Extra-cerebral oxygenation influence on near-infrared-spectroscopy-determined frontal lobe oxygenation in healthy volunteers: a comparison between INVOS-4100 and NIRO-200NX.

INTRODUCTION: Frontal lobe oxygenation (Sc O2 ) is assessed by spatially resolved near-infrared spectroscopy (SR-NIRS) although it seems influenced by extra-cerebral oxygenation. We aimed to quantify the impact of extra-cerebral oxygenation on two SR-NIRS derived Sc O2 . METHODS: Multiple regression analysis estimated the influence of extra-cerebral oxygenation as exemplified by skin oxygenation (Sskin O2 ) on Sc O2 in 21 healthy subjects exposed to whole-body exercise in hypoxia (Fi O2  = 12%; n = 10) and normoxia (n = 12), whole-body heating, hyperventilation (n = 21), administration of norepinephrine with and without petCO2 -correction (n = 15), phenylephrine and head-up tilt (n = 7). Sc O2 was assessed simultaneously by NIRO-200NX (Sniro O2 ) and INVOS-4100 (Sinvos O2 ). Arterial (Sa O2 ) and jugular bulb oxygen saturations (Sj O2 ) were obtained. RESULTS: The regression analysis indicated that Sinvos O2 reflects 46% arterial, 14% jugular, 35% skin and 4% oxygenation of tissues not interrogated. Sinvos O2 follows a calculated estimate of cerebral capillary oxygenation (r = 0·67; P<0·0001). In contrast, the NIRO-200NX-determined Sc O2 did not correlate with the estimate of cerebral oxygenation (r = 0·026; P = 0·71). CONCLUSION: For all interventions, 35% of the INVOS-4100 signal reflected extra-cerebral oxygenation while, on the other hand, NIRO-200NX did not follow changes in a calculated estimate of cerebral capillary oxygenation. Thus, the NIRO-200NX and INVOS-4100 do not provide for unbiased evaluation of the cerebral signal.

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise.

We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac(-)](B)) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation ([Formula: see text]). Prior to the intervention, the MLSS [lac(-)](B) was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L(-1) in the IMT and control groups, respectively. During volitional hyperpnoea, [Formula: see text] increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min(-1) at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min(-1) in IMT and control groups, respectively; [lac(-)](B) concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L(-1) (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.

Effects of different respiratory muscle training regimes on fatigue-related variables during volitional hyperpnoea.

We compared the effects of the most commonly used respiratory muscle (RM) training regimes: RM endurance training (RMET; normocapnic hyperpnoea) and inspiratory resistive training (IMT), on RM performance. Twenty-six healthy men were randomized into 3 groups performing 4 weeks of RMET, IMT or sham-training. Lung function, RM strength and endurance were tested before and after training. RM fatigue during intermittent hyperpnoea was assessed by twitch oesophageal (P(oes,tw)) and gastric pressures with cervical and thoracic magnetic stimulation. Respiratory sensations (visual analogue scale, 0-10) and blood lactate concentrations ([La]) were assessed during hyperpnoea. RMET increased maximal voluntary ventilation while IMT increased maximal inspiratory pressure. Both RMET and IMT increased vital capacity and RM endurance, but only RMET improved the development of inspiratory muscle fatigue (from -31% to -21% P(oes,tw)), perception of respiratory exertion (4.2+/-0.1 to 2.3+/-2.3 points) and [La] (1.8+/-0.4 to 1.3+/-0.3 mmol l(-1)) during hyperpnoea. Whether these specific RMET-induced adaptations observed during hyperpnoea would translate into greater improvements in exercise performance compared to IMT remains to be investigated.

Brain pH response to hyperventilation in panic disorder: preliminary evidence for altered acid-base regulation.

OBJECTIVE: Previous findings of excess brain lactate and delayed end-tidal CO(2) (pCO(2)) recovery in subjects with panic disorder during hyperventilation suggested altered acid-base regulation. Two models were posited to explain these results: 1) subjects with panic disorder demonstrate greater alkalosis to hyperventilation, implicating increased lactate as directly compensatory, or 2) subjects with panic disorder demonstrate reduced or blunted alkalosis, implicating increased lactate as overly compensatory to a normal pH response. In both models, delayed pCO(2) recovery in subjects with panic disorder could reflect slower pH normalization in the recovery phase. METHOD: Asymptomatic medicated patients with panic disorder were studied during regulated hyperventilation. Phosphorous spectroscopy was used to measure brain pH every 2 minutes. Nine subjects with panic disorder were compared to 11 healthy subjects at baseline (five scans), during regulated hyperventilation (five scans), and across recovery (10 scans). Anxiety symptoms were assessed with standard ratings. RESULTS: No subject had a panic attack before hyperventilation. Subjects with panic disorder had lower pCO(2) during hyperventilation and slower pCO(2) recovery across the posthyperventilation interval. Despite this different respiratory response in the panic disorder group, brain pH increases were not significantly greater during hyperventilation, nor was pH return to baseline slowed during posthyperventilation. A linear regression model derived from data of healthy subjects showed pH blunting in the panic disorder group. CONCLUSIONS: Although subjects with panic disorder had greater hypocapnea during hyperventilation, their observed pH response, not altered from comparison levels, implicated exaggerated buffering. It is suggested that increased lactate could account for these findings.

Lack of a relation between serum potassium concentration and exercise hyperpnea in patients with chronic heart disease.

Exertional dyspnea, a major symptom of patients with chronic heart failure, mainly stems from an abnormally high ventilatory response to exercise. However, there has been considerable controversy surrounding the mechanisms of respiratory control during exercise, especially regarding the role of serum potassium. We investigated the relation between serum potassium concentration [K+] and ventilation (VE) during exercise before and after oral supplements of potassium chloride in cardiac patients. Thirteen patients with chronic heart disease performed a 6-min constant-work-rate exercise (65.8+/-11.1 W) with respiratory gas measurements before initiating oral supplements of potassium chloride, 4 weeks after continued supplements, and 4 weeks after discontinuing supplements. Blood was sampled from a forearm vein at rest before exercise and at the end of exercise for measurement of [K+] and blood gases. The [K+] at rest was 3.66+/-0.30 mmol/L before oral supplements of potassium and significantly increased to 4.08+/-0.31 mmol/L (p<0.01) after supplements. In spite of the significant increases in the [K+], resting VE was not changed. While serum [K+] during exercise was significantly higher after potassium supplements than before, exercise VE was not influenced by the changes in [K+] throughout the study period. The findings of the present study strongly suggest that the chronic increase in the serum [K+] has no influence on the resting or exercise VE in patients with heart disease.

Refractoriness of eucapnic hyperventilation-induced bronchoconstriction in rabbits.

The mechanism of refractoriness in bronchoconstriction after repeated hyperventilation was investigated in 18 sensitized rabbits. Rabbits were separated into three groups: an untreated control group (n = 7), a cimetidine-treated group (n = 6), and an indomethacin-treated group (n = 5). After anesthetization, hyperventilation was performed for 15 min (120 breaths/min, 7 ml/kg tidal volume) with dry air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before (baseline) and after hyperventilation challenge. After RL and Cdyn had returned to baseline values, the hyperventilation challenge was repeated. In the control group maximal increase in percent RL (max %RL) was 49 +/- 9% after the first challenge, but 16 +/- 4% after the second challenge, indicating refractoriness. A similar tendency was observed in percent Cdyn. In the cimetidine- and indomethacin-treated groups, max %RL were 42 +/- 3% and 60 +/- 15% after the first challenge, and 35 +/- 8% and 60 +/- 7% after the second challenge, respectively, indicating no refractoriness. These results suggest that the H2-receptor and bronchodilating prostanoids play an important role in producing the refractoriness to bronchoconstriction observed in sensitized rabbits after repeated hyperventilation.

Hyperventilation and panic attacks.

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.

Effect of respiratory alkalosis during exercise on blood lactate.

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.

Erythrocyte adenosine triphosphate depletion during voluntary hyperventilation.

Chronic hypophosphatemia in humans is associated with a slow depletion of adenosine triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG) in erythrocytes, combined with shape alteration, impaired deformability, and viability of the cells. Likewise, incubation of erythrocytes in alkaline solution is associated with ATP depletion. Since in hyperventilation both hypophosphatemia and alkalosis are present, we have investigated red cell organic phosphates, shape, deformability, and osmotic fragility before, during, and after 20 min of voluntary hyperventilation. On the average, red cell ATP decreased by 42%, the blood pH increased by 0.2 units, and plasma inorganic phosphorus decreased by 46% compared with the initial values. Red cell 2,3-DPG, shape, deformability, and osmotic fragility remained unchanged. After the end of hyperventilation ATP increased rapidly to control values in parallel with the normalization of the blood pH, whereas inorganic plasma phosphorus remained at the low level observed during hyperventilation. It is concluded that the combined effects of hypophosphatemia and alkalosis in acute hyperventilation lead to an isolated fall of red cell ATP, which occurs as rapid as after total inhibition of red cell glycolysis in vitro.

Effect of hyperventilation on total calcium, ionized calcium, and serum phosphorus in neonates.

The effect of alkalosis (pH greater than 7.55) on total calcium, ionized calcium, and serum phosphorus was studied in seven infants with persistent pulmonary hypertension (PPH) before, during, and after hyperventilation. Hyperventilation-induced alkalosis resulted in marked decreases in total calcium, phosphorus, and ionized calcium. There was an inverse correlation between plasma Ca+2 and pH; a 0.1-unit increase in blood pH decreased Ca+2 by 0.42 mg/dl. Two of the study infants had ionized calcium concentrations less than 2.5 mg/dl during hyperventilation. These disturbing changes in total calcium, ionized calcium, and serum phosphorus could have potentially detrimental effects on neonates with PPH.