Phlebotomy eliminates the maximal cardiac output response to six weeks of exercise training

Bonne, Thomas Christian; Doucende, Grégory; Flück, Daniela; Jacobs, Robert A.; Nordsborg, Nikolai Baastrup; Robach, Paul; Walther, Guillaume; Lundby, Carsten

doi:10.1152/ajpregu.00028.2014

Cited by 74 publications

(111 citation statements)

References 57 publications

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“…A recent paper documented a 7% (P Ͻ 0.05) increase in BV accompanied with a 10% (P Ͻ 0.05) increased V O 2peak following 6 wk of endurance training (5). The investigators then removed, via phlebotomy, the training-induced BV and observed V O 2peak returned to a level not differing from pretraining values.…”

Section: Discussionmentioning

confidence: 96%

Peak exercise oxygen uptake during and following long-duration spaceflight

Moore

Downs

Lee

et al. 2014

Journal of Applied Physiology

104

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This investigation was designed to measure aerobic capacity (V̇o2peak) during and after long-duration International Space Station (ISS) missions. Astronauts (9 males, 5 females: 49 ± 5 yr, 77.2 ± 15.1 kg, 40.6 ± 6.4 ml·kg(-1)·min(-1) [mean ± SD]) performed peak cycle tests ∼90 days before flight, 15 days after launch, every ∼30 days in-flight, and on recovery days 1 (R + 1), R + 10, and R + 30. Expired metabolic gas fractions, ventilation, and heart rate (HR) were measured. Data were analyzed using mixed-model linear regression. The main findings of this study were that V̇o2peak decreased early in-flight (∼17%) then gradually increased during flight but never returned to preflight levels. V̇o2peak was lower on R + 1 and R + 10 than preflight but recovered by R + 30. Peak HR was not different from preflight at any time during or following flight. A sustained decrease in V̇o2peak during and/or early postflight was not a universal finding in this study, since seven astronauts were able to attain their preflight V̇o2peak levels either at some time during flight or on R + 1. Four of these astronauts performed in-flight exercise at higher intensities compared with those who experienced a decline in V̇o2peak, and three had low aerobic capacities before flight. These data indicate that, while V̇o2peak may be difficult to maintain during long-duration ISS missions, aerobic deconditioning is not an inevitable consequence of long-duration spaceflight.

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Section: Discussionmentioning

confidence: 96%

Peak exercise oxygen uptake during and following long-duration spaceflight

Moore

Downs

Lee

et al. 2014

Journal of Applied Physiology

104

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“…Studies employing acute expansion of blood volume by intravenous infusion of dextran (198,236) or albumin (115) have demonstrated that increased blood volume significantly influences cardiac performance by increasing cardiac preload, ventricular filling and stroke volume. Reestablishing blood volume to a level similar to that observed before a 6-week training intervention by phlebotomy, abolished the training-induced change in maximal cardiac output, suggesting that the training-induced change in maximal cardiac output following a short period of exercise training is a consequence of an increase in blood volume (39). Furthermore, a large part of the difference in stroke volume between trained and untrained has also been suggested to be related to differences in blood volume (198,236).…”

Section: Blood Volume Response To Exercise Trainingmentioning

confidence: 89%

Cardiovascular Adaptations to Exercise Training

Hellsten

Nyberg

2015

Comprehensive Physiology

210

185

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Aerobic exercise training leads to cardiovascular changes that markedly increase aerobic power and lead to improved endurance performance. The functionally most important adaptation is the improvement in maximal cardiac output which is the result of an enlargement in cardiac dimension, improved contractility, and an increase in blood volume, allowing for greater filling of the ventricles and a consequent larger stroke volume. In parallel with the greater maximal cardiac output, the perfusion capacity of the muscle is increased, permitting for greater oxygen delivery. To accommodate the higher aerobic demands and perfusion levels, arteries, arterioles, and capillaries adapt in structure and number. The diameters of the larger conduit and resistance arteries are increased minimizing resistance to flow as the cardiac output is distributed in the body and the wall thickness of the conduit and resistance arteries is reduced, a factor contributing to increased arterial compliance. Endurance training may also induce alterations in the vasodilator capacity, although such adaptations are more pronounced in individuals with reduced vascular function. The microvascular net increases in size within the muscle allowing for an improved capacity for oxygen extraction by the muscle through a greater area for diffusion, a shorter diffusion distance, and a longer mean transit time for the erythrocyte to pass through the smallest blood vessels. The present article addresses the effect of endurance training on systemic and peripheral cardiovascular adaptations with a focus on humans, but also covers animal data.

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“…relaxes quickly and fills to a large end-diastolic volume, but a decreased vascular resistance could also contribute (54). In healthy volunteers, the initial (6 wk) exercise training-induced increase in SV seems to be the product of increased blood volume rather than structural changes within the myocardium (9). Remarkably, 1 yr of exercise training in previously untrained individuals induced morphological adaptations similar to those observed in athletes, including augmented LV mass from 168 Ϯ 38 to 203 Ϯ 46 g; surprisingly, this did not alter Q max as much as could have been expected (from 20.1 Ϯ 5.1 to 21.9 Ϯ 5.4 l/min) since Starling and pressure/volume curves approached but did not match those of elite athletes (3).…”

Section: How and By How Muchmentioning

confidence: 99%