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.

Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation

1994 ◽  
Vol 77 (2) ◽  
pp. 912-917 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie ◽  
R. B. Schoene ◽  
R. W. Glenny ◽  
H. T. Robertson
Keyword(s):  
Gas Exchange ◽  
Aerobic Capacity ◽  
Maximal Exercise ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Inert Gases ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Maximal Aerobic Capacity ◽  
Arterial Blood

To investigate pulmonary gas exchange during exercise in athletes, 10 high aerobic capacity athletes (maximal aerobic capacity = 5.15 +/- 0.52 l/min) underwent testing on a cycle ergometer at rest, 150 W, 300 W, and maximal exercise (372 +/- 22 W) while trace amounts of six inert gases were infused intravenously. Arterial blood samples, mixed expired gas samples, and metabolic data were obtained. Indexes of ventilation-perfusion (VA/Q) mismatch were calculated by the multiple inert gas elimination technique. The alveolar-arterial difference for O2 (AaDO2) was predicted from the inert gas model on the basis of the calculated VA/Q mismatch. VA/Q heterogeneity increased significantly with exercise and was predicted to increase the AaDO2 by > 17 Torr during heavy and maximal exercise. The observed AaDO2 increased significantly more than that predicted by the inert gas technique during maximal exercise (10 +/- 10 Torr). These data suggest that this population develops diffusion limitation during maximal exercise, but VA/Q mismatch is the most important contributor (> 60%) to the wide AaDO2 observed.

Effects of two successive maximal exercise tests on pulmonary gas exchange in athletes

1996 ◽  
Vol 74 (1-2) ◽  
pp. 141-147 ◽  
Author(s):  
Corinne F. Caillaud ◽  
Florence M. Anselme ◽  
Christian G. Prefaut
Keyword(s):  
Gas Exchange ◽  
Maximal Exercise ◽  
Pulmonary Gas Exchange ◽  
Exercise Tests

scholarly journals The Influence of Oxygen Saturation on the Relationship Between Hemoglobin Mass and VO2max

2018 ◽  
Vol 02 (04) ◽  
pp. E98-E104 ◽  
Author(s):  
Jesse Goodrich ◽  
Benjamin Ryan ◽  
William Byrnes
Keyword(s):  
Negative Relationship ◽  
Cycle Ergometer ◽  
Endurance Athletes ◽  
Moderate Altitude ◽  
Exercise Tests ◽  
Graded Exercise ◽  
Males And Females ◽  
Hemoglobin Mass ◽  
Exercise Induced ◽  
The Relationship

AbstractHemoglobin mass (tHb) is a key determinant of maximal oxygen uptake (VO2max). We examined whether oxyhemoglobin desaturation (ΔSaO2) at VO2max modifies the relationship between tHb and VO2max at moderate altitude (1,625 m). Seventeen female and 16 male competitive, endurance-trained moderate-altitude residents performed two tHb assessments and two graded exercise tests on a cycle ergometer to determine VO2max and ΔSaO2. In males and females respectively, VO2max (ml·kg−1·min−1) ranged from 62.5–83.0 and 44.5–67.3; tHb (g·kg−1) ranged from 12.1–17.5 and 9.1–13.0; and SaO2 at VO2max (%) ranged from 81.7–94.0 and 85.7–95.0. tHb was related to VO2max when expressed in absolute terms and after correcting for body mass (r=0.94 and 0.86, respectively); correcting by ΔSaO2 did not improve these relationships (r=0.93 and 0.83). Additionally, there was a negative relationship between tHb and SaO2 at VO2max (r=–0.57). In conclusion, across a range of endurance athletes at moderate altitude, the relationship between tHb and VO2max was found to be similar to that observed at sea level. However, correcting tHb by ΔSaO2 did not explain additional variability in VO2max despite significant variability in ΔSaO2; this raises the possibility that tHb and exercise-induced ΔSaO2 are not independent in endurance athletes.

scholarly journals Pulmonary gas exchange at maximal exercise in Danish lowlanders during 8 wk of acclimatization to 4,100 m and in high-altitude Aymara natives

2004 ◽  
Vol 287 (5) ◽  
pp. R1202-R1208 ◽  
Author(s):  
Carsten Lundby ◽  
Jose A. L. Calbet ◽  
Gerrit van Hall ◽  
Bengt Saltin ◽  
Mikael Sander
Keyword(s):  
Gas Exchange ◽  
High Altitude ◽  
Sea Level ◽  
Maximal Exercise ◽  
Acute Hypoxia ◽  
Pulmonary Gas Exchange ◽  
Maximum Exercise ◽  
Altitude Acclimatization ◽  
Ventilatory Equivalent ◽  
High Altitude Natives

We aimed to test effects of altitude acclimatization on pulmonary gas exchange at maximal exercise. Six lowlanders were studied at sea level, in acute hypoxia (AH), and after 2 and 8 wk of acclimatization to 4,100 m (2W and 8W) and compared with Aymara high-altitude natives residing at this altitude. As expected, alveolar Po2 was reduced during AH but increased gradually during acclimatization (61 ± 0.7, 69 ± 0.9, and 72 ± 1.4 mmHg in AH, 2W, and 8W, respectively), reaching values significantly higher than in Aymaras (67 ± 0.6 mmHg). Arterial Po2 (PaO2) also decreased during exercise in AH but increased significantly with acclimatization (51 ± 1.1, 58 ± 1.7, and 62 ± 1.6 mmHg in AH, 2W, and 8W, respectively). PaO2 in lowlanders reached levels that were not different from those in high-altitude natives (66 ± 1.2 mmHg). Arterial O2 saturation (SaO2) decreased during maximum exercise compared with rest in AH and after 2W and 8W: 73.3 ± 1.4, 76.9 ± 1.7, and 79.3 ± 1.6%, respectively. After 8W, SaO2 in lowlanders was not significantly different from that in Aymaras (82.7 ± 1%). An improved pulmonary gas exchange with acclimatization was evidenced by a decreased ventilatory equivalent of O2 after 8W: 59 ± 4, 58 ± 4, and 52 ± 4 l·min·l O2−1, respectively. The ventilatory equivalent of O2 reached levels not different from that of Aymaras (51 ± 3 l·min·l O2−1). However, increases in exercise alveolar Po2 and PaO2 with acclimatization had no net effect on alveolar-arterial Po2 difference in lowlanders (10 ± 1.3, 11 ± 1.5, and 10 ± 2.1 mmHg in AH, 2W, and 8W, respectively), which remained significantly higher than in Aymaras (1 ± 1.4 mmHg). In conclusion, lowlanders substantially improve pulmonary gas exchange with acclimatization, but even acclimatization for 8 wk is insufficient to achieve levels reached by high-altitude natives.

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.

Augmented Hyperventilation Via Normoxic Helium Breathing Does Not Prevent Exercise-Induced Hypoxemia

1996 ◽  
Vol 21 (4) ◽  
pp. 264-270 ◽  
Author(s):  
Michael J. Buono ◽  
Richard Maly
Keyword(s):  
Oxygen Saturation ◽  
Maximal Exercise ◽  
Arterial Oxygen Saturation ◽  
Ambient Air ◽  
Cycle Ergometer ◽  
Endurance Athletes ◽  
Arterial Oxygen ◽  
Volitional Exhaustion ◽  
Graded Exercise ◽  
Exercise Induced

The purpose of this study was to determine if augmented hyperventilation produced via normoxic helium breathing would reduce exercise-induced hypoxemia (EIH). Seven highly trained endurance athletes with a mean maximum oxygen uptake of 65 ml∙kg−1∙min−1, performed two cycle ergometer tests to volitional exhaustion. During one of the tests the subjects breathed ambient air, while during the other they breathed normoxic helium (21% O2, 79% He). Mean maximum expired ventilation significantly (p <.05) increased from 139 L∙min−1 during the ambient trial to 168 L∙min−1 while breathing normoxic helium. Mean arterial oxygen saturation obtained at maximum exercise, however, was not significantly different for the two trials (ambient = 90%, helium = 89%). These results suggest that significantly augmenting exercise hyperventilation by 21% essentially had no effect on EIH in endurance athletes. Thus, the data do not support the hypothesis that inadequate hyperventilation is an important mechanism for arterial oxygen desaturation during graded exercise to exhaustion in highly trained individuals. Key words: arterial oxygen saturation, endurance athletes, maximal exercise

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

Neuropeptide Y release from human heart is enhanced during prolonged exercise in hypoxia

1994 ◽  
Vol 76 (3) ◽  
pp. 1346-1349 ◽  
Author(s):  
L. Kaijser ◽  
J. Pernow ◽  
B. Berglund ◽  
J. Grubbstrom ◽  
J. M. Lundberg
Keyword(s):  
Neuropeptide Y ◽  
Coronary Sinus ◽  
Cycle Ergometer ◽  
Air Breathing ◽  
Ergometer Exercise ◽  
The Difference ◽  
Exercise Induced ◽  
Arterial O2 Saturation ◽  
Net Release ◽  
Coronary Sinus Blood

To evaluate the effect of hypoxemia on cardiac release of neuropeptide Y-like immunoreactivity (NPY-LI) and norepinephrine (NE), arterial and coronary sinus blood was sampled and coronary sinus blood flow was measured by thermodilution in nine healthy volunteers at rest and during supine cycle ergometer exercise while they breathed air and 12% O2, which reduced arterial O2 saturation to approximately 68%. Five subjects started to exercise for 30 min breathing air and continued for 30 min breathing 12% O2; four subjects breathed 12% O2 and air in the reverse order. The load was adjusted to give the same heart rate during O2 and air breathing. No significant cardiac net release of NPY-LI or NE was seen at rest. Exercise induced release of NPY-LI and NE. The net release of NPY-LI was 0.7 +/- 0.4 pmol/min during air breathing (average 12 and 30 min) and 2.8 +/- 0.6 pmol/min during 12% O2 breathing. The difference was not influenced by the order of the breathing periods. The NE coronary sinus-arterial difference was not significantly different between 12% O2 and air breathing, whereas the net release was significantly larger during 12% O2 breathing (0.6 +/- 0.1 vs. 0.4 +/- 0.1 nmol/min). Thus, NPY is released with NE from the heart during exercise. Arterial hypoxemia seems to be an additional stimulus of preferential NPY release.

Design and Evaluation of a Modified Underwater Cycle Ergometer

1996 ◽  
Vol 21 (2) ◽  
pp. 134-148 ◽  
Author(s):  
An A. Chen ◽  
Glen P. Kenny ◽  
Chad E. Johnston ◽  
Gordon G. Giesbrecht
Keyword(s):  
Power Output ◽  
Maximal Exercise ◽  
Exercise Duration ◽  
Cycle Ergometer ◽  
Gear Ratio ◽  
Upright Position ◽  
Exercise Tests ◽  
Maximal Power Output ◽  
Power Outputs ◽  
Key Words Core Temperature

An underwater cycle ergometer was designed consisting of an aluminum cycle frame in water connected with a 1:1 gear ratio to a mechanically braked standard cycle ergometer supported above the water. Three progressive maximal exercise tests were performed (n = 10): (a) the underwater ergometer in water (UEW), (b) underwater ergometer in air (UEA), and (c) a standard cycle ergometer in air (SEA). At submaximal power outputs, oxygen consumption [Formula: see text] and heart rate (HR) were generally lower in the SEA condition (p <.05), indicating that exercise in the upright position was more efficient. Exercise in water (UEW) resulted in lower total exercise duration, maximal HR, and maximal Tes than in air conditions. The upright position (SEA) resulted in greater total exercise duration and maximal power output than the semirecumbent positions. Because of positional differences between the standard and underwater ergometers, air-water comparisons should be made by using the underwater ergometer in water and on land. Key words: core temperature, esophageal temperature, skin temperature, exercise, resistance, work, power output, heat balance, heat loss, heat production, thermoregulation

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