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    <title><![CDATA[Medicine & Science in Sports & Exercise - Featured Articles - Featured Articles]]></title>
    <link>http://journals.lww.com/acsm-msse/</link>
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    <language>en-us</language>
    <lastBuildDate>Sun, 22 Nov 2009 08:56:14 -0600</lastBuildDate>
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      <title><![CDATA[Medicine & Science in Sports & Exercise - Featured Articles - Featured Articles]]></title>
      <link>http://journals.lww.com/acsm-msse/</link>
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      <link>http://journals.lww.com/acsm-msse/Fulltext/2009/12000/Metabolic_Syndrome_and_Insulin_Resistance_in.1.aspx</link>
      <author>BORCHERS, JAMES R.; CLEM, KELLEY L.; HABASH, DIANE L.; NAGARAJA, HAIKADY N.; STOKLEY, LISA M.; BEST, THOMAS M.</author>
      <category>Clinical Sciences</category>
      <title><![CDATA[Metabolic Syndrome and Insulin Resistance in Division 1 Collegiate Football Players]]></title>
      <description><![CDATA[Purpose: To estimate the prevalence of metabolic syndrome and insulin resistance in a cohort of Division 1 collegiate football players.
Methods: Ninety football players were evaluated in a cross-sectional study to estimate the prevalence of metabolic syndrome, insulin resistance, and associated risk factors. Obesity was defined as a body fat >=25% determined by BOD POD measurements. The National Cholesterol Education Program Adult Treatment Panel III criteria were used to estimate prevalence of metabolic syndrome. Quantitative insulin sensitivity check index calculations were performed to estimate prevalence of insulin resistance. Linear regression techniques were used to determine association between body fat percentage and other measured continuous parameters. Fisher exact test was used to determine association between nominal variables, and one-way ANOVA compared the three groups defined by position.
Results: Summary measures showed a small prevalence of abnormal individual measurements. There was an association between body fat percentage and most evaluated parameters (P < 0.05). The prevalence of obesity, insulin resistance, and metabolic syndrome was 21%, 21%, and 9%, respectively. Obesity is closely associated with metabolic syndrome (P < 0.0001) and insulin resistance (P < 0.0001) in this population. All subjects with metabolic syndrome were obese, and the odds for insulin resistance in the obese group are 10.6 times the odds for the nonobese group. Linemen (n = 29) had 19 of the 19 obese subjects, 13 of the 19 subjects with insulin resistance, and all subjects with metabolic syndrome.
Conclusions: There is a strong association between obesity and both metabolic syndrome and insulin resistance in Division 1 collegiate football players. Linemen are at significant risk for metabolic syndrome and insulin resistance compared with other positions. This may be predictive of future health problems in Division 1 collegiate football players, especially linemen.
(C)2009The American College of Sports Medicine]]></description>
      <pubDate>12/1/2009 12:00:00 AM</pubDate>
      <guid isPermaLink="false">00005768-200912000-00001</guid>
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      <link>http://journals.lww.com/acsm-msse/Fulltext/2009/12000/Long_Term_Exercise_Stabilizes_Atherosclerotic.4.aspx</link>
      <author>PELLEGRIN, MAXIME; MIGUET-ALFONSI, CAROLE; BOUZOURENE, KARIMA; AUBERT, JEAN-FRANÇOIS; DECKERT, VALÉRIE; BERTHELOT, ALAIN; MAZZOLAI, LUCIA; LAURANT, PASCAL</author>
      <category>Basic Sciences</category>
      <title><![CDATA[Long-Term Exercise Stabilizes Atherosclerotic Plaque in ApoE Knockout Mice]]></title>
      <description><![CDATA[Purpose: Exercise is known to reduce cardiovascular mortality. However, the precise mechanisms are still unknown. Because atherosclerotic plaque destabilization and rupture leads to dramatic cardiovascular events, stabilization of plaque might be regarded as an important goal of an exercise preventive therapy. The present study examined the plaque-stabilizing effect of long-term exercise in experimental atherosclerosis using apolipoprotein E-deficient mice (ApoE-/-).
Methods: ApoE-/- mice were subjected to 6 months of swimming exercise. A group of sedentary animals were used as controls. Morphometry and characteristics of atherosclerotic plaque stability were assessed in aortic sinus by immunohistochemistry. Aortic levels of total protein kinase Akt (protein kinase B), phosphorylated Akt at Ser473 (p-Akt), total endothelial nitric oxide synthase (eNOS), and phosphorylated eNOS at Ser1177 (p-eNOS) were assessed by Western blotting.
Results: Exercised mice developed a more stable plaque phenotype as shown by decreased macrophage and increased smooth muscle cell content. Protein expressions of Akt, p-Akt, eNOS, and p-eNOS were not modulated by exercise.
Conclusions: Long-term exercise promotes plaque stability in ApoE-/- mice. The Akt-mediated eNOS phosphorylation pathway seems not to be the primary molecular mechanism.
(C)2009The American College of Sports Medicine]]></description>
      <pubDate>12/1/2009 12:00:00 AM</pubDate>
      <guid isPermaLink="false">00005768-200912000-00004</guid>
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      <link>http://journals.lww.com/acsm-msse/Fulltext/2009/12000/Effects_of_Stride_Length_and_Running_Mileage_on_a.10.aspx</link>
      <author>EDWARDS, W. BRENT; TAYLOR, DAVID; RUDOLPHI, THOMAS J.; GILLETTE, JASON C.; DERRICK, TIMOTHY R.</author>
      <category>Applied Sciences</category>
      <title><![CDATA[Effects of Stride Length and Running Mileage on a Probabilistic Stress Fracture Model]]></title>
      <description><![CDATA[The fatigue life of bone is inversely related to strain magnitude. Decreasing stride length is a potential mechanism of strain reduction during running. If stride length is decreased, the number of loading cycles will increase for a given mileage. It is unclear if increased loading cycles are detrimental to skeletal health despite reductions in strain.
Purpose: To determine the effects of stride length and running mileage on the probability of tibial stress fracture.
Methods: Ten male subjects ran overground at their preferred running velocity during two conditions: preferred stride length and 10% reduction in preferred stride length. Force platform and kinematic data were collected concurrently. A combination of experimental and musculoskeletal modeling techniques was used to determine joint contact forces acting on the distal tibia. Peak instantaneous joint contact forces served as inputs to a finite element model to estimate tibial strains during stance. Stress fracture probability for stride length conditions and three running mileages (3, 5, and 7 miles[middle dot]d-1) were determined using a probabilistic model of bone damage, repair, and adaptation. Differences in stress fracture probability were compared between conditions using a 2 x 3 repeated-measures ANOVA.
Results: The main effects of stride length (P = 0.017) and running mileage (P = 0.001) were significant. Reducing stride length decreased the probability of stress fracture by 3% to 6%. Increasing running mileage increased the probability of stress fracture by 4% to 10%.
Conclusions: Results suggest that strain magnitude plays a more important role in stress fracture development than the total number of loading cycles. Runners wishing to decrease their probability for tibial stress fracture may benefit from a 10% reduction in stride length.
(C)2009The American College of Sports Medicine]]></description>
      <pubDate>12/1/2009 12:00:00 AM</pubDate>
      <guid isPermaLink="false">00005768-200912000-00010</guid>
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