Oxygen transport to exercising leg in chronic hypoxia

1988 ◽  
Vol 65 (6) ◽  
pp. 2592-2597 ◽  
Author(s):  
P. R. Bender ◽  
B. M. Groves ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
S. Y. Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sea Level ◽  
Chronic Hypoxia ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Leg Blood Flow ◽  
State Cycle ◽  
O2 Delivery

Residence at high altitude could be accompanied by adaptations that alter the mechanisms of O2 delivery to exercising muscle. Seven sea level resident males, aged 22 +/- 1 yr, performed moderate to near-maximal steady-state cycle exercise at sea level in normoxia [inspired PO2 (PIO2) 150 Torr] and acute hypobaric hypoxia (barometric pressure, 445 Torr; PIO2, 83 Torr), and after 18 days' residence on Pikes Peak (4,300 m) while breathing ambient air (PIO2, 86 Torr) and air similar to that at sea level (35% O2, PIO2, 144 Torr). In both hypoxia and normoxia, after acclimatization the femoral arterial-iliac venous O2 content difference, hemoglobin concentration, and arterial O2 content, were higher than before acclimatization, but the venous PO2 (PVO2) was unchanged. Thermodilution leg blood flow was lower but calculated arterial O2 delivery and leg VO2 similar in hypoxia after vs. before acclimatization. Mean arterial pressure (MAP) and total peripheral resistance in hypoxia were greater after, than before, acclimatization. We concluded that acclimatization did not increase O2 delivery but rather maintained delivery via increased arterial oxygenation and decreased leg blood flow. The maintenance of PVO2 and the higher MAP after acclimatization suggested matching of O2 delivery to tissue O2 demands, with vasoconstriction possibly contributing to the decreased flow.

Oxygen transport during steady-state submaximal exercise in chronic hypoxia

1991 ◽  
Vol 70 (3) ◽  
pp. 1129-1136 ◽  
Author(s):  
E. E. Wolfel ◽  
B. M. Groves ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. S. Mazzeo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Steady State ◽  
Sea Level ◽  
Vascular Resistance ◽  
Barometric Pressure ◽  
Submaximal Exercise ◽  
Leg Blood Flow ◽  
Total Body ◽  
O2 Delivery

Arterial O2 delivery during short-term submaximal exercise falls on arrival at high altitude but thereafter remains constant. As arterial O2 content increases with acclimatization, blood flow falls. We evaluated several factors that could influence O2 delivery during more prolonged submaximal exercise after acclimatization at 4,300 m. Seven men (23 +/- 2 yr) performed 45 min of steady-state submaximal exercise at sea level (barometric pressure 751 Torr), on acute ascent to 4,300 m (barometric pressure 463 Torr), and after 21 days of residence at altitude. The O2 uptake (VO2) was constant during exercise, 51 +/- 1% of maximal VO2 at sea level, and 65 +/- 2% VO2 at 4,300 m. After acclimatization, exercise cardiac output decreased 25 +/- 3% compared with arrival and leg blood flow decreased 18 +/- 3% (P less than 0.05), with no change in the percentage of cardiac output to the leg. Hemoglobin concentration and arterial O2 saturation increased, but total body and leg O2 delivery remained unchanged. After acclimatization, a reduction in plasma volume was offset by an increase in erythrocyte volume, and total blood volume did not change. Mean systemic arterial pressure, systemic vascular resistance, and leg vascular resistance were all greater after acclimatization (P less than 0.05). Mean plasma norepinephrine levels also increased during exercise in a parallel fashion with increased vascular resistance. Thus we conclude that both total body and leg O2 delivery decrease after arrival at 4,300 m and remain unchanged with acclimatization as a result of a parallel fall in both cardiac output and leg blood flow and an increase in arterial O2 content.(ABSTRACT TRUNCATED AT 250 WORDS)

Why is V˙o 2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?

2003 ◽  
Vol 284 (2) ◽  
pp. R304-R316 ◽  
Author(s):  
J. A. L. Calbet ◽  
R. Boushel ◽  
G. Rådegran ◽  
H. Søndergaard ◽  
P. D. Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Sea Level ◽  
Chronic Hypoxia ◽  
Maximal Exercise ◽  
Acute Hypoxia ◽  
Hemoglobin Concentration ◽  
Cycle Ergometry ◽  
The Other ◽  
Circulatory Effects

Acute hypoxia (AH) reduces maximal O2 consumption (V˙o 2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]),V˙o 2 max remains low. To determine why, seven lowlanders were studied at V˙o 2 max(cycle ergometry) at sea level (SL), after 9–10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (Fi O2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by ∼15% in both AH and CH ( P < 0.05). At maximal exercise, arterial [O2] in AH was 31% lower than at SL ( P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. PulmonaryV˙o 2 max (4.1 ± 0.3 l/min at SL) fell to 2.2 ± 0.1 l/min in AH ( P < 0.05) and was only 2.4 ± 0.2 l/min in CH ( P < 0.05). These data suggest that the failure to recoverV˙o 2 max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptations to High-Altitude Hypoxia

2021 ◽  
Author(s):  
Cynthia M. Beall ◽  
Kingman P. Strohl
Keyword(s):  
High Altitude ◽  
Oxygen Delivery ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Extreme Environment ◽  
Indigenous Populations ◽  
East African ◽  
Short Term

Biological anthropologists aim to explain the hows and whys of human biological variation using the concepts of evolution and adaptation. High-altitude environments provide informative natural laboratories with the unique stress of hypobaric hypoxia, which is less than usual oxygen in the ambient air arising from lower barometric pressure. Indigenous populations have adapted biologically to their extreme environment with acclimatization, developmental adaptation, and genetic adaptation. People have used the East African and Tibetan Plateaus above 3,000 m for at least 30,000 years and the Andean Plateau for at least 12,000 years. Ancient DNA shows evidence that the ancestors of modern highlanders have used all three high-altitude areas for at least 3,000 years. It is necessary to examine the differences in biological processes involved in oxygen exchange, transport, and use among these populations. Such an approach compares oxygen delivery traits reported for East African Amhara, Tibetans, and Andean highlanders with one another and with short-term visitors and long-term upward migrants in the early or later stages of acclimatization to hypoxia. Tibetan and Andean highlanders provide most of the data and differ quantitatively in biological characteristics. The best supported difference is the unelevated hemoglobin concentration of Tibetans and Amhara compared with Andean highlanders as well as short- and long-term upward migrants. Moreover, among Tibetans, several features of oxygen transfer and oxygen delivery resemble those of short-term acclimatization, while several features of Andean highlanders resemble the long-term responses. Genes and molecules of the oxygen homeostasis pathways contribute to some of the differences.

Leg crossing with muscle tensing, a physical counter-manoeuvre to prevent syncope, enhances leg blood flow

2007 ◽  
Vol 112 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jan T. Groothuis ◽  
Nynke van Dijk ◽  
Walter ter Woerds ◽  
Wouter Wieling ◽  
Maria T. E. Hopman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Orthostatic Intolerance ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Head Up Tilt

In patients with orthostatic intolerance, the mechanisms to maintain BP (blood pressure) fail. A physical counter-manoeuvre to postpone or even prevent orthostatic intolerance in these patients is leg crossing combined with muscle tensing. Although the central haemodynamic effects of physical counter-manoeuvres are well documented, not much is known about the peripheral haemodynamic events. Therefore the purpose of the present study was to examine the peripheral haemodynamic effects of leg crossing combined with muscle tensing during 70° head-up tilt. Healthy subjects (n=13) were monitored for 10 min in the supine position followed by 10 min in 70° head-up tilt and, finally, for 2 min of leg crossing with muscle tensing in 70° head-up tilt. MAP (mean arterial BP), heart rate, stroke volume, cardiac output and total peripheral resistance were measured continuously by Portapres. Leg blood flow was measured using Doppler ultrasound. Leg vascular conductance was calculated as leg blood flow/MAP. A significant increase in MAP (13 mmHg), stroke volume (27%) and cardiac output (18%), a significant decrease in heart rate (−5 beats/min) and no change in total peripheral resistance during the physical counter-manoeuvre were observed when compared with baseline 70° head-up tilt. A significant increase in leg blood flow (325 ml/min) and leg vascular conductance (2.9 arbitrary units) were seen during the physical counter-manoeuvre when compared with baseline 70° head-up tilt. In conclusion, the present study indicates that the physical counter-manoeuvre of leg crossing combined with muscle tensing clearly enhances leg blood flow and, at the same time, elevates MAP.

Ventilation-perfusion inequality in normal humans during exercise at sea level and simulated altitude

1985 ◽  
Vol 58 (3) ◽  
pp. 978-988 ◽  
Author(s):  
G. E. Gale ◽  
J. R. Torre-Bueno ◽  
R. E. Moon ◽  
H. A. Saltzman ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Statistical Significance ◽  
Barometric Pressure ◽  
Bicycle Ergometer ◽  
Lung Model ◽  
Inert Gas ◽  
Topographical Distribution ◽  
Normal Humans

To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.

Operation Everest II: maximal oxygen uptake at extreme altitude

1989 ◽  
Vol 66 (5) ◽  
pp. 2446-2453 ◽  
Author(s):  
A. Cymerman ◽  
J. T. Reeves ◽  
J. R. Sutton ◽  
P. B. Rock ◽  
B. M. Groves ◽  
...  
Keyword(s):  
Sea Level ◽  
Chronic Hypoxia ◽  
Rank Order ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Arterial Pco2 ◽  
Altitude Exposure ◽  
Extreme Altitude ◽  
Maximum Effort ◽  
Arterial O2 Saturation

Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188–1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1–15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.

Effect of reduced hemoglobin concentration on leg oxygen uptake during maximal exercise in humans

1993 ◽  
Vol 75 (2) ◽  
pp. 491-498 ◽  
Author(s):  
W. Schaffartzik ◽  
E. D. Barton ◽  
D. C. Poole ◽  
K. Tsukimoto ◽  
M. C. Hogan ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Venous Blood ◽  
Hemoglobin Concentration ◽  
Random Order ◽  
Barometric Pressure ◽  
Whole Body ◽  
Cell Spacing ◽  
O2 Delivery

Maximum oxygen uptake (VO2max) is affected by hemoglobin concentration ([Hb]). Whether this is simply due to altered convection of O2 into the muscle microcirculation or also to [Hb]-dependent diffusive transport of O2 out of the muscle capillary is unknown in humans. To examine this, seven healthy volunteers performed four maximal cycle exercise bouts at sea level immediately after 8 wk at altitude (3,801 m, barometric pressure 485 Torr), a sojourn designed to increase [Hb]. The first two bouts were at ambient [Hb] of 15.9 +/- 0.7 g/100 ml breathing 21 or 12% O2 in random order. [Hb] was then decreased to a prealtitude level of 13.8 +/- 0.6 g/100 ml by venesection and isovolemic replacement with 5% albumin in 0.9% saline, and the exercise bouts were repeated. At whole body VO2max, PO2, PCO2, pH, and O2 saturation were measured in radial arterial and femoral venous blood. Femoral venous thermodilution blood flow was determined for calculation of leg VO2. Mean muscle capillary PO2 and muscle diffusing capacity (DO2) were computed by Bohr integration between measured arterial and femoral venous PO2. Averaged over both fractional concentrations of inspired O2, leg VO2 at maximum decreased by 17.7 +/- 4.3% as [Hb] was lowered while leg O2 delivery decreased by 17.5 +/- 2.6% and DO2 decreased by 10.7 +/- 2.7% (all P < 0.05). The relative contributions of decreases in leg O2 delivery and DO2 to the decrease in VO2max were computed to be 64 and 36%, respectively. These findings suggest that [Hb] is an important determinant of O2 diffusion rates into working muscle in humans. Possible mechanisms include 1) dependence of DO2 on intracapillary red blood cell spacing, 2) changes in the total rate of dissociation of O2 from [Hb], and 3) increased red blood cell flow heterogeneity as [Hb] is reduced.

Effects of hyperoxia on leg blood flow and metabolism during exercise

1977 ◽  
Vol 42 (3) ◽  
pp. 385-390 ◽  
Author(s):  
H. G. Welch ◽  
F. Bonde-Petersen ◽  
T. Graham ◽  
K. Klausen ◽  
N. Secher
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Aerobic Capacity ◽  
Power Output ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
Maximal Aerobic Capacity ◽  
Leg Blood Flow ◽  
O2 Delivery

These experiments were designed to investigate the effects of O2 breathing on limb blood flow and metabolism during exercise. Six subjects took part in the study. Four subjects breathed air or 100% O2 while pedaling a Krogh bicycle at 150 W (55–70% of maximal aerobic capacity). Two subjects breathed either 60% or 100% O2 while working at a power output at or slightly in excess of their maximal aerobic capacities. The major findings of the study were 1) leg blood flow is reduced during exercise when comparing hyperoxia with normoxia; 2) VO2 of the exercising limb is not different during hyperoxia; 3) O2 delivery to the leg (the product of blood flow and arteriovenous O2 difference) is not significantly different in the two conditions; and 4) blood pressure is not markedly affected in the experiments at 150 W. Since BP was not different during hyperoxia, at a time when flow was reduced by 11%, this suggests an increased resistance to flow in the exercising limb. In general, these findings are consistent with those reported for the in situ dog muscle but are at variance with results of experiments with humans, especially the reports indicating substantial increases in O2 uptake during hypertoxic conditions.

Effect of blood flow reduction on maximal O2 uptake in canine gastrocnemius muscle in situ

1993 ◽  
Vol 74 (4) ◽  
pp. 1742-1747 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
P. D. Wagner
Keyword(s):  
Blood Flow ◽  
Gastrocnemius Muscle ◽  
Muscle Blood Flow ◽  
Lactate Concentration ◽  
Blood Gases ◽  
Hemoglobin Concentration ◽  
Random Order ◽  
O2 Uptake ◽  
O2 Delivery ◽  
Severe Ischemia

The purpose of this study was to decrease O2 delivery to maximally working muscle by reductions in muscle blood flow (Q), while maintaining hemoglobin concentration and the arterial PO2 (PaO2) constant, to investigate how the decreases in maximal O2 uptake (VO2max) that occur with ischemia are related to changes in the estimated effective muscle O2 diffusing capacity (DO2). Additionally, the relationships among Q, DO2, O2 uptake (VO2), and effluent venous PO2 (PVO2) were used to infer whether the reductions in Q occur uniformly throughout the muscle or whether a nonuniform (greater heterogeneity of Q to VO2) pattern develops. Isolated dog gastrocnemius muscle (n = 6) was stimulated maximally at three levels of muscle blood flow (controlled by pump perfusion): control [C; 119 +/- 3 ml.100 g-1.min-1 (SE)], moderate ischemia (MI; 80 +/- 6), and severe ischemia (SI; 45 +/- 6) in random order. Arterial and venous samples were taken to measure blood gases, O2 concentration, and lactate concentration, whereas a Bohr integration technique using a model based on Fick's law of diffusion was used to estimate mean capillary PO2 and DO2 for each Q condition. VO2max fell progressively (P < 0.05) with Q, even though the O2 extraction ratio (VO2/O2 delivery) increased significantly (C = 67%, MI = 84%, SI = 90%). PVO2 and VO2max fell in proportion to each other from C to MI, but there was not a significant fall in PVO2 from MI to SI. Thus the calculated DO2 did not change between C and MI but fell in proportion to Q between MI and SI. These results suggest that with moderate Q reduction, perfusion falls relatively uniformly throughout the muscle, whereas more severe ischemia leads to nonuniform changes in Q distribution with some areas being poorly perfused to allow more adequate perfusion to other areas.

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