Effect of obesity and metabolic syndrome on hypoxic vasodilation

This study was designed to test whether obese adults and adults with metabolic syndrome (MetSyn) exhibit altered hyperemic responses to hypoxia at rest and during forearm exercise when compared with lean controls. We hypothesized blood flow responses due to hypoxia would be lower in young obese subjects (n = 11, 24 ± 2 years, BMI 36 ± 2 kg m⁻²) and subjects with MetSyn (n = 8, 29 ± 3 years BMI 39 ± 2 kg m⁻²) when compared with lean adults (n = 13, 29 ± 2 years, BMI 24 ± 1 kg m⁻²). We measured forearm blood flow (FBF, Doppler Ultrasound) and arterial oxygen saturation (pulse oximetry) during rest and steady-state dynamic forearm exercise (20 contractions/min at 8 and 12 kg) under two conditions: normoxia (0.21 F_iO₂, ~98% S_aO₂) and hypoxia (~0.10 F_iO₂, 80% S_aO₂). Forearm vascular conductance (FVC) was calculated as FBF/mean arterial blood pressure. At rest, the percent change in FVC with hypoxia was greater in adults with MetSyn when compared with lean controls (p = 0.02); obese and lean adult responses were not statistically different. Exercise increased FVC from resting levels in all groups (p < 0.05). Hypoxia caused an additional increase in FVC (p < 0.05) that was not different between groups; responses to hypoxia were heterogeneous within and between groups. Reporting FVC responses as absolute or percent changes led to similar conclusions. These results suggest adults with MetSyn exhibit enhanced hypoxic vasodilation at rest. However, hypoxic responses during exercise in obese adults and adults with MetSyn were not statistically different when compared with lean adults. Individual hypoxic vasodilatory responses were variable, suggesting diversity in vascular control.     

Intracellular hyperhydration induced by a 7-day endurance race

A group of 15 competitive male cyclists [mean peak oxygen uptake, V˙O_2peak 68.5 (SEM 1.5?ml?· kg^?1?·?min^?1)] exercised on a cycle ergometer in a protocol which began at an intensity of 150?W and was increased by 25?W every 2?min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (S _aO₂), with all values corrected for rectal temperature. The S _a O₂ was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (P _aO₂) was seen at the first exercise intensity (150?W, about 40% V˙O_2peak). A further significant decrease in P _aO₂ occurred at 200?W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350?W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (P _aCO₂) was unchanged up to an exercise intensity of 250?W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375?W [34.5 (SEM 0.5) mmHg]. During both the first (150?W) and final exercise intensities (V˙O_2peak) P _aO₂ was correlated significantly with both partial pressure of oxygen in alveolar gas (P _AO₂, r?=?0.81 and r?=?0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P _A?aO₂, r?=?0.63 and r?=?0.86, respectively) but not with P _aCO₂. At V˙O_2peak P _aO₂ was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r?=?0.58 and r?=?0.53, respectively). When both P _AO₂ and P _A?aO₂ were combined in a multiple linear regression model, at least 95% of the variance in P _aO₂ could be explained at both 150?W and V˙O_2peak. A significant downward trend in S _aO₂ was seen with increasing exercise intensity with the lowest value at 375?W [94.6 (SEM 0.3)%]. Oximetry estimates of S _aO₂ were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350?W. The significant correlations between P _aO₂ and P _AO₂ with the first exercise intensity and at V˙O_2peak led to the conclusion that inadequatehyperventilation is a major contributor to exercise-induced hypoxaemia.     

Effects of breathing control on cardiocirculatory modulation in Caucasian lowlanders and Himalayan Sherpas

This study was performed to investigate the influence of breathing control on the autonomic cardiac regulation at high altitude in adapted and non-adapted awake subjects. We recorded electrocardiogram and pulse oximetry in 14 short-term acclimatized lowlanders and 14 Himalayan Sherpas during resting conditions at an altitude of 5,050 m. Spectrum analysis was performed on synchronized 15 min periods of R-R intervals and the oxygen saturation of arterial blood (S_aO₂). Despite mean S_aO₂ being similar in lowlanders and Himalayan Sherpas [78.5 (SD 7.0)% compared to 79.4 (SD5.8)%, respectively], fluctuations in S_aO₂ were significantly increased in lowlanders compared to Sherpas, thus indicating an unstable regulation of respiration control in lowlanders. Regression analysis demonstrated a significant relationship between spectrum power of S_aO₂ and the relative power of R-R intervals in the frequency band between 0.01 and 0.08 Hz in lowlanders, but not in Sherpas. Our results demonstrate differences in respiratory and autonomic cardiac control between non-adapted lowlanders and Himalayan high-altitude residents and indicate that unstable breathing control during chronic hypobaric hypoxia is significantly correlated with the autonomic cardiocirculatory regulation. Accepted: 11 September 2000     

Influence of hypoxic ventilatory response on arterial O2 saturation during maximal exercise in acute hypoxia

The aim of this study was to evaluate the influence of peripheral chemosensitivity estimated by hypoxic ventilatory response (HVR) on arterial oxygen saturation (S _aO₂) during maximal exercise in acute hypoxia. A group of 16 healthy men performed maximal exercise in two conditions of partial pressure of inspired oxygen (P _IO₂/149 and 70 mm Hg, 19.8 and 9.3 kPa). Measurements of maximal oxygen uptake ( ) andS _aO₂ using an ear-oximeter were carried out in both conditions ofP _IO₂. The HVR was measured at rest by progressive isocapnic hypoxia and evaluated by the slope of the linear regression between the ventilatory flow ( ) and theS _aO₂ ( ). The absolute value of HVR (in litres per minute per percentage saturation per kilogram) was correlated to maximal expired (r = 0.85,P < 0.001), ventilatory equivalent for CO₂ (r = 0.83,P < 0.001) andS _aO₂ (r = 0.60,P < 0.05) determined during maximal exercise in hypoxia: a significant decrease in (37%) andS _aO₂ (32%) forP _IO₂ of 70 mm Hg (9.3 Pa) was observed (P < 0.001). The correlation between the decline of and arterial oxygen desaturation failed to reach statistical significance (r = 0.47, P = 0.1). The present findings indicated that the peripheral ventilatory chemosensitivity contributed to the interindividual variability of andS _aO₂ during maximal exercise in acute hypoxia.     

Effect of acute normobaric hypoxia on quadriceps integrated electromyogram and blood metabolites during incremental exercise to exhaustion

This investigation analysed the effects of environmental hypoxia (EH) on changes in quadriceps integrated electromyogram (iEMG) and metabolite accumulation during incremental cycle ergometry. Trained male subjects (n = 14) were required to complete two maximal oxygen uptake tests, one test during EH (F _IO₂ = 0.135), the other during normoxia (F _IO₂ = 0.2093). The EMG were recorded at each exercise intensity from the vastus lateralis, rectus femoris and vastus medialis muscles over 60 cycle revolutions. Mean integral values were then calculated. Blood was collected from the radial vein of consenting subjects (n = 8) at the end of each exercise intensity. Oxygen saturation of arterial blood (S _aO₂) was estimated using pulse oximetry. Gas exchange variables were collected on-line every 15 s. The results indicated that, without exception, EH significantly reduced total exercise time. Mean time to exhaustion in EH was 26.34 (SD 2.58) min compared with 35.25 (SD 4.21) min during N. The S _aO₂ values indicated that severe arterial desaturation had been achieved by EH. Mean values for obtained in EH were 49 ml·kg·min^–1, compared with 59 ml · kg· min^–1 attained in N. Plasma lactate and ammonia concentrations were both significantly higher in EH. Increases in lactate and ammonia concentration were highly correlated in both N and EH. The onset of plasma lactate and ammonia accumulation occurred at the same exercise intensity in N. The iEMG responses of all three quadriceps muscles tended to be greater in the EH trials, although this difference was not significant. The basis for iEMG nonsignificance may have been related to large within sample variation in iEMG, sample size and the severity of the hypoxia induced.     

Exercise stimulus increases ventilation from maximal to supramaximal intensity

This study investigated the influence of an exercise stimulus on pulmonary ventilation (V _E) during severe levels of exercise in a group of ten athletes. The altered ventilation was assessed in relation to its effect on blood gas status, in particular to the incidence and severity of exercise induced hypoxaemia. Direct measurements of arterial blood were made at rest and during the last 15 s of two intense periods of cycling; once at an intensity found to elicit maximal oxygen uptake (VO_2max; MAX) and once at an intensity established to require 115% ofVO_2max (SMAX). Oxygen uptake (VO₂) and ventilatory markers were continually recorded during the exercise and respiratory flow-volume loops were measured at rest and during the final 30 s of each minute for both exercise intensities. When compared to MAX exercise, the subjects had higher ventilation and partial pressure of arterial oxygen (P _aO₂) during the SMAX intensity. Regression analysis for both conditions indicated the levels ofP _aO₂ and oxygen saturation of arterial blood (S _aO₂) were positively correlated with relative levels of ventilation during exercise. It was apparent that mechanical constraints to ventilate further were not present during the MAX test since the subjects were able to elevateV _E during SMAX and attenuate the level of hypoxaemia. This was also confirmed by analysis of the flow volume recordings. These data support the conclusions firstly, that overwhelming mechanical constraints onV _E were not present during the MAX exercise, secondly, the subjects exhibiting the most severe hypoxaemia had no consistent relationship with any measure of expiratory flow limitation, and thirdly, ventilatory patterns during intense exercise are strong predictors of blood gas status.     

Effect of acute hypoxia on muscle blood flow, VO2p, and [HHb] kinetics during leg extension exercise in older men

The adjustment of pulmonary oxygen uptake (VO_2p), heart rate (HR), limb blood flow (LBF), and muscle deoxygenation [HHb] was examined during the transition to moderate-intensity, knee-extension exercise in six older adults (70 ± 4 years) under two conditions: normoxia (FIO₂ = 20.9 %) and hypoxia (FIO₂ = 15 %). The subjects performed repeated step transitions from an active baseline (3 W) to an absolute work rate (21 W) in both conditions. Phase 2 VO_2p, HR, LBF, and [HHb] data were fit with an exponential model. Under hypoxic conditions, no change was observed in HR kinetics, on the other hand, LBF kinetics was faster (normoxia 34 ± 3 s; hypoxia 28 ± 2), whereas the overall [HHb] adjustment ( $ \tau^{\prime } = {\text{TD}} + \tau $ ) was slower (normoxia 28 ± 2; hypoxia 33 ± 4 s). Phase 2 VO_2p kinetics were unchanged (p < 0.05). The faster LBF kinetics and slower [HHb] kinetics reflect an improved matching between O₂ delivery and O₂ utilization at the microvascular level, preventing the phase 2 VO_2p kinetics from become slower in hypoxia. Moreover, the absolute blood flow values were higher in hypoxia (1.17 ± 0.2 L min^?1) compared to normoxia (0.96 ± 0.2 L min^?1) during the steady-state exercise at 21 W. These findings support the idea that, for older adults exercising at a low work rate, an increase of limb blood flow offsets the drop in arterial oxygen content (CaO₂) caused by breathing an hypoxic mixture.     

Effect of supplemental oxygen on post-exercise inflammatory response and oxidative stress

This investigation explored the influence of supplemental oxygen administered during the recovery periods of an interval-based running session on the post-exercise markers of reactive oxygen species (ROS) and inflammation. Ten well-trained male endurance athletes completed two sessions of 10 × 3 min running intervals at 85 % of the maximal oxygen consumption velocity (vVO_2peak) on a motorised treadmill. A 90-s recovery period was given between each interval, during which time the participants were administered either a hyperoxic (HYP) (Fraction of Inspired Oxygen (F_IO₂) 99.5 %) or normoxic (NORM) (F_IO₂ 21 %) gas, in a randomized, single-blind fashion. Pulse oximetry (S_pO₂), heart rate (HR), blood lactate (BLa), perceived exertion (RPE), and perceived recovery (TQRper) were recorded during each trial. Venous blood samples were taken pre-exercise, post-exercise and 1 h post-exercise to measure Interleukin-6 (IL-6) and Isoprostanes (F₂-IsoP). The S_pO₂ was significantly lower than baseline following all interval repetitions in both experimental trials (p < 0.05). The S_pO₂ recovery time was significantly quicker in the HYP when compared to the NORM (p < 0.05), with a trend for improved perceptual recovery. The IL-6 and F₂-IsoP were significantly elevated immediately post-exercise, but had significantly decreased by 1 h post-exercise in both trials (p < 0.05). There were no differences in IL-6 or F₂-IsoP levels between trials. Supplemental oxygen provided during the recovery periods of interval based exercise improves the recovery time of S_PO₂ but has no effect on post-exercise ROS or inflammatory responses.     

Exercise-induced oxidative stress and hypoxic exercise recovery

Hypoxia due to altitude diminishes performance and alters exercise oxidative stress responses. While oxidative stress and exercise are well studied, the independent impact of hypoxia on exercise recovery remains unknown. Accordingly, we investigated hypoxic recovery effects on post-exercise oxidative stress. Physically active males (n = 12) performed normoxic cycle ergometer exercise consisting of ten high:low intensity intervals, 20 min at moderate intensity, and 6 h recovery at 975 m (normoxic) or simulated 5,000 m (hypoxic chamber) in a randomized counter-balanced cross-over design. Oxygen saturation was monitored via finger pulse oximetry. Blood plasma obtained pre- (Pre), post- (Post), 2 h post- (2Hr), 4 h post- (4Hr), and 6 h (6Hr) post-exercise was assayed for Ferric Reducing Ability of Plasma (FRAP), Trolox Equivalent Antioxidant Capacity (TEAC), Lipid Hydroperoxides (LOOH), and Protein Carbonyls (PC). Biopsies from the vastus lateralis obtained Pre and 6Hr were analyzed by real-time PCR quantify expression of Heme oxygenase 1 (HMOX1), Superoxide Dismutase 2 (SOD2), and Nuclear factor (euthyroid-derived2)-like factor (NFE2L2). PCs were not altered between trials, but a time effect (13 % Post-2Hr increase, p = 0.044) indicated exercise-induced blood oxidative stress. Plasma LOOH revealed only a time effect (p = 0.041), including a 120 % Post-4Hr increase. TEAC values were elevated in normoxic recovery versus hypoxic recovery. FRAP values were higher 6Hr (p = 0.045) in normoxic versus hypoxic recovery. Exercise elevated gene expression of NFE2L2 (20 % increase, p = 0.001) and SOD2 (42 % increase, p = 0.003), but hypoxic recovery abolished this response. Data indicate that recovery in a hypoxic environment, independent of exercise, may alter exercise adaptations to oxidative stress and metabolism.     

Respiratory muscle endurance training in humans increases cycling endurance without affecting blood gas concentrations

Isolated respiratory muscle endurance training (RMT) can prolong constant-intensity cycling performance. We tested whether RMT affects O₂ supply during exercise, i.e. whether the partial pressure of oxygen in arterial blood (P _aO₂) and/or its oxygen saturation (S _aO₂) are higher during exercise after RMT than before. A group of 28 sedentary subjects were randomly assigned to either an RMT (n=13) or a control group (n=15). The RMT consisted of 40×30 min sessions of normocapnic hyperpnoea. The control group did not perform any training. Breathing and cycling endurance time as well as P _aO₂ and S _aO₂ during cycling at a constant intensity of 70% maximum power output were measured before and after the RMT or the control period. Mean breathing endurance increased significantly after RMT compared to control [RMT 5.2 (SD 2.9) vs 38.1 (SD 6.8) min, control 6.5 (SD 5.7) vs 6.4 (SD 7.6) min; P<0.01], as did mean cycling endurance [RMT 35.6 (SD 11.9) vs 44.0 (SD 17.2) min, control 32.8 (SD 11.6) vs 31.4 (SD 14.4) min; P<0.05]. The RMT did not affect P _aO₂ which ranged from 11.6 to 12.3 kPa (87–92 mmHg), and S _aO₂ which ranged from 96% to 98% throughout all tests. In conclusion, RMT substantially increased breathing and cycling endurance in sedentary subjects. These changes, however, cannot be attributed to increased O₂ supply, as neither P _aO₂ nor S _aO₂ were increased during exercise after RMT. Electronic Publication     

Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (V˙O_{2 max} ) 3.39 (SEM 0.21) l?·?min^?1] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA?·?day^?1. Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (P _aO₂), partial pressure of carbon dioxide in arterial blood (P _aCO₂), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in P _aO₂ (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% V˙O_{2 max} in Ctrl reaching 75.9 (SEM 2.1) at V˙O_{2 max} . PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P?P _aO₂–oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P _(A?a)O₂) at V˙O_{2 max} [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while P _aCO₂, remained unchanged. Indomethacin had no effect on either P _aO₂, ideal partial pressure of oxygen in alveolar gas or P _(A?a)O₂ in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while V˙CO₂, P _aCO₂ and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise P _aO₂ behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.     

Muscle metabolism from near infrared spectroscopy during rhythmic handgrip in humans

The rate of metabolism in forearm flexor muscles (MO₂) was derived from near-infrared spectroscopy (NIRS-O₂) during ischaemia at rest rhythmic handgrip at 15% and 30% of maximal voluntary contraction (MVC), post-exercise muscle ischaemia (PEMI), and recovery in seven subjects. The MO₂ was compared with forearm oxygen uptake (O₂) [flow?×?(oxygen saturation in arnterial blood-oxygen saturation in venous blood, S _aO₂?S _vO₂)], and with the ³¹P-magnetic resonance spectroscopy-determined ratio of inorganic phosphate to phosphocreatine (P_I:PCr). During ischaemia at rest, the fall in NIRS-O₂ was more pronounced [76 (SEM 3) to 3 (SEM 1)%] than in S _vO₂ [71 (SEM 3) to 59 (SEM 2)%]. During the handgrip, NIRS-O₂ was lower at 30% compared to 15% MVC [58 (SEM 3) vs 67 (SEM 3)%] while the S _vO₂ was similar [29 (SEM 3) vs 31 (SEM 4)%]. Accordingly, MO₂ as well as P_I:PCr increased twofold, while V˙O₂ increased only 30%. During PEMI after 15% and 30% MVC, NIRS-O₂ fell to 9 (SEM 1)% and “0”, but the use of oxygen by forearm muscles was not reflected in S _vO₂. During reperfusion after PEMI, the peak NIRS-O₂ was lowest after intense exercise, while for S _vO₂ the reverse was seen. The discrepancies between NIRS-O₂ and S _vO₂, and therefore between the estimates of the metabolic rate, would suggest significant limitations in sampling venous blood which is representative of the flexor muscle capillaries. In support of this contention, S _vO₂ and venous pH decreased during the first seconds of reperfusion after PEMI. To conclude, NIRS-O₂ of forearm flexor muscles closely reflected the exercise intensity and the metabolic rate determined by magnetic resonance spectroscopy but not that rate derived from flow and the arterio-venous oxygen difference.     

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis

We have previously demonstrated a prolonged (65?min or longer) elevated plateau of esophageal temperature (T _es ) (0.5–0.6°C above pre-exercise values) in humans following heavy dynamic exercise (70% maximal oxygen consumption, V˙O_2max) at a thermoneutral temperature (T _a) of 29°C. The elevated T _es value was equal to the threshold T _es at which active skin vasodilation was initiated during exercise (Th_dil). A subsequent observation, i.e., that successive exercise/recovery cycles (performed at progressively increasing pre-exercise T _es levels) produced parallel increases of Th_dil and the post-exercise T _es, further supports a physiological relationship between these two variables. However, since all of these tests have been conducted at the same T _a (29°C) and exercise intensity (70% V˙O_2max) it is possible that the relationship is limited to a narrow range of T _a/exercise intensity conditions. Therefore, five male subjects completed 18?min of treadmill exercise followed by 20?min of recovery in the following T _a/exercise intensity conditions: (1) cool with light exercise, T _a?=?20°C, 45% V˙O_2max (CL); (2) temperature with heavy exercise, T _a?=?24°C, 75% O_{2 max} (TH); (3) warm with heavy exercise, T _a?=?29°C, 75% V˙O_2max (WH); and (4) hot with light exercise, T _a?=?40°C, 45% V˙O_2max (HL). An abrupt decrease in the forearm-to-finger temperature gradient (T _fa??T _fi) was used to identify the Th_dil during exercise. Mean pre-exercise T _es values were 36.80, 36.60, 36.72, and 37.20°C for CL, TH, WH, and HL conditions respectively. T _es increased during exercise, and end post-exercise fell to stable values of 37.13, 37.19, 37.29, and 37.55°C for CL, TH, WH, and HL trials respectively. Each plateau value was significantly higher than pre-exercise values (P?dil values (i.e., 37.20, 37.23, 37.37, and 37.48°C for CL, TH, WH, and HL) were comparable to the post-exercise T _es values for each condition. The relationship between Th_dil and post-exercise T _es remained intact in all T _a/exercise intensity conditions, providing further evidence that the relationship between these two variables is physiological and not coincidental.     

Rapidity of responding to a hypoxic challenge during exercise

The ability to modify power output (PO) in response to a changing stimulus during exercise is crucial for optimizing performance involving an integration system involving a performance template and feedback from peripheral receptors. The rapidity with which PO is modified has not been established, but would be of interest relative to understanding how PO is regulated. The objective is to determine the rapidity of changes in PO in response to a hypoxic challenge, and if change in PO is linked to changes in arterial O₂ saturation (S _aO₂). Well-trained cyclists performed randomly ordered 5-km time trials. Subjects began the trials breathing room air and switched to hypoxic (HYPOXIC, F_IO₂ = 0.15) or room (CONTROL, F_IO₂ = 0.21) air at 2 km, then to room air at 4 km. The time delay to begin decreasing S _aO₂ and PO and to recover S _aO₂ and PO on to room air was compared, along with the half time (t _1/2) during the HYPOXIC trial. Mean S _aO₂ and PO between 2 and 4 km were significantly different between CONTROL and HYPOXIC (94 ± 2 vs. 83 ± 2% and 285 ± 16 vs. 245 ± 19 W, respectively). There was no difference between the time delay for S _aO₂ (31.5 ± 12.8 s) and in PO (25.8 ± 14.4 s) or the recovery of S _aO₂ (29.0 ± 7.7 s) and PO (21.5 ± 12.4 s). The half time for decreases in S _aO₂ (56.6 ± 14.4 s) and in PO (62.7 ± 20.8 s) was not significantly different. Modifications of PO due to the abrupt administration of hypoxic air are related to the development of arterial hypoxemia, and begin within ~30 s.     

Arterial hypoxemia and performance during intense exercise

In order to determine the level of hypoxemia which is sufficient to impair maximal performance, seven well-trained male cyclists [maximum oxygen consumption (VO_2max)51·min^–1 or 60 ml·kg^–1·min^–1] performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia [percentage of arterial oxyhemoglobin saturation (%S _a O₂)>94%], and artificially induced mild (%S _aO₂=90±1%) and moderate (%S _aO₂=87±1%) hypoxemia. Performance, evaluated as the total work output (Work_tot) performed in the 5-min cycle test, progressively decreased with decreasing %S _aO₂ [mean (SE) Work_tot=107.40 (4.5) kJ, 104.07 (5.6) kJ, and 102.52 (4.7) kJ, under normoxemia, mild, and moderate hypoxemia, respectively]. However, only performance in the moderate hypoxemia condition was significantly different than in normoxemia (P=0.02). Mean oxygen consumption and heart rate were similar in the three conditions (P=0.18 andP=0.95, respectively). End-tidal partial pressure of CO₂ was significantly lower (P=0.005) during moderate hypoxemia compared with normoxemia, and ventilatory equivalent of CO₂ was significantly higher (P=0.005) in both hypoxemic conditions when compared with normoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an %S _aO₂ level of 87% but not under a milder desaturation level of 90%.     

Effects of prolonged bed rest on cardiovascular oxygen transport during submaximal exercise in humans

The hypothesis was tested that prolonged bed rest impairs O₂ transport during exercise, which implies a lowering of cardiac output Q˙ _c and O₂ delivery (_aO₂). The following parameters were determined in five males at rest and at the steady-state of the 100-W exercise before (B) and after (A) 42-day bed rest with head-down tilt at ?6°: O₂ consumption (V˙O₂), by a standard open-circuit method; Q˙ _c, by the pressure pulse contour method, heart rate (?f _c), stroke volume (Q _h), arterial O₂ saturation, blood haemoglobin concentration ([Hb]), arterial O₂ concentration (C _aO₂), and Q˙ _aO₂. The V˙O₂ was the same in A and in B, as was the resting f _c. The f _c at 100?W was higher in A than in B (+17.5%). The Q _h was markedly reduced (?27.7% and ?22.2% at rest and 100?W, respectively). The Q˙ _c was lower in A than in B [?27.6% and ?7.8% (NS) at rest and 100?W, respectively]. The C _aO₂ was lower in A than in B because of the reduction in [Hb]. Thus also Q˙ _aO₂ was lower in A than in B (?32.0% and ?11.9% at rest and at 100?W, respectively). The present results would suggest a down-regulation of the O₂ transport system after bed rest.     

The influence of PaO2, pH and SaO2 on maximal oxygen uptake

Influence of arterial oxygen pressure (P_aO₂) and pH on haemoglobin saturation (S_aO₂) and in turn on O₂ uptake (VO ₂) was evaluated during ergometer rowing (156, 276 and 376 W; VO _2max, 5.0 L min^?1; n = 11). During low intensity exercise, neither pH nor S_aO₂ were affected significantly. In response to the higher work intensities, ventilations (V_E) of 129 ± 10 and 155 ± 8 L min^?1 enhanced the end tidal PO₂ (P_ETO₂) to the same extent (117 ± 2 mmHg), but P_aO₂ became reduced (from 102 ± 2 to 78 ± 2 and 81 ± 3 mmHg, respectively). As pH decreased during maximal exercise (7.14 ± 0.02 vs. 7.30 ± 0.02), S_aO₂ also became lower (92.9 ± 0.7 vs. 95.1 ± 0.1%) and arterial O₂ content (C_aO₂) was 202 ± 3 mL L^?1. An inspired O₂ fraction (F_IO₂) of 0.30 (n = 8) did not affect V_E, but increased P_ETO₂ and P_aO₂ to 175 ± 4 and 164 ± 5 mmHg and the P_ETO₂–P_aO₂ difference was reduced (21 ± 4 vs. 36 ± 4 mmHg). pH did not change when compared with normoxia and S_aO₂ remained within 1% of the level at rest in hyperoxia (99 ± 0.1%). Thus, C_aO₂ and VO _2max increased to 212 ± 3 mL L^?1 and 5.7 ± 0.2 L min^?1, respectively. The reduced P_aO₂ became of importance for S_aO₂ when a low pH inhibited the affinity of O₂ to haemoglobin. An increased F_IO₂ reduced the gradient over the alveolar-arterial membrane, maintained haemoglobin saturation despite the reduction in pH and resulted in increases of the arterial oxygen content and uptake.     

Cardiopulmonary and metabolic responses in healthy elderly humans during a 1-week hiking programme at high altitude

Worldwide there are approximately 100 million visitors to high altitude annually and about 15% of those are elderly. Nevertheless, basic information on the cardiopulmonary and metabolic responses to physical activity at high altitude in the elderly is scarce. Therefore, we studied 20 voluntary healthy elderly subjects (55–77 years) who were randomly assigned to a low- (600 m) or a high altitude (2,000 m) group. Both groups increased the duration of their daily hiking from 2.5 to 5 h during a period of 1 week. Pre- and post-hiking cardiopulmonary variables at rest were measured daily. Exercise tests (3 min step test) were performed on days 1, 4 and 7. Of the morning values at rest, only arterial oxygen saturation (S _aO₂) had decreased after the 1st night at high altitude. After hiking however, S _aO₂ was diminished on all days at high altitude. Post-hiking heart rates increased from baseline on days 1 and 2 in the low- and on days 1–5 in the high-altitude group. Exercising S _aO₂ (%) in the three tests was decreased [84.9 (SD 2.8), 88.1 (SD 2.1), 87.2 (SD 2.3)] compared to baseline [93.2 (SD 2.0); P<0.05] and blood lactate concentrations were increased [3.1 (SD 0.7), 3.4 (SD 0.3), 3.3 (SD 0.2)] compared to baseline [2.7 (SD 0.6); P<0.05] in all tests at high altitude. The 1-week hiking programme was well tolerated by the healthy elderly at both low and high altitudes. Ventilatory adaptation to high altitude in the elderly seemed to have been completed within the first 2 days during the measurements at rest. However, cardiopulmonary and metabolic responses to exercise were increased and recovery from exercise was delayed during the 1-week hiking programme at high altitude. Heart rate and S _aO₂ measurements are considered to be highly sensitive in estimating the state of acclimatisation and for monitoring exercise intensity and duration at high altitude. Electronic Publication     

Pulmonary gas exchange during apnoea in exercising men

There is indirect evidence that cardiovascular responses to apnoea result in a temporary slowing of the O₂ uptake in the lungs in exercising humans. The present study was undertaken in an attempt to determine directly to what extent this occurs, and whether the magnitude of this slowing is such that it must be the result of concomitant cardiovascular readjustments and not merely a result of an isolated apnoea-induced fall in the arterial O₂ saturation (S _aO₂). Eight men performed 120 W leg exercise and performed repeated apnoeas of 10–40 s duration. Heart rate, S _aO₂, and breath-by-breath gas exchange were determined. Pulmonary O₂ uptake fell gradually as breath-holds proceeded by [mean (SEM)] 74 (3)% of the pre-apnoea O₂ uptake. This decrease was significantly larger than could be accounted for by the fall in S _aO₂ alone [S _aO₂ fall –30 (3)%], which it is estimated would have resulted in a fall of pulmonary O₂ uptake of –54 (5)%. We conclude that cardiovascular responses to apnoea contribute significantly to reducing pulmonary O₂ uptake during apnoea in exercising men. Electronic Publication     

The oxygen affinity of sickle hemoglobin

The right-shifted oxyhemoglobin dissociation curve of sickle cell disease (SCD) has been thought to result in abnormally low arterial oxygen saturation (S(o)(2)), even when oxygen partial pressure (P(o)(2)) is normal. However, without polymer formation (minimal under normoxic conditions), HbS oxygen affinity is normal. We hypothesized that in SCD, in vivo S(o)(2) is normal when P(o)(2) is normal. We retrospectively examined 50 blood gas and COoximetry samples from SCD patients and from controls matched for pH, P(o)(2), and carboxyhemoglobin. Control data fell close to the Severinghaus curve, as did non-hypoxemic ( [Formula: see text] ) SCD data. In contrast, hypoxemic (S(o)(2)) < 92.5% SCD data fell well below the standard curve. Thus, although SCD patients' oxygen affinity is low under hypoxic conditions, it is normal at normal arterial S(o)(2). Therefore, a finding of abnormally low saturation demonstrates that P(o)(2) is abnormally low. Given our previous finding that pulse oximetry faithfully reflects saturation in SCD, low pulse oximeter readings in SCD constitute reliable evidence of impaired gas exchange.