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      Cardio-Respiratory Reference Data in 4631 Healthy Men and Women 20-90 Years: The HUNT 3 Fitness Study

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          Abstract

          Purpose

          To provide a large reference material on key cardio-respiratory variables in a healthy population of Norwegian men and women aged 20–90 years.

          Methods

          Sub maximal and peak levels of cardio-respiratory variables were measured using cardiopulmonary exercise testing during treadmill running.

          Results

          The highest peak ventilation among men (141.9±24.5 L·min −1) and women (92.0±16.5 L·min −1) was observed in the youngest age group (20–29 years, sex differences p<0.001) with an average 7% reduction per decade. The highest tidal volumes were observed in the 30–39 and 40–49 year age groups among men (2.94±0.46 L) and women (2.06±0.32 L) (sex differences p<0.001), with a subsequent average 6% reduction per decade. Ventilatory threshold and respiratory compensation point were observed at approximately 77% and 87% of peak oxygen uptake (VO 2peak) among men and women, respectively. The best ventilatory efficiency (EqVCO 2Than) was observed in the youngest age group (20–29 years) in both men (26.2±2.8) and woman (27.5±2.7) (sex differences p<0.001) with an average 3% deterioration in ventilatory efficiency per decade.

          Conclusion

          This is the largest European reference material of cardio-respiratory variables in healthy men and women aged 20–90 years, establishing normal values for, and associations between key cardio-respiratory parameters. This will be useful in clinical decision making when evaluating cardiopulmonary health in similar populations.

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          Most cited references58

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          Normal standards for an incremental progressive cycle ergometer test.

          One hundred healthy subjects (50 male and 50 female), selected to provide an even distribution of age (15 to 71 yr) and height (165 to 194 cm in males and 152 to 176 cm in females), underwent a progressively incremental (100 kpm/min each min) exercise test to a symptom-limited maximum. Measurements were made of O2 intake and CO2 output, ventilation and breathing pattern, heart rate and blood pressure, and rating of perceived exertion. The ventilatory anaerobic threshold was identified. Predictive data were derived for measurements at maximal and submaximal exercise. Maximal power output (Wmax) and oxygen intake (VO2max) varied with sex (0, male; 1, female), age (yr), and height (Ht, cm): Wmax = 20.4 (Ht) - 8.74 (Age) - 288 (Sex) - 1,909 kpm/min (SEE, 216; r, 0.858); VO2max = 0.046 (Ht) - 0.021 (Age) - 0.62 (Sex) - 4.31 L/min (SEE, 0.458; r, 0.869). The extent of leisure time activity exerted a positive influence on VO2max (r, 0.47; p less than 0.001); VO2max was also related to lean thigh volume (r, 0.79). Maximal heart rate (HR) declined as a function of age: HRmax = 202 - 0.72 (Age) beats/min (SEE, 10.3; r, 0.72). Maximal O2 pulse (O2Pmax) was related to height and was systematically higher in males than in females: O2Pmax = 0.28 (Ht) - 3.3 (Sex) - 26.7 ml/beat (SEE, 2.8; r, 0.86). Ventilation was closely related to CO2 output, and the maximal tidal volume was related to vital capacity. The VO2 increased linearly with power throughout the test; in an individual subject, the intercept of this relationship was positively influenced by weight and height.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Ventilatory efficiency during exercise in healthy subjects.

            When evaluating dyspnea in patients with heart or lung disease it is useful to measure the quantity of ventilation needed to eliminate metabolically produced CO2 (i.e., the ventilatory efficiency). Mathematically, the relationship between ventilation (VE) and CO2 output is determined by the arterial CO2 pressure and the physiologic dead space-tidal volume ratio. We decided to determine how age, sex, size, fitness, and the type of ergometer influenced ventilatory efficiency in normal subjects. Three methods were compared for expressing this relationship: (1) the VE versus CO2 output slope below the ventilatory compensation point, commonly used by cardiologists for estimating the severity of heart failure; (2) the VE/CO2 output ratio at the anaerobic threshold, commonly used by pulmonologists; and (3) the lowest VE/CO2 output ratio during exercise, the latter parameter not previously reported. We studied 474 healthy adults, between 17 and 78 years of age during incremental cycle and treadmill cardiopulmonary exercise tests at three test sites, correcting the total VE for the equipment dead space. The lowest VE/CO2 output ratio was insignificantly different from the ratio at the anaerobic threshold, less variable than that for the slope relationship, and unaffected by the site, ergometer, and gas exchange measurement systems. The regression equation for the lowest VE/CO2 output ratio was 27.94 + 0.108 x age + (0.97 = F, 0.0 = M) - 0.0376 x height, where age is in years and height is in centimeters. We conclude that the lowest VE/CO2 output ratio is the preferred noninvasive method to estimate ventilatory inefficiency.
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              Exercise-induced arterial hypoxemia.

              Exercise-induced arterial hypoxemia (EIAH) at or near sea level is now recognized to occur in a significant number of fit, healthy subjects of both genders and of varying ages. Our review aims to define EIAH and to critically analyze what we currently understand, and do not understand, about its underlying mechanisms and its consequences to exercise performance. Based on the effects on maximal O(2) uptake of preventing EIAH, we suggest that mild EIAH be defined as an arterial O(2) saturation of 93-95% (or 3-4% 25-30 Torr) and inadequate compensatory hyperventilation (arterial PCO(2) >35 Torr) commonly contribute to EIAH, as do acid- and temperature-induced shifts in O(2) dissociation at any given arterial PO(2). In turn, expiratory flow limitation presents a significant mechanical constraint to exercise hyperpnea, whereas ventilation-perfusion ratio maldistribution and diffusion limitation contribute about equally to the excessive A-a DO(2). Exactly how diffusion limitation is incurred or how ventilation-perfusion ratio becomes maldistributed with heavy exercise remains unknown and controversial. Hypotheses linked to extravascular lung water accumulation or inflammatory changes in the "silent" zone of the lung's peripheral airways are in the early stages of exploration. Indirect evidence suggests that an inadequate hyperventilatory response is attributable to feedback inhibition triggered by mechanical constraints and/or reduced sensitivity to existing stimuli; but these mechanisms cannot be verified without a sensitive measure of central neural respiratory motor output. Finally, EIAH has detrimental effects on maximal O(2) uptake, but we have not yet determined the cause or even precisely identified which organ system, involved directly or indirectly with O(2) transport to muscle, is responsible for this limitation.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2014
                26 November 2014
                : 9
                : 11
                : e113884
                Affiliations
                [1 ]K.G. Jebsen Center of Exercise in Medicine at Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway
                [2 ]Valnesfjord Rehabilitation Center, Valnesfjord, Norway
                [3 ]Department of Thoracic Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
                VU University Medical Center, Netherlands
                Author notes

                Competing Interests: This study was funded in part by Roche Norway Incorporated Center. There are no disclosures to report or any conflicts of interest. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.

                Conceived and designed the experiments: UW. Performed the experiments: UW. Analyzed the data: HL SS UW. Contributed reagents/materials/analysis tools: HL SS UW. Wrote the paper: HL SS UW. Contributed substantially to design, analysis and interpretation of data, final approval of manuscript and was accountable for all aspects of the work: HL SS UW. Drafted manuscript: HL. Critical revision of manuscript for important intellectual content: SS UW. Conception and acquisition of work: UW.

                Article
                PONE-D-14-21691
                10.1371/journal.pone.0113884
                4245230
                25426954
                dab0d9fe-6df2-45a4-87a3-052e47006105
                Copyright @ 2014

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 15 May 2014
                : 31 October 2014
                Page count
                Pages: 22
                Funding
                This study was funded by K.G. Jebsen Foundation, The Norwegian Council on Cardiovascular Disease, The Research Council of Norway, Foundation for Cardiovascular Research at St. Olav's Hospital, Norwegian State Railways, Roche Norway Incorporated and Valnesfjord Rehabilitation Center. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology and Life Sciences
                Physiology
                Cardiovascular Physiology
                Physiological Parameters
                Physiological Properties
                Respiratory Physiology
                Medicine and Health Sciences
                Epidemiology
                Clinical Epidemiology
                Sports and Exercise Medicine
                Exercise
                Custom metadata
                The authors confirm that, for approved reasons, some access restrictions apply to the data underlying the findings. Data from the HUNT3 fitness study are stored at the HUNT-Research Center's databank and can be accessed by request. Contact information: Hunt Research center, Forskningsveien 2, 7600 Levanger, Norway. phone: +4774075180/+4774019240; mail: hunt@ 123456medisin.ntnu.no . Contact authors: Henrik Loe, ( henrikl@ 123456ntnu.no ); Sigurd Steinshamn ( sigurd.steinshamn@ 123456ntnu.no ); Ulrik Wisløff ( ulrik.wisloff@ 123456ntnu.no ).

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