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Biomedical subjects

G J Heigenhauser

Publications and source records attributed to G J Heigenhauser.

At least 73 records · Page 4Linked to original sources
PubMed1995

K+ and Lac- distribution in humans during and after high-intensity exercise: role in muscle fatigue attenuation?

This review describes processes for the distribution of K+ ([K+]) and lactate concentrations ([Lac-]) that are released from contracting muscle at high rates during high-intensity exercise. This results in increased interstitial and venous [K+] and [Lac-] in contracting muscle. Large and rapid increases in plasma [K+] and [Lac-] result in the transport of these ions into red blood cells (RBCs). These ions are distributed to noncontracting tissues within both the plasma and RBC compartments of blood. The extraction of K+ and Lac- from the circulation by noncontracting tissue serves to markedly attenuate exercise-induced increases in plasma [K+] and [Lac-]. This apparent regulation of the plasma compartment by noncontracting tissues helps to maintain favorable concentration gradients for the net movement of [K+] and [Lac-] into the venous side of the microcirculation from interstitial fluids of contracting muscle. This provides conditions that 1) reduce the increase in interstitial [K+], thereby decreasing the magnitude and rate of sarcolemmal depolarization, and 2) favor the sarcolemmal transport of Lac- from within contracting muscle cells, thereby regulating intracellular osmolality and H+ concentration. On cessation of exercise, net K+ uptake by recovering muscle is rapid, with 90-95% recovery of intracellular [K+] within 3.5 min, indicating a very high rate of Na+-K+ pump activity. The K+ extracted by noncontracting tissues during exercise may be slowly released during recovery. During the initial minutes of recovery, recovering muscle continues to release Lac- into the circulation, and noncontracting tissues continue to extract Lac- for up to 30 min. The uptake of Lac- by noncontracting tissues results in elevated intracellular [Lac-]. There is no evidence that Lac- extracted by noncontracting tissues is subsequently released; it is probably metabolized within these cells. We conclude that the uptake of K+ and Lac- by RBCs and noncontracting tissues regulates ion homeostasis within plasma and the interstitial and intracellular compartments of contracting muscle. The regulatory processes help to maintain the function of active muscles by delaying the onset of fatigue during exercise and to restore homeostasis during recovery.

Humans↗
PubMed1995

Drink composition and the electrolyte balance of children exercising in the heat.

Twelve 9- to 12-year-old children (6 boys, 6 girls) performed four exercise-in-heat (35 degrees C, 45% RH) trials which differed in the composition of the fluids they drank. In each trial, subjects cycled for one 20-min and two 15-min bouts at 50% peak VO2 with 10-min rest periods in between. In a fourth bout, they cycled at 90% peak VO2 until exhaustion. Drinks had the same grape flavor and were assigned in a double-blind design and in a Latin-square order. Subjects drank 7 ml.kg-1.h-1 to keep them euhydrated. Three of the drinks had 6% carbohydrates (CHO), with different [Na+]: 0, 8.8, 18.5 mmol.l-1 and one drink had neither CHO nor Na+ (WATER). Among drink trials, there were no differences in the increase in rectal temperature, HR, or performance time to exhaustion. Despite the larger Na+ deficit induced by the Na(+)-free drinks compared with the Na+ drinks (11.8 +/- 1.4 vs 5.7 +/- 0.9 mmol.h-1), neither plasma [Na+] nor osmolality were affected. These results suggest that electrolyte, as in the above conditions, did not affect electrolyte balance, thermoregulatory responses, or aerobic performance of children exercising in the heat. The greater Na+ deficit induced by ion-free drinks was of minor biological importance.

Blood Glucose↗
PubMed1994

Plasma volume and ion regulation during exercise after low- and high-carbohydrate diets.

This study compared plasma volume (PV) and ion regulation during prolonged exercise in control vs. glycogen-depleted (GD) conditions, with emphasis on the initial minutes of exercise. In two trials separated by 1-2 wk, four adult males cycled at 75% of peak oxygen consumption (VO2) until exhaustion (50 +/- 7 min for GD) or until the GD exhaustion time in the control trial. Blood was sampled from catheters placed in the brachial artery and retrograde in the femoral vein (fv). Arterial PV decreased rapidly and by 15 min PV was 83% (control) and 88% (GD) of initial. The decrease in PV was accompanied by a net osmotic flux of water from plasma and inactive tissues to contracting muscles. The significantly greater decrease in PV in control compared with GD was associated with a higher muscle lactate content (Lac-; 36 vs. 17 mumol/g dry wt, respectively). Increases in plasma [Cl-] and [Na+] were less than predicted from decreased PV, indicating net loss of these ions from the plasma compartment. Increases in arterial and fv [K+] were 50% greater than could be accounted for by decreased PV, corresponding with increased arterial and fv plasma K+ contents. The rapid net release of K+ and Lac- from contracting muscle during the first few minutes of exercise in both trials was abolished (control) or reversed (GD) within 15 min of beginning exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effect of chronic acetazolamide administration on gas exchange and acid-base control after maximal exercise.

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1994

A simple isokinetic cycle for measurement of leg muscle function.

The measurement of net pedaling torque during isokinetic cycling allows for the evaluation of leg muscle strength and work capacity over fixed time intervals. However, the expense and difficulty of constructing an isokinetic cycle have limited the widespread application of this useful research tool. We have modified a simple commercially available isokinetic cycle that uses hydraulics to maintain pedaling velocity. A strain gauge on the flywheel axle strut measures the torsion on the strut caused by pedaling. To evaluate this device, seven healthy subjects (3 males and 4 females) were each tested twice at 60, 90, and 120 rpm for peak power during a 10-s sprint and at 100 rpm for total work performed during a 30-s sprint. These results were compared with predicted values for age, height, and sex developed on a more complicated isokinetic cycle. Subjects also performed a progressive cycle ergometry test. For the group, peak power was 97.30 +/- 12.64% of predicted (males 883.70 +/- 202.76 W; females 657.00 +/- 66.42 W) and work output was 107.70 +/- 15.75% of predicted (males 15.50 +/- 2.85 kJ; females 11.70 +/- 2.17 kJ), whereas maximal progressive exercise capacity was 126.40 +/- 25.84% (males 245.30 +/- 56.58 W; females 212.30 +/- 35.49 W). The relatively lower work values generated on this cycle (compared with the maximal progressive exercise capacity) can be attributed to the location of the strain gauge, resulting in measurement of effective work output on the flywheel.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Integrated responses to exhaustive exercise and recovery in rainbow trout white muscle: acid-base, phosphogen, carbohydrate, lipid, ammonia, fluid volume and electrolyte metabolism.

White muscle and arterial blood plasma were sampled at rest and during 4 h of recovery from exhaustive exercise in rainbow trout. A compound respiratory and metabolic acidosis in the blood was accompanied by increases in plasma lactate (in excess of the metabolic acid load), pyruvate, glucose, ammonia and inorganic phosphate levels, large elevations in haemoglobin concentration and haematocrit, red cell swelling, increases in the levels of most plasma electrolytes, but no shift of fluid out of the extracellular fluid (ECF) into the intracellular fluid (ICF) of white muscle. The decrease in white muscle pHi was comparable to that in pHe; both recovered by 4 h. Creatine phosphate and ATP levels were both reduced by 40% after exercise, the former recovering within 0.25 h, whereas the latter remained depressed until 4 h. Changes in creatine concentration mirrored those in creatine phosphate, whereas changes in IMP and ammonia concentration mirrored those in ATP. White muscle glycogen concentration was reduced 90% primarily by conversion to lactate; recovery was slow, to only 40% of resting glycogen levels by 4 h. During this period, most of the lactate and metabolic acid were retained in white muscle and there was excellent conservation of carbohydrate, suggesting that in situ glycogenesis rather than oxidation was the major fate of lactate. The redox state ([NAD+]/[NADH]) of the muscle cytoplasm, estimated from ICF lactate and pyruvate levels and pHi, remained unchanged from resting levels, challenging the traditional view of the 'anaerobic' production of lactate. Furthermore, the membrane potential, estimated from levels of ICF and ECF electrolytes using the Goldman equation, remained unchanged throughout, challenging the view that white muscle becomes depolarized after exhaustive exercise. Indeed, ICF K+ concentration was elevated. Lactate was distributed well out of electrochemical equilibrium with either the membrane potential (Em) or the pHe-pHi difference, supporting the view that lactate is actively retained in white muscle. In contrast, H+ was actively extruded. Ammonia was distributed passively according to Em rather than pHe-pHi throughout recovery, providing a mechanism for retaining high ICF ammonia levels for adenylate resynthesis in situ. Although lipid is not traditionally considered to be a fuel for burst exercise, substantial decreases in free carnitine and elevations in acyl-carnitines and acetyl-CoA concentrations indicated an important contribution of fatty acid oxidation by white muscle during both exercise and recovery.

Acid-Base Equilibrium↗
PubMed1994

Is heparin the ideal anticoagulant for cardiopulmonary bypass? Dermatan sulphate may be an alternate choice.

Performance of cardiopulmonary bypass (CPB) during cardiac surgery requires the administration of high dose heparin to prevent CPB pump occlusion. However, this heparin use is associated with bleeding side-effects. Moreover, at the end of CPB, the heparin must be neutralized with protamine sulphate, which is also associated with adverse side-effects. A number of recent studies suggest that dermatan sulphate may be useful as an alternate anticoagulant to heparin. We determined whether CPB could be performed using dermatan sulphate instead of heparin, in an adult pig CPB model. When heparin was used, a high dose (> 200 U/kg, which generated > 3 anti-thrombin U/ml of plasma), was required to perform successful CPB and to maintain CPB pump patency. This dose was associated with a post CPB bleeding of approximately 600 ml/2 h. In contrast, successful CPB could be achieved when the pigs were given lower doses of dermatan sulphate than heparin, which in turn, were associated with less bleeding. We conclude that dermatan sulphate may be an alternate anticoagulant for cardiac surgery.

Animals↗
PubMed1993

Maximal short-term exercise performance and ion regulation in cystic fibrosis.

Controversy exists over whether defects in electrolyte transport exist in erythrocytes from cystic fibrosis (CF) patients. We hypothesized that differences in ion regulation in CF would affect skeletal muscle performance during intense exercise. Seven well-nourished CF patients were compared with seven healthy age-matched control subjects. Skeletal muscle performance was assessed during a 30-s sprint on an isokinetic cycle ergometer. Ion regulation was evaluated from arterialized venous blood sampled at rest, at peak exercise, and after 5 min of recovery. There was no difference in sprint performance between the CF (total work, 93.7 +/- 30.02% predicted; endurance, 30.6 +/- 9.93% decline) and control (109.7 +/- 19.48%; 35.6 +/- 14.76%) groups. The changes in plasma and erythrocyte ions and blood gases did not differ between the groups. There was a suggestion that the CF group may have had an inadequate ventilatory response to the metabolic challenge of short-term maximal exercise. The contribution of decreases in the strong ion difference to increases in plasma hydrogen ion concentrations was less in the CF group. This may be due to alterations in ionic regulation in CF, but the influence of inadequate arterialization of the blood samples could not be ruled out.

Adult↗
PubMed1993

Pyruvate dehydrogenase activity and acetyl group accumulation during exercise after different diets.

Pyruvate dehydrogenase activity (PDHa) and acetyl group accumulation were examined in human skeletal muscle at rest and during exercise after different diets. Five males cycled at 75% of maximal O2 uptake (VO2 max) to exhaustion after consuming a low-carbohydrate diet (LCD) for 3 days and again 1-2 wk later for the same duration after consuming a high-carbohydrate diet (HCD) for 3 days. Resting PDHa was lower after a LCD (0.20 +/- 0.04 vs. 0.69 +/- 0.05 mmol.min-1.kg wet wt-1; P < 0.05) and coincided with a greater intramuscular acetyl-CoA-to-CoASH ratio, acetyl-CoA content, and acetylcarnitine content. PDHa increased during exercise in both conditions but at a lower rate in the LCD condition compared with the HCD condition (1.46 +/- 0.25 vs. 2.65 +/- 0.23 mmol.min-1.kg wet wt-1 at 16 min and 1.88 +/- 0.20 vs. 3.11 +/- 0.14 at the end of exercise; P < 0.05). During exercise muscle acetyl-CoA and acetylcarnitine content and the acetyl-CoA-to-CoASH ratio decreased in the LCD condition but increased in the HCD condition. Under resting conditions PDHa was influenced by the availability of fat or carbohydrate fuels acting through changes in the acetyl-CoA-to-CoASH ratio. However, during exercise the activation of PDHa occurred independent of changes in the acetyl-CoA-to-CoASH ratio, suggesting that other factors are more important.

Acetyl Coenzyme A↗
PubMed1993

Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling.

Six male subjects received either a saline (control) or Intralipid infusion during 30 min rest and 15 min cycling at 85% maximal O2 uptake (VO2max) to examine the regulation of fat-carbohydrate interaction (glucose-fatty acid cycle) in skeletal muscle. Muscle biopsies were sampled immediately before and at 3 and 15 min of exercise in both trials. A muscle biopsy was also taken at -30 min rest in the Intralipid trial. Intralipid infusion significantly elevated plasma free fatty acids above control during rest (0.21 +/- 0.04 to 0.94 +/- 0.09 mM) and exercise (5 min: 1.27 +/- 0.15 mM; 15 min: 1.42 +/- 0.13 mM). Muscle glycogen degradation was significantly lower in the Intralipid trial (109.7 +/- 29.3 vs. 194.7 +/- 32.1 mmol/kg dry muscle). Muscle lactate accumulation after 15 min was similar in both trials (control, 60.7 +/- 12.2 and Intralipid, 60.9 +/- 12.4 mmol/kg dry muscle). Muscle citrate increased at rest during Intralipid (0.32 +/- 0.06 to 0.58 +/- 0.06 mmol/kg dry muscle) but was not different between trials at 3 min (control, 0.73 +/- 0.07 and Intralipid, 0.68 +/- 0.06 mmol/kg dry muscle) and 15 min of cycling. Resting acetyl-CoA was unaffected by Intralipid and increased similarly in both trials at 3 min of cycling (control, 59.0 +/- 10.3 and Intralipid, 50.7 +/- 13.6 mumol/kg dry muscle) and remained unchanged at 15 min. Pyruvate dehydrogenase activity increased five- to sevenfold during exercise and was similar in both trials (15 min: control, 2.42 +/- 0.30 and Intralipid, 2.79 +/- 0.41 mmol.min-1 x kg wet wt-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyl Coenzyme A↗
PubMed1993

Comparison of three techniques for body composition analysis in cystic fibrosis.

Body composition analysis is an important component of nutritional assessment in cystic fibrosis (CF). No gold standard of measurement exists, and techniques applicable to healthy populations may be unsuitable for CF patients. We assessed lean body mass (LBM) in 12 children with CF by skinfold (SK) measurements, bioelectrical impedance analysis (BIA), and dual-photon absorptiometry (DPA) and repeated these measures in 10 subjects 6 mo later. SK and DPA measures in eight older CF patients and eight healthy controls were compared to evaluate any effect of disease on estimates of LBM by use of DPA. Good agreement between the measures was seen at baseline and 6 mo by use of concordance plots. However, the limits of agreement between measures ranged up to 19% of SK-derived LBM measures (baseline: SK and DPA, 2.63 to -3.93 kg; SK and BIA, 2.36 to -1.24 kg; BIA and DPA, 1.88 to -4.28 kg; 6 mo: SK and DPA, 2.10 to -3.58 kg; SK and BIA, 6.28 to -5.49 kg; BIA and DPA, 5.53 to -7.79 kg). The change in LBM over 6 mo did not correlate among the three measures. Only BIA change in LBM correlated with weight change (r = 0.716, P < 0.02), probably due to the inclusion of weight in the regression equations for determining LBM from impedance. The relationship between SK and DPA measures did not differ between the CF and control groups, suggesting that there was no effect of disease on the DPA measure. The results suggest that none of these methods is precise enough to follow short-term changes in the nutritional status of CF patients longitudinally.

Absorptiometry, Photon↗
PubMed1993

Respiratory and peripheral muscle function in cystic fibrosis.

Respiratory muscle strength (RMS) and endurance are often preserved in cystic fibrosis (CF) despite malnutrition, chronic airflow limitation, and hyperinflation. Inspiratory muscle function may be relatively preserved due to a selective "training stimulus" from chronic lung disease. Respiratory and peripheral muscle function were evaluated in 14 stable CF patients and 16 healthy control subjects. RMS was measured using static maximal pressures performed at FRC. Respiratory fatigue (RF) was assessed using 18 repeated static efforts (10 s on/5 s off) over 4.5 min. Peripheral function was evaluated by leg strength (LS) and leg fatigue (LF) measured during sprint efforts on an isokinetic cycle ergometer. Despite a lower weight (mean +/- SD, 94 +/- 9.6% ideal wt for CF patients versus 107 +/- 14.6% for controls) and elevated residual volume (RV)/TLC ratio (38 +/- 13.0 versus 22 +/- 5.3), the CF group maintained RMS (inspiratory 96 +/- 23.2 versus 114 +/- 33.2; expiratory 105 +/- 28.3 versus 123 +/- 40.9 cm H2O) but had decreased LS (590 +/- 201.7 versus 813 +/- 167.1 W). There were no differences between the groups with respect to RF or LF. For the control group, inspiratory and expiratory RMS correlated with LS (p < 0.01) and lean body mass (p < 0.01). For the CF group, while expiratory RMS (p < 0.05) and LS (p < 0.01) correlated with lean body mass and each other (p < 0.01), inspiratory RMS was independent of lean body mass and LS (p > 0.1). Female CF patients appeared to have a better preservation of inspiratory RMS than males with CF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Analysis of factors limiting maximal exercise performance in cystic fibrosis.

1. Maximal exercise capacity in cystic fibrosis is influenced by both pulmonary and nutritional factors: lung disease by limiting maximal achievable ventilation, and malnutrition through a loss of muscle mass. The associated reduction in everyday activities may result in peripheral muscle deconditioning. 2. We studied 14 stable patients with cystic fibrosis (six males, eight females) and 14 healthy control subjects (seven males, seven females) in order to assess the influence of these factors on exercise performance. Subjects underwent anthropometry to estimate muscle mass, spirometry to assess ventilatory capacity, a 30 s sprint on an isokinetic cycle ergometer to assess maximal leg muscle performance, and progressive cycle ergometry to assess overall exercise capacity. 3. Compared with control subjects, the patients with cystic fibrosis were of similar age and height but weighed proportionately less [% ideal weight (mean +/- SD): 94.3 +/- 9.64 versus 109.5 +/- 11.82] and showed evidence of airflow limitation [forced expiratory volume in 1.0 s (FEV1.0) 72.5 +/- 24.78 versus 112.6 +/- 14.25% of predicted]. 4. The patients with cystic fibrosis did less absolute (5.1 +/- 1.89 versus 7.3 +/- 1.97 kJ) but similar relative maximal (11.5 +/- 3.41 versus 13.1 +/- 3.55 kJ/kg lean body mass) sprint work. During progressive exercise, the group with cystic fibrosis achieved lower absolute [maximal O2 consumption (VO2max.) 1.8 +/- 0.527 versus 3.0 +/- 0.655 litres/min] and relative (VO2max./kg lean body mass: 40.5 +/- 9.23 versus 53.0 +/- 11.62 ml min-1 kg-1) work levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Erythrocyte ion regulation across inactive muscle during leg exercise.

Ion concentration changes in whole blood, plasma, and erythrocytes across inactive muscle were examined in eight healthy males performing four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Blood was sampled from the arm brachial artery and deep antecubital vein during the intermittent exercise period and for 90 min of recovery. Arterial and venous erythrocyte lactate concentration ([Lac-]) increased from 0.3 +/- 0.1 to 12.5 +/- 1.3 (p < 0.01) and 1.1 +/- 0.4 to 8.5 +/- 1.5 mmol/L (p < 0.01), respectively, returning to control values during recovery. Arterial and venous plasma [Lac-] increased from 1.5 +/- 0.2 to 27.7 +/- 1.8 and from 1.3 +/- 0.4 to 25.7 +/- 3.5 mmol/L, respectively, and was greater than erythrocyte [Lac-] throughout exercise and recovery. Arterial and venous [K+] increased in erythrocytes from 119.5 +/- 5.1 to 125.4 +/- 4.6 (p < 0.01) and from 113.6 +/- 1.7 to 120.6 +/- 7.1 mmol/L, respectively, decreasing to control during recovery. In arterial and venous plasma, [K+] increased from 4.3 +/- 0.1 to 6.1 +/- 0.2 (p < 0.01) and from 4.5 +/- 0.2 to 5.3 +/- 0.2 mmol/L (p < 0.01), respectively, decreasing to control during recovery. The efflux of Lac- out of erythrocytes against an electrochemical concentration gradient suggests the presence of an active transport system. Efflux of K+ from erythrocytes as blood passes across inactive muscle affords an important adaptation to the K+ release from muscle activated in heavy exercise.

Acid-Base Equilibrium↗
PubMed1992

Blood ion regulation during repeated maximal exercise and recovery in humans.

We investigated the ionic changes in arterial (a) and femoral venous (fv) blood that accompany muscle fatigue with repeated maximal exercise. Measurements were made on separated plasma and hemolysed whole blood to quantify the relative contributions of plasma and erythrocytes to this acid-base challenge. Five healthy males performed four 30-s bouts of maximal isokinetic cycling exercise, with 4 min of rest between bouts, and recovery was followed for 90 min. In whole blood, maximal increases in [K+]a amounted to 10 +/- 2.0 meq/l and in [K+]fv to 7 +/- 4.3 meq/l and occurred at the end of bout 2. Whole blood lactate concentration ([Lac-]) peaked at 15.3 +/- 1.39 ([Lac-]a) and 16.7 +/- 1.59 meq/l ([Lac-]fv) at the end of bout 4. In plasma, peak [Lac-]a and [Lac-]fv were both 21 meq/l at the end of bout 4. Plasma [H+]a increased from 36 +/- 1.0 neq/l at rest to 44 +/- 2.9 neq/l at the end of the first bout of exercise; 80% of this increase was due to a 2.9 meq/l decrease in arterial strong ion difference ([SID]), and 20% was due to an increase in plasma protein ([Atot]a); a reduction in arterial PCO2 to 29 mmHg had an alkalinizing effect. In contrast, plasma [H+]fv increased from 39 +/- 0.5 neq/l at rest to 93 +/- 4.1 neq/l, with an increase in PfvCO2 to 97 +/- 7 mmHg contributing 75%, a decrease in [SID]fv 15%, and an increase in [Atot]fv 10% to the increase in [H+]fv. In later exercise bouts, the relative contributions of [SID]a, [Atot]a, and arterial PCO2 to plasma [H+]a were similar, but the contribution of [SID]fv to [H+]fv increased and that of femoral venous PCO2 decreased, with the contribution of [Atot]fv remaining unchanged (8-12%). During exercise and recovery, the changes in both arterial and femoral venous PCO2 and [K+] were more rapid than changes in [Lac-], and the time course of whole blood [K+] was slower than that of plasma [K+]. Erythrocytes may play an important role in regulating plasma [Lac-] and [K+] with intense exercise.

Adult↗
PubMed1992

Effect of acetazolamide on gas exchange and acid-base control after maximal exercise.

To investigate the interactions between the systems that contribute to acid-base homeostasis after severe exercise, we studied the effects of carbonic anhydrase inhibition on exchange of strong ions and CO2 in six subjects after 30 s of maximal isokinetic cycling exercise. Each subject exercised on two randomly assigned occasions, a control (CON) condition and 30 min after intravenous injection of 1,000 mg acetazolamide (ACZ) to inhibit blood carbonic anhydrase activity. Leg muscle power output was similar in the two conditions; peak O2 uptake (VO2) after exercise was lower in ACZ (2,119 +/- 274 ml/min) than in CON (2,687 +/- 113, P less than 0.05); peak CO2 production (VCO2) was also lower (2,197 +/- 241 in ACZ vs. 3,237 +/- 87 in CON, P less than 0.05) and was accompanied by an increase in the recovery half-time from 1.7 min in CON to 2.3 min in ACZ. Whereas end-tidal PCO2 was lower in ACZ than in CON, arterial PCO2 (PaCO2) was higher, and a large negative end-tidal-to-arterial difference (less than or equal to 20 Torr) was present in ACZ on recovery. In ACZ, postexercise increases in arterial plasma [Na+] and [K+] were greater but [La-] was lower. Arteriovenous differences across the forearm showed a greater uptake of La- and Cl- in CON than in ACZ. Carbonic anhydrase inhibition with ACZ, in addition to impairing equilibration of the CO2 system to the acid-base challenge of exercise, was accompanied by changes in equilibration of strong inorganic ions. A lowered plasma [La-] was not accompanied by greater uptake of La- by inactive muscle.

Acetazolamide↗
PubMed1992

Gas exchange, metabolite status and excess post-exercise oxygen consumption after repetitive bouts of exhaustive exercise in juvenile rainbow trout.

Juvenile rainbow trout (approximately 6 g) were exercised to exhaustion in two 5 min bouts given 6 h apart. Resting levels of whole-body lactate and glycogen were restored prior to the second bout. The rate of O2 consumption increased about threefold 5 min after each bout of exercise, while recovery time decreased from 4 h after the first bout to 2-3 h after the second. The excess post-exercise oxygen consumption, i.e. 'oxygen debt', was significantly reduced by 40% after the second exercise bout, despite almost identical rates of lactate clearance and glycogen resynthesis. The rates of CO2 and ammonia excretion increased sixfold and threefold, and recovery times decreased from 4-6 h to 3 h and from 3 h to 1.5 h, respectively. After the first bout, whole-body lactate levels peaked at 5 min post-exercise at about 8.5 times pre-exercise levels. After the second bout, lactate levels peaked at 0 min post-exercise and fell more rapidly during recovery. Whole-body glycogen levels decreased by 70% and 80% and ATP levels decreased by 75% and 65% after the first and second bouts, respectively, while glucose levels increased about 1.5-fold immediately after both bouts. Creatine phosphate levels decreased by 70% and 80% after the first and second bouts, respectively. After 6 h of recovery, creatine phosphate levels were higher after the second bout than after the first. These findings suggest that exhaustive exercise may cause a 'non-specific' increase in metabolic rate not directly related to the processing of metabolites, which is reduced upon a subsequent exercise bout. This is in contrast with the classical 'oxygen debt hypothesis', which states that the oxygen debt and lactate clearance are linked. Furthermore, it appears that two sequential exercise bouts are sufficient to induce a 'training effect', i.e. improved rates of metabolic recovery.

Adenosine Triphosphate↗