scholarly journals Determinants of maximal oxygen uptake in severe acute hypoxia

2003 ◽  
Vol 284 (2) ◽  
pp. R291-R303 ◽  
Author(s):  
J. A. L. Calbet ◽  
R. Boushel ◽  
G. Rådegran ◽  
H. Søndergaard ◽  
P. D. Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Acute Hypoxia ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Leg Blood Flow ◽  
Ergometer Exercise

To unravel the mechanisms by which maximal oxygen uptake (V˙o 2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2(hypoxia, ∼5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31–34 mmHg and arterial O2 content (CaO2 ) was reduced by 35% ( P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (Pi O2 ) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia ( P < 0.05). Hypoxia caused a 47% decrease inV˙o 2 max (a greater fall than accountable by reduced CaO2 ). Peak cardiac output decreased by 17% ( P < 0.01), due to equal reductions in both peak heart rate and stroke volume ( P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia ( P < 0.001) correlating closely with V˙o 2 max( r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction ofV˙o 2 max in severe acute hypoxia: 1) reduction of Pi O2 , 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss inV˙o 2 max.

Central and peripheral adaptations of the gas transport system to one-leg training

1981 ◽  
Vol 59 (11) ◽  
pp. 1146-1154 ◽  
Author(s):  
S. G. Thomas ◽  
D. A. Cunningham ◽  
M. J. Plyley ◽  
D. R. Boughner ◽  
R. A. Cook
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Maximal Oxygen Uptake ◽  
Enzyme Activities ◽  
Cardiovascular Responses ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Enzyme Analysis ◽  
Ergometer Exercise

The role of central and peripheral adaptations in the response to endurance training was examined. Changes in cardiac structure and function, oxygen extraction, and muscle enzyme activities following one-leg training were studied.Eleven subjects (eight females, three males) trained on a cycle ergometer 4 weeks with one leg (leg 1), then 4 weeks with the second leg (leg 2). Cardiovascular responses to exercise with both legs and each leg separately were evaluated at entry (T1), after 4 weeks of training (T2), and after a second 4 weeks of training (T3). Peak oxygen uptake ([Formula: see text] peak) during exercise with leg 1 (T1 to T2 increased 19.8% (P < 0.05) and during exercise with leg 2 (T2 to T3 increased 16.9% (P < 0.05). Maximal oxygen uptake with both legs increased 7.9% from T1 to T2 and 9.4% from T2 to T3 (P < 0.05). During exercise at 60% of [Formula: see text] peak, cardiac output [Formula: see text] was increased significantly only when the trained leg was exercised. [Formula: see text] increased 12.2% for leg 1 between T1 and T2 and 13.0% for leg 2 between T2 and T3 (P < 0.05). M-mode echocardiographic assessment of left ventricular internal diameter at diastole and peak velocity of circumferential fibre shortening at rest or during supine cycle ergometer exercise at T1 and T3 revealed no training induced changes in cardiac dimensions or function. Enzyme analysis of muscle biopsy samples from the vastus lateralis (At T1, T2, T3) revealed no consistent pattern of change in aerobic (malate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase) or anaerobic (phosphofructokinase, lactate dehydroginase, and creatine kinase) enzyme activities. Increases in cardiac output and maximal oxygen uptake which result from short duration endurance training can be achieved, therefore, without measurable central cardiac adaptation. The absence of echocardio-graphically determined changes in cardiac dimensions and contractility and the absence of an increase in cardiac output during exercise with the nontrained leg following training of the contralateral limb support this conclusion.

Is pulmonary gas exchange during exercise in hypoxia impaired with the increase of cardiac output?

2008 ◽  
Vol 33 (3) ◽  
pp. 593-600 ◽  
Author(s):  
José A.L. Calbet ◽  
Paul Robach ◽  
Carsten Lundby ◽  
Robert Boushel
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Exercise Intensity ◽  
Acute Hypoxia ◽  
Mean Transit Time ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Oxygen Binding ◽  
Diffusion Limitation ◽  
Absolute Level

During exercise in humans, the alveolar–arterial O2 tension difference ((A–a)DO2) increases with exercise intensity and is an important factor determining the absolute level of oxygen binding to hemoglobin and therefore the level of systemic oxygen transport. During exercise in hypoxia, the (A–a)DO2 is accentuated. Using the multiple inert gas elimination technique it has been shown that during exercise in acute hypoxia the contribution of ventilation–perfusion inequality to (A–a)DO2 is rather small and in the absence of pulmonary edema intrapulmonary shunts can be ruled out. This implies that the main mechanism limiting pulmonary gas exchange is diffusion limitation. It is presumed that an elevation of cardiac output during exercise in acute hypoxia should increase the (A–a)DO2. However, no studies have examined how variations in cardiac output independently affect pulmonary diffusion with increases in exercise intensity. We have consistently observed that during steady-state, submaximal (100–120 W) exercise on the cycle ergometer in hypoxia the lung can accommodate an increase in cardiac output of ~2 L·min–1 without any significant effect on pulmonary gas exchange. This result contrasts with the predicted effect of cardiac output on (A–a)DO2 using the model of Piiper and Scheid, and thus indicates that an elevation of cardiac output is not necessarily accompanied by a reduction of mean transit time and (or) diffusion limitation during submaximal exercise in acute hypoxia. It remains to be determined what is the influence of changes in cardiac output per se on pulmonary gas exchange during high-intensity exercise.

Exercise training enhances leg vasodilatory capacity of 65-yr-old men and women

1990 ◽  
Vol 69 (5) ◽  
pp. 1804-1809 ◽  
Author(s):  
W. H. Martin ◽  
W. M. Kohrt ◽  
M. T. Malley ◽  
E. Korte ◽  
S. Stoltz
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Exercise Training ◽  
Oxygen Uptake ◽  
Endurance Exercise ◽  
Maximal Oxygen Uptake ◽  
Statistical Significance ◽  
Tissue Loss ◽  
Leg Blood Flow ◽  
Endurance Exercise Training

To determine whether extremity vasodilatory capacity may be augmented in older persons by endurance exercise training, lower leg blood flow and conductance were characterized plethysmographically at rest and during maximal hyperemia in 9 men and 10 women aged 64 +/- 3 (SD) yr before and after 31 +/- 6 wk of walking and jogging at 70-90% of maximal oxygen uptake for 45 min 3-5 days/wk. Maximal oxygen uptake expressed as milliliters per kilogram per minute improved 25% in men and 21% in women (P less than 0.01). Maximal leg blood flow and conductance increased in all nine men by an average of 39 +/- 33 (P less than 0.001) and 42 +/- 44% (P less than 0.004), respectively. Results were more variable in women and achieved unequivocal statistical significance only for maximal blood flow (+33 +/- 54% for blood flow and +29 +/- 55% for conductance; P less than 0.02 and P = 0.05, respectively). Body weight and skinfold adiposity declined in both sexes (P less than 0.05). Enhancement of vasodilatory capacity was related to weight loss in men and adipose tissue loss in women (r = 0.61 and 0.51, respectively; P less than 0.05). There were no significant changes in exercise capacity, body weight, or maximal blood flow in four male and three female controls aged 66 +/- 4 yr. Thus adaptability of the lower limb circulation to endurance exercise training is retained to at least age 65 yr.

Effects of incomplete pulmonary gas exchange on VO2 max

1989 ◽  
Vol 66 (6) ◽  
pp. 2491-2495 ◽  
Author(s):  
S. K. Powers ◽  
J. Lawler ◽  
J. A. Dempsey ◽  
S. Dodd ◽  
G. Landry
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Maximal Exercise ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Endurance Athletes ◽  
Healthy Male ◽  
Exercise Tests ◽  
Ergometer Exercise ◽  
Exercise Induced

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)

AltitudeOmics: impaired pulmonary gas exchange efficiency and blunted ventilatory acclimatization in humans with patent foramen ovale after 16 days at 5,260 m

2015 ◽  
Vol 118 (9) ◽  
pp. 1100-1112 ◽  
Author(s):  
Jonathan E. Elliott ◽  
Steven S. Laurie ◽  
Julia P. Kern ◽  
Kara M. Beasley ◽  
Randall D. Goodman ◽  
...  
Keyword(s):  
Gas Exchange ◽  
High Altitude ◽  
Sea Level ◽  
Patent Foramen Ovale ◽  
Acute Mountain Sickness ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Foramen Ovale ◽  
Ergometer Exercise ◽  
High Altitude Acclimatization

A patent foramen ovale (PFO), present in ∼40% of the general population, is a potential source of right-to-left shunt that can impair pulmonary gas exchange efficiency [i.e., increase the alveolar-to-arterial Po2 difference (A-aDO2)]. Prior studies investigating human acclimatization to high-altitude with A-aDO2 as a key parameter have not investigated differences between subjects with (PFO+) or without a PFO (PFO−). We hypothesized that in PFO+ subjects A-aDO2 would not improve (i.e., decrease) after acclimatization to high altitude compared with PFO− subjects. Twenty-one (11 PFO+) healthy sea-level residents were studied at rest and during cycle ergometer exercise at the highest iso-workload achieved at sea level (SL), after acute transport to 5,260 m (ALT1), and again at 5,260 m after 16 days of high-altitude acclimatization (ALT16). In contrast to PFO− subjects, PFO+ subjects had 1) no improvement in A-aDO2 at rest and during exercise at ALT16 compared with ALT1, 2) no significant increase in resting alveolar ventilation, or alveolar Po2, at ALT16 compared with ALT1, and consequently had 3) an increased arterial Pco2 and decreased arterial Po2 and arterial O2 saturation at rest at ALT16. Furthermore, PFO+ subjects had an increased incidence of acute mountain sickness (AMS) at ALT1 concomitant with significantly lower peripheral O2 saturation (SpO2). These data suggest that PFO+ subjects have increased susceptibility to AMS when not taking prophylactic treatments, that right-to-left shunt through a PFO impairs pulmonary gas exchange efficiency even after acclimatization to high altitude, and that PFO+ subjects have blunted ventilatory acclimatization after 16 days at altitude compared with PFO− subjects.

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