Non-invasive cardiac output evaluation during a maximal progressive exercise test, using a new impedance cardiograph device

Richard, Ruddy; Lonsdorfer‐Wolf, Evelyne; Charloux, Anne; Doutreleau, Stéphane; Buchheit, Martin; Oswald‐Mammosser, Monique; Lampert, Eliane; Mettauer, Bertrand; Gény, Bernard; Lonsdorfer, J.

doi:10.1007/s004210100458

Cited by 218 publications

(180 citation statements)

References 9 publications

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“…Stroke volume was measured by bioimpedance, whereas heart rate was simultaneously estimated from the electrocardiogram first derivative (Manatec type PF05L1; Physio Flow, Paris, France). The accuracy of this bioimpedance device has previously been established against the direct Fick method during maximal incremental exercise in healthy subjects (36). Calibration of the impedance device was done using a procedure based on 24 consecutive heartbeats recorded with the subject resting on the ergometer (10).…”

Section: Methodsmentioning

confidence: 99%

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

Ponsot

Dufour

Doutreleau

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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This study investigates the role of central vs. peripheral factors in the limitation of maximal oxygen uptake (V O2max) with moderate hypoxia [inspired fraction (FI O 2 ) ϭ14.5%]. Fifteen endurance-trained athletes performed maximal cycle incremental tests to assess V O2max, maximal cardiac output (Q max), and maximal arteriovenous oxygen (a-vO2) difference in normoxia and hypoxia. Muscle biopsies of vastus lateralis were taken 1 wk before the cycling tests to evaluate maximal muscle oxidative capacity (V max) and sensitivity of mitochondrial respiration to ADP (Km) on permeabilized muscle fibers in situ. Those athletes exhibiting the largest reduction of V O2max in moderate hypoxia (Severe Loss group: Ϫ18 Ϯ 2%) suffered from significant reductions in Q max (Ϫ4 Ϯ 1%) and maximal a-vO2 difference (Ϫ14 Ϯ 2%). Athletes who well tolerated hypoxia, as attested by a significantly smaller drop of V O2max with hypoxia (Moderate Loss group: Ϫ7 Ϯ 1%), also display a blunted Q max (Ϫ9 Ϯ 2%) but, conversely, were able to maintain maximal a-vO 2 difference (ϩ1 Ϯ 2%). Though V max was similar in the two experimental groups, the smallest reduction of V O2max with moderate hypoxia was observed in those athletes presenting the lowest apparent Km for ADP in the presence of creatine (KmϩCr). In already-trained athletes with high muscular oxidative capacities, the qualitative, rather than quantitative, aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising at low FIO 2 , presumably through the functional coupling between the mitochondrial creatine kinase and ATP production. This study suggests a potential role for peripheral factors, including the alteration of cellular homeostasis in active muscles, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.exercise; cardiac output HYPOXIC ENVIRONMENTS HAVE repeatedly been observed to depress maximal oxygen uptake (V O 2max ) during whole body exercise in humans, and the magnitude of this reduction is thought to be proportional to the hypoxia-induced diminution of arterial oxygen content (15). Although this phenomenon is well described, a wide interindividual variability in the magnitude of reduction of V O 2max at a given level of hypoxia has been reported by several laboratories (8,14,28,31,37). Of note is the observation that the hypoxia-induced reduction in V O 2max is greater in endurance athletes than in sedentary subjects (28). However, the mechanisms involved in the fitness-specific limitation of maximal aerobic metabolism with moderate hypoxia [inspired fraction (FI O 2 ) ϭ ϳ14.5% or 2,000 -3,000 m] remain unclear, as changes in oxygen extraction may play a role to maintain arteriovenous oxygen (a-vO 2 ) difference and aerobic power. For instance, despite being the two determinants of V O 2max during whole body exercise in athletes, little is known about the respective contribution of cardiac output (Q ) and a-vO 2 difference in the individual hypoxia tolerance, especially within a hom...

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Section: Methodsmentioning

confidence: 99%

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

Ponsot

Dufour

Doutreleau

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Stroke volume (SV) was estimated beat by beat by impedence cardiography (Physio Flow, Manatec, Paris, France) (33). The accuracy of this device has been previously evaluated during incremental exercise in healthy subjects against the direct Fick method (33); in that study, the correlation coefficient between the two methods was r ϭ 0.946 (P Ͻ 0.01), and the mean difference was equal to Ϫ2.78 Ϯ 12.33% (2 SD). Overall, the accuracy of this method can be considered "acceptable" for the purpose of the study, which is to demonstrate that the cardiac involvement during KE was not "maximal" also at peak exercise (as confirmed also from HR measurements).…”

Section: Measurementsmentioning

confidence: 99%

Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training

Salvadego

Domenis

Lazzer

et al. 2013

Journal of Applied Physiology

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Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA; body mass 102.6 Ϯ 7.3 kg, mean Ϯ SD) and 11 controls (CTRL; body mass 77.8 Ϯ 6.0 kg). Pulmonary O2 uptake (V O2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross-sectional area, volume (determined by magnetic resonance imaging), and strength were greater in RTA vs. CTRL (by ϳ40%, ϳ33%, and ϳ20%, respectively). V O2peak during CE was higher in RTA vs. CTRL (4.05 Ϯ 0.64 vs. 3.56 Ϯ 0.30 l/min); no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE), V O2 peak was lower (by 15-20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, during both CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.7 Ϯ 23.7 pmol O2·s Ϫ1 ·mg Ϫ1 ww) vs. CTRL (35.7 Ϯ 10.2 pmol O2·s Ϫ1 ·mg Ϫ1 ww) and a tighter coupling of oxidative phosphorylation. In RTA, the greater muscle mass and maximal force and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise and unchanged efficiency and O 2 cost at submaximal exercise, despite a much greater body mass. skeletal muscle hypertrophy; mitochondrial respiration; oxidative metabolism during exercise RESISTANCE TRAINING PROGRAMS have been developed with the aim of improving variables of muscle function such as strength, power, speed, local muscular endurance, coordination, and flexibility (21). Resistance training is now considered an important part of training and rehabilitation programs for healthy subjects and for various types of patients, such as cardiac patients (45), patients with pulmonary diseases (10), patients undergoing prolonged bed-rest periods (2), or elderly subjects (28). In these populations, the combination of resistance training with the more conventional endurance exercise improves the patients' outcomes and quality of life (45).An increase in the cross-sectional area of skeletal muscle fibers and a shift of fiber-type distribution toward type 2 fibers are typical adaptations induced by resistance training; these adaptations enhance the muscle force-generating potential (12) but could represent an impairment to skeletal muscle oxidative metabolism. On the other hand, muscles with higher maximal force would need to recruit a lower number of motor units, and therefore more oxidative (and more efficient) muscle fibers (20,26). According to other authors, strength training may increas...

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“…The algorithm that is used does not require basal thoracic impedance measurement or the estimation of blood resistivity and the position of the electrodes is not critical for the accuracy of the measurements. Previous studies showed that Physioflow provides accurate cardiac output measurements during steady-state and maximal exercise in healthy subjects (8,34). However, in patients with chronic obstructive pulmonary disease (COPD), cardiac output was systematically overestimated (7).…”

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confidence: 99%

Evaluation of two methods for continuous cardiac output assessment during exercise in chronic heart failure patients

Kemps¹,

Thijssen²,

Schep³

et al. 2008

Journal of Applied Physiology

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Non-invasive cardiac output evaluation during a maximal progressive exercise test, using a new impedance cardiograph device

Cited by 218 publications

References 9 publications

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

Impairment of maximal aerobic power with moderate hypoxia in endurance athletes: do skeletal muscle mitochondria play a role?

Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training

Evaluation of two methods for continuous cardiac output assessment during exercise in chronic heart failure patients

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