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Am J Physiol Heart Circ Physiol 277: H1045-H1052, 1999;
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Vol. 277, Issue 3, H1045-H1052, September 1999

Cerebral desaturation during exercise reversed by O2 supplementation

H. B. Nielsen, R. Boushel, P. Madsen, and N. H. Secher

Copenhagen Muscle Research Center, Department of Anesthesia, Rigshospitalet, University of Copenhagen, 2100 Copenhagen Ø, Denmark


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation (ScO2) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 ± 1 mmHg; mean ± SE) and O2 pressure (77 ± 2 mmHg) as well as the hemoglobin saturation (91.9 ± 0.7%) were reduced (P < 0.05). ScO2 was reduced from 80 ± 2 to 63 ± 2% (P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (Delta Hb) and oxyhemoglobin (Delta HbO2) of the vastus lateralis muscle increased 22 ± 3 µM and decreased 14 ± 3 µM, respectively (P < 0.05). Increasing the inspired O2 fraction to 0.30 did not affect ventilation (174 ± 4 l/min), but arterial CO2 pressure (37 ± 2 mmHg), O2 pressure (165 ± 5 mmHg), and hemoglobin O2 saturation (99 ± 0.1%) increased (P < 0.05). ScO2 remained close to the resting level during exercise (79 ± 2 vs. 81 ± 2%), and although the muscle Delta Hb (18 ± 2 µM) and Delta HbO2 (-12 ± 3 µM) were similar to those established without O2 supplementation, work capacity increased from 389 ± 11 to 413 ± 10 W (P < 0.05). These results indicate that an elevated inspiratory O2 fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.

arterial oxygen saturation; arterial oxygen pressure; hyperoxia; lactate; near-infrared spectroscopy; pH


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

IN RESPONSE TO exhaustive exercise athletes have been observed to exhibit decreased cognitive abilities (7). Such manifestations could represent a lack of homeostasis of cerebral physiology, i.e., reduced blood flow and oxygenation. Exercise hyperventilation lowers the arterial CO2 pressure, which, with constriction of cerebral vessels, reduces cerebral perfusion (26). Cerebral O2 supply may also be affected by intense exercise due to reduction of the arterial O2 pressure (11, 35). During exercise involving a large muscle mass, e.g., during rowing, blood pH may be as low as 6.74 (34). Thus hemoglobin O2 saturation may decrease below 85% (13, 34, 35). During rowing, such arterial desaturation may be critical for the cerebral oxygenation. The exercise-induced increase in cerebral perfusion (20, 21) is small during rowing (41) because of the large stroke-related fluctuations in blood pressure as the oarsmen perform a Valsalva-like maneuver at the catch of each stroke (9). Cerebral O2 oxygenation (ScO2) determined by near-infrared spectroscopy reflects changes in regional cerebral blood flow (12, 23, 36). We considered that during exercise (rowing) associated with hypocapnia, hypoxemia, and only a small increase in cerebral blood flow, ScO2 may be reduced.

With an elevated inspired O2 fraction, the arterial CO2 pressure and hemoglobin O2 saturation increase (35), and we hypothesize that moderate hyperoxia would maintain ScO2 close to resting levels. Such an effect could help to explain the enhanced exercise capacity with hyperoxia (38), because O2 delivery to muscle appears to remain at the level obtained during exercise in normoxia (48).


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Eleven competitive male oarsmen [median age 24 yr (range 20-29 yr), median body wt 76 kg (range 72-82 kg), median height 183 cm (range 177-194 cm)] participated in the study as approved by the Ethics Committee of Copenhagen (KF 01-276/97). Among the subjects, one was an Olympic gold medal winner, two were world champions, two had each won a silver medal at the world championships in rowing, and four ranked within the "top ten." The Olympic medalist won the world championship in ergometer rowing (a 2,000-m effort in a record time of 6 min, 4 s). Five subjects ranked within the top 62 according to the 1997 Concept II World Record List. None of the subjects had any disease or injury 3 wk before the experiment, and none was taking any medication. The reproducibility of repeated maximal rowing tests for elite rowers is high. Nineteen national team oarsmen were tested three times in 1 yr (333 ± 13 days) with at least 4 mo between the tests. The maximal O2 uptake reached 5.5 ± 0.1, 5.5 ± 0.1, and 5.6 ± 0.1 l/min, respectively; thus rowing test variability was <1%.

The subjects in the present study were randomized in a double-blind manner to an inspired O2 fraction of either 0.21 or 0.30 in a crossover design with 7 days between trials. A catheter (1.0-mm inner diameter, 19 gauge) was inserted in the radial artery of the nondominant arm, and another catheter (1.7-mm inner diameter, 16 gauge) was advanced to the superior caval vein. The catheters were connected to a pressure monitoring kit (Baxter Healthcare, Maurepas, France) positioned at the level of the heart with continuous infusion of isotonic saline (3 ml/h). To simulate an on-water competition, the subjects performed a 10-min warm-up row followed by a 6-min "all-out" row using a wind-braked rowing ergometer (Concept II, Morrisville, VT). The subjects were encouraged to beat their personal records, and a ranking list, which included the power for each trial, ensured interindividual competition. After the second trial, the subjects were asked after which of the two rows they had felt better.

On another test day, five oarsmen [median age 23 yr (range 20-28 yr), median body wt 77 kg (range 70-81 kg), median height 181 cm (range 175-194 cm)] performed cycle ergometry in ambient air conditions for evaluation of ScO2 during exercise that did not involve the large fluctuations in blood pressure that occurred during rowing (9) and thus would be less likely to affect the arterial O2 pressure and hemoglobin O2 saturation. The pedaling rate was maintained at 60 rpm, and power was increased by 100 W every third minute until the power matched the power developed during the rowing trial. At the highest workload, the pedaling rate was increased to a supramaximal level and maintained until the subject was exhausted.

The subjects breathed through a two-way low-resistance T valve (model 2700, Hans Rudolph, Kansas City, MO) with humidified air delivered from a Douglas bag. The flow rate, O2, and CO2 were continuously analyzed by a cardiopulmonary exercise test system (2001, Medical Graphics, St. Paul, MN). Measurements were made with an electrochemical O2 analyzer and a CO2 infrared analyzer. After a 5-min rest period to stabilize ventilation, the subject breathed ambient air and thereafter air with an inspired O2 fraction of either 0.21 or 0.30 for 5 min while seated on the ergometer. Breath-by-breath measurements of O2 consumption (VO2), ventilation (VE), respiratory rate (RR), expired CO2 (VCO2), and end-tidal partial pressures for O2 and CO2 were averaged every 30 s. The peak VO2 was taken to reflect the maximum VO2 (VO2 max), because such a VO2 max value is similar to or slightly higher than that obtained during cycling (10). The respiratory variables were averaged at rest with the peak values presented during exercise.

Blood samples for the measurement of bicarbonate, CO2 pressure, O2 pressure, pH, base excess, hemoglobin, and lactate in arterial and venous blood were obtained anaerobically (QS50, Radiometer, Copenhagen, Denmark). Samples were taken at rest, during the last minute of exercise, and 1-2 min into the recovery period. During cycling, arterial sampling was made at each workload. All blood samples were stored on ice and analyzed within 15 min (ABL-615, Radiometer). Lactate in plasma was determined (YSI 2300, Yellow Springs Instruments, Yellow Springs, OH) after centrifugation of samples for 10 min at 5°C. The O2 content in arterial (CaO2) and venous blood (CvO2) was calculated as the sum of bound (1.39 × hemoglobin O2 saturation) and dissolved O2 (0.003 × PO2). At rest and during the last minute of exercise, plasma catecholamines were determined in a single-isotope radioenzymatic method (Waters HPLC, Waters Chromatography Division, Millford, MA) with an average variability <1%.

Arterial pressure was assessed invasively through the arterial line connected with a transducer (Baxter) and a monitor, with results stored on a computer hard disk. Mean arterial pressure was averaged at rest and during exercise. A lightweight portable heart rate meter (model PE 3000 Sport Tester, Polar Electro, Kempele, Finland) was used to record heart rate every 15 s.

Cardiac output (Q) was estimated by dye dilution and by the Fick principle using the VO2 and the CaO2-CvO2 difference. Indocyanine green (5 mg; Cardio-Green, Becton Dickinson, Cockeysville, MO) was injected rapidly into the venous catheter, followed by a 10-ml flush of isotonic saline. Measurements were made twice at rest when the subjects were breathing air from the Douglas bag. During rowing, indocyanine green injections were made two to four times after the third minute of exercise. Blood from the artery was sampled at 30 ml/min by a Harvard pump through a photodensitometer (Waters Instruments, Rochester, MN). The dye dilution curve was recorded, and withdrawn blood was reinfused immediately into the vein. The indocyanine green dilution curves were calibrated on each day of experiments using 10 ml of indocyanine green (5 mg/ml) in 10 ml of whole blood. The area of the dilution curve was determined by planimetry (Digiplan, Haff, Pfronten, Germany). The Q values derived from dye dilution were averaged at rest and during exercise.

A cerebral near-infrared spectroscopy oximeter (INVOS 3100 Cerebral Oximeter, Somanetics, Troy, WI) was used to measure the absorbance changes of two light wavelengths. This provides an index of ScO2, which is the ratio of oxyhemoglobin (810 nm) to the sum of oxyhemoglobin and deoxyhemoglobin (730 nm). The near-infrared spectroscopy sensor (two separate light receivers and a miniature light-emitting diode) was placed on the forehead just below the hairline. The photons pass through the scalp, the skull, and the brain tissue to a depth of several centimeters with the signal weighted toward the cortical tissue of the brain (19, 32). This technique has shown only a minimal influence of the skin blood flow (32). Thus microvasculature saturation of the frontal lobe was measured at rest and during and after exercise. With this placement of the near-infrared spectroscopy probe, ScO2 responds to manipulation of arterial CO2 pressure in normal humans (28, 40) similar to the way it responds to coronary bypass surgery (3) and liver transplantation (46). Values were documented when the readout remained stable for 10 s.

Muscle oxygenation was assessed by a fast time-resolved near-infrared spectroscopy apparatus (NIRO500, Hamamatsu phototonics, Hamamatsu, Japan). The two optodes were positioned on the vastus lateralis muscle of the left leg at the midpoint of a line between the anterior superior iliac spine and the superior part of the fibula bone. Hair on the leg was removed for maximal optode contact. A black rubber holder eliminated background light and also secured the distance (4 cm) between the optodes. The same position of the probe was used in both trials. With the use of four wavelengths (775, 826, 850, and 910 nm), chromophore concentration changes (in µM) in oxyhemoglobin (Delta HbO2), deoxyhemoglobin (Delta Hb), and cytochrome-c oxidase (Delta CtOx) were calculated by a modified Lambert-Beer law (50). A running average integrated over 10 s was used, and results were presented as the overall means at rest and during exercise. The variables were averaged until the time of dye injection (first 3 min of exercise), because indocyanine green has a peak spectral absorption in blood similar to that of CtOx and such a change in chromophores affects the calculation of Delta Hb, Delta HbO2, and Delta CtOx (Fig. 1, arrows).


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  		Fig. 1.   Representative data of concentration changes in deoxy- (Delta Hb) and oxyhemoglobin (Delta HbO2) and cytochrome-c oxidase (Delta CtOx) from 1 subject in response to a 6-min all-out ergometer row. Delta CtOx increased after injections of indocyanine green (arrows). Horizontal bar corresponds to an expanded time scale.

Data are expressed as means ± SE. Comparisons among multiple samples were evaluated by the Friedman analysis of variance (SYSTAT, Evanston, IL). This test included the effect of exercise and comparisons between the two trials. Significant effects resulted in a Wilcoxon test by rank for locating significant pairwise differences, and a P value <0.05 was considered statistically significant.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Inspired O2 fraction of 0.21. During rowing, the power was 389 ± 11 W and resulted in markedly elevated RR and VE, reduced end-tidal and arterial CO2 pressure, and increased VCO2 (Table 1). The end-tidal O2 pressure also increased, but arterial O2 pressure decreased, and the end-tidal arterial O2 pressure difference was elevated. The concentration of arterial lactate increased and arterial pH decreased. In one subject, lactate concentration was as high as 24 mM, and pH decreased to 6.98 immediately after rowing. The lowest arterial and central venous O2 saturations were 88 and 10%, respectively. There were similar increases in arterial and venous hemoglobin concentrations, and CaO2 was higher during exercise than at rest. Also, the increase in plasma concentration of catecholamines was pronounced during rowing. VO2 max was 5.0 ± 0.3 l/min, and Q was 30 ± 2 l/min with no significant difference between the two estimates of Q.

                              
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  		Table 1.   Effects of inspired O2 fraction of 0.21 or 0.30 at rest and during rowing

At rest, muscle oxygenation and ScO2 remained stable. In response to rowing, ScO2 decreased 17% (Fig. 2). Delta Hb increased and Delta HbO2 decreased, whereas Delta CtOx was not affected (Table 1). Also, the concentration change in total hemoglobin was not significantly affected by exercise. However, throughout the 6-min trial, Delta Hb, Delta HbO2, and Delta CtOx fluctuated in a cyclic manner over a period of ~2 s (Fig. 1). This temporal cycle was related to the vigorous muscle contractions during each stroke, because the rowing rate was close to 30 strokes/min.


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  		Fig. 2.   Cerebral oxygenation (ScO2) in ambient air, with an inspired O2 fraction of 0.21 (open circle ) or 0.30 () at rest, during a 6-min maximal row (exercise), and at 2 and 4 min into recovery after exercise. * P < 0.05 vs. control (rest); dagger  P < 0.05 vs. trial with O2 supplementation.

During the recovery from exercise, ScO2 remained depressed for 2 min and was followed by an increase to a level above the resting value. At 2 and 4 min after exercise, VE had decreased to 79 ± 7 and 50 ± 6 l/min, respectively, but arterial CO2 pressure (32.6 ± 0.8 mmHg) and pH (7.12 ± 0.04) continued to decrease to below the exercise levels. At 1 min after exercise, arterial O2 saturation (95.7 ± 0.4%) increased toward the resting level as arterial O2 pressure was elevated to 116 ± 2 mmHg.

Inspired O2 fraction of 0.30. Power was 413 ± 10 W, a level 2.4 ± 0.6% higher than the power reached during exercise at an inspired O2 fraction of 0.21. One world champion oarsman was able to beat his personal record by 2 m. The subjects expressed an enhanced ability to maintain rowing rhythm and pressure on the "oar," and they all "felt better" after this exercise than they did during control exercise.

The VE and RR values were not significantly different from those during control exercise, but the end-tidal and arterial CO2 pressure and VCO2 were increased (Table 1). The end-tidal and arterial O2 pressure were elevated but not significantly affected by hyperoxic exercise, thus reducing the end-tidal arterial O2 pressure difference. At rest, arterial hemoglobin O2 saturation was elevated, and only a minimal reduction occurred during exercise, whereas the central venous hemoglobin O2 saturation was not significantly affected by the elevated inspired O2 fraction. Thus, with an increase in hemoglobin similar to that obtained during exercise in normoxia, CaO2 became elevated by 7 ± 1%. These changes resulted in an elevated VO2 max (5.7 ± 0.3 l/min; 13 ± 2%) although Q, as confirmed by dye dilution, was not significantly different from that in control exercise (30 ± 1 l/min).

With an elevated inspired O2 fraction, ScO2 at rest increased from 79 ± 2 to 82 ± 2%. During exercise, ScO2 was not affected significantly. Supplementation with O2 did not affect Delta Hb, Delta HbO2, or Delta CtOx at rest or during exercise. In both arterial and venous blood, the concentration of lactate reached levels similar to those reached with an inspired O2 fraction of 0.21. Also, pH, base excess, bicarbonate, and the concentration of catecholamines were not affected significantly by an elevated inspired O2 fraction.

Cycling. With an elevated RR and VE, end-tidal and arterial CO2 pressure remained at the resting level, whereas arterial O2 pressure was reduced to 88 ± 2 mmHg with no marked acidosis (pH 7.31); arterial hemoglobin O2 saturation remained >95% throughout cycling (Table 2). ScO2 was not reduced below resting level; in fact, ScO2 had a tendency to become elevated during intense exercise. In one subject, the highest cycling intensity was associated with an arterial O2 pressure, pH, and hemoglobin O2 saturation of 86 mmHg, 7.25, and 93.7%, respectively, and even with hyperventilation (arterial CO2 pressure at 39 mmHg) ScO2 was not significantly lower than at rest.

                              
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  		Table 2.   Effects of incremental cycling ergometry in ambient air


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Cerebral oxygenation and arterial hemoglobin O2 saturation were reduced during exercise with an intensity that elicited a low blood pH and a catecholamine level surpassing that previously reported in trained humans (15, 18, 22). When exercise was performed with an elevated inspired O2 fraction (0.30 vs. 0.21), both blood and cerebral oxygenation remained at the resting levels during exercise, whereas pH decreased to an extent similar to that measured during exercise in normoxia. In contrast, the reduction in muscle oxygenation was not significantly affected with O2 supplementation. Thus, after moderate hyperoxia in highly trained oarsmen, an increase in work capacity by 2.4% was related to enhanced cerebral, rather than muscle, oxygenation.

Blood oxygenation. During exercise, an elevated VE maintained the alveolar O2 pressure, but arterial O2 pressure decreased and, in combination with the influence of pH on the affinity of O2 to hemoglobin, arterial hemoglobin O2 saturation was reduced (13, 14, 35, 42, 44). In contrast, when acidosis was modest during cycling, hemoglobin O2 saturation remained at the resting level even though arterial O2 pressure decreased to <90 mmHg. These observations support the hypothesis that two mechanisms work in concert to develop hypoxemia during exercise: a pulmonary O2 diffusion limitation that lowers arterial O2 pressure and a pH effect on the affinity of O2 to hemoglobin.

Dempsey et al. (11) considered that, with a large increase in cardiac output, the time that the erythrocytes remain in the pulmonary capillary is critical for O2 equilibration. In response to submaximal ergometer rowing, cardiac output reaches 17 l/min (45), whereas a maximal intensity increases cardiac output to almost twice that value, corresponding to a predicted value from VO2 max (18). The large increase in cardiac output is achieved with decreased peripheral resistance as indicated by a low diastolic pressure after the Valsalva-like maneuver performed at the catch of each stroke (9, 25). With the same increase in cardiac output during exercise, an inspired O2 fraction of 0.30 attenuated the widened alveolar-arterial O2 pressure difference by ~75% (35), indicating that a ventilation-perfusion mismatch (16) comprises <25% of a pulmonary limitation to O2 diffusion.

Muscle oxygenation. Because the use of a femoral catheter is not practical during all-out rowing, an alternative approach to evaluate oxygenation in the muscle capillary bed is to use near-infrared spectroscopy. In a study by Chance et al. (8), all-out rowing provoked an immediate desaturation in the vastus lateralis muscle that reached a steady state in the first minute, with an abrupt resaturation after cessation of exercise. Chance et al. (8) described the desaturation as a percent change in absorbance and emphasized that the near-infrared spectroscopy response of muscles reflects only hemoglobin in the capillary bed. In support, the near-infrared spectroscopy-determined desaturation during exercise appears not to be related to desaturation of myoglobin (32). In response to a moderate cycling intensity, the concentration change in total hemoglobin is elevated 8 µM with no change in Delta HbO2 (17) as muscle blood volume becomes enhanced (37).

The increase in Delta Hb by 22 µM during rowing reflects muscle hemoglobin desaturation of 10% (4, 5), similar to the central venous O2 saturation obtained in the present study. Also, Mancini et al. (32) showed a correlation between muscle hemoglobin desaturation and venous O2 saturation in blood from a forearm vein that drained the exercising muscle. The level of muscle desaturation during rowing may represent the level of capillary O2 extraction when a large increase in cardiac output and, in turn, the muscle blood flow decreases the red cell transit time in the muscle capillaries. This is illustrated by the observation that the hemoglobin desaturation was <2% of that obtained by circulatory arrest (6, 8), indicating that the homeostatic adjustments are insufficient to maintain the muscle O2 concentration, especially during the vigorous muscle contraction involved in rowing. The expected sequential O2 desaturation of Hb and cytochrome aa3 (Ref. 8 and Fig. 2) implies a pronounced imbalance of O2 supply and demand. During the all-out rowing protocol, the muscle blood volume, expressed as the concentration change in total hemoglobin, is affected by limb motion and muscle contraction (8), and the present results correspond to the pulsating muscle blood flow during exercise (2). However, it should be considered that muscle contractions may affect the geometry of the muscle and, in turn, the scattering of light.

During exercise with an elevated inspired O2 fraction, arterial O2 saturation remained at the resting level and CaO2 was elevated by 7%, yet the oxygenation in the capillary bed of muscle reached a level similar to that reached with intense arterial desaturation. Even during exercise involving a small muscle mass, such as leg kicking, muscle O2 desaturation is not influenced by pronounced hyperoxia or moderate hypoxia associated with a reduction in arterial hemoglobin O2 saturation to 85% (27). It could be that near-infrared spectroscopy does not detect small changes in blood O2 saturation. However, Elwell et al. (12) demonstrated that near-infrared spectroscopy responds to an abrupt change in arterial O2 hemoglobin saturation from 90 to 100%, which is within the range of arterial desaturation in the present study. Thus, because the near-infrared spectroscopy signal reflects light attenuation to a depth of several centimeters, these results suggest that during exercise, when an elevated inspired O2 fraction increases CaO2, the O2 delivery to the muscles is not elevated.

Previous studies on hyperoxia have demonstrated that blood flow to the working muscles may decrease (48) or remain unchanged (24) during exercise involving only the legs. This should be considered in view of only a small increase in power (35, 38) and an increase in femoral venous O2 pressure proportionally greater than the increase in leg VO2 max (24). Although it could be argued that the small increases in O2 uptake and exercise capacity were attributable to an increase in O2 extraction, the present results suggest that an enhanced performance with O2 supplementation may also relate to other mechanisms, i.e., attenuated cerebral hypoxemia.

Cerebral oxygenation. The cerebral oximeter reflects cerebral hypoperfusion during central hypovolemia induced by head-up tilt (28), in which oxygenated hemoglobin decreases 5 µM (29). Also, ScO2 decreases with a reduction in arterial O2 pressure (33, 39). However, although both arterial hemoglobin O2 saturation and ScO2 decrease during exercise, ScO2 is influenced by hypo- and hypercapnia (28, 40). On the basis of earlier data incorporating hyperventilation and CO2-supplemented ventilation, the reduction in arterial CO2 pressure during rowing is too small to account for the changes in ScO2 (28). Thus, in the present study, with cycling associated with modest hypocapnia and arterial hemoglobin O2 saturation maintained at the resting level, ScO2 was not affected. Furthermore, in the immediate recovery from rowing ScO2 increased above baseline, although it was reduced to levels below that obtained during exercise. The decreased ScO2 during exercise corresponds to the level of cerebral hypoxemia observed during hypovolemic shock and congestive heart failure (30).

It may be that, regardless of arterial CO2 pressure levels, ScO2 is influenced by regional changes in cerebral blood flow in response to activation of the motor area (23, 47). Transcranial Doppler measures have demonstrated a 20% increase in middle cerebral artery blood flow velocity during dynamic exercise (21, 26, 31), whereas that of the anterior cerebral artery was not changed (20). The heterogeneity of cerebral blood flow is illustrated in that, during a unilateral finger-opposition task, Delta Hb and Delta HbO2 of the contralateral sensorimotor area become reduced and increased, respectively, whereas only minor changes are seen in the "inactive" motor area (23). When several muscle groups are involved in exercise, other parts of the brain may suffer from a decrease in blood flow, because global cerebral blood flow and O2 uptake are not affected by exercise (31). This may be the case during rowing, because transcranial Doppler measures demonstrate only a 12% increase in middle cerebral artery blood flow velocity (41). Furthermore, the blood flow velocity mimicked a sinusoidal function with the maximum when force was highest and with the minimum during the recovery phase of rowing (41).

Limitations to the study. First, although venous blood sampling does not represent true mixed venous values, the level of arterial-venous O2 difference corresponds to that reported during exercise associated with an O2 uptake >5 l/min (1). Second, the O2 uptake tends to be overestimated during hyperoxia (49); however, the exercise test system used in the present study has proven reliable with an inspired O2 fraction of 0.30 (43). Third, in terms of perfusion, near-infrared spectroscopy is demonstrated to reflect changes in cerebral blood flow (30), but the differential cerebral flow distribution has not been determined during exercise involving a large muscle mass. Also, near-infrared spectroscopy-determined muscle O2 saturation during exercise in hyperoxic conditions has been evaluated in only one other study (27). Muscle O2 saturation in normoxia reflects muscular metabolism (4, 5), but only to a tissue depth of a few centimeters (30).

We conclude that during maximal exercise arterial hemoglobin O2 saturation and regional cerebral oxygenation decrease to be maintained at resting levels with moderate hyperoxia. Exercise performance was also elevated without a change in muscle oxygenation, indicating that cerebral hypoxemia appears to be a contributing factor for limitation of exercise capacity.


    ACKNOWLEDGEMENTS

Heidi Hansen and Victor Feddersen are acknowledged for excellent technical assistance. Benny Larsson is thanked for the rowing variability results.


    FOOTNOTES

H. B. Nielsen was funded by the Copenhagen Muscle Research Center. The study was supported by The Danish National Research Foundation Grant No. 504-14. We also acknowledge the Danish Sports Research Council and Team Denmark.

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: H. B. Nielsen, Dept. of Anesthesia, 2041, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark (E-mail: h.bay{at}dadlnet.dk).

Received 11 November 1998; accepted in final form 30 April 1999.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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12.   Elwell, C. E., M. Cope, A. D. Edwards, J. S. Wyatt, D. T. Delpy, and E. O. R. Reynolds. Quantification of adult cerebral hemodynamics by near-infrared spectroscopy. J. Appl. Physiol. 77: 2753-2760, 1994[Abstract/Free Full Text].

13.   Hanel, B., P. S. Clifford, and N. H. Secher. Restricted postexercise pulmonary diffusion capacity does not impair maximal transport for O2. J. Appl. Physiol. 77: 2408-2412, 1994[Abstract/Free Full Text].

14.   Hanel, B., I. Teunissen, A. Rabøl, J. Warberg, and N. H. Secher. Restricted postexercise pulmonary diffusion capacity and central blood volume depletion. J. Appl. Physiol. 83: 11-17, 1997[Abstract/Free Full Text].

15.   Holmqvist, N., N. H. Secher, K. Sander-Jensen, U. Knigge, J. Warberg, and T. W. Schwartz. Sympathoadrenal and parasympathetic responses to exercise. J. Sports Sci. 4: 123-128, 1986[Medline].

16.   Hopkins, S. R., D. C. McKenzie, R. B. Schoene, R. W. Glenny, and H. T. Robertson. Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation. J. Appl. Physiol. 77: 912-917, 1994[Abstract/Free Full Text].

17.   Ide, K., F. Pott, J. J. Van Lieshout, and N. H. Secher. Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass. Acta Physiol. Scand. 162: 13-20, 1998[Medline].

18.   Jensen, K., T. S. Nielsen, Å. Fiskestrand, J. O. Lund, N. J. Christensen, and N. H. Secher. High-altitude training does not increase maximal oxygen uptake or work capacity at sea level in rowers. Scand. J. Med. Sci. Sports 3: 256-262, 1993.

19.   Jöbsis, F. F. Noninvasive, infrared monitoring of cerebral and myocardial oxygen sufficiency and circulatory parameters. Science 198: 1264-1267, 1977[Abstract/Free Full Text].

20.   Jørgensen, L. G., G. Perko, and N. H. Secher. Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans. J. Appl. Physiol. 73: 1825-1830, 1992[Abstract/Free Full Text].

21.   Jørgensen, L. G., M. Perko, B. Hanel, T. V. Schroeder, and N. H. Secher. Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans. J. Appl. Physiol. 72: 1123-1132, 1992[Abstract/Free Full Text].

22.   Kjaer, M., N. J. Christensen, B. Sonne, E. A. Richter, and H. Galbo. Effect of exercise on epinephrine turnover in trained and untrained male subjects. J. Appl. Physiol. 59: 1061-1067, 1985[Abstract/Free Full Text].

23.   Kleinschmidt, A., H. Obrig, M. Requardt, K. D. Merboldt, U. Dirnagl, A. Villringer, and J. Frahm. Simultaneous recording of cerebral blood oxygenation changes during human brain activation by magnetic resonance imaging and near-infrared spectroscopy. J. Cereb. Blood Flow Metab. 16: 817-826, 1996[Medline].

24.   Knight, D. R., W. Schaffartzik, D. C. Poole, M. C. Hogan, D. E. Bebout, and P. D. Wagner. Effects of hyperoxia on maximal leg O2 supply and utilization in men. J. Appl. Physiol. 75: 2586-2594, 1993[Abstract/Free Full Text].

25.   Lassen, A., J. H. Mitchell, D. R. Reeves, Jr., H. B. Rogers, and N. H. Secher. Cardiovascular responses to brief static contractions in man with topical nervous blockade. J. Physiol. (Lond.) 409: 333-341, 1989[Abstract/Free Full Text].

26.   Linkis, P., L. G. Jørgensen, H. L. Olesen, P. L. Madsen, N. A. Lassen, and N. H. Secher. Dynamic exercise enhances regional cerebral artery mean flow velocity. J. Appl. Physiol. 78: 12-16, 1995[Abstract/Free Full Text].

27.   MacDonald, M. J., M. A. Tarnopolsky, H. J. Green, and R. L. Hughson. Comparison of femoral blood gases and muscle near-infrared spectroscopy at exercise onset in humans. J. Appl. Physiol. 86: 687-693, 1999[Abstract/Free Full Text].

28.   Madsen, P., F. Lyck, M. Pedersen, H. L. Olesen, H. B. Nielsen, and N. H. Secher. Brain and muscle oxygen saturation during head-up-tilt-induced central hypovolaemia in humans. Clin. Physiol. 15: 523-533, 1995[Medline].

29.   Madsen, P., F. Pott, S. B. Olsen, H. B. Nielsen, I. Burcev, and N. H. Secher. Near-infrared spectrophotometry determined brain oxygenation during fainting. Acta Physiol. Scand. 162: 501-507, 1998[Medline].

30.   Madsen, P. L., and N. H. Secher. Near-infrared oximetry of the brain. Prog. Neurobiol. 58: 541-560, 1999[Medline].

31.   Madsen, P. L., B. K. Sperling, T. Warming, J. F. Schmidt, N. H. Secher, G. Wildschiødtz, S. Holm, and N. A. Lassen. Middle cerebral artery blood velocity and cerebral blood flow and O2 uptake during dynamic exercise. J. Appl. Physiol. 74: 245-250, 1993[Abstract/Free Full Text].

32.   Mancini, D. M., L. Bolinger, H. Li, K. Kendrick, B. Chance, and J. R. Wilson. Validation of near-infrared spectroscopy in humans. J. Appl. Physiol. 77: 2740-2747, 1994[Abstract/Free Full Text].

33.   McCormick, P. W., M. Stewart, M. G. Goetting, and G. Balakrishnan. Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans. Stroke 22: 596-602, 1991[Abstract/Free Full Text].

34.   Nielsen, H. B. pH after competitive rowing: the lower physiological range? Acta Physiol. Scand. 165: 113-114, 1999[Medline].

35.   Nielsen, H. B., P. Madsen, L. B. Svendsen, R. C. Roach, and N. H. Secher. The influence of PaO2, pH and SaO2 on maximal oxygen uptake. Acta Physiol. Scand. 164: 89-97, 1998[Medline].

36.   Obrig, H., C. Hirth, J. G. Junge-Hulsing, C. Doge, T. Wolf, U. Dirnagl, and A. Villringer. Cerebral oxygenation changes in response to motor stimulation. J. Appl. Physiol. 81: 1174-1183, 1996[Abstract/Free Full Text].

37.   Pawelczyk, J. A., B. Hanel, R. A. Pawelczyk, J. Warberg, and N. H. Secher. Leg vasoconstriction during dynamic exercise with reduced cardiac output. J. Appl. Physiol. 73: 1838-1846, 1992[Abstract/Free Full Text].

38.   Peltonen, J. E., J. Rantamäki, S. P. T. Niittymäki, K. Sweins, J. T. Viitasalo, and H. K. Rusko. Effects of oxygen fraction in inspired air on rowing performance. Med. Sci. Sports Exerc. 27: 573-579, 1995[Medline].

39.   Pollard, V., D. S. Prough, A. E. DeMelo, D. J. Deyo, T. Uchida, and H. F. Stoddart. Validation in volunteers of near-infrared spectroscope for monitoring brain oxygenation in vivo. Anesth. Analg. 82: 269-277, 1996[Abstract].

40.   Pollard, V., D. S. Prough, A. E. DeMelo, D. J. Deyo, T. Uchida, and R. Widman. The influence of carbon dioxide and body position on near-infrared spectroscopic assessment of cerebral hemoglobin oxygen saturation. Anesth. Analg. 82: 278-287, 1996[Abstract].

41.   Pott, F., L. Knudsen, M. Nowak, H. B. Nielsen, B. Hanel, and N. H. Secher. Middle cerebral artery blood velocity during rowing. Acta Physiol. Scand. 160: 251-255, 1997[Medline].

42.   Powers, S. K., L. Lawler, J. A. Dempsey, S. Dodd, and G. Landry. Effects of incomplete pulmonary gas exchange on VO2 max. J. Appl. Physiol. 66: 2491-2495, 1989[Abstract/Free Full Text].

43.   Prieur, F., T. Busso, J. Castells, R. Bonnefoy, H. Benoit, A. Geyssant, and C. Denis. Validity of oxygen uptake measurements during exercise under moderate hyperoxia. Med. Sci. Sports Exerc. 30: 958-962, 1998[Medline].

44.   Rasmussen, J., B. Hanel, B. Diamant, and N. H. Secher. Muscle mass effect on arterial desaturation after maximal exercise. Med. Sci. Sports Exerc. 23: 1349-1352, 1991[Medline].

45.   Rosiello, R. A., D. A. Mahler, and J. L. Ward. Cardiovascular responses to rowing. Med. Sci. Sports Exerc. 19: 239-245, 1987[Medline].

46.   Skak, C., A. Rasmussen, P. Kirkegaard, and N. H. Secher. Cerebral oxygen saturation and blood flow during liver transplantation. Anesth. Analg. 84: 730-733, 1997[Abstract].

47.   Weiler, C., M. Jüptner, S. Fellows, M. Rijntjes, G. Leonhardt, S. Kiebel, S. Müller, H. C. Diener, and A. F. Thilmann. Brain representation of active and passive movements. Neuroimage 4: 105-110, 1996[Medline].

48.   Welch, H. G., F. Bonde-Petersen, T. Graham, K. Klausen, and N. H. Secher. Effect of hyperoxia on leg blood flow and metabolism during exercise. J. Appl. Physiol. 42: 385-390, 1977[Abstract/Free Full Text].

49.   Welch, H. G., and P. K. Pedersen. Measurement of metabolic rate in hyperoxia. J. Appl. Physiol. 51: 725-731, 1981[Abstract/Free Full Text].

50.   Wray, S., M. Cope, D. T. Delpy, J. S. Wyatt, and E. O. Reynolds. Characterization of the near infrared absorption spectra of cytochrome aa3 and haemoglobin for the non-invasive monitoring of cerebral oxygenation. Biochim. Biophys. Acta 933: 184-192, 1988[Medline].

Am J Physiol Heart Circ Physiol 277(3):H1045-H1052
0002-9513/99 $5.00 Copyright © 1999 the American Physiological Society


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