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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 397 (1982), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1439-6327
    Keywords: Key words Fatigue ; Antioxidant enzymes ; Non-protein thiols ; Lipid peroxidation ; Oxidative stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Endurance exercise training promotes a small but significant increase in antioxidant enzyme activity in the costal diaphragm (DIA) of rodents. It is unclear if these training-induced improvements in muscle antioxidant capacity are large enough to reduce oxidative stress during prolonged contractile activity. To test the hypothesis that training-related increases in DIA antioxidant capacity reduces contraction-induced lipid peroxidation, we exercise trained adult female Sprague-Dawley (n = 7) rats on a motor-driven treadmill for 12 weeks at ≈ 75% maximal O2 consumption (90 min/day). Control animals (n = 8) remained sedentary during the same 12-week period. After training, DIA strips from animals in both experimental groups were excised and subjected to an in vitro fatigue contractile protocol in which the muscle was stimulated for 60 min at a frequency of 30 Hz, every 2 s, with a train duration of 330 m. Compared to the controls, endurance training resulted in an increase (P 〈 0.05) in diaphragmatic non-protein thiols and in the activity of the antioxidant enzyme superoxide dismutase. Following the contractile protocol, lipid peroxidation was significantly lower (P 〈 0.05) in the trained DIA compared to the controls. These data support the hypothesis that endurance exercise training-induced increases in DIA antioxidant capacity protect the muscle against contractile-related oxidative stress.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 52 (1984), S. 173-177 
    ISSN: 1439-6327
    Keywords: Anaerobic threshold ; Ventilatory threshold ; Exercise ventilation ; Gas exchange ; Blood lactate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Anaerobic threshold has been defined as the oxygen uptake ( $$\dot V_{{\text{O}}_{\text{2}} }$$ ) at which blood lactate (La) begins to rise systematically during graded exercise (Davis et al. 1982). It has become common practice in the literature to estimate the anaerobic threshold by using ventilatory and/or gas exchange alterations. However, confusion exists as to the validity of this practice. The purpose of this study was to examine the precision with which ventilatory and gas exchange techniques for determining anaerobic threshold predicted the anaerobic threshold resolved by La criteria. The anaerobic threshold was chosen using three criteria: (1) systematic increase in blood La (ATLa), (2) systematic increase in ventilatory equivalent for O2 with no change in the ventilatory equivalent for CO2 ( $${\text{AT}}_{\dot V_{\text{E}} } /\dot V_{{\text{O}}_{\text{2}} }$$ ), and (3) non-linear increase in expired ventilation graphed as a function of $$\dot V_{{\text{O}}_{\text{2}} }$$ ( $${\text{AT}}_{\dot V_{\text{E}} }$$ ). Thirteen trained male subjects performed an incremental cycle ergometer test to exhaustion in which the load was increased by 30 W every 3 minutes. Ventilation, gas exchange measures, and blood samples for La analysis were obtained every 3rd min throughout the test. In five of the thirteen subjects tested the anaerobic threshold determined by ventilatory and gas exchange alterations did not occur at the same $$\dot V_{{\text{O}}_{\text{2}} }$$ as the ATLa. The highest correlation between a gas exchange anaerobic threshold and ATLa was found for $${\text{AT}}_{\dot V_{\text{E}} } /\dot V_{{\text{O}}_{\text{2}} }$$ and was r=0.63 (P〈0.05). These data provide evidence that the ATLa and $${\text{AT}}_{\dot V_{\text{E}} }$$ do not always occur simultaneously and suggest limitations in using ventilatory or gas exchange measures to estimate the ATla.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 74 (1996), S. 391-396 
    ISSN: 1439-6327
    Keywords: Key words β(2)-Adrenoceptor agonist ; Skeletal muscle ; Fiber type ; Myosin heavy chain isoforms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This study examined the effects of 6 weeks of treatment with the β(2)-adrenoceptor agonist, clenbuterol, on the soleus muscle of adult female Sprague-Dawley rats. Animals (4 months old) were divided into two groups: clenbuterol treated (CL, n=7) (2 mg·kg–1 body mass injected subcutaneously every other day), and control (CON, n=7) (injected with isotonic saline). Post-treatment body weights were ≈5% greater in the CL group compared to CON (P〈0.05). Polyacrylamide gel electrophoresis (SDS-PAGE) of soleus myofibrillar protein indicated a clenbuterol-induced decrease (P〈0.05) in the relative percentage of type I myosin heavy chain (MHC) with a concomitant increase (P〈0.05) in type IIdx MHC, while the proportion of type IIa MHC was unaffected. ATPase fiber typing revealed increases (P〈0.05) in the proportion of type II fibers expressed both as a percentage of total fiber number and total cross-sectional area (CSA). Finally, mean type II fiber CSA was ≈25% greater (P〈0.05) in the CL groups as compared to the CON group. These data indicate that clenbuterol treatment results in alterations in the MHC phenotype and an increased proportion of type II fiber CSA in the soleus of adult rats. These observations were due to an increase in the total number of type II fibers, as well as hypertrophy of these fibers. Thus, the relative increase in the number of histochemically determined type II fibers and the emergence of the normally unexpressed type IIdx MHC isoform in the soleus suggest a clenbuterol-induced transition of muscle fiber phenotype as well as selective hypertrophy of the type II fibers.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 74 (1996), S. 391-396 
    ISSN: 1439-6327
    Keywords: β(2)-Adrenoceptor agonist ; Skeletal muscle ; Fiber type ; Myosin heavy chain isoforms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examined the effects of 6 weeks of treatment with theβ (2)-adrenoceptor agonist, clenbuterol, on the soleus muscle of adult female Sprague-Dawley rats. Animals (4 months old) were divided into two groups: clenbuterol treated (CL,n=7) (2 mg kg−1 body mass injected subcutaneously every other day), and control (CON,n=7) (injected with isotonic saline). Post-treatment body weights were ≈ 5% greater in the CL group compared to CON (P〈0.05). Polyacrylamide gel electrophoresis (SDS-PAGE) of soleus myofibrillar protein indicated a clenbuterol-induced decrease (P〈0.05) in the relative percentage of type I myosin heavy chain (MHC) with a concomitant increase (P〈0.05) in type IIdx MHC, while the proportion of type IIa MHC was unaffected. ATPase fiber typing revealed increases (P〈0.05) in the proportion of type II fibers expressed both as a percentage of total fiber number and total cross-sectional area (CSA). Finally, mean type II fiber CSA was ≈25% greater (P〈0.05) in the CL groups as compared to the CON group. These data indicate that clenbuterol treatment results in alterations in the MHC phenotype and an increased proportion of type II fiber CSA in the soleus of adult rats. These observations were due to an increase in the total number of type II fibers, as well as hypertrophy of these fibers. Thus, the relative increase in the number of histochemically determined type II fibers and the emergence of the normally unexpressed type IIdx MHC isoform in the soleus suggest a clenbuterol-induced transition of muscle fiber phenotype as well as selective hypertrophy of the type 11 fibers.
    Type of Medium: Electronic Resource
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