Carvedilol reduces exercise‐induced hyperventilation: A benefit in normoxia and a problem with hypoxia

Agostoni, Piergiuseppe; Contini, Mauro; Magini, Alessandra; Apostolo, Anna; Cattadori, Gaia; Bussotti, Maurizio; Veglia, Fabrizio; Andreini, Daniele; Palermo, Pietro

doi:10.1016/j.ejheart.2006.02.001

Cited by 55 publications

(54 citation statements)

References 37 publications

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“…This did not translate into improved exercise capacity; however, it did not result in any adverse effect nor in a reduction of physical performance. This is at variance from other antihypertensive drugs suggested to be used at altitude, such as some beta blockers, that may have a negative impact on ventilatory control and exercise capacity in hypoxic conditions 25, 26, 27. Moreover, the slope of the VO 2 /work relationship was unaffected by high altitude (3260 m) both in the active treatment group and in the placebo group, suggesting that during effort, compensatory mechanisms allow oxygen delivery to muscles to remain stable.…”

Section: Discussionmentioning

confidence: 89%

Upward Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

Caravita

Faini

Baratto

et al. 2018

JAHA

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BackgroundAcute exposure to high‐altitude hypobaric hypoxia induces a blood pressure rise in hypertensive humans, both at rest and during exercise. It is unclear whether this phenomenon reflects specific blood pressure hyperreactivity or rather an upward shift of blood pressure levels. We aimed at evaluating the extent and rate of blood pressure rise during exercise in hypertensive subjects acutely exposed to high altitude, and how these alterations can be counterbalanced by antihypertensive treatment.Methods and ResultsFifty‐five subjects with mild hypertension, double‐blindly randomized to placebo or to a fixed‐dose combination of an angiotensin‐receptor blocker (telmisartan 80 mg) and a calcium‐channel blocker (nifedipine slow release 30 mg), performed a cardiopulmonary exercise test at sea level and after the first night's stay at 3260 m altitude. High‐altitude exposure caused both an 8 mm Hg upward shift (P<0.01) and a 0.4 mm Hg/mL/kg per minute steepening (P<0.05) of the systolic blood pressure/oxygen consumption relationship during exercise, independent of treatment. Telmisartan/nifedipine did not modify blood pressure reactivity to exercise (blood pressure/oxygen consumption slope), but downward shifted (P<0.001) the relationship between systolic blood pressure and oxygen consumption by 26 mm Hg, both at sea level and at altitude. Muscle oxygen delivery was not influenced by altitude exposure but was higher on telmisartan/nifedipine than on placebo (P<0.01).ConclusionsIn hypertensive subjects exposed to high altitude, we observed a hypoxia‐driven upward shift and steepening of the blood pressure response to exercise. The effect of the combination of telmisartan/nifedipine slow release outweighed these changes and was associated with better muscle oxygen delivery.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01830530.

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Section: Discussionmentioning

confidence: 89%

Upward Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

Caravita

Faini

Baratto

et al. 2018

JAHA

Self Cite

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“…Pulmonary function may also be impaired. 109 Treatment with ␤-blockers reduces exercise-induced hyperventilation in hypoxia 110 and is associated with a fall in PaO 2 .…”

Section: Pathophysiologymentioning

confidence: 99%

Effect of Altitude on the Heart and the Lungs

2007

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T his review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the highaltitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. Effects of Exposure to High Altitude on the Normal Cardiovascular System CirculationThe major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors. 1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues 2,3 ; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs of the tissue. These mechanisms may decrease with prolonged stay at high altitude when oxygen content of the blood increases because of ventilatory acclimatization, an increase in hematocrit associated with plasma volume reduction, and an increase in red blood cell mass due to erythropoiesis.Peripheral chemoreceptor afferent activity rises hyperbolically as hypoxia increases. 4 Ventilation and sympathetic activity are augmented, as demonstrated by increased urinary and plasma concentration of catecholamines 5 and skeletal muscle sympathetic activity. 6 With exposure over days to weeks, the sensitivity of the peripheral chemoreceptors to hypoxia increases, leading to further enhancement of ventilation (ventilatory acclimatization). This presumably also accounts for the further increase of sympathetic activity documented by microneurography after 3 weeks at 5200 m 6 and elevated catecholamines in urine and plasma. 5 As shown in Figure 1, there is antagonism between the direct effects of hypoxia on the resistance vessels ...

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“…This is at variance from other antihypertensive drugs suggested to be used at altitude, such as some beta blockers, that may have a negative impact on ventilatory control and exercise capacity in hypoxic conditions. [25][26][27] Moreover, the slope of the VO 2 /work relationship was unaffected by high altitude (3260 m) both in the active treatment group and in the placebo group, suggesting that during effort, compensatory mechanisms allow oxygen delivery to muscles to remain stable. There are several possible compensatory mechanisms, including blood flow redistribution, increased oxygen extraction, and increased cardiac output for a given work rate.…”

mentioning

confidence: 87%

Upward-Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

Baratto

Caravita

Faini

et al. 2018

Journal of Hypertension

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Background--Acute exposure to high-altitude hypobaric hypoxia induces a blood pressure rise in hypertensive humans, both at rest and during exercise. It is unclear whether this phenomenon reflects specific blood pressure hyperreactivity or rather an upward shift of blood pressure levels. We aimed at evaluating the extent and rate of blood pressure rise during exercise in hypertensive subjects acutely exposed to high altitude, and how these alterations can be counterbalanced by antihypertensive treatment.Methods and Results--Fifty-five subjects with mild hypertension, double-blindly randomized to placebo or to a fixed-dose combination of an angiotensin-receptor blocker (telmisartan 80 mg) and a calcium-channel blocker (nifedipine slow release 30 mg), performed a cardiopulmonary exercise test at sea level and after the first night's stay at 3260 m altitude. High-altitude exposure caused both an 8 mm Hg upward shift (P<0.01) and a 0.4 mm Hg/mL/kg per minute steepening (P<0.05) of the systolic blood pressure/oxygen consumption relationship during exercise, independent of treatment. Telmisartan/nifedipine did not modify blood pressure reactivity to exercise (blood pressure/oxygen consumption slope), but downward shifted (P<0.001) the relationship between systolic blood pressure and oxygen consumption by 26 mm Hg, both at sea level and at altitude. Muscle oxygen delivery was not influenced by altitude exposure but was higher on telmisartan/nifedipine than on placebo (P<0.01).Conclusions--In hypertensive subjects exposed to high altitude, we observed a hypoxia-driven upward shift and steepening of the blood pressure response to exercise. The effect of the combination of telmisartan/nifedipine slow release outweighed these changes and was associated with better muscle oxygen delivery. In previous articles, we demonstrated that acute exposure to high-altitude hypobaric hypoxia induces a blood pressure (BP) rise in subjects with hypertension, both at rest over the 24 hours and during exercise, 1-3 likely through chemoreflex-induced sympathetic activation.4-6 Moreover, we also showed that the combination treatment with telmisartan and sustained-release formulation of nifedipine gastrointestinal therapeutic system formulation (GITS) is able to lower BP levels during exercise not only at sea level but also at high altitude, as compared with placebo. However, we previously Indeed, it is a common experience that a given task (eg, climbing stairs, which may correspond to a given workload) may engender extremely different responses in terms of dyspnea, fatigue, or palpitations when conducted either at sea level or at high altitude. For these reasons, in a previous report of ours, we also tried to normalize BP for oxygen consumption (VO 2 ), the latter being acknowledged as a more precise indicator of cardiac output and metabolic needs imposed by exercise than is the measure of workload. However, we assessed this ratio only at peak exercise and not dynamically throughout the different exercise steps. Thus, it remains debated whe...

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Carvedilol reduces exercise‐induced hyperventilation: A benefit in normoxia and a problem with hypoxia

Cited by 55 publications

References 37 publications

Upward Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

Upward Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

Effect of Altitude on the Heart and the Lungs

Upward-Shift and Steepening of the Blood Pressure Response to Exercise in Hypertensive Subjects at High Altitude

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