Role of lungs and inactive muscle in acid-base control after maximal exercise

The pulmonary responses and changes in plasma acid-base status occurring across the inactive forearm muscle were examined after 30 s of intense exercise in six male subjects exercising on an isokinetic cycle ergometer. Arterial and deep forearm venous blood were sampled at rest and during 10 min after exercise; ventilation and pulmonary gas exchange variables were measured breath by breath during exercise and recovery. Immediately after exercise, ventilation and CO2 output increased to 124 +/- 17 1/min and 3.24 +/- 0.195 l/min, respectively. The subsequent decrease in CO2 output was slower than the decrease in O2 intake (half time of 105 +/- 15 and 47 +/- 4 s, respectively); the respiratory exchange ratio was greater than 1.0 throughout the 10 min of recovery. Arterial plasma concentrations of Na+, K+, and Ca2+ increased transiently after exercise. Arterial lactate ion concentration ([La-]) increased to 14-15 meq/l within 1.5 min and remained at this level for the rest of the study. Throughout recovery there was a positive arteriovenous [La-] difference of 4-5 meq/l, associated with an increase in the arteriovenous strong ion difference ([SID]) and by a large increase in the venous Pco2 and [HCO3-]. These findings were interpreted as indicating uptake of La- by the inactive muscle, leading to a fall in the muscle [SID] and increase in plasma [SID], associated with an increase in muscle PCO2. The venoarterial CO2 content difference was 38% greater than could be accounted for by metabolism of La- alone, suggesting liberation of CO2 stored in muscle, possibly as carbamate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood lactate changes during isocapnic buffering in sprinters and long distance runners

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation.     

Factors influencing hydrogen ion concentration in muscle after intense exercise

To assess the importance of factors influencing the resolution of exercise-associated acidosis, measurements of acid-base variables were made in nine healthy subjects after 30 s of maximal exercise on an isokinetic cycle ergometer. Quadriceps muscle biopsies (n = 6) were taken at rest, immediately after exercise, and at 3.5 and 9.5 min of recovery; arterial and femoral venous blood were sampled (n = 3) over the same time. Intracellular and plasma inorganic strong ions were measured by neutron activation and ion-selective electrodes, respectively; lactate concentration ([La-]) was measured enzymatically, and plasma PCO2 and pH were measured by electrodes. Immediately after exercise, intracellular [La-] increased to 47 meq/l, almost fully accounting for a reduction in intracellular strong ion difference ([SID]) from 154 to 106 meq/l. At the same time, femoral venous PCO2 increased to 100 Torr and plasma [La-] to 9.7 meq/l; however, plasma [SID] did not change because of a concomitant increase in inorganic [SID] secondary to increases in [K+], [Na+], and [Ca2+]. During recovery, muscle [La-] fell to 26 meq/l by 9.5 min; [SID] remained low (101 and 114 meq/l at 3.5 and 9.5 min, respectively) due almost equally to the elevated [La-] (30 and 26 meq/l) and reductions in [K+] (from 142 meq/l at rest to 123 and 128 meq/l). Femoral venous PCO2 rose to 106 Torr at 0.5 min postexercise and fell to resting values at 9.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood lactate responses in incremental exercise as predictors of constant load performance

Seven trained male cyclists (VO2max = 4.42 +/- 0.23 l.min-1; weight 71.7 +/- 2.7 kg, mean +/- SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the "individual anaerobic threshold" (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% VO2max, the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La-]av) and deep venous blood ([La-]v) of the resting forearm. The av-v lactate gradient across the inactive forearm muscle was -0.08 mmol.l-1 at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol.l-1 (*P less than 0.05). The gradients after 10 min at these same work rates were -0.09, +0.24 and +1.03* mmol.l-1. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P less than 0.05). The [La-]av was consistently higher during prolonged exercise at both 60 and 80% VO2max than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La-] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater av-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

Water and electrolyte balance in the vascular space during graded exercise in humans

We analyzed the changes in water content and electrolyte concentrations in the vascular space during graded exercise of short duration. Six male volunteers exercised on a cycle ergometer at 20 degrees C (relative humidity = 30%) as exercise intensity was increased stepwise until voluntary exhaustion. Blood samples were collected at exercise intensities of 29, 56, 70, and 95% of maximum aerobic power (VO2max). A curvilinear relationship between exercise intensity and Na+ concentration in plasma ([Na+]p) was observed. [Na+]p significantly increased at 70% VO2max and at 95% VO2max was approximately 8 meq/kgH2O higher than control. The change in lactate concentration in plasma ([Lac-]p) was closely correlated with the change in [Na+]p (delta[Na+]p = 0.687 delta[Lac-]p + 1.79, r = 0.99). The change in [Lac-]p was also inversely correlated with the change in HCO3- concentration in plasma (delta[HCO3-]p = -0.761 delta[Lac-]p + 0.22, r = -1.00). At an exercise intensity of 95% VO2max, 60% of the increase in plasma osmolality (Posmol) was accounted for by an increase in [Na+]p. These results suggest that lactic acid released into the vascular space from active skeletal muscles reacts with [HCO3-]p to produce CO2 gas and Lac-. The data raise the intriguing notion that increase in [Na+]p during exercise may be caused by elevated Lac-.     

Blood glucose responses in humans mirror lactate responses for individual anaerobic threshold and for lactate minimum in track tests

The equilibrium point between blood lactate production and removal (La-(min)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-]b, catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc]b, this study investigated the [Glc] and [La-]b responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum (Glc(min)) in addition to IAT and La-(min) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v3km); IAT and IGT - 8 x 800 m runs at velocities between 84% and 102% of v3km; La-(min) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 6 x 800 m at intensities between 87% and 97% of v3km; endurance test (ET) - 30 min at the velocity of IAT. Capillary blood (25 microl) was collected for [La-]b and [Glc]b measurements. The IAT and IGT were determined by [La-]b and [Glc]b kinetics during the second test. The La-(min) and Glc(min) were determined considering the lowest [La-] and [Glc]b during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21) m. x min(-1); r = 0.096; P < 0.001] and between La-(min) [285 (SD 21)] and Glc(min) [287 (SD 20) m. x min(-1) r = 0.77; P < 0.05]. During ET, the [La-]b reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol x l(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min) as well as by IAT and La-(min).     

Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.     

Recovery from an activity-induced metabolic acidosis in the American alligator, Alligator mississippiensis

The metabolic acidosis resulting from an intense exercise bout is large in crocodilians. Here we studied recovery from this pH perturbation in the American alligator. Metabolic rate, minute ventilation, arterial pH and gases, and strong ion concentration were measured for 10 h after exhaustion to elucidate the mechanisms and time course of recovery. Exhaustion resulted in a significant increase in lactate, metabolic rate, and ventilation, and a decrease in arterial PCO2), pH and bicarbonate. By 15 min after exhaustion, oxygen consumption returned to rest though carbon dioxide excretion remained elevated for 30 min. Arterial PO2), [Na+], and [K+], increased following exhaustion and recovered by 30 min post-exercise. Minute ventilation, tidal volume, [Cl-], and respiratory exchange ratio returned to resting values by 1 h. The air convection requirement for oxygen was elevated between 15 and 60 min of recovery. Breathing frequency and pH returned to resting values by 2 h of recovery. Lactate levels remained elevated until 6 h post-exercise. Arterial PCO2) and [HCO3-] were depressed until 8 h post-exercise. Compensation during recovery of acid-base balance was achieved by altering ventilation: following the initial metabolic acidosis and titration of bicarbonate, a relative hyperventilation prevented a further decrease in pH.     

Acid-base balance during repeated cycling sprints in boys and men.

The aim of this study was to investigate the acid-base balance during repeated cycling sprints in children and adults. Eleven boys (9.6 +/- 0.7 yr) and ten men (20.4 +/- 0.8 yr) performed ten 10-s sprints on a cycle ergometer separated by 30-s passive recovery intervals. To measure the time course of lactate ([La]), hydrogen ions ([H(+)]), bicarbonate ions ([HCO(3)(-)]), and base excess concentrations and the arterial partial pressure of CO(2), capillary blood samples were collected at rest and after each sprint. Ventilation and CO(2) output were continuously measured. After the 10th sprint, concentrations of boys vs. men were as follows: [La], 8.5 +/- 2.1 vs. 15.4 +/- 2.0 mmol/l; [H(+)], 43.8 +/- 1.3 vs. 66.9 +/- 9.9 nmol/l (P < 0.001). Significant correlations showed that, for a given [La], [H(+)] was lower in the boys compared with the men (P < 0.001). Significant relationships also indicated that, for a given [La], [HCO(3)(-)] and base excess concentration were similar in the boys compared with the men. Moreover, significant relationships revealed that, for a given [H(+)] or [HCO(3)(-)], arterial partial pressure of CO(2) was lower in the boys compared with the men (P < 0.001). The ventilation-to-CO(2) output ratio was higher in the boys during the first five rest intervals and was then higher in the men during the last five sprints. To conclude, during repeated sprints, the ventilatory regulation related to the change in acid-base balance induced by lactic acidosis was more important during the first rest intervals in the boys compared with the men.     

Cardiorespiratory effects of forced activity and digestion in toads

Digestion and physical activity are associated with large and sometimes opposite changes in several physiological parameters. Gastric acid secretion during digestion causes increased levels of plasma bicarbonate ([HCO-3](pl)), whereas activity leads to a metabolic acidosis with increased lactate and decrease in plasma bicarbonate. Here we describe the combined effects of feeding and activity in the toad Bufo marinus to investigate whether the increased bicarbonate buffering capacity during digestion (the so-called alkaline tide) protects the acid-base disturbance during activity and enhances the subsequent recovery. In addition, we describe the changes in arterial oxygen levels and plasma ion composition, as well as rates of gas exchange, heart rates, and blood pressures. Toads were equipped with catheters in the femoral artery and divided into four experimental regimes: control, digestion, forced activity, and forced activity during the postprandial period (N=6 in each). Digestion induced a significant metabolic alkalosis with increased [HCO-3](pl) that was completely balanced by a respiratory acidosis; that is, increased arterial Pco(2) (P(a)co(2)), so that arterial pH (pH(a)) did not change. Forced activity led to a substantial reduction in pH(a) by 0.43 units, an increase in plasma lactate concentration by 12.5 mmol L(-1), and a reduction in [HCO-3](pl) of similar magnitude. While digesting animals had higher P(a)co(2) and [HCO-3](pl) at rest, the magnitude and duration of the changes in arterial acid-base parameters were similar to those of fasting animals, although the reduction in pH(a) was somewhat lower (0.32 units). In conclusion, while recovery from the acidosis following exercise did not seem to be affected by digestion, the alkaline tide did slightly dampen the reduction in pH(a) during activity.     

Pulmonary gas exchange and acid-base state at 5,260 m in high-altitude Bolivians and acclimatized lowlanders.

Pulmonary gas exchange and acid-base state were compared in nine Danish lowlanders (L) acclimatized to 5,260 m for 9 wk and seven native Bolivian residents (N) of La Paz (altitude 3,600-4,100 m) brought acutely to this altitude. We evaluated normalcy of arterial pH and assessed pulmonary gas exchange and acid-base balance at rest and during peak exercise when breathing room air and 55% O2. Despite 9 wk at 5,260 m and considerable renal bicarbonate excretion (arterial plasma HCO3- concentration = 15.1 meq/l), resting arterial pH in L was 7.48 +/- 0.007 (significantly greater than 7.40). On the other hand, arterial pH in N was only 7.43 +/- 0.004 (despite arterial O2 saturation of 77%) after ascent from 3,600-4,100 to 5,260 m in 2 h. Maximal power output was similar in the two groups breathing air, whereas on 55% O2 only L showed a significant increase. During exercise in air, arterial PCO2 was 8 Torr lower in L than in N (P < 0.001), yet PO2 was the same such that, at maximal O2 uptake, alveolar-arterial PO2 difference was lower in N (5.3 +/- 1.3 Torr) than in L (10.5 +/- 0.8 Torr), P = 0.004. Calculated O2 diffusing capacity was 40% higher in N than in L and, if referenced to maximal hyperoxic work, capacity was 73% greater in N. Buffering of lactic acid was greater in N, with 20% less increase in base deficit per millimole per liter rise in lactate. These data show in L persistent alkalosis even after 9 wk at 5,260 m. In N, the data show 1) insignificant reduction in exercise capacity when breathing air at 5,260 m compared with breathing 55% O2; 2) very little ventilatory response to acute hypoxemia (judged by arterial pH and arterial PCO2 responses to hyperoxia); 3) during exercise, greater pulmonary diffusing capacity than in L, allowing maintenance of arterial PO2 despite lower ventilation; and 4) better buffering of lactic acid. These results support and extend similar observations concerning adaptation in lung function in these and other high-altitude native groups previously performed at much lower altitudes.     

A new method for detecting anaerobic threshold by gas exchange

Excess CO2 is generated when lactate is increased during exercise because its [H+] is buffered primarily by HCO-3 (22 ml for each meq of lactic acid). We developed a method to detect the anaerobic threshold (AT), using computerized regression analysis of the slopes of the CO2 uptake (VCO2) vs. O2 uptake (VO2) plot, which detects the beginning of the excess CO2 output generated from the buffering of [H+], termed the V-slope method. From incremental exercise tests on 10 subjects, the point of excess CO2 output (AT) predicted closely the lactate and HCO-3 thresholds. The mean gas exchange AT was found to correspond to a small increment of lactate above the mathematically defined lactate threshold [0.50 +/- 0.34 (SD) meq/l] and not to differ significantly from the estimated HCO-3 threshold. The mean VO2 at AT computed by the V-slope analysis did not differ significantly from the mean value determined by a panel of six experienced reviewers using traditional visual methods, but the AT could be more reliably determined by the V-slope method. The respiratory compensation point, detected separately by examining the minute ventilation vs. VCO2 plot, was consistently higher than the AT (2.51 +/- 0.42 vs. 1.83 +/- 0.30 l/min of VO2). This method for determining the AT has significant advantages over others that depend on regular breathing pattern and respiratory chemosensitivity.     

Roles of CO2, O2, and acid in arteriovenous [H+] difference during muscle contractions

To determine the origins of the arteriovenous [H+] difference of muscle during contractions, arterial and muscle venous blood sample pairs were taken before and after 0.5, 5.0, and 30.0 min of 4/s isometric twitches of the gastrocnemius-plantaris muscle group of anesthetized dogs. These samples were analyzed for PO2, PCO2, and pH, the concentrations of O2, CO2, K+, Na+, La-, and Cl- in whole blood, and La-, K+, Na+, and Cl- in plasma. Whole blood was hemolyzed and analyzed for PO2, PCO2, and pH. Net O2 uptake, CO2 output, L, K+, Na+, and Cl- were calculated in addition to net output of non-CO2 acid (HA) and strong ion difference ([SID]) and common ion [SID] ([K+] + [Na+] - [Cl-] - [La-]). From these data we partitioned the origins of the arteriovenous [H+] difference via the common PCO2-pH diagram and via a [H+]-PCO2 diagram and determined whether true plasma arteriovenous [H+] differences reflect plasma and cell arteriovenous [H+] differences. The arteriovenous [H+] differences of plasma and hemolyzed blood were the same, showing that true plasma does reflect plasma and cells. K+ showed a small significant but transient output. Na+ was not significant, whereas Cl- showed a significant transient uptake. Lactate output and HA, calculated for dog blood acid-base, showed transient outputs and were the same. At 5.0 min when the arteriovenous difference was largest, CO2 alone would have increased [H+] 15.9 nmol/l whereas desaturation of Hb would have decreased [H+] 4.2 nmol/l and lactate could have raised [H+] 1.0 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute hypobaric hypoxia on acid-base status of fowl blood

Arterial blood Po/, Pco2, lactate levels and Cl- ion concentration as well as pH were measured on the time course in chickens (Gallus domesticus) as they settled in normoxic conditions and during exposure to acute hypobaric hypoxia (Pb = 450 Torr). Hypoxia provoked at first a CO2 increased output from blood and a brief stage of deep metabolic acidosis during which lactate levels suddenly increased. This acidosis was then compensated producing a return to the initial pH and a decrease in [HCO3-] + [CO3(2-)] after 60 min. Subsequently respiratory alkalosis associated with an increase in [HCO-3] + [CO3(2-)], a decrease in cl- ion concentration and a small decrease in lactate levels were observed. Prolonged exposure to hypoxia (16 h) resulted in a new return to the initial pH, a decrease in concentration of [HCO3-] + [CO3(2-)] and a high lactate level. The hematocrit value, the Hb concentration, and the plasma Na+, K+, Ca++ and Mg++ ion concentration did not change significantly.     

Effect of expertise on postmaximal long sprint blood metabolite responses

The aim of this study was to describe and compare the blood metabolic responses obtained after a single maximal exercise in elite and less-successful athletes and to investigate whether these responses are related to sprint performance. Eleven elite (ELI) and 14 regional (REG) long sprint runners performed a 300-m running test as fast as possible. Blood samples were taken at rest and at 4 minutes after exercise for measurements of blood lactate concentration [La] and acid-base status. The blood metabolic responses of ELI subjects compared to those of REG subjects for pH (7.07 ± 0.05 vs. 7.14 ± 1.5), sodium bicarbonate concentration ([HCO(3)(-)], 8.1 ± 1.5 vs. 9.8 ± 1.8 mmol·L(-1)), hemoglobin O(2) saturation (SaO(2)) (94.7 ± 1.8 vs. 96.2 ± 1.6%) were significantly lower (p < 0.05), and [La] was significantly higher in ELI (21.1 ± 2.9 vs. 19.1 ± 1.2 mmol·L(-1), p < 0.05). The 300-m performance (in % world record) was negatively correlated with pH (r = -0.55, p < 0.01), SaO2 (r = -0.64, p < 0.001), [HCO(3)(-)] (r = -0.40, p < 0.05), and positively correlated with [La] (r = 0.44, p < 0.05). In conclusion, for the same quantity of work, the best athletes are able to strongly alter their blood acid-base balance compared to underperforming runners, with larger acidosis and lactate accumulation. To obtain the pH limits with acute maximal exercise, coaches must have their athletes perform a distance run with duration of exercise superior to 35 seconds. The blood lactate accumulation values (mmol·L(-1)·s(-1)) recorded in this study indicate that the maximal glycolysis rate obtained in the literature from short sprint distances is maintained, but not increased, until 35 seconds of exercise.     

Relationship between ventilation and arterial potassium concentration during incremental exercise and recovery

The purpose of this study was to compare the relationship of ventilation (VE) with pH, arterial concentrations of potassium [( K+]a), bicarbonate [( HCO3-]a), lactate [( la]a), and acid-base parameters which would affect hyperpnoea during exercise and recovery. To assess this relationship, ten healthy male subjects exercised with intensity increasing as a ramp function of 20 W.min-1 until voluntary exhaustion and they were then allowed a 5-min recovery period. Breath-by-breath gas exchange data, [HCO3-]a, pH, [la]a, [K+]a and blood gases were determined during both exercise and recovery. Using a linear regression method, the VE/[K+]a relationship was analysed during both exercise and recovery. Several interesting results were obtained: a significant relationship between [K+]a and VE was observed during recovery as well as during exercise; the VE at any given values of [K+]a was significantly higher during recovery than during exercise and out of those factors affecting exercise hyperpnoea, only [K+]a had a similar time-course to VE during recovery. Changes in [K+]a during recovery were shown to occur significantly faster than VE with an [K+]a time constant of 70.0 s, SD 16.2 as opposed to 105.5 s, SD 10.0 for VE (P less than 0.01). These results provided further evidence that [K+]a might play an important role as a substance which can stimulate exercise hyperpnoea as has been suggested by other workers. The present study also showed that during recovery [K+]a contributed significantly to the control of VE.     

The effects of exogenous extracellular carbonic anhydrase on CO2 excretion in rainbow trout (Oncorhynchus mykiss): role of plasma buffering capacity

The buffering capacity (beta) of rainbow trout (Oncorhynchus mykiss) plasma was manipulated prior to intravascular injection of bovine carbonic anhydrase to test the idea that proton (H+) availability limits the catalysed dehydration of HCO3- within the extracellular compartment. An extracorporeal blood shunt was employed to continuously monitor blood gases in vivo in fish exhibiting normal plasma beta (-3.9+/-0.3 mmol 1(-1) pH unit(-1)), and in fish with experimentally (using N-[2-hydroxyethyl]piperazine-N'-[2-ethanesulfonic acid]) elevated plasma beta (-12.1+/-1.1 mmol 1(-1) pH unit(-1)). An injection of 5 mg kg(-1) carbonic anhydrase equally reduced (after 90 min) the arterial partial pressure of CO2 in trout with regular (-0.23+/-0.05 Torr) or high (-0.20+/-0.05 Torr) plasma beta; saline injection was without effect. Because ventilation and venous blood gases were unaffected by carbonic anhydrase, the effect of extracellular carbonic anhydrase in lowering arterial partial pressure of CO2 was likely caused solely by a specific enhancement of CO2 excretion owing to acceleration of HCO3- dehydration within the plasma. The lowering of arterial partial pressure of CO2 in trout after injection of exogenous carbonic anhydrase provides the first in vivo evidence that the accessibility of plasma HCO3- to red blood cell carbonic anhydrase constrains CO2 excretion under resting conditions. Because the velocity of red blood cell Cl-/HCO3- exchange governs HCO3- accessibility to red blood cell carbonic anhydrase, the present study also provides evidence that CO2 excretion at rest is limited by the relatively slow rate of Cl-/HCO3- exchange. The effect of carbonic anhydrase in lowering arterial partial pressure of CO2 was unrelated to plasma buffering capacity. While these data could suggest that H+ availability does not limit extracellular HCO3- dehydration in vivo at resting rates of CO2 excretion, it is more likely that the degree to which plasma beta was elevated in the present study was insufficient to drive a substantially increased component of HCO3- dehydration through the plasma.     

Catecholamine responses to high intensity cycle ergometer exercise: Body mass or body composition?

The purpose of this study was to compare the sympathoadrenergic and metabolic responses following 30 s of maximal high intensity cycle ergometry exercise when cradle resistive forces were derived from total-body mass (TBM) or fat-free mass (FFM). Increases in peak power output (PPO) and pedal velocity were recorded when resistive forces reflected FFM (953 +/- 114 W vs 1020 +/- 134 W; 134 +/- 8 rpm vs 141 +/- 7 rpm ; P < 0.05). No differences were observed between mean power output (MPO), fatigue index (FI%), work done (WD) or heart rate (HR) when the TBM and FFM protocols were compared. There were no differences between the TBM and FFM protocols for adrenaline (A), noradrenaline (NA) or blood lactate concentrations ([La-]B) recorded at rest, immediately post or 24 h post exercise. However, increases in blood concentrations of A and NA (P < 0.05) were recorded for both the TBM and FFM protocol immediately post exercise. Significant correlations (P < 0.05) were recorded between PPOs, immediate post- exercise NA and [La-]B for both the TBM and FFM protocols. [La-]B levels were also significantly elevated (P < 0.01) immediately post exercise for both the TBM and FFM protocols. The results from this study suggest that greater peak power outputs are obtainable with no subsequent differences in neurophysiological or metabolic stress as determined by plasma A, NA and [La-]B concentrations when resistive forces reflect FFM and not TBM during loading procedures. The findings also indicate that immediate post exercise concentrations return to resting levels 24 h post exercise.