18 research outputs found

    Decline of oxygen uptake (VO<sub>2</sub>) relative to age.

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    <p>Mean and SD for each age group is presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0064319#pone-0064319-t002" target="_blank">Table 2</a>.</p

    Correlations between workload (Watts) and oxygen uptake (VO<sub>2</sub>) and correlations between Watts and heart rate (f<sub>c</sub>).

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    <p>Correlations between workload (Watts) and oxygen uptake (VO<sub>2</sub>) and correlations between Watts and heart rate (f<sub>c</sub>).</p

    Physical and physiological characteristics of participants in the HUNT 3 Fitness study.

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    <p>Data is presented as arithmetic mean ±SD. VO<sub>2max</sub>: maximal oxygen uptake, O<sub>2</sub> pulse: oxygen uptake per heartbeat, CO<sub>2</sub>: Carbon dioxide, R: respiratory exchange ratio, f<sub>c</sub>: cardiac frequency, workload: treadmill exercise load, BORG: subjective perception of fatigue (6–20), Physical activity index: A weighted product score between training- intensity, duration and frequency.</p

    Relationships between perceived exertion, VO<sub>2max</sub> and f<sub>cmax</sub> in the HUNT 3 fitness study.

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    <p>Borgscale: subjective perception of perceived exertion (6–20), CI: confidence interval, %f<sub>cmax</sub>: percent of maximal heart frequency, %VO<sub>2max</sub>: percent of maximal oxygen uptake.</p

    Correlations between physical activity index score and oxygen uptake (VO<sub>2</sub>).

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    <p>Correlations between physical activity index score and oxygen uptake (VO<sub>2</sub>).</p

    O<sub>2</sub>-pulse in the HUNT 3 Fitness study stratified by intensity levels, sex and age groups.

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    <p>Data is presented as arithmetic mean ± SD. O<sub>2</sub>-pulse: oxygen pulse, VO<sub>2</sub>: oxygen uptake, %f<sub>cmax</sub>: percent of maximum heart frequency, Workload: treadmill exercise load.</p

    Mitochondrial Respiration after One Session of Calf Raise Exercise in Patients with Peripheral Vascular Disease and Healthy Older Adults

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    <div><p>Purpose</p><p>Mitochondria are essential for energy production in the muscle cell and for this they are dependent upon a sufficient supply of oxygen by the circulation. Exercise training has shown to be a potent stimulus for physiological adaptations and mitochondria play a central role. Whether changes in mitochondrial respiration are seen after exercise in patients with a reduced circulation is unknown. The aim of the study was to evaluate the time course and whether one session of calf raise exercise stimulates mitochondrial respiration in the calf muscle of patients with peripheral vascular disease.</p><p>Methods</p><p>One group of patients with peripheral vascular disease (n = 11) and one group of healthy older adults (n = 11) were included. Patients performed one session of continuous calf raises followed by 5 extra repetitions after initiation of pain. Healthy older adults performed 100 continuous calf raises. Gastrocnemius muscle biopsies were collected at baseline and 15 minutes, one hour, three hours and 24 hours after one session of calf raise exercise. A multi substrate (octanoylcarnitine, malate, adp, glutamate, succinate, FCCP, rotenone) approach was used to analyze mitochondrial respiration in permeabilized fibers. Mixed-linear model for repeated measures was used for statistical analyses.</p><p>Results</p><p>Patients with peripheral vascular disease have a lower baseline respiration supported by complex I and they increase respiration supported by complex II at one hour post-exercise. Healthy older adults increase respiration supported by electron transfer flavoprotein and complex I at one hour and 24 hours post-exercise.</p><p>Conclusion</p><p>Our results indicate a shift towards mitochondrial respiration supported by complex II as being a pathophysiological component of peripheral vascular disease. Furthermore exercise stimulates mitochondrial respiration already after one session of calf raise exercise in patients with peripheral vascular disease and healthy older adults.</p><p>Trial Registration</p><p>ClinicalTrials.gov <a href="https://clinicaltrials.gov/ct2/show/NCT01842412" target="_blank">NCT01842412</a></p></div

    Effect of one session of calf raises upon mitochondrial function in patients with PVD.

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    <p><b>(A)</b>: oxphos coupling efficiency (1 - (ETF+CI)<sub>L</sub> / (ETF+CI)<sub>P</sub>) <b>(B)</b>: Excess ETS-phophorylation capacity factor (1 - (CI+CII+ETF)P / (CI+CII+ETF)<sub>E</sub>) <b>(C)</b>: complex II control factor (1 - (CI+ETF)<sub>P</sub> / (CI+CII+ETF)P)White (baseline); black (post-exercise). Values are mean and standard error of the mean, n = 11. * Significantly different from pre (P < 0.05), ** Significantly different from pre (P < 0.01), *** Significantly different from pre (P < 0.001).</p

    Mitochondrial respiration, efficiency and mitochondrial respiration per international unit of citrate synthase activity at baseline.

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    <p>Mitochondrial respiration (pmol O<sub>2</sub>/s/ mg wet weight of muscle fibers). <b>(A)</b> (ETF+CI)L is the LEAK state electron transfer through electron transferring flavoprotein (ETF) and complex I after addition of the substrates octanoylcarnitin (0.2mM) + malate (2mM), in the absence of ADP; (ETF+CI)P is fatty acid oxphos capacity after addition of ADP (2.5mM); (CI+ETF)<sub>P</sub> is electron transfer through complex I and ETF reaching complex I oxphos capacity after addition of glutamate (10mM); (CI+II+ETF)P is electron transfer through complex I, II and ETF reaching complex I and II oxphos capacity after addition of succinate (10mM) and ADP (5mM); (CI+II+ETF)E is electron transfer through complex I, II and ETF reaching ETS capacity after FCCP titrations (0.5M max. 3M) to uncouple oxidation from phosphorylation; (CII)<sub>E</sub> is ETS capacity supported by complex II after addition of rotenone (0.5M), which inhibits complex I. The subscripts L,P,E indicate the LEAK state, OXPHOS and ETS capacity <b>(B)</b> Mitochondrial efficiency at baseline: OCE: oxphos coupling efficiency (1 - (ETF+CI)<sub>L</sub> / (ETF+CI)<sub>P</sub>); EEPCF: Excess ETS-phophorylation capacity factor (1 - (CI+CII+ETF)<sub>P</sub> / (CI+CII+ETF)<sub>E</sub>), CII CF: complex II control factor (1 - (CI+ETF)<sub>P</sub> / (CI+CII+ETF)<sub>P</sub>) <b>(C)</b> Mitochondrial respiration per international unit of citrate synthase (CS). Black (patients with PVD n = 11), White (healthy older adults n = 11). Values are mean and standard error of the mean, comparison between groups, Significant differences between groups * Significantly different between groups (P < 0.05), ** Significantly different between groups (P < 0.01), *** Significantly different between groups (P < 0.001)</p
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