Effects of Beta-Blockade on Exercise Performance at High Altitude

Summary Aims Exposure to high altitude (HA) hypoxia decreases exercise performance in healthy subjects. Although β-blockers are known to affect exercise capacity in normoxia, no data are available comparing selective and nonselective β-adrenergic blockade on exercise performance in healthy subjects acutely exposed to HA hypoxia. We compared the impact of nebivolol and carvedilol on exercise capacity in healthy subjects acutely exposed to HA hypobaric hypoxia. Methods In this double-blind, placebo-controlled trial, 27 healthy untrained sea-level (SL) residents (15 males, age 38.3 ± 12.8 years) were randomized to placebo (n = 9), carvedilol 25 mg b.i.d. (n = 9), or nebivolol 5 mg o.d. (n = 9). Primary endpoints were measures of exercise performance evaluated by cardiopulmonary exercise testing at sea level without treatment, and after at least 3 weeks of treatment, both at SL and shortly after arrival at HA (4559 m). Results HA hypoxia significantly decreased resting and peak oxygen saturation, peak workload, VO2, and heart rate (HR) (P < 0.01). Changes from SL (no treatment) differed among treatments: (1) peak VO2 was better preserved with nebivolol (–22.5%) than with carvedilol (–37.6%) (P < 0.01); (2) peak HR decreased with carvedilol (–43.9 ± 11.9 beats/min) more than with nebivolol (–24.8 ± 13.6 beats/min) (P < 0.05); (3) peak minute ventilation (VE) decreased with carvedilol (–9.3%) and increased with nebivolol (+15.2%) (P= 0.053). Only peak VE changes independently predicted changes in peak VO2 at multivariate analysis (R= 0.62, P < 0.01). Conclusions Exercise performance is better preserved with nebivolol than with carvedilol under acute exposure to HA hypoxia in healthy subjects

Disappearance of isocapnic buffering period during increasing work rate exercise at high altitude

Background At sea level, ventilation kinetics are characterized during a ramp exercise by three progressively steeper slopes, the first from the beginning of exercise to anaerobic threshold, the second from anaerobic threshold to respiratory compensation point, and the third from respiratory compensation point to peak exercise. In the second ventilation phase, body CO2 stores are used to buffer acidosis owing to lactate production; it has been suggested that this extra CO2 production drives the ventilation increase. At high altitude, ventilation increases owing to hypoxia. We hypothesize that ventilation increase reduces body CO2 stores affecting ventilation kinetics during exercise. Design In eight healthy participants, we studied the ventilation kinetics during an exercise performed at sea level and at high altitude (4559 m). Methods We used 30 W/2 min step incremental protocol both at sea level and high altitude. Tests were done on a cycloergometer with breath-by-breath ventilation and inspiratory and expiratory gas measurements. We evaluated cardiopulmonary data at anaerobic threshold, respiratory compensation point, peak exercise and the VE/VCO2 slope. Results At high altitude: (a) peak Vo(2) decreased from 2595 +/- 705 to 1745 +/- 545mi/min (P < 0.001); (b) efficiency of ventilation decreased (VE/VCO2 slope from 25 +/- 2 to 38 +/- 4, P < 0.0001); (c) at each exercise step end-tidal pressure change for CO2 was lower; and (d) the isocapnic buffering period disappeared in seven over eight participants and was significantly shortened in the remaining participant. Conclusion Exercise performed at high altitude is characterized by two, instead of three, ventilation slopes

A novel wearable sensor system for multi-lead ECG measurement

This work is concerned with the development of a wireless low-power wearable system to be used for multi-lead ECG monitoring. Potential applications can range from sport and fitness to healthcare.Query The paper aims to present the architecture of the system and its performance, along with in vivo results achieved with carbon based smart textiles

Plasma adenosine and neurally mediated syncope: ready for clinical use

International audienceEither central or peripheral baroreceptor reflex abnormalities and/or alterations in neurohumoral mechanisms play a pivotal role in the genesis of neurally mediated syncope. Thus, improving our knowledge of the biochemical mechanisms underlying specific forms of neurally mediated syncope (more properly termed 'neurohumoral syncope') might allow the development of new therapies that are effective in this specific subgroup. A low-adenosine phenotype of neurohumoral syncope has recently been identified. Patients who suffer syncope without prodromes and have a normal heart display a purinergic profile which is the opposite of that observed in vasovagal syncope patients and is characterized by very low-adenosine plasma level values, low expression of A2A receptors and the predominance of the TC variant in the single nucleotide c.1364 C>T polymorphism of the A2A receptor gene. The typical mechanism of syncope is an idiopathic paroxysmal atrioventricular block or sinus bradycardia, most often followed by sinus arrest. Since patients with low plasma adenosine levels are highly susceptible to endogenous adenosine, chronic treatment of these patients with theophylline, a non-selective adenosine receptor antagonist, is expected to prevent syncopal recurrences. This hypothesis is supported by results from series of cases and from observational controlled studies

Effects of Beta-Blockade on Exercise Performance at High Altitude: A Randomized, Placebo-Controlled Trial Comparing the Efficacy of Nebivolol versus Carvedilol in Healthy Subjects

Aims Exposure to high altitude (HA) hypoxia decreases exercise performance in healthy subjects. Although beta-blockers are known to affect exercise capacity in normoxia, no data are available comparing selective and nonselective beta-adrenergic blockade on exercise performance in healthy subjects acutely exposed to HA hypoxia. We compared the impact of nebivolol and carvedilol on exercise capacity in healthy subjects acutely exposed to HA hypobaric hypoxia. Methods In this double-blind, placebo-controlled trial, 27 healthy untrained sea-level (SL) residents (15 males, age 38.3 +/- 12.8 years) were randomized to placebo (n = 9), carvedilol 25 mg b.i.d. (n = 9), or nebivolol 5 mg o.d. (n = 9). Primary endpoints were measures of exercise performance evaluated by cardiopulmonary exercise testing at sea level without treatment, and after at least 3 weeks of treatment, both at SL and shortly after arrival at HA (4559 m). Results HA hypoxia significantly decreased resting and peak oxygen saturation, peak workload, VO2, and heart rate (HR) (P < 0.01). Changes from SL (no treatment) differed among treatments: (1) peak VO2 was better preserved with nebivolol (22.5%) than with carvedilol (37.6%) (P < 0.01); (2) peak HR decreased with carvedilol (43.9 +/- 11.9 beats/min) more than with nebivolol (24.8 +/- 13.6 beats/min) (P < 0.05); (3) peak minute ventilation (VE) decreased with carvedilol (9.3%) and increased with nebivolol (+15.2%) (P= 0.053). Only peak VE changes independently predicted changes in peak VO2 at multivariate analysis (R= 0.62, P < 0.01). Conclusions Exercise performance is better preserved with nebivolol than with carvedilol under acute exposure to HA hypoxia in healthy subjects

Study variables assessed at high altitude in baseline condition, after 15 minutes of slow breathing exercise and after 5 and 30 minutes of recovery.

<p>Data are separately shown for Study A and B.</p>*<p>-p<0.05, **-p<0.01, ***, p<0.001 vs. baseline; † - p<0.05, †† - p<0.01, †††, p<0.001 vs. slow breathing.</p><p>Sp_O2, blood oxygen saturation; p_tO2– transcutaneous oxygen partial pressure; pt_CO2– transcutaneous CO₂ partial pressure; Et_CO2– end tidal CO₂ pressure in the exhaled air; SBP – systolic blood pressure; DBP – diastolic blood pressure; PP – pulse pressure; HR – heart rate; sPAP – systolic pulmonary artery pressure; RF – respiratory frequency; Vt – tidal volume; VE – minute ventilation; VA – alveolar volume; Dl_CO - pulmonary CO diffusion; TFC – thoracic fluid content.</p

Schematic representation of the sequence of data collection in studies A and B.

<p>Sp_O2, blood oxygen saturation; Pt_O2, transcutaneous oxygen partial pressure; Pt_CO2, transcutaneous CO₂ partial pressure; HR, heart rate; BP, blood pressure; RF, respiratory frequency; PAP, pulmonary artery pressure; Vt, tidal volume; VE, minute ventilation; Dl_CO, pulmonary CO diffusion; VA = alveolar volume; TFC, thoracic fluid content; Pet_CO2, end tidal CO₂ pressure in the exhaled air.</p