The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

Ferretti, Guido; Licker, Marc; Anchisi, Sara; Moia, Christian; Суста, Давиде; Morel, Denis R.

doi:10.1007/s00421-005-1393-5

Cited by 11 publications

(13 citation statements)

References 39 publications

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“…At rest, in which there is predominant vagal control of heart rate (Fagraeus and Linnarsson 1976;Lador et al 2006;Malliani et al 1991;Perini and Veicsteinas 2003), the data lie below those obtained at exercise, compatibly with a lower _ Q vO 2 value. This agrees with previous observations, both during cycling (Anchisi et al 2001;Ferretti et al 2005) and during two-legged knee extension exercise (Koskolou et al 1997;Roach et al 1999). In Fig.…”

Section: The Cardiovascular Responses To Exercisesupporting

confidence: 92%

“…This implies that the vertical difference between the two lines, corresponding to the oxygen flow in mixed venous blood ( _ Q vO 2 ), is a constant, independent of _ Q and _ V O 2 , and thus of the exercise intensity. Later, _ Q vO 2 was found to depend SaO 2 (Anchisi et al 2001) and on the activation state of the autonomic nervous system (Ferretti et al 2005).…”

Section: The Cardiovascular Responses To Exercisementioning

confidence: 98%

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Aerobic Metabolism and the Steady-State Concept

Ferretti

2015

Energetics of Muscular Exercise

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This chapter contains an analysis of the steady-state concept, as it is applied during light exercise. In this case, oxygen consumption increases upon exercise onset to attain a steady level, which can be maintained for a long period of time. The steady-state oxygen consumption is proportional to the exerted mechanical power. Under these circumstances, there is neither accumulation of lactate in blood nor changes in muscle phosphocreatine concentration: aerobic metabolism sustains the entire energy requirement of the exercising body. Once the steady state has been attained, the flow of oxygen is the same at all levels along the respiratory system. The quantitative relations determining the flow of oxygen across the alveoli and in blood are discussed. Special attention is given to the effects of ventilation-perfusion inequality and to the diffusion-perfusion interaction equations. The cardiovascular responses at exercise steady state are analysed in the context of the equilibrium between systemic oxygen delivery and systemic oxygen return. The relationship between oxygen consumption and power is discussed, along with the distinction between external and internal work during cycling. The concepts of mechanical efficiency of exercise and energy cost of locomotion are analysed. Concerning the latter, the distinction between aerodynamic work and frictional work is introduced. The roles of the cross-sectional surface area on the frontal plane and of air density in aerodynamic work are discussed. To end with, an equation linking ventilation, circulation and metabolism at exercise in a tight manner is developed, around the notion that the homeostasis of the respiratory system at exercise is maintained around given values of the constant oxygen return. This equation tells that, as long as we are during steady-state exercise in normoxia, any increase in the exercise metabolic rate requires an increase in ventilation that is proportional to that in oxygen consumption only if the pulmonary respiratory quotient stays invariant does not change, and an increase in cardiac output that is not proportional to the corresponding increase in oxygen consumption. At intense exercise, when lactate accumulation also occurs and hyperventilation superimposes, a new steady state would be attained only at P A CO 2 values lower than 40 mmHg: the homeostasis of the respiratory system would be modified. This new steady state, however, is never attained in fact, for reasons that are discussed in Chap. 3.

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Section: The Cardiovascular Responses To Exercisesupporting

confidence: 92%

Section: The Cardiovascular Responses To Exercisementioning

confidence: 98%

Aerobic Metabolism and the Steady-State Concept

Ferretti

2015

Energetics of Muscular Exercise

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“…HR during exercise in hypoxia was higher compared with that in normoxia (Ferretti et al 2005;Leuenberger et al 2005;Boussuges et al 2000;Hopkins et al 2003). Hypoxia-induced sympathetic activation is a …”

Section: Discussionmentioning

confidence: 83%

“…Normoxia Hypoxia possible explanation for this HR elevation (Ferretti et al 2005). The hypoxia-induced higher HR during exercise shortens the diastolic cardiac function time interval and hence the time in which LV Wlling might occur (Gledhill et al 1994).…”

Section: Sv (Ml)mentioning

confidence: 98%

The effect of acute hypoxia on left ventricular function during exercise

Yan

et al. 2007

Eur J Appl Physiol

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The eVect of acute hypoxia on the human left ventricular function during exercise was evaluated by 2D and Doppler echocardiography on 11 healthy male college students. Each subject completed 6-min moderate intensity (100 W) supine cycling exercises in normoxia and hypoxia, respectively. The concentration of inspired O 2 was adjusted to keep arterial hemoglobin O 2 concentration (SpO 2 ) at 88-92% during hypoxia. Doppler indices obtained were compared between normoxia and hypoxia. The left ventricular myocardial diastolic function was increased during exercise in hypoxia compared with normoxia. The peak velocity of early Wlling wave increased at rest (P < 0.05) and during exercise (P < 0.05 at second minute, and P < 0.01 at sixth minute) in hypoxia. The heart rate (P < 0.01) and cardiac output (P < 0.001) were elevated markedly at rest during hypoxia. The left ventricular systolic function variables, such as stroke volume, ejection fraction, and end-systolic volume were relatively unaltered during hypoxia compared with normoxia. The results suggest that acute hypoxia increases the left ventricular myocardial diastolic function during moderate intensity supine cycling exercise without aVecting the systolic function.

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“…A potential explanation is that beta‐blockade reduces cardiovascular compensation during exercise resulting in reduced oxygen delivery when the respiratory system is impaired. This is supported by evidence that beta‐blockade exaggerates exercise‐induced oxygen desaturation at altitude and reduces cardiovascular oxygen flow in hypoxia 32,33 . It has been postulated that there is beta‐adrenoceptor‐mediated vasodilation in hypoxic exercise states and that blockade of these receptors may lead to significant tissue hypoxia 34 .…”

Section: Discussionmentioning

confidence: 94%