Ventilatory and cardiac responses to hypoxia at submaximal exercise are independent of altitude and exercise intensity

2012 ◽  
Vol 112 (4) ◽  
pp. 566-570 ◽  
Author(s):  
François J. Lhuissier ◽  
Maxime Brumm ◽  
Didier Ramier ◽  
Jean-Paul Richalet

The hypoxic exercise test combining a 4,800-m simulated altitude and a cycloergometer exercise at 30% of normoxic maximal aerobic power (MAP) is used to evaluate the individual chemosensitivity to hypoxia in submaximal exercise conditions. This test allows the calculation of three main parameters: the decrease in arterial oxygen saturation induced by hypoxia at exercise (ΔSae) and the ventilatory (HVRe) and cardiac (HCRe) responses to hypoxia at exercise. The aim of this study was to determine the influence of altitude and exercise intensity on the values of ΔSae, HVRe, and HCRe. Nine subjects performed hypoxic tests at three simulated altitudes (3,000 m, 4,000 m, and 4,800 m) and three exercise intensities (20%, 30%, and 40% MAP). ΔSae increased with altitude and was higher for 40% MAP than for 20% or 30% ( P < 0.05). For a constant heart rate, the loss in power output induced by hypoxia, relative to ΔSae, was independent of altitude (4,000–4,800 m) and of exercise intensity. HVRe and HCRe were independent of altitude (3,000–4,800 m) and exercise intensity (20%-40% MAP). Moreover, the intraindividual variability of responses to hypoxia was lower during moderate exercise than at rest ( P < 0.05 to P < 0.001). Therefore, we suggest that HVRe and HCRe are invariant parameters that can be considered as intrinsic physiological characteristics of chemosensitivity to hypoxia.

2001 ◽  
Vol 90 (4) ◽  
pp. 1431-1440 ◽  
Author(s):  
Keisho Katayama ◽  
Yasutake Sato ◽  
Yoshifumi Morotome ◽  
Norihiro Shima ◽  
Koji Ishida ◽  
...  

The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (SaO2 ) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and SaO2 during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (V˙o 2), expired minute ventilation (V˙e), and SaO2 were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2(V˙e/V˙o 2) and SaO2 during submaximal exercise. There were significant correlations among the changes in HVR at rest and inV˙e/V˙o 2 and SaO2 during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.


2002 ◽  
Vol 93 (2) ◽  
pp. 576-580 ◽  
Author(s):  
Kevin D. Monahan ◽  
Chester A. Ray

We determined the interaction between the vestibulosympathetic reflex and the arterial chemoreflex in 12 healthy subjects. Subjects performed three trials in which continuous recordings of muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP), heart rate (HR), and arterial oxygen saturation were obtained. First, in prone subjects the otolith organs were engaged by use of head-down rotation (HDR). Second, the arterial chemoreflex was activated by inspiration of hypoxic gas (10% O2 and 90% N2) for 7 min with HDR being performed during minute 6. Third, hypoxia was repeated (15 min) with HDR being performed during minute 14. HDR [means ± SE; increase (Δ)7 ± 1 bursts/min and Δ50 ± 11% for burst frequency and total MSNA, respectively; P < 0.05] and hypoxia (Δ6 ± 2 bursts/min and Δ62 ± 29%; P < 0.05) increased MSNA. Additionally, MSNA increased when HDR was performed during hypoxia (Δ11 ± 2 bursts/min and Δ127 ± 57% change from normoxia; P < 0.05). These increases in MSNA were similar to the algebraic sum of the individual increase in MSNA elicited by HDR and hypoxia (Δ13 ± 1 bursts/min and Δ115 ± 36%). Increases in MAP (Δ3 ± 1 mmHg) and HR (Δ19 ± 1 beats/min) during combined HDR and hypoxia generally were smaller ( P < 0.05) than the algebraic sum of the individual responses (Δ5 ± 1 mmHg and Δ24 ± 2 beats/min for MAP and HR, respectively; P < 0.05). These findings indicate an additive interaction between the vestibulosympathetic reflex and arterial chemoreflex for MSNA. Therefore, it appears that MSNA outputs between the vestibulosympathetic reflex and arterial chemoreflex are independent of one another in humans.


2009 ◽  
Vol 31 (2) ◽  
pp. 135-151 ◽  
Author(s):  
Fabio E. Fontana ◽  
Oldemar Mazzardo ◽  
Comfort Mokgothu ◽  
Ovande Furtado ◽  
Jere D. Gallagher

The aim of this study was to examine the decision-making performance of experienced and inexperienced soccer players at four exercise intensities (rest, 40%, 60%, and 80% maximal aerobic power). The decision-making performance of inexperienced players was expected to demonstrate an inverted-U shape with increasing levels of exercise. For the experienced players, decision making was predicted to show no change in performance with increased exercise intensity. Thirty-two adult soccer players (16 experienced, 16 inexperienced) were asked to answer seven decision-making questions as quickly and accurately as possible for each exercise intensity. Results indicated that exercise does not affect the accuracy of decision making; however, the speed of decision making for experienced and inexperienced players improved with increased exercise intensity. These results suggest that physiologically induced arousal only affects speed of decision making.


1992 ◽  
Vol 145 (4_pt_1) ◽  
pp. 817-826 ◽  
Author(s):  
James D. Anholm ◽  
A. C. Peter Powles ◽  
Ralph Downey ◽  
Charles S. Houston ◽  
John R. Sutton ◽  
...  

2010 ◽  
Vol 108 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Laura Banks ◽  
Zion Sasson ◽  
Marco Busato ◽  
Jack M. Goodman

We examined the effect of intensity during prolonged exercise (PE) on left (LV) and right ventricular (RV) function. Subjects included 18 individuals (mean ± SE: age = 28.1 ± 1.1 yr, maximal aerobic power = 55.1 ± 1.6 ml · kg−1 · min−1), who performed 150 min of exercise at 60 and 80% maximal aerobic power on two separate occasions. Transthoracic echocardiography assessed systolic and diastolic performance, and blood sampling assessed hydration status and noradrenaline levels before (pre), during (15 and 150 min), and 60 min following (post) PE. β-Adrenergic sensitivity pre- and post-PE was assessed by dobutamine stress. High-intensity PE (15 vs. 150 min) induced reductions in LV ejection fraction (69.3 ± 1.3 vs. 63.5 ± 1.3%, P = 0.000), LV strain (−23.5 ± 0.6 vs. −22.3 ± 0.6%, P = 0.034), and RV strain (−26.3 ± 0.6 vs. −23.0 ± 0.6%, P < 0.01). Both exercise intensities induced diastolic reductions (pre vs. post) in the ratio of septal early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (2.15 ± 0.15 vs. 1.62 ± 0.09; 2.21 ± 0.15 vs. 1.48 ± 0.10), ratio of lateral early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (3.84 ± 0.42 vs. 2.49 ± 0.20; 3.56 ± 0.32 vs. 2.08 ± 0.18), ratio of early to late LV strain rate (2.42, ± 0.16 vs. 1.97 ± 0.13; 2.30 ± 0.15 vs. 1.81 ± 0.11), and ratio of early to late RV strain rate (2.03 ± 0.17 vs. 1.51 ± 0.09; 2.16 ± 0.16 vs. 1.44 ± 0.11) ( P < 0.001). Evidence of β-adrenergic sensitivity was supported by a decreased strain, strain rate, ejection fraction, and systolic pressure-volume ratio response to dobutamine ( P < 0.05) with elevated noradrenaline ( P < 0.01). PE-induced reductions in LV and RV systolic function were related to exercise intensity and β-adrenergic desensitization. The clinical significance of exercise-induced cardiac fatigue warrants further research.


2011 ◽  
Vol 26 (3) ◽  
pp. 102-106 ◽  
Author(s):  
B Sperlich ◽  
M Haegele ◽  
M Krüger ◽  
T Schiffer ◽  
H-C Holmberg ◽  
...  

Objective The effects of knee-high socks that applied different levels of compression (0, 10, 20, 30 and 40 mmHg) on various cardio-respiratory and metabolic parameters during submaximal running were analysed. Methods Fifteen well-trained, male endurance athletes (age: 22.2 ± 1.3 years; peak oxygen uptake: 57.2 ± 4.0 mL/minute/kg) performed a ramp test to determine peak oxygen uptake. Thereafter, all athletes carried out five periods of submaximal running (at approximately 70% of peak oxygen uptake) with and without compression socks that applied the different levels of pressure. Cardiac output and index, stroke volume, arterio-venous difference in oxygen saturation, oxygen uptake, arterial oxygen saturation, heart rate and blood lactate were monitored before and during all of these tests. Results Cardiac output ( P = 0.29) and index ( P = 0.27), stroke volume ( P = 0.50), arterio-venous difference in oxygen saturation ( P = 0.11), oxygen uptake ( P = 1.00), arterial oxygen saturation ( P = 1.00), heart rate ( P = 1.00) and arterial lactate concentration ( P = 1.00) were unaffected by compression (effect sizes = 0.00–0.65). Conclusion This first evaluation of the potential effects of increasing levels of compression on cardio-respiratory and metabolic parameters during submaximal exercise revealed no effects whatsoever.


2006 ◽  
Vol 110 (6) ◽  
pp. 683-692 ◽  
Author(s):  
Charles S. Fulco ◽  
Steven R. Muza ◽  
Dan Ditzler ◽  
Eric Lammi ◽  
Steven F. Lewis ◽  
...  

Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20±1 years of age; mean±S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25±2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43±0.01 with placebo compared with 7.34±0.01 with acetazolamide; P<0.05) and altitude (7.48±0.03 with placebo compared with 7.37±0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48±4 min with placebo compared with 36±5 min with acetazolamide; P<0.05), but not altitude (17±2 min with placebo compared with 20±3 min with acetazolamide; P=not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89±1 compared with 86±1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.


2013 ◽  
Vol 8 (3) ◽  
pp. 319-322 ◽  
Author(s):  
Dionne A. Noordhof ◽  
Thijs Schoots ◽  
Derk H. Hoekert ◽  
Jos J. de Koning

Purpose:The purpose of this study was to test the assumption that gross efficiency (GE) at sea level (SL) is representative of GE at altitude (AL). It was hypothesized that an increased cost of ventilation and heart rate, combined with a higher respiratory-exchange ratio, at AL might result in a decrease in GE.Methods:Trained men (N = 16) completed 2 maximal incremental tests and 2 GE tests, 1 at SL and 1 at an acute simulated AL of 1500 m (hypobaric chamber). GE was determined during submaximal exercise at 45%, 55%, and 65% of the altitude-specific power output attained at VO2max.Results:GE determined at the highest submaximal exercise intensity with a mean RER ≤1.0, matched for both conditions, was significantly lower at AL (AL 20.7% ± 1.1% and SL 21.4% ± 0.8%, t15 = 2.9, P < .05).Conclusion:These results demonstrate that moderate AL resulted in a significantly lower GE during cycling exercise than SL. However, it might be that the lower GE at AL is caused by the lower absolute exercise intensity.


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