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      Similar pattern of change in V̇o2 kinetics, vascular function, and tissue oxygen provision following an endurance training stimulus in older and young adults

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          Abstract

          <p class="first" id="d12269981e222">The purpose of this study was to examine the time course of changes in the oxygen uptake (V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub>) kinetics response subsequent to short-term exercise training (i.e., 24, 48, 72, and 120 h posttraining) and examine the relationship with the time course of changes in microvascular [deoxygenated hemoglobin concentration ([HHb])-to-V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub> ratio ([HHb])/V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub>)] and macrovascular [flow-mediated dilation (FMD)] O <sub>2</sub> delivery to the active tissues/limbs. Seven healthy older [OA; 74 ± 6 (SD) yr] and young men (YA; 25 ± 3 yr) completed three endurance cycling exercise training sessions at 70% V̇ <span style="font-variant: small-caps">o</span> <sub>2peak</sub>. Moderate-intensity exercise on-transient V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub> (measured breath by breath) and [HHb] (measured by near-infrared spectroscopy) were modeled with a monoexponential and normalized (0–100% of response), and the [HHb])/V̇ <span style="font-variant: small-caps">o</span> <sub>2 </sub>was calculated. Ultrasound-derived FMD of the popliteal artery was assessed after 5 min of cuff occlusion. %FMD was calculated as the greatest percent change in diameter from baseline. Time constant of V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub> (τV̇ <span style="font-variant: small-caps">o</span> <sub>2</sub>) was significantly reduced in both OA (~18%) and YA (~23%) at 24 h ( <i>P</i> &lt; 0.001) posttraining and remained decreased at 48 h before returning toward pretraining (PRE) values. Both groups showed a significant decrease in the [HHb])/V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub> at 24, 48, and 72 h ( <i>P</i> = 0.001, 0.01, and 0.03, respectively) posttraining before returning toward PRE values at 120 h. %FMD followed a similar time course to that of changes in the [HHb])/V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub>, being significantly greater in both OA (by ~64%) and YA (by ~26%) at 24 h ( <i>P</i> &lt; 0.001), remaining increased at 48 and 72 h ( <i>P</i> = 0.02 and 0.03, respectively), and returning toward PRE values at 120 h. These data suggest the rate of adjustment of V̇ <span style="font-variant: small-caps">o</span> <sub>2</sub> may be constrained by O <sub>2</sub> availability in the active tissues. </p>

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          Decline in skeletal muscle mitochondrial function with aging in humans.

          Cumulative mtDNA damage occurs in aging animals, and mtDNA mutations are reported to accelerate aging in mice. We determined whether aging results in increased DNA oxidative damage and reduced mtDNA abundance and mitochondrial function in skeletal muscle of human subjects. Studies performed in 146 healthy men and women aged 18-89 yr demonstrated that mtDNA and mRNA abundance and mitochondrial ATP production all declined with advancing age. Abundance of mtDNA was positively related to mitochondrial ATP production rate, which in turn, was closely associated with aerobic capacity and glucose tolerance. The content of several mitochondrial proteins was reduced in older muscles, whereas the level of the oxidative DNA lesion, 8-oxo-deoxyguanosine, was increased, supporting the oxidative damage theory of aging. These results demonstrate that age-related muscle mitochondrial dysfunction is related to reduced mtDNA and muscle functional changes that are common in the elderly.
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            Effect of interbreath fluctuations on characterizing exercise gas exchange kinetics.

            Breathing has inherent irregularities that produce breath-to-breath fluctuations ("noise") in pulmonary gas exchange. These impair the precision of characterizing nonsteady-state gas exchange kinetics during exercise. We quantified the effects of this noise on the confidence of estimating kinetic parameters of the underlying physiological responses and hence of model discrimination. Five subjects each performed eight transitions from 0 to 100 W on a cycle ergometer. Ventilation, CO2 output, and O2 uptake were computed breath by breath. The eight responses were interpolated uniformly, time aligned, and averaged for each subject; and the kinetic parameters of a first-order model (i.e., the time constant and time delay) were then estimated using three methods: linear least squares, nonlinear least squares, and maximum likelihood. The breath-by-breath noise approximated an uncorrelated Gaussian stochastic process, with a standard deviation that was largely independent of metabolic rate. An expression has therefore been derived for the number of square-wave repetitions required for a specified parameter confidence using methods b and c; method a being less appropriate for parameter estimation of noisy gas exchange kinetics.
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              Influence of repeated sprint training on pulmonary O2 uptake and muscle deoxygenation kinetics in humans.

              We hypothesized that a short-term training program involving repeated all-out sprint training (RST) would be more effective than work-matched, low-intensity endurance training (ET) in enhancing the kinetics of oxygen uptake (Vo(2)) and muscle deoxygenation {deoxyhemoglobin concentration ([HHb])} following the onset of exercise. Twenty-four recreationally active subjects (15 men, mean +/- SD: age 21 +/- 4 yr, height 173 +/- 9 cm, body mass 71 +/- 11 kg) were allocated to one of three groups: RST, which completed six sessions of four to seven 30-s RSTs; ET, which completed six sessions of work-matched, moderate-intensity cycling; and a control group (CON). All subjects completed moderate-intensity and severe-intensity "step" exercise transitions before (Pre) and after the 2-wk intervention period (Post). Following RST, [HHb] kinetics were speeded, and the amplitude of the [HHb] response was increased during both moderate and severe exercise (P < 0.05); the phase II Vo(2) kinetics were accelerated for both moderate (Pre: 28 +/- 8, Post: 21 +/- 8 s; P < 0.01) and severe (Pre: 29 +/- 5, Post: 23 +/- 5 s; P < 0.05) exercise; the amplitude of the Vo(2) slow component was reduced (Pre: 0.52 +/- 0.19, Post: 0.40 +/- 0.17 l/min; P < 0.01); and exercise tolerance during severe exercise was improved by 53% (Pre: 700 +/- 234, Post: 1,074 +/- 431 s; P < 0.01). None of these parameters was significantly altered in the ET and CON groups. Six sessions of RST, but not ET, resulted in changes in [HHb] kinetics consistent with enhanced fractional muscle O(2) extraction, faster Vo(2) kinetics, and an increased tolerance to high-intensity exercise.
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                Author and article information

                Journal
                American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
                American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
                American Physiological Society
                0363-6119
                1522-1490
                April 2017
                April 2017
                : 312
                : 4
                : R467-R476
                Affiliations
                [1 ]Canadian Centre for Activity and Aging, London, Ontario, Canada;
                [2 ]School of Kinesiology, The University of Western Ontario, London, Ontario, Canada; and
                [3 ]Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada
                Article
                10.1152/ajpregu.00399.2016
                5407081
                28122720
                ba5db8a6-774b-4c39-b024-033f10772dd1
                © 2017
                History

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