Effect of induced acute metabolic alkalosis on the V̇E/V̇CO2 response to exercise in healthy adults.

We tested the hypothesis that increasing the respiratory control systems' arterial PCO2 equilibrium point via induced acute metabolic alkalosis by ingestion of sodium bicarbonate (NaHCO3, 0.3 g/kg) would decrease the ventilatory equivalent for CO2 (V̇E/V̇CO2) at its lowest point ("nadir") during constant-load cycle exercise testing performed at 80 % of peak power output in 18 healthy young adults. Compared to the sodium chloride (4 g) control condition, ingestion of NaHCO3: increased arterialized venous pH, HCO3- and PCO2 at rest by 0.05 ± 0.01 units (mean ± SE), 6.4 ± 0.4 mEq/L and 4.3 ± 0.7 mmHg, respectively (all p < 0.0001); and decreased the V̇E/V̇CO2 nadir during exercise by 9.4 % (p < 0.0001) secondary to a 4.7 ± 1.8 L/min decrease in V̇E (p = 0.019). In conclusion, induced acute metabolic alkalosis by ingestion of NaHCO3 decreased the V̇E/V̇CO2 response to strenuous exercise in healthy adults.

Mechanisms of acid-base regulation following respiratory alkalosis in red drum (Sciaenops ocellatus).

Respiratory acidosis and subsequent metabolic compensation are well-studied processes in fish exposed to elevated CO2 (hypercapnia). Yet, such exposures in the marine environment are invariably accompanied by a return of environmental CO2 to atmospheric baselines. This understudied phenomenon has the potential to cause a respiratory alkalosis that would necessitate base excretion. Here we sought to explore this question and the associated physiological mechanisms that may accompany base excretions using the red drum (Sciaenops ocellatus). As expected, when high pCO2 (15,000 µatm CO2) acclimated red drum were transferred to normal pCO2, their net H+ excretion shifted from positive (0.157 ± 0.044 µmol g-1 h-1) to negative (-0.606 ± 0.116 µmol g-1 h-1) in the 2 h post-transfer period. Net H+ excretion returned to control rates during the 3 to 24 h flux period. Gene expression and enzyme activity assays demonstrated that while the acidosis resulted in significant changes in several relevant transporters, no significant changes accompanied the alkalosis phase. Confocal microscopy was used to assess alkalosis-stimulated translocation of V-type H+ ATPase to the basolateral membrane previously seen in other marine species; however, no apparent translocation was observed. Overall, these data demonstrate that fluctuations in environmental CO2 result in both acidic and alkalotic respiratory disturbances; however, red drum maintain sufficient regulatory capacity to accommodate base excretion. Furthermore, this work does not support a role for basolateral VHA translocation in metabolic compensation from a systemic alkalosis in teleosts.

Distúrbios ácido-base nas doenças hepáticas / Acid-base disorders in liver diseases

O objetivo deste artigo foi abordar as controvérsias científicas acerca dos distúrbios ácido-base nas doenças hepáticas. Nos estágios avançados da doença hepática, os distúrbios ácido-base atuam de forma complexa, comprometendo a qualidade de vida do paciente e desafiando o manejo clínico. A literatura apresenta a alcalose respiratória como uma das principais alterações, porém há uma longa discussão sobre o mecanismo fisiopatológico; em especial, citam-se a hipóxia, a hipocapnia e o nível de progesterona. Nas desordens metabólicas, com destaque para a acidose, os estudos apontam principalmente o lactato, os unmeasured ions ou íons não medidos e as alterações hidroeletrolíticas, mas cada componente desse sobressai-se dependendo da fase da doença estudada, compensada ou descompensada. As controvérsias dos distúrbios ácido-base nas doenças hepáticas devem-se ora à complexidade da fisiopatologia da própria doença, ora à necessidade de mais estudos esclarecedores.

The aim of this study is to address the scientific controversy about acid-base disorders in liver diseases. In the end stage of liver diseases, the acid-base disorder has a complex performance, impairing the patient's quality of life and challenging the clinic management. Although the literature shows respiratory alkalosis as one of the main alterations, there is a long discussion about the pathophysiological mechanism, specially regarding hypoxia, hypocapnia, and progesterone level. In metabolic disorders, especially acidosis, the studies mainly indicate the lactate, unmeasured ions, and hydroelectrolytic alterations, but, depending on the disease phase, either compensated or decompensated, each element has a particular action. The controversy about acid-base disorders in liver diseases is associated with the complexity of this condition, as well as with the necessity of more specialized research.

The effect of inspiratory muscle fatigue on acid-base status and performance during race-paced middle-distance swimming.

The aim of this study was to investigate the effect of pre-induced inspiratory muscle fatigue (IMF) on race-paced swimming and acid-base status. Twenty-one collegiate swimmers performed two discontinuous 400-m race-paced swims on separate days, with (IMF trial) and without (control trial) pre-induced IMF. Swimming characteristics, inspiratory and expiratory mouth pressures, and blood parameters were recorded. IMF and expiratory muscle fatigue (P < 0.05) were evident after both trials and swimming time was slower (P < 0.05) from 150-m following IMF inducement. Pre-induced IMF increased pH before the swim (P < 0.01) and reduced bicarbonate (P < 0.05) and the pressure of carbon dioxide (PCO2) (P < 0.05). pH (P < 0.05), bicarbonate (P < 0.01) and PCO2 (P < 0.05) were lower during swimming in the IMF trial. Blood lactate was similar before both trials (P > 0.05) but was higher (P < 0.01) in the IMF trial after swimming. Pre-induced IMF induced respiratory alkalosis, reduced bicarbonate buffering capacity and slowed swimming speed. Pre-induced and propulsion-induced IMF reflected metabolic acidosis arising from dual role breathing and propulsion muscle fatigue.

Hyperventilation Syndrome and Sustained Hyperchloremia After Kidney Transplant: Time-Sequence Swing of Acid-Base Interpretation.

An interaction between regained renal function in a transplanted kidney and hyperventilation syndrome may interfere with correct diagnosis of acid-base status in patients with preoperative nongap acidosis. Here, we present a patient with glomerular nephritis and hyperchloremia who underwent kidney transplant. Progressively increasing bicarbonate reabsorption by the renal graft, which thereby changed the arterial carbon dioxide tension-to-bicarbonate ratio, resulted in a time-sequence swing of an acid-base interpretation despite persistent mixed respiratory alkalosis due to hyperventilation syndrome and nongap metabolic acidosis due to preexisting hyperchloremia. Specifically, the sequence was mixed primary metabolic acidosis and primary respiratory acidosis immediately after surgery, primary metabolic acidosis and secondary respiratory alkalosis on postoperative days 1 and 2, mixed primary hyperchloremic metabolic acidosis and primary respiratory alkalosis on postoperative day 3, and finally primary respiratory alkalosis and secondary hyperchloremic metabolic acidosis on postoperative day 7. This swing in the acid-base interpretation indicates that the acid-base imbalance described here does not fit the empirical relationship for calculating the expected bicarbonate or carbon dioxide tension value, suggesting that "correct" interpretation of acid-base status may not lead to "correct" diagnosis of acid-base status. It should be remembered that not every acid-base imbalance fits the empirical relationship.

The venous-arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers.

The venous-arterial difference in CO2 (ΔCO2) has been proposed as an index of the adequacy of tissue perfusion in shock states. We hypothesized that the variation in PaCO2 (hyper- or hypocapnia) could impact ΔCO2, partly through microcirculation adaptations. Fifteen healthy males volunteered to participate. For hypocapnia condition (hCO2), the subjects were asked to hyperventilate, while they were asked to breathe a gas mixture containing 8 % CO2 for hypercapnia condition (HCO2). The 2 conditions were randomly assigned. Blood gases were measured at baseline before each condition, and after 5-7 min of either hCO2 or HCO2 condition. Microcirculation was assessed by the muscle reoxygenation slope measured with near infrared spectroscopy following a vascular occlusion test and by skin circulation with in vivo reflectance confocal microscopy. ΔCO2 was significantly increased with hCO2 while it tended to decrease with HCO2 (non-significant). HCO2 induced a moderate increase of the resaturation slope of NIRS oxygenation. Skin microcirculatory blood flow significantly dropped with hCO2, while it remained unchanged with hypercapnia. Our results warrant cautious interpretation of ΔCO2 as an indicator of tissue perfusion during respiratory alkalosis.

A Quick Reference on Respiratory Alkalosis.

Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco2, increases in pH, and compensatory decreases in blood HCO3- levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO3- and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO3-; the arterial pH can approach near-normal values.

[Disorders of the acid-base balance and the anion gap]. / Störungen des Säure-Basen-Haushaltes und der Anionenlücke.

The regulation of the acid-base balance and pH is critical for the organism. The most important buffer system is CO2 / HCO3-. The kidney controls systemic bicarbonate and therefore the metabolic regulation and the lung is relevant for respiratory regulation by an effective CO2 elimination. There are four acid-base disorders with two metabolic and two respiratory disorders (acidosis and alkalosis). The anion gap enables a further workup of metabolic acidosis.

VESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia.

This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈4,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the VESTPD at RER <1.0 was significantly lower and the VEBTPS was higher because of higher breathing frequency; at VO2max, both VESTPD and VEBTPS were not significantly different. As percent of VO2max, the VEBTPS was nearly identical and VESTPD was 30% lower throughout the exercise at 455 mmHg. The lower VESTPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where VESTPD at submaximal workloads was maintained or increased above that at sea level. The lower VESTPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO2 (≈0.17 pHa units), reduction in PACO2 (≈5 mmHg) and higher PAO2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict VESTPD from VO2 and PB in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in VESTPD at low workloads after arrival at altitude.

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation.

UNLABELLED: Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. PURPOSE: To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). METHODS: 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. RESULTS: Compared with the control condition, hyperventilation reduced (all P < .01) pCO2 (40.5 ± 2.8 vs 22.5 ± 1.6 mm Hg) and HCO3 - (25.5 ± 1.7 vs 22.7 ± 1.6 mmol/L) and increased (all P < .01) pH (7.41 ± 0.01 vs 7.61 ± 0.03) and actual base excess (1.4 ± 1.4 vs 3.2 ± 1.6 mmol/L) pre-WAnT with an ergogenic effect on WAnT average power (681 ± 41 vs 714 ± 44 W) and total metabolic energy (138 ± 12 vs. 144 ± 13 kJ) based on an increase in glycolytic energy (81 ± 13 vs 88 ± 13 kJ). CONCLUSION: Hyperventilation-induced respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Acid-base disturbance in patients with cirrhosis: relation to hemodynamic dysfunction.

PURPOSE: Acid-base disturbances were investigated in patients with cirrhosis in relation to hemodynamic derangement to analyze the hyperventilatory effects and the metabolic compensation. METHODS: A total of 66 patients with cirrhosis and 44 controls were investigated during a hemodynamic study. RESULTS: Hyperventilatory hypocapnia was present in all patients with cirrhosis and progressed from Child class A to C (P<0.01). Arterial pH increased significantly from class A to C (P<0.001) and was correlated inversely to the mean arterial blood pressure (r=-0.30, P<0.02), systemic vascular resistance (r=-0.25, P<0.05), indocyanine green clearance (r=-0.37, P<0.005), and serum sodium (r=-0.38, P<0.002). Metabolic compensation was shown by a reduced standard base excess in all patients (P<0.001). Standard base excess contained elements related to changes in serum albumin, water dilution, and effects of unidentified ions (all P<0.001). A significant hepatic component in the acid-base disturbances could not be identified. CONCLUSION: Hypocapnic alkalosis is related to disease severity and hyperdynamic systemic circulation in patients with cirrhosis. The metabolic compensation includes alterations in serum albumin and water retention that may result in a delicate acid-base balance in these patients.

Longitudinal cerebrovascular reactivity during pregnancy: a case study.

Normal cerebrovascular adaptation during pregnancy is poorly understood. We document a case study of progressively increased cerebrovascular reactivity to CO2, despite no change in resting blood flow, from prepregnancy to late gestation in a 36-year-old normotensive participant. Increased cerebral reactivity was related to progressive chronic respiratory alkalosis and specifically elevated pH and reduced HCO3(-). These novel data serve as important indicators of normative maternal cerebral adaptation and highlight novel areas of future study.

Effect of airway acidosis and alkalosis on airway vascular smooth muscle responsiveness to albuterol.

BACKGROUND: In vitro and animal experiments have shown that the transport and signaling of ß2-adrenergic agonists are pH-sensitive. Inhaled albuterol, a hydrophilic ß2-adrenergic agonist, is widely used for the treatment of obstructive airway diseases. Acute exacerbations of obstructive airway diseases can be associated with changes in ventilation leading to either respiratory acidosis or alkalosis thereby affecting albuterol responsiveness in the airway. The purpose of this study was to determine if airway pH has an effect on albuterol-induced vasodilation in the airway. METHODS: Ten healthy volunteers performed the following respiratory maneuvers: quiet breathing, hypocapnic hyperventilation, hypercapnic hyperventilation, and eucapnic hyperventilation (to dissociate the effect of pH from the effect of ventilation). During these breathing maneuvers, exhaled breath condensate (EBC) pH and airway blood flow response to inhaled albuterol (ΔQ̇aw) were assessed. RESULTS: Mean ± SE EBC pH (units) and ΔQ̇aw (µl.min(-1).mL(-1)) were 6.4 ± 0.1 and 16.8 ± 1.9 during quiet breathing, 6.3 ± 0.1 and 14.5 ± 2.4 during eucapnic hyperventilation, 6.6 ± 0.2 and -0.2 ± 1.8 during hypocapnic hyperventilation (p = 0.02 and <0.01 vs. quiet breathing), and 5.9 ± 0.1 and 2.0 ± 1.5 during hypercapnic hyperventilation (p = 0.02 and <0.02 vs quiet breathing). CONCLUSIONS: Albuterol responsiveness in the airway as assessed by ΔQ̇aw is pH sensitive. The breathing maneuver associated with decreased and increased EBC pH both resulted in a decreased responsiveness independent of the level of ventilation. These findings suggest an attenuated response to hydrophilic ß2-adrenergic agonists during airway disease exacerbations associated with changes in pH. TRIAL REGISTRATION: Registered at clinicaltrials.gov: NCT01216748 .

Hyperventilation-induced respiratory alkalosis falls short of countering fatigue during repeated maximal isokinetic contractions.

PURPOSE: Hyperventilation, implemented during recovery of repeated maximal sprints, has been shown to attenuate performance decrement. This study evaluated the effects of hyperventilation, using strength exercises, on muscle torque output and EMG amplitude. METHODS: Fifteen power-trained athletes underwent maximal isokinetic knee extensions consisting of 12 repetitions × 8 sets at 60°/s and 25 repetitions × 8 sets at 300°/s. The inter-set interval was 40 s for both speeds. For the control condition, subjects breathed spontaneously during the interval period. For the hyperventilation condition, subjects hyperventilated for 30 s before each exercise set (50 breaths/min, PETCO2: 20-25 mmHg). EMG was recorded from the vastus medialis and lateralis muscles to calculate the mean amplitude for each contraction. RESULTS: Hyperventilation increased blood pH by 0.065-0.081 and lowered PCO2 by 8.3-10.3 mmHg from the control values (P < 0.001). Peak torque declined with repetition and set numbers for both speeds (P < 0.001), but the declining patterns were similar between conditions. A significant, but small enhancement in peak torque was observed with hyperventilation at 60°/s during the initial repetition phase of the first (P = 0.032) and fourth sets (P = 0.040). EMG amplitude also declined with set number (P < 0.001) for both speeds and muscles, which was, however, not attenuated by hyperventilation. CONCLUSION: Despite a minor ergogenic effect in peak torque at 60°/s, hyperventilation was not effective in attenuating the decrement in torque output at 300°/s and decrement in EMG amplitude at both speeds during repeated sets of maximal isokinetic knee extensions.

Hypoxia silences retrotrapezoid nucleus respiratory chemoreceptors via alkalosis.

In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby C1 neurons with Arch (PRSx8-ArchT-EYFP-LVV) and measured the cardiorespiratory consequences of Arch activation (10 s) in conscious rats during normoxia, hypoxia, or hyperoxia. RTN photoinhibition reduced breathing equally during non-REM sleep and quiet wake. Compared with normoxia, the breathing frequency reduction (Δf(R)) was larger in hyperoxia (65% FiO2), smaller in 15% FiO2, and absent in 12% FiO2. Tidal volume changes (ΔV(T)) followed the same trend. The effect of hypoxia on Δf(R) was not arousal-dependent but was reversed by reacidifying the blood (acetazolamide; 3% FiCO2). Δf(R) was highly correlated with arterial pH up to arterial pH (pHa) 7.5 with no frequency inhibition occurring above pHa 7.53. Blood pressure was minimally reduced suggesting that C1 neurons were very modestly inhibited. In conclusion, RTN neurons regulate eupneic breathing about equally during both sleep and wake. RTN neurons are the first putative CRCs demonstrably silenced by hypocapnic hypoxia in conscious mammals. RTN neurons are silent above pHa 7.5 and increasingly active below this value. During hyperoxia, RTN activation maintains breathing despite the inactivity of the carotid bodies. Finally, during hypocapnic hypoxia, carotid body stimulation increases breathing frequency via pathways that bypass RTN.

[Every mountain too high when Nausea strikes: gastrointestinal function at high altitude]. / Wenn der Berg auf den Magen schlägt: Magen-Darm-Funktion in der Höhe.

For people unaccustomed to high altitude, exposure to height often leads to Acute Mountain Sickness, with headaches, difficulty breathing and gastrointestinal symptoms. Nausea and loss of appetite may result in less calorie intake and weight loss. At altitudes greater than 4000 m about 50-80% of people are affected. After only short exposure, gastrointestinal mucosal lesions can occur, potentially leading to gastrointestinal bleeding and lessened hunger. Patients with inflammatory bowel disorders may develop an acute exacerbation. At high altitude, an induction of numerous metabolic processes can be observed, including increased iron absorption. While the pathophysiology of hypobaric hypoxia has been well documented for the respiratory and cardiovascular system, this Mini-Review summarizes the current literature concerning the gastrointestinal function in high altitude.

Pour les personnes non habituées à, l'exposition à de hautes altitudes provoque souvent le mal aigu des montagnes, avec des céphalées, de la dyspnée et des symptômes digestifs. Des nausées et une perte de l'appétit peuvent entrainer une diminution de l'apport calorique et une perte de poids. À des altitudes supérieures à 4000 m, approximativement 50­80% des gens sont en sont affectés. Même après une exposition de courte durée des lésions de la muqueuse gastrointestinale peuvent apparaître, provoquant potentiellement un saignement gastrointestinal et une perte de l'appétit. Les malades souffrant d'affections inflammatoires du tube digestif peuvent être sujets à une exacerbation aiguë de leur affection. A haute altitude l'induction de nombreux processus métaboliques peuvent être observés, y compris une augmentation de l'absorption du fer. Alors que la physiopathologie de l'hypoxie hypobare a été bien documentée pour le système respiratoire et le système cardiovasculaire, il n'en est pas de même pour le système digestif. La présente revue a pour but de résumé ce qui est connu en ce qui concerne l'altitude et la fonction gastrointestinale.

Hyperventilation provokes symptoms of carpal tunnel syndrome.

Hyperventilation causes respiratory alkalosis. The nervous system is more excitable in alkalosis. This phenomenon can be observed as paraesthesia in fingers and toes as well as around the lips in anxious patients breathing rapidly. We wanted to test this phenomenon on already irritable nerves like the median nerve in carpal tunnel syndrome (CTS). We deployed 50 patients who came in to the day case unit for carpal tunnel decompression with electro-physiologically proven diagnosis. We devised a test whereby patients were made to hyperventilate under prescribed conditions and repeated Phalen's test and Tinel's sign for comparison. These were compared with a control group chosen randomly among hospital staff. 86% patients had a positive result which was just behind Phalen's test in sensitivity. It was also 100% specific as there were no false positives. Hyperventilation is a phenomenon which provokes carpal tunnel syndrome. Its clinical value remains to be seen due to cumbersome method and probable patient non-compliance but it is a new discovery. It may be useful in other irritable-nerve-syndromes as a test to add to our available armament. It may be an additional factor or a primary reason for nocturnal paraesthesias in CTS patients.

Short-term exposure to hypoxia for work and leisure activities in health and disease: which level of hypoxia is safe?

INTRODUCTION: Exposures to natural and simulated altitudes entail reduced oxygen availability and thus hypoxia. Depending on the level of hypoxia, the duration of exposure, the individual susceptibility, and preexisting diseases, health problems of variable severity may arise. Although millions of people are regularly or occasionally performing mountain sport activities, are transported by airplanes, and are more and more frequently exposed to short-term hypoxia in athletic training facilities or at their workplace, e.g., with fire control systems, there is no clear consensus on the level of hypoxia which is generally well tolerated by human beings when acutely exposed for short durations (hours to several days). CONCLUSIONS: Available data from peer-reviewed literature report adaptive responses even to altitudes below 2,000 m or corresponding normobaric hypoxia (F(i)O(2) > 16.4%), but they also suggest that most of exposed subjects without severe preexisting diseases can tolerate altitudes up to 3,000 m (F(i)O(2) > 14.5%) well. However, physical activity and unusual environmental conditions may increase the risk to get sick. Large interindividual variations of responses to hypoxia have to be expected, especially in persons with preexisting diseases. Thus, the assessment of those responses by hypoxic challenge testing may be helpful whenever possible.

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise.

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO(2) rebreathing, alkalosis by hyperventilation, or control. The Pco(2), pH, K(+) concentration ([K(+)]), and Na(+) concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis (P < 0.001). The venous [K(+)] rose to similar maximum values in all conditions (6.2 ± 0.8 mmol/l). The acidification reduced the decline in contraction speed (P < 0.001) but decreased the M-wave area to 73.4 ± 19.8% (P < 0.001) of the initial value. After the first exercise cycle, the M-wave area was smaller with acidosis than with alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition (P < 0.001). The duration of the M-wave was not affected. Acidification diminished the reduction in performance, although the M-wave area during exercise was decreased. Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.