of tricarboxylic acid (TCA) cycle and glycolytic metabolites with microfluorometric enzymatic cycling assays. When the normal values were established, further changes that occur as a result of the induction of apoptosis by exposure to high-glucose conditions were examined. From the 2-cell to the blastocyst stage, the embryos experienced an increase in TCA metabolites and a dramatic increase in fructose 1,6-bisphosphate (FBP). The high TCA metabolites may result from accumulation of substrate due to a slowing of TCA cycle metabolism as glycolysis predominates. Embryos exposed to elevated glucose conditions experienced significantly lower FBP, suggesting decreased glycolysis, significantly higher pyruvate, suggesting increased pyruvate uptake by the embryos in response to decreased glycolysis, and increased TCA metabolites, suggesting an inability to oxidize the pyruvate and a slowing of the TCA cycle. We speculate that the glycolytic changes lead to dysfunction of the outer mitochondrial membrane that results in the abnormal TCA metabolite pattern and triggers the apoptotic event.

Glucose transporter 8 expression and translocation are critical for murine blastocyst survival.

Glucose transporter (GLUT) 8 is an insulin-responsive facilitative glucose transporter expressed predominantly in the murine blastocyst. To determine the physiologic role of GLUT8, two-cell embryos were cultured to a blastocyst stage in antisense or sense oligonucleotides to GLUT8. Apoptosis was assessed using the TUNEL techniques and recorded as the percentage of TUNEL-positive nuclei/total nuclei. Embryos cultured in GLUT8 antisense experienced increased TUNEL-positive nuclei, whereas sense embryos did not. Embryos cultured in a control AS oligonucleotide, specific for heat shock protein 70-2, showed a rate of apoptosis similar to sense. To determine the outcome of these apoptotic embryos, blastocysts exposed to sense vs. antisense were transferred back into foster mice and the pregnancy continued until Day 14.5, at which time the uteri were examined for normal gestational sacs and resorptions. Embryos exposed to GLUT8 antisense experienced higher rates of resorptions and lower normal pregnancy rates compared to embryos cultured in GLUT8 sense. To examine the insulin growth factor (IGF)-1/insulin intracellular signaling pathways involved in GLUT8 translocation, IGF-1 receptor (IGF-1R) expression was decreased in the blastocysts with antisense oligonucleotides. Using confocal immunofluorescent microscopy, GLUT8 translocation in response to insulin was observed. Exposure to insulin in the embryos exposed to IGF-1R sense induced translocation of GLUT8 from intracellular compartments to the plasma membrane. Blastocysts exposed to IGF-1R antisense, however, failed to demonstrate any change in the intracellular location of GLUT8 with insulin treatment. The IGF-1R antisense embryos also displayed significantly greater TUNEL staining compared to sense embryos. These data suggest that GLUT8 expression and translocation in response to insulin are critical for blastocyst survival.