Intermittent hypoxia reduces cerebrovascular sensitivity to isocapnic hypoxia in humans

The purpose of this study was to determine the changes in human cerebrovascular function associated with intermittent poikilocapnic hypoxia (IH). Healthy men (n=8; 24+/-1 years) were exposed to IH for 10 days (12% O(2) for 5min followed by 5min of normoxia for 1h). During the hypoxic exposures, oxyhemoglobin saturation (SaO(2)) was 85% and the end-tidal partial pressure of CO(2) was permitted to fall as a result of hypoxic hyperventilation. Pre- and post-IH intervention subjects underwent a progressive isocapnic hypoxic test where ventilation, blood pressure, heart rate, and cerebral blood flow velocity (middle cerebral artery, transcranial Doppler) were measured to determine the ventilatory, cardiovascular and cerebrovascular sensitivities to isocapnic hypoxia. When compared to the pre-IH trial, cerebrovascular sensitivity to hypoxia significantly decreased (pre-IH=0.28+/-0.15; post-IH=0.16+/-0.14cms(-1)%SaO(2)(-1); P<0.05). No changes in ventilatory, blood pressure or heart rate sensitivity were observed (P>0.05). We have previously shown that the ability to oxygenate cerebral tissue measured using spatially resolved near infrared spectroscopy is significantly reduced following IH in healthy humans. Our collective findings indicate that intermittent hypoxia can blunt cerebrovascular regulation. Thus, it appears that intermittent hypoxia has direct cerebrovascular effects that can occur in the absence of changes to the ventilatory and neurovascular control systems.     

Effects of five nights of normobaric hypoxia on the ventilatory responses to acute hypoxia and hypercapnia

This study examined the effects of five nights of normobaric hypoxia on ventilatory responses to acute isocapnic hypoxia (AHVR) and hyperoxic hypercapnia (AHCVR). Twelve male subjects (26.6 +/- 4.1 years, standard deviation (S.D.)) slept 8-9 h per day overnight for 5 consecutive days at a simulated altitude of 4,300 m (FiO2= approximately 13.8%). Using the technique of dynamic end-tidal forcing, the AHVR and AHCVR were assessed twice prior to, immediately after, and 5 days following the hypoxic exposure. Immediately following the exposure, AHVR was increased by 1.6 +/- 1.3 L min(-1) %(-1) (P<0.01) when compared with control values. Likewise, after the exposure, ventilation in hyperoxia was increased (P<0.001) and was associated with both an increase in the slope (1.5 +/- 1.4 L min(-1) Torr(-1); P<0.05) and decrease in the intercept (-2.7 +/- 4.3 Torr; P<0.05) of the AHCVR. These results show that five nights of hypoxia can elicit similar perturbations, in both AHVR and AHCVR, as have been reported during more chronic altitude exposures.     

Protocol to measure acute cerebrovascular and ventilatory responses to isocapnic hypoxia in humans

This study describes a protocol to determine acute cerebrovascular and ventilatory (AHVR) responses to hypoxia. Thirteen subjects undertook a protocol twice, 5 days apart. The protocol started with 8 min of eucapnic euoxia (end-tidal P(CO2) (PET(CO2)= 1.5 Torr) above rest; end-tidal P(O2) (PET(O2)) = 88 Torr) followed by six descending 90 s hypoxic steps (PET(O2) = 75.2, 64.0, 57.0, 52.0, 48.2, 45.0 Torr). Then, PET(O2) was elevated to 300 Torr for 10 min while PET(O2) remained at eucapnia (5 min) then raised by 7.5 Torr (5 min). Peak blood flow velocity in the middle cerebral artery (MCA) and regional cerebral oxygen saturation (Sr(O2)) were measured with transcranial Doppler ultrasound and near-infrared spectroscopy, respectively, and indices of acute hypoxic sensitivity were calculated (AHR(CBF) and AHRSr(O2)). Values for AHR(CBF), AHRSr(O2) and AHVR were 0.43 cm s(-1) % desaturation(-1), 0.80% % desaturation(-1) and 1.24l min(-1) % desaturation(-1), respectively. Coefficients of variation for AHR(CBF), AHRSr(O2) and AHVR were small (range = 8.0-15.2%). This protocol appears suitable to quantify cerebrovascular and ventilatory responses to acute isocapnic hypoxia.     

Effect of raised potassium on ventilation in euoxia, hypoxia and hyperoxia at rest and during light exercise in man.

The purpose of this study was to determine whether changes in arterial plasma potassium concentration [K+]a affect expired ventilation (VE) in euoxia, hypoxia and hyperoxia during rest and light exercise in humans. Three periods of ventilatory measurements were undertaken in eight healthy subjects at rest and in seven other subjects during cycle ergometry (70 W). The first period of measurement was before the ingestion of 64 mmol of potassium chloride (KCl), the second 20 min after ingestion of KCl when [K+]a levels were elevated, and the third 3 h after the ingestion of KCl when [K+]a had returned substantially to normal. During each period, end-tidal PO2 was cycled between euoxia, hypoxia and hyperoxia, whilst the end-tidal PCO2 was maintained constant. The acute ventilatory response to hypoxia (AHVR) was calculated as the difference in VE during hypoxia and hyperoxia within each period of measurement. Oral KCl produced a 1.3 +/- 0.2 mM (mean +/- S.E.M.) increase in [K+]a at rest and a 0.8 +/- 0.2 mM increase during exercise. There was no significant difference in ventilation during euoxia between the three periods of measurement at rest or during exercise. There was a significant increase in AHVR with the rise in [K+]a of 21 min-1 mM-1 at rest (arterial PO2 during hypoxia ca 57 Torr) and 10 l min-1 mM-1 during exercise (arterial PO2 during hypoxia ca 52 Torr). There was a significant difference in the absolute increase in AHVR with [K+]a between rest and exercise, but this difference was not significant if the increase in AHVR with [K+]a was expressed as a percentage of the initial AHVR. We conclude that changes in [K+]a of the order of 1 mM have little effect on euoxic ventilation at rest or during light exercise in humans. We also conclude that [K+]a changes of this order increase AHVR at rest and during light exercise and that increases in [K+]a contribute to the increase in AHVR with exercise in humans.     

Prior sustained hypoxia attenuates interaction between hypoxia and exercise as ventilatory stimuli in humans

Both exercise and hypoxia increase pulmonary ventilation. However, the combined effects of the two stimuli are more than additive, such that exercise may be considered to potentiate the acute ventilatory response to hypoxia (AHVR), and vice versa. Exposure to sustained hypoxia of 8 h duration or more has been shown to increase the acute chemoreflex responses to hypoxia and hypercapnia. The purpose of this study was to determine whether sustained exposure to hypoxia also changed the stimulus interaction between the effects of exercise and hypoxia on ventilation. Ten subjects undertook two main protocols on two separate days. On one day, subjects were exposed to isocapnic hypoxia (IH) at an end-tidal partial pressure of O(2) of 55 mmHg and on the other day, subjects were exposed to air as a control (C). Before and after each exposure, the sensitivity of AHVR was assessed during both resting conditions and exercise at 35% of the subjects' maximal oxygen uptake capacity. Average values (means +/- s.d.) obtained for the sensitivity of AHVR from protocol IH were 0.85 +/- 0.35 (rest, prehypoxic exposure), 1.60 +/- 0.66 (exercise, prehypoxic exposure), 1.69 +/- 0.63 (rest, posthypoxic exposure) and 1.81 +/- 0.86 l min(-1) %(-1) (exercise, posthypoxic exposure). A non-dimensional variable, Phi, was used to quantify the interaction present between exercise and hypoxia. The variable Phi fell significantly following the sustained exposure to hypoxia (P < 0.02, ANOVA), indicating that the degree of stimulus interaction between acute hypoxia and exercise had declined. We suggest that the mechanisms by which sustained hypoxia modifies peripheral chemoreflex function may also modify the effects of exercise on the peripheral chemoreflex.     

The effect of hypoxia on pulmonary O2 uptake, leg blood flow and muscle deoxygenation during single-leg knee-extension exercise

The effect of hypoxic breathing on pulmonary O(2) uptake (VO(2p)), leg blood flow (LBF) and O(2) delivery and deoxygenation of the vastus lateralis muscle was examined during constant-load single-leg knee-extension exercise. Seven subjects (24 +/- 4 years; mean +/-s.d.) performed two transitions from unloaded to moderate-intensity exercise (21 W) under normoxic and hypoxic (P(ET)O(2)= 60 mmHg) conditions. Breath-by-breath VO(2p) and beat-by-beat femoral artery mean blood velocity (MBV) were measured by mass spectrometer and volume turbine and Doppler ultrasound (VingMed, CFM 750), respectively. Deoxy-(HHb), oxy-, and total haemoglobin/myoglobin were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). VO(2p) data were filtered and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. MBV data were filtered and averaged to 2 s bins (1 contraction cycle). LBF was calculated for each contraction cycle and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. VO(2p) was significantly lower in hypoxia throughout the period of 20, 40, 60 and 120 s of the exercise on-transient. LBF (l min(-1)) was approximately 35% higher (P > 0.05) in hypoxia during the on-transient and steady-state of KE exercise, resulting in a similar leg O(2) delivery in hypoxia and normoxia. Local muscle deoxygenation (HHb) was similar in hypoxia and normoxia. These results suggest that factors other than O(2) delivery, possibly the diffusion of O(2,) were responsible for the lower O(2) uptake during the exercise on-transient in hypoxia.     

Noninvasive determination of brain tissue oxygenation during sleep in obstructive sleep apnea: a near-infrared spectroscopic approach

STUDY OBJECTIVES: Recurrent apneas and hypoxemia during sleep in obstructive sleep apnea (OSA) are associated with profound changes in cerebral blood flow to the extent that cerebral autoregulation may be insufficient to protect the brain. Since the brain is sensitive to hypoxia, the cerebrovascular morbidity seen in OSA could be due to chronic, cumulative effects of intermittent hypoxia. Near-infrared spectroscopy (NIRS) has the potential to noninvasively monitor brain tissue oxygen saturation (SO2), and changes in concentration of oxyhemoglobin [O2Hb], deoxyhemoglobin [HHb] and total hemoglobin [tHb] with real-time resolution. We hypothesized that brain tissue oxygenation would be worse during sleep in OSA relative to controls and sought to determine the practical use of NIRS in the sleep laboratory. DESIGN: We evaluated changes in brain tissue oxygenation using NIRS during overnight polysomnography. SETTING: Studies were conducted at University of Illinois, Chicago and Carle Hospital, Urbana, Illinois. PATIENTS: Nineteen subjects with OSA and 14 healthy controls underwent continuous NIRS monitoring during polysomnography. MEASUREMENTS AND RESULTS: We observed significantly lower indexes of brain tissue oxygenation (SO2: 57.1 +/- 4.9 vs. 61.5 +/- 6.1), [O2Hb]: 22.8 +/- 7.7 vs. 31.5 +/- 9.1, and [tHb]: 38.6 +/- 11.2 vs. 48.6 +/- 11.4 micromol/L) in OSA than controls (all P < 0.05). However, multivariate analysis showed that the differences might be due to age disparity between the two groups. CONCLUSIONS: NIRS is an effective tool to evaluate brain tissue oxygenation in OSA. It provides valuable data in OSA assessment and has the potential to bridge current knowledge gap in OSA.     

Muscle oxygenation trends during dynamic exercise measured by near infrared spectroscopy.

During the last decade, NIRS has been used extensively to evaluate the changes in muscle oxygenation and blood volume during a variety of exercise modes. The important findings from this research are as follows: (a) There is a strong correlation between the lactate (ventilatory) threshold during incremental cycle exercise and the exaggerated reduction in muscle oxygenation measured by NIRS. (b) The delay in steady-state oxygen uptake during constant work rate exercise at intensities above the lactate/ventilatory threshold is closely related to changes in muscle oxygenation measured by NIRS. (c) The degree of muscle deoxygenation at the same absolute oxygen uptake is significantly lower in older persons compared younger persons; however, these changes are negated when muscle oxygenation is expressed relative to maximal oxygen uptake values. (d) There is no significant difference between the rate of biceps brachii and vastus lateralis deoxygenation during arm cranking and leg cycling exercise, respectively, in males and females. (e) Muscle deoxygenation trends recorded during short duration, high-intensity exercise such as the Wingate test indicate that there is a substantial degree of aerobic metabolism during such exercise. Recent studies that have used NIRS at multiple sites, such as brain and muscle tissue, provide useful information pertaining to the regional changes in oxygen availability in these tissues during dynamic exercise.     

Cerebral oxygenation during intermittent supramaximal exercise

This study examined cerebral deoxygenation during intermittent supramaximal exercise in six healthy male subjects (age: 27.2 +/- 0.6 years (mean +/- S.E.). The subjects performed seven times exercise at an intensity corresponding to 150% of maximal oxygen uptake (VO2max) on cycle ergometer (30 s exercise/15 s rest). Cerebral oxygenation was measured by near-infrared spectroscopy (NIRS). The peak blood lactate concentration after exercise was 15.3 +/- 0.2 mmol/l. Cerebral oxygenation increased in first repetition compared with at rest (+ 5.7 +/- 0.6 microM; P < 0.05), but then decreased with time. Thus, in the last repetition cerebral oxygenation was - 8.5 +/- 0.4 microM (P < 0.05). There was no significant change in arterial oxygen saturation (99.6 +/- at rest, 98.4 +/- 0.2 at the final set of intermittent exercise), and there was no correlated change in end-tidal CO2 concentration with cerebral oxygenation (P > 0.05). These findings suggest that the fatigue resulting from dynamic severe exercise related to a decrease in the cerebral oxygenation level.     

Very mild exposure to hypoxia for 8 h can induce ventilatory acclimatization in humans

Ventilatory acclimatization to altitude is associated with a progressive increase in ventilation, a progressive decrease in end-tidal PCO2 and a progressive increase in the acute ventilatory sensitivity to hypoxia. Ventilatory acclimatization has been observed with mild exposure to hypoxia when the duration of exposure has been of some length (e.g. days), and with shorter duration exposures (e.g. 8 h) when the degree of hypoxia has been more severe. The purpose of this study was to determine whether short-duration exposures to very mild hypoxia, such as are commonly associated with the reduction in cabin pressure during commercial airline flight, can also induce some degree of ventilatory acclimatization. Twelve subjects were exposed in a chamber to both 8 h mild hypoxia (inspired PO2 127 mmHg) and 8 h air-breathing as a control. Exposures were on different days in random order. Following the hypoxic exposure, there was a significant reduction in end-tidal PCO2 during air breathing (from 39.2+/-1.8 to 38.11+/-1.5 mmHg, mean +/- SD, P<0.05), and a significant increase in ventilatory sensitivity to hypoxia (from 0.84+/-0.54 l/min/% to 1.13+/-0.66 l/min/%, P<0.05). We conclude that shortterm exposures to very mild hypoxia do induce significant acclimatization within the respiratory control system.     

Alveolar gas exchange and tissue deoxygenation during exercise in type 1 diabetes patients and healthy controls

We used near-infrared spectroscopy to investigate whether leg and arm skeletal muscle and cerebral deoxygenation differ during incremental cycling exercise in men with type 1 diabetes (T1D, n=10, mean±SD age 33±7 years) and healthy control men (matched by age, anthrometry, and self-reported physical activity, CON, n=10, 32±7 years) to seek an explanation for lower aerobic capacity (˙VO2peak) often reported in T1D. T1D had lower ˙VO2peak (35±4mlkg(-1)min(-1) vs. 43±8mlkg(-1)min(-1), P<0.01) and peak work rate (219±33W vs. 290±44W, P<0.001) than CON. Leg muscle deoxygenation (↑ [deoxyhemoglobin]; ↓ tissue saturation index) was greater in T1D than CON at a given absolute submaximal work rate, but not at peak exercise, while arm muscle and cerebral deoxygenation were similar. Thus, in T1D compared with CON, faster leg muscle deoxygenation suggests limited circulatory ability to increase O(2) delivery as a plausible explanation for lower ˙VO2peak and earlier fatigue in T1D.     

Cardiac and respiratory effects of digitalis during chronic hypoxia in intact conscious dogs.

The arrhythmogenic and respiratory effects of ouabain during chronic hypoxia were studied in 10 unanesthetized dogs in a hypobaric chamber (446 mmHg) following 7-19 (mean 14.7) days of continuous exposure at this altitude. Another 15 dogs studied at sea level comprised the normoxic control group. In both groups, a 7.5-mug/kg loading dose of ouabain was followed by infusion of ouabain at 3.0 mug/kg per min to ECG evidence of toxicity. Mean arterial Po2 was 46 +/- 5 mmHg in chronically hypoxic dogs as compared to 86 +/- 7 mmHg in normoxic animals (P less than 0.001). Mean hematocrit was 54 +/- 1% in hypoxic and 43 +/- 2% in normoxic groups (P less than 0.001). In five dogs studied first at sea level and subsequently under conditions of chronic hypoxia, mean maximum left ventricular dP/dt and peak (dP/dt)P-1 were unchanged. Marked hyperventilation during ouabain infusion was observed. In normoxic dogs mean arterial pH rose from 7.43 +/- 0.05 to 7.70 +/- 0.02 U, and Pco2 fell from 41 +/- 4 to 15 +/- 1 mmHg during ouabain administration (P less than 0.001). Similar changes were observed in hypoxic dogs. There was no significant difference in the mean toxic dose of ouabain in chronically hypoxic (71 +/- 11 mug/kg) versus normoxic (78 +/- 12 mug/kg) animals. Thus, in contrast to acute hypoxia, chronic hypoxia in unanesthetized dogs was not associated with a significant reduction in the dose of ouabain required to produce toxic arrhythmias. Chronic hypoxia was also not associated with alterations in left ventricular performance.     

Acute hypoxic ventilatory response and exercise-induced arterial hypoxemia in men and women

Recent studies claim a higher prevalence of exercise-induced arterial hypoxemia (EIAH) in women relative to men and that diminished peripheral chemosensitivity is related to the degree of arterial desaturation during exercise in male endurance athletes. The purpose of this study was to determine the relationship between the acute ventilatory response to hypoxia (AHVR) and EIAH and the potential influence of gender in trained endurance cyclists and untrained individuals. Healthy untrained males (n = 9) and females (n = 9) and trained male (n = 11) and female (n = 10) cyclists performed an isocapnic AHVR test followed by an incremental cycle test to exhaustion. Oxyhemoglobin saturation (Sa(O(2)) was lower in trained men (91.4 +/- 0.9%) and women (91.3 +/- 0.9%) compared to their untrained counterparts (94.4 +/- 0.8% versus 94.3 +/- 0.7%) (P < 0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P < 0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P > 0.05). We conclude that resting AHVR does not have a significant role in maintaining Sa(O(2)) during sea-level maximal cycle exercise in men or women.     

Muscle microvascular hemoglobin concentration and oxygenation within the contraction-relaxation cycle

Inability to directly measure microvascular oxygen distribution and extraction in striated muscle during a contraction/relaxation cycle limits our understanding of oxygen transport to and utilization by contracting muscle. We examined muscle microvascular hemoglobin concentration (total [Hb/Mb]) and oxygenation within the contraction-relaxation cycle to determine if microvascular RBC volume would be preserved and if oxygen extraction continued during the actual contraction phase. Eight subjects performed dynamic knee extension exercise (40 contractions/min) at moderate ( approximately 30% of peak work rate) and heavy ( approximately 80% of peak) work rates. Total hemoglobin/myoglobin (total [Hb/Mb]) and deoxy-hemoglobin/myoglobin (deoxy-[Hb/Mb]) were measured in the rectus femoris using NIRS to determine if microvascular total [Hb/Mb] would be preserved during the contraction, and to estimate microvascular oxygen extraction, respectively. Mean values during the relaxation (RP) and contractile phases and the peak values during the contractile phase for both moderate and heavy exercise were calculated. Total [Hb/Mb] increased from rest to steady-state exercise (6.36+/-5.08 microM moderate; 5.72+/-4.46 microM heavy exercise, both P<0.05), but did not change significantly within the contraction/relaxation cycle. Muscle contractions were associated with a significant (1.29+/-0.98 microM moderate; 2.16+/-2.12 microM heavy exercise, P<0.05) increase in deoxy-[Hb/Mb] relative to RP. We conclude that (a) microvascular RBC volume is preserved during muscle contractions (i.e., RBCs are present in the capillaries), and (b) the cyclical pattern of deoxygenation/oxygenation during the respective contraction/relaxation phases of the contraction cycle suggests that oxygen extraction is not restricted to the relaxation phase but continues to occur during muscle contractions.     

Ventilatory and cerebrovascular responses to hypercapnia in patients with obstructive sleep apnoea: effect of CPAP therapy

The purpose of this study was to assess whether the cerebrovascular response to hypercapnia is blunted in OSA patients and if this could alter the ventilatory response to hypercapnia before and after CPAP therapy. We measured the cerebrovascular, cardiovascular and ventilatory responses to hypercapnia in 8 patients with OSA (apnoea-hypopnoea index=101+/-10) before and after 4-6 weeks of CPAP therapy and in 10 control subjects who did not undergo CPAP therapy. The cerebrovascular and ventilatory responses to hypercapnia were not different between OSA and controls at baseline or follow-up. The cardiovascular response to hypercapnia was significantly increased in the OSA group by CPAP therapy (mean arterial pressure response: 1.30+/-0.16 vs. 2.04+/-0.36 mmHg Torr(-1); p=0.007). We conclude that in normocapnic, normotensive OSA patients without cardiovascular disease, the ventilatory, cerebrovascular, and cardiovascular responses to hypercapnia are normal, but the cardiovascular response to hypercapnia is heightened following 1 month of CPAP therapy.     

Influence of indomethacin on the ventilatory and cerebrovascular responsiveness to hypoxia

Indomethacin (INDO) has the potential to be a useful tool to explore the influence of cerebral blood flow and its responses to CO₂ on ventilatory control. However, the effect of INDO on the cerebrovascular and ventilatory response to hypoxia remains unclear; therefore, we examined the effect of INDO on ventilatory and cerebrovascular sensitivity to hypoxia and hypercapnia. We measured end-tidal gases, ventilation ([(V)\dot]_\textE ), (\dot{V}_{\text{E}} ), and middle cerebral artery velocity (MCAv) before and 90 min following INDO (100 mg) in 12 healthy participants at rest and during hyperoxic hypercapnia and isocapnic hypoxia. Following INDO, resting [(V)\dot]_\textE \dot{V}_{\text{E}} and end-tidal gases were unaltered (P > 0.05), whilst MCAv was lowered by 25 ± 19% (P < 0.001). INDO ingestion reduced MCAv-CO₂ reactivity by 46 ± 29% (2.9 ± 0.9 vs. 1.7 ± 0.9 cm s⁻¹ mmHg⁻¹; P < 0.001) and enhanced the [(V)\dot]_\textE \dot{V}_{\text{E}} -CO₂ sensitivity by 0.5 ± 0.5 L min⁻¹ mmHg⁻¹ (1.9 ± 1.5 vs. 2.3 ± 1.6 L min⁻¹ mmHg⁻¹; P < 0.05). No changes were observed in either the MCAv or [(V)\dot]_\textE \dot{V}_{\text{E}} responsiveness to isocapnic hypoxia following INDO ingestion (P > 0.05). These findings indicate that INDO does not alter cerebrovascular and ventilatory responsiveness to hypoxia, indicating a preserved peripheral chemoreflex in response to this pharmacological agent.     

Role of respiratory system impedance in the difference of ventilatory control between children and adults

How children are able to adapt their ventilation to the intensity of exercise faster than adults remain unclear. We hypothesized that differences of VE observed between children and adults depend on either peripheral chemoreceptors or central command activity. We examined ventilatory control parameters in either normoxic or hypoxic condition (FI 02 =0.15). We analyzed the adaptability of the respiratory exchanges by (i) the measurement of ventilatory kinetics time-constant and (ii) the central command by the mouth-occlusion pressure (P0.1). A group of nine pre-pubescent children (mean age 9.5+/-1 years) and a group of eight adults (mean age 24+/-3.1 years) performed a constant-load exercise. In normoxia, children had significantly shorter time-constant (tau) VCO2 (respectively, 38.5+/-4.3 and 53.1+/-5.3s; P<0.001), tau VE (respectively, 52.5+/-13.1s vs. 66.1+/-12.3s; P<0.001), and tau P0.1 (57.4+/-15.4 and 61.0+/-12.9s, respectively; P<0.001) than adults. In hypoxia, children exhibited shorter tau P0.1/VT/Ti compare to adults. Reinforced by the significant correlation between tau VE and tau P0.1/VT/Ti for children but not adults, we concluded that ventilatory response differences could be due in part to the respiratory system impedance.     

Regional cerebral blood flow distribution during exercise: Influence of oxygen

We investigated regional changes in cerebral artery velocity during incremental exercise while breathing normoxia (21% O(2)), hyperoxia (100% O(2)) or hypoxia (16% O(2)) [n=10; randomized cross over design]. Middle cerebral and posterior cerebral arterial velocities (MCAv and PCAv) were measured continuously using transcranial Doppler ultrasound. At rest, only PCAv was reduced (-7%; P=0.016) with hyperoxia. During low-intensity exercise (40% workload maximum [Wmax]) MCAv (+17cms(-1); +14cms(-1)) and PCAv (+9cms(-1); +14cms(-1)) were increased above baseline with normoxia and hypoxia, respectively (P<0.05). The absolute increase from rest in MCAv was greater than the increase in PCAv between 40 and 80% Wmax with normoxia; this greater increase in MCAv was also evident at 60% Wmax with hypoxia and hyperoxia. Hyperoxic exercise resulted in larger absolute (+19cms(-1)) and relative (+40%) increases in PCAv compared with normoxia. Our findings highlight the selective changes in PCAv during hyperoxic incremental exercise.     

Interstitial glycerol concentrations in human skeletal muscle and adipose tissue during graded exercise

AIM: It is not clear how lipolysis changes in skeletal muscle and adipose tissue during exercise of different intensities. We aimed at estimating this by microdialysis and muscle biopsy techniques. METHODS: Nine healthy, young men were kicking with both legs at 25% of maximal power (Wmax) for 45 min and then simultaneously with one leg at 65% and the other leg at 85% Wmax for 35 min. RESULTS: Glycerol concentrations in skeletal muscle and adipose tissue interstitial fluid and in arterial plasma increased (P<0.001) during low intensity exercise and increased (P<0.05) even more during moderate intensity exercise. The difference between interstitial muscle and arterial plasma water glycerol concentration, which indicates the direction of the glycerol flux, was positive (P<0.05) at rest (21 +/- 9 microM) and during exercise at 25% Wmax (18 +/- 6 microM). The difference decreased (P<0.05) with increasing exercise intensity and was not significantly different from zero during exercise at 65% (-11 +/- 17 microM) and 85% (-12 +/- 13 microM) Wmax. In adipose tissue, the difference between interstitial and arterial plasma water glycerol increased (P<0.001) with increasing intensity. The net triacylglycerol breakdown, measured chemically from the biopsy, did not differ significantly from zero at any exercise intensity although directional changes were similar to microdialysis changes. CONCLUSIONS: Skeletal muscle releases glycerol at rest and at low exercise intensity but not at higher intensities. This can be interpreted as skeletal muscle lipolysis peaking at low exercise intensities but could also indicate that glycerol is taken up in skeletal muscle at a rate which is increasing with exercise intensity.     

Respiratory, cerebrovascular and cardiovascular responses to isocapnic hypoxia

We simultaneously measured respiratory, cerebrovascular and cardiovascular responses to 10-min of isoxic hypoxia at three constant CO(2) tensions in 15 subjects. We observed four response patterns, some novel, for ventilation, middle cerebral artery blood flow velocity, heart rate and mean arterial blood pressure. The occurrence of the response patterns was correlated between some measures. Isoxic hyperoxic and hypoxic ventilatory sensitivities to CO(2) derived from these responses were equivalent to those measured with modified (Duffin) rebreathing tests, but cerebrovascular sensitivities were not. We suggest the different ventilatory response patterns reflect the time course of carotid body afferent activity; in some individuals, carotid body function changes during hypoxia in more complex ways than previously thought. We concluded that isoxic hyperoxic and hypoxic ventilatory sensitivities to CO(2) can be measured using multiple hypoxic ventilatory response tests only if care is taken choosing the isocapnic CO(2) levels used, but a similar approach to measuring the cerebrovascular response to isocapnic hyperoxia and hypoxia is unfeasible.