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Biomedical subjects

G J Heigenhauser

Publications and source records attributed to G J Heigenhauser.

At least 91 records · Page 5Linked to original sources
PubMed1992

Cardiac output determination during progressive exercise in cystic fibrosis.

Cardiac output (Q) determination using the equilibrium CO2-rebreathe indirect Fick technique (Equil) to estimate mixed venous PCO2 (Pv-CO2) has been validated during steady state (SS) exercise in subjects with lung disease. A modification of the exponential method using a low concentration of CO2 with an exponential rise in PEt-CO2 (Ex) during rebreathing to estimate Pv-CO2 has been validated during nonsteady state exercise. The purpose of the present study was to validate the Ex method in subjects with lung disease. Q was measured by Ex at every second work load during Prog. Q was measured after 5 min of SS exercise by both Ex and Equil. Arterial PCO2 was estimated from PEtCO2. There was no significant difference in the Q-VO2 relationship during Prog exercise between the combined control and mild (FEV1 > 70%) CF subjects or the moderate and severe CF subjects. Q can be determined in the nonsteady state using the exponential CO2-rebreathe indirect Fick technique in subjects with CF, allowing for noninvasive examination of cardiopulmonary interaction during exercise at a wide range of work loads.

Adult↗
PubMed1992

Sweat electrolyte loss during exercise in the heat: effects of gender and maturation.

Humans may lose large amounts of water and electrolytes from sweat during prolonged exercise in a hot climate. Gender and maturational differences for the total sweat electrolyte losses have not been reported. The purpose of this study was to compare sweat electrolyte losses of prepubescent (PP), pubescent (P) and young adult (YA) males and females, under the same environmental conditions and relative exercise intensities. Twenty-five females (8 PP, 9 P, 8 YA) and 26 males (10 PP, 8 P, 8 YA) cycled for two 20-min bouts at 50% of their peak VO2 in a climatic chamber (42 degrees C, 18% relative humidity). Sweat was collected from a plastic bag attached to the lower back. Total body sweat loss was calculated from the differences in nude body weight corrected for fluid intake, urine, and respiratory water loss. Sweat [Na+] and [Cl-] tended to increase with maturation while sweat [K+] was lower in YA compared with that of PP. Children had a lower sweating rate than YA, even when corrected for body surface area. As a result, total Na+ and Cl- losses per kg body weight from sweat (mEq.kg-1.h-1) were higher in YA compared with those of PP and P; however, no maturational difference was found in K+ losses. Within the same maturational group, there were no gender differences in any of the electrolyte losses. These results may be useful in recommending "optimal" fluid-electrolyte drinks for children exercising in the heat.

Adolescent↗
PubMed1991

The oxygen debt hypothesis in juvenile rainbow trout after exhaustive exercise.

A 5 min bout of exhaustive exercise in 2-3 g rainbow trout resulted in a 2.0-2.5 fold increase in oxygen consumption (MO2), a 5-fold increase in whole-body lactate (LAC) levels and a near depletion in whole-body glycogen (GLY), ATP and creatine phosphate (CP) stores; glucose, ADP and AMP did not change. Recovery of MO2 and LAC was complete by 6 h, by which time GLY had stabilized at about 65% resting levels without further recovery through 24 h. Complete recovery of ATP required 1.0-1.5 h, whereas restoration of CP required only 5 min. The MO2 recovery curve was resolved into an initial fast component (t1/2 = 0.23 h) and a second slower component (t1/2 = 2.1 h), comprising approximately 20% and 80% respectively of the excess post-exercise oxygen consumption (EPOC). The fast component was satisfactorily accounted for by the standard components of the 'alactacid O2 debt'. However, the slow component could not be completely explained by changes in whole body LAC and GLY during recovery based on scenarios of either oxidation or GLY resynthesis as the primary fate of LAC. The classical 'O2 dept hypothesis' (Hill and Lupton, Quart, J. Med. 16: 135-171, 1923; Margaria et al., Am. J. Physiol. 106: 689-715, 1933) cannot be the complete explanation of EPOC in the trout.

Adenosine Triphosphate↗
PubMed1991

The roles of ion fluxes in skeletal muscle fatigue.

Intense muscle contractions result in large changes in the intracellular concentrations of electrolytes. The purpose of this study was to examine the contributions of changes in intracellular strong ions to calculated changes in steady-state membrane potential (Em) and muscle intracellular H+ concentration ([H+]i). A physicochemical model is used to examine the origin of the changes in [H+]i during intense muscle contraction. The study used the isolated perfused rat hindlimb intermittently stimulated to contract at high intensity for 5 min. This resulted in significant K+ depletion of both slow (soleus) and fast (white gastrocnemius, WG) muscle fibers and a release of K+ and lactate (Lac-) into venous perfusate. The major contributor to a 12- to 14-mV depolarization of Em in soleus and WG was the decrease in intracellular K+ concentration ([K+]i). The major independent contributors to [H+]i are changes in the concentrations of strong and weak ions and in CO2. Significant decreases in the strong ion difference [( SID]i) in both soleus and WG contributed substantially to the increase in [H+]i during stimulation. In WG the model showed that the decrease in [SID]i accounted for 35% of the increase in [H+]i (133-312 nequiv/L; pHi = 6.88-6.51) at the end of stimulation. Of the main contributors to decreased [SID]i, increased [Lac-]i and decreased [K+]i contributed 40 and 60%, respectively, to increased [H+]i, whereas a decrease in [PCr2-]i contributed to reduced [H+]i. It is concluded that decreased muscle [K+]i during intense contractions is the single most important contributor to reduced Em and increased [H+]i. Depletion of PCr2- simultaneous to the changes in [Lac-]i and [K+]i prevents larger increases in [H+]i and helps maintain the intracellular acid-base state.

Animals↗
PubMed1991

Factors contributing to increased muscle fatigue with beta-blockers.

beta-Adrenoceptor blockers are widely used clinically and can be classified as nonselective (beta 1 and beta 2) or selective (beta 1). Impairment of exercise performance is a well-known side effect of this group of drugs. This paper reviews mechanisms that could potentially be responsible for this impairment. In addition to cardiovascular and metabolic effects, beta-blockade inhibits Na(+)-K+ ATPase pumps controlling ion movement between muscle and plasma and thus may contribute to muscle fatigue through this mechanism. To investigate the relationship between the change in plasma [K+] and exercise performance, we studied healthy male subjects taking propranolol. Eight subjects performed maximal incremental cycle ergometer exercise tests during control (no drug), low dose (LD) (40 mg daily), and high dose (HD) (265 +/- 4.3 (SE) mg daily) of propranolol. The control plasma [K+] (5.8 +/- 0.12 mequiv./L) during exercise was significantly lower than either the LD (6.4 +/- 0.05 mequiv./L) or HD (6.1 +/- 0.16 mequiv./L) values. There was no significant difference between plasma [K+] for the LD and HD of propranolol. However, maximum oxygen uptake was reduced only while taking the HD of propranolol. Six of the subjects also performed three 30-s bouts of high intensity exercise on an isokinetic cycle ergometer while taking the LD and HD of propranolol. There was no significant difference between doses for the increase in plasma [K+] (LD, 7.8 +/- 0.35 mequiv./L vs. HD, 7.6 +/- 0.36 mequiv./L) during exercise. However, exercise performance was significantly reduced during HD compared with LD. These results suggest that the increases in plasma [K+] with propranolol did not play a direct significant role in the reduced performance observed during the HD.

Adrenergic beta-Antagonists↗
PubMed1991

Contribution of erythrocytes to the control of the electrolyte changes of exercise.

Five healthy males performed four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Arterial and femoral venous blood was sampled during and for 90 min following exercise. During exercise, arterial erythrocyte [K+] increased from 117.0 +/- 6.6 mequiv./L at rest to 124.2 +/- 5.9 mequiv./L after the second exercise bout. Arterial erythrocyte [K+] returned to the resting values during the first 5 min of recovery. No significant change was observed in femoral venous erythrocyte [K+]. Arterial erythrocyte lactate concentration ([Lac-]) increased during exercise from 0.2 +/- 0.1 mequiv./L peaking at 9.5 +/- 1.5 mequiv./L at 5 min of recovery, after which the values returned to control. Femoral venous erythrocyte [Lac-] changed in a similar fashion. Arterial erythrocyte [Cl-] rose during exercise to 76 +/- 3 mequiv./L and returned to resting values (70 +/- 2 mequiv./L) by 25 min recovery. During exercise there was a net flux of Cl- into the erythrocyte. We conclude that erythrocytes are a sink for K+ ions leaving working muscles. Furthermore, erythrocytes function to transport Lac- from working muscle and reduce plasma acidosis by uptake of Cl-. The erythrocyte uptake of K+, Lac-, and Cl- helps to maintain a concentration difference between plasma and muscle, facilitating diffusion of Lac- and K+ from the interstitial space into femoral venous plasma.

Acid-Base Equilibrium↗
PubMed1991

Lactate metabolism in inactive skeletal muscle during lactacidosis.

Contributions of carbohydrate and fat metabolism to the removal of a lactate (Lac-) load were quantified in inactive soleus (SL), plantaris (PL), and white gastrocnemius (WG) rat hindlimb muscle. Male Sprague-Dawley rats were perfused for 60 min with normal perfusate (NP, n = 8) or a high-lactate perfusate (LP, n = 8), simulating ionic conditions found in arterial blood and plasma after intense exercise: Lac- = 11.0 mM, K+ = 7.88 mM, and pH = 7.15. Metabolite fluxes across the hindlimb were calculated from blood flow and arteriovenous differences. In NP, Lac- was continuously released (2.9 +/- 0.2 mumol.min-1 x 100 g-1). However, in LP, a rapid and significant uptake of Lac- increased muscle Lac- fivefold to 39.6 +/- 1.1, 33.1 +/- 2.2, and 28.8 +/- 1.7 mumol/g dry wt in SL, PL, and WG, respectively. Glucose and O2 uptakes were similar during LP and NP perfusion. Glycerol release increased eightfold to 3.3 +/- 0.7 mumol.min-1 x 100 g-1 in response to LP. Muscle ATP, creatine phosphate, glycogen, glycolytic intermediate, and triacylglycerol concentrations did not change. However, muscle lactate-to-pyruvate ratios were elevated in all muscles of the LP group postperfusion, indicating changes in the mass action ratio at the pyruvate dehydrogenase reaction. In LP, of 80 mumol of Lac- taken up, 11% was accounted for by increased muscle Lac-, 12-24% was oxidized, and 5% may have been involved in glycerol release. The remaining Lac- may have been involved in metabolic cycling along the glyconeogenic-glycolytic pathway and/or in triacylglycerol-free fatty acid substrate cycling.

Acidosis, Lactic↗
PubMed1991

Accuracy of measurements of small changes in soft tissue mass by use of dual-photon absorptiometry.

Dual-photon absorptiometry (DPA) has recently been applied to the assessment of body composition. To evaluate the accuracy of DPA in detecting small changes in the lean soft tissue mass, we performed DPA with the use of the Norland 2600 Dichromatic densitometer on six healthy adult males before and after a 30-ml/kg transfusion of saline and before and after exercise in a warm environment, resulting in a greater than or equal to 1-kg weight loss. Absolute weight [baseline pretransfusion r2 = 0.999, standard error of estimate (SEE) = 590 g; posttransfusion r2 = 0.999, SEE = 300 g; baseline pretranspiration r2 = 0.999, SEE = 230 g; posttranspiration r2 = 0.999, SEE = 240 g] was accurately reflected in DPA total mass. Weight changes due to transfusion were poorly reflected by changes in DPA total mass (r2 = 0.417, SEE = 404 g). However, changes posttranspiration were accurately reflected in the DPA total mass (r2 = 0.886, SEE = 106 g posttranspiration). Similarly, weight changes due to transfusion were poorly measured by changes in DPA soft mass (r2 = 0.478, SEE = 365 g), but changes posttranspiration were highly correlated with DPA soft mass changes (r2 = 0.909, SEE = 92 g). Weight changes were not reflected by changes in the DPA lean soft tissue mass (r2 = 0.006, SEE = 1,737 posttransfusion, r2 = 0.094, SEE = 1,038 g posttranspiration). DPA-derived nonfat mass was highly correlated with skinfold-derived nonfat mass (r2 = 0.96, SEE = 2,400 g). Accuracy of total and soft tissue measurements implied correct mineral mass assessment.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1990

Effects of alkalosis on muscle ions at rest and with intense exercise.

The effects of metabolic and respiratory alkalosis (MALK and RALK) on intracellular strong ion concentrations ([ion]i) and muscle to blood ion fluxes were examined at rest and during 5 min of intense, intermittent tetanic stimulation in the isolated, perfused rat hindlimb. Compared with the control (C), perfusion of resting skeletal muscle during MALK and RALK significantly increased [Cl-]i and [Na+]i, and RALK significantly lowered [K+]i; these changes, however, did not affect initial hindlimb force production. In both resting and stimulated muscle, the intracellular ion changes corresponded to appropriate perfusate to muscle ion fluxes. At rest, changes in slow-twitch soleus were greater than in fast-twitch white gastrocnemius (WG), but stimulation-induced changes in [Lac]i and [K+]i were greater in WG. At the end of stimulation [K+]i and [Mg2+]i had decreased less in MALK than in C and RALK, particularly in plantaris and WG muscles. Compared with C, the muscle to perfusate flux of Lac- increased by 37% in MALK and 27% in RALK. This was associated with significantly less Lac- accumulation in all muscles in MALK than in RALK, which, in turn, had significantly less lactate than C. Lactate efflux from contracting skeletal muscle was significantly correlated with an uptake of Cl- by muscle. It is concluded that extracellular alkalosis alters skeletal muscle intracellular ionic composition and increases Lac- efflux from skeletal muscle. In agreement with other studies, lactate release appears to occur by both ionic and molecular transport processes. Alkalosis had no apparent effect on muscle performance with this preparation.

Alkalosis↗
PubMed1990

Role of nonworking muscle on blood metabolites and ions with intense intermittent exercise.

The exchange of ions between blood and inactive muscle was studied in healthy males (n = 11) who performed four 30-s bouts of maximum isokinetic leg exercise, with 4 min of rest between bouts; recovery was followed for 90 min. Blood was sampled from the brachial artery and antecubital vein from inactive arm, and biopsies were taken from the nonworking deltoid muscles. During exercise, whole blood and plasma arteriovenous (a-v) differences across the arm showed increased net uptake of lactate (Lac-), K+, Na+, Cl-, glycerol, and O2. Arm glucose uptake also increased during exercise and the last 30 min of recovery, but there was no change in muscle glycogen content. Deltoid intracellular Lac- concentration [( Lac-]) increased 2.5-fold to 8.2 +/- 1.4 meq/l during exercise and 25 min of recovery. Despite evidence of uptake from blood and plasma a-v differences, deltoid intracellular K+, Na+, and Cl- concentrations did not change. During recovery, arm a-v differences showed no Lac- release, but Cl- and Na+ were released to venous blood for at least 90 min of recovery. During repeated exercise, the elevated Lac- uptake (a-v [Lac-] is 5-8 meq/l) and a HCO3- release (a-v HCO3- concentration is -8-11 meq/l) by the arm was suggestive of a possible anion exchange (Lac-/HCO3-). It is concluded that during heavy exercise non-working muscles take up and oxidize significant amounts of Lac-. Other inactive tissues also play a role in the regulation of ion and metabolite concentrations of blood.

Adult↗
PubMed1990

High-intensity endurance training in 20- to 30- and 60- to 70-yr-old healthy men.

Factors contributing to maximal incremental and short-term exercise capacity were measured before and after 12 wk of high-intensity endurance training in 12 old (60-70 yr) and 10 young (20-30 yr) sedentary healthy males. Peak O2 uptake in incremental cycle ergometer exercise increased from 1.60 +/- 0.073 to 2.21 +/- 0.073 (SE) l/min (38% increase) in the old subjects and from 2.54 +/- 0.141 to 3.26 +/- 0.181 l/min (29%) in the young subjects. Peak cardiac output, estimated by extrapolation from a series of submaximal measurements by the CO2 rebreathing method, increased by 30% (from 12.7 to 16.5 l/min) in the old subjects, associated with a 6% increase (from 126 to 135 ml/l) in arteriovenous O2 difference; in the young subjects there were equal 14% increases in both variables (18.0 to 20.5 l/min and 140 to 159 ml/l, respectively). Submaximal mean arterial pressure and cardiac output were lower posttraining in the old subjects; total vascular conductance and cardiac stroke volume increased. Although peak power at the start of a short-term maximal isokinetic test did not change, total work accomplished in 30 s at a pedaling frequency of 110 revolutions/min increased in both groups, from 11.2 to 12.6 kJ and from 15.7 to 16.9 kJ in the old and young, respectively; fatigue during the 30-s test was less, and postexercise plasma lactate concentrations were lower. In older subjects, increases in aerobic power after high-intensity endurance training are at least as large as in younger subjects and are associated with increases in vascular conductance, maximal cardiac output, and stroke volume.

Adult↗
PubMed1989

Renal responses to exercise-induced lactic acidosis.

Five healthy males performed four 30-s bouts of maximal exercise, separated by 4 min of rest, on an isokinetic cycle ergometer. Arterial blood and urine samples were taken from indwelling catheters at rest, immediately postexercise, and for 90 min of recovery. Inulin was continuously infused to measure glomerular filtration rate (GFR). Arterial plasma [Na+], [K+], and [Cl-] increased (P less than 0.05) with exercise; plasma lactate concentration ([Lac-]) increased from 1.3 +/- 0.2 to 21.0 +/- 1.0 (SE) meq/l (P less than 0.05). A significant decrease in the GFR occurred after exercise and during recovery associated with reductions in renal Na+ and K+ excretion (P less than 0.05). Renal excretion of Lac- reached a maximum of 293 +/- 79.4 mu eq.kg-1.h-1 (P less than 0.05), with Cl- excretion reaching a minimum of 4.8 +/- 0.95 mu eq.kg-1.h-1 (P less than 0.05). Urine [Lac-] was 189 +/- 25.6 meq/l, and urine [Cl-] was 6 +/- 1.7 meq/l at 30 min of recovery. There was a curvilinear relationship between urine [Cl-] and [Lac-] (r = -0.86; P less than 0.0001). Net Lac- production was estimated from arterial [Lac-] and after assuming a distribution volume. Less than 2% (13.1 meq) of the total estimated Lac- produced (678 meq) was excreted in the urine. Decreases in urine [Cl-] act to limit the fall in urine pH that accompanies increases in urine [Lac-].

Acidosis, Lactic↗
PubMed1989

Muscle glycogenolysis and H+ concentration during maximal intermittent cycling.

The relationships between muscle glycogenolysis, glycolysis, and H+ concentration were examined in eight subjects performing three 30-s bouts of maximal isokinetic cycling at 100 rpm. Bouts were separated by 4 min of rest, and muscle biopsies were obtained before and after bouts 2 and 3. Total work decreased from 20.5 +/- 0.7 kJ in bout 1 to 16.1 +/- 0.7 and 13.2 +/- 0.6 kJ in bouts 2 and 3. Glycogenolysis was 47.2 and 15.1 mmol glucosyl U/kg dry muscle during bouts 2 and 3, respectively. Lower accumulations of pathway intermediates in bout 3 confirmed a reduced glycolytic flux. In bout 3, the work done represented 82% of the work in bout 2, whereas glycogenolysis was only 32% of that in bout 2. Decreases in ATP and phosphocreatine contents were similar in the two bouts. Muscle [H+] increased from 195 +/- 12 to 274 +/- 19 nmol/l during bout 2, recovered to 226 +/- 8 nmol/l before bout 3, and increased to 315 +/- 24 nmol/l during bout 3. Muscle [H+] could not be predicted from lactate content, suggesting that ion fluxes are important in [H+] regulation in this exercise model. Low glycogenolysis in bout 3 may be due to an inhibitory effect of increased [H+] on glycogen phosphorylase activity. Alternately, reduced Ca2+ activation of fast-twitch fibers (including a possible H+ effect) may contribute to the low overall glycogenolysis. Total work in bout 3 is maintained by a greater reliance on slow-twitch fibers and oxidative metabolism.

Adenosine Triphosphate↗
PubMed1989

Measurement of cardiac output by carbon dioxide rebreathing methods.

Cardiac output may be measured noninvasively by applying the Fick principle to CO2; CO2 output is measured by expired gas analysis and the veno-arterial CO2 content difference is obtained from estimates of PVCO2 and PaCO2. PVCO2 is determined using the lung as a tonometer for the equilibration of CO2; two main methods are available. In the Defares or exponential method, a low concentration of CO2 is initially rebreathed. Complete equilibration is not reached between the lung and rebreathing bag and the PvCO2 is calculated as the asymptote of the exponential rise in PETCO2 during rebreathing and prior to recirculation. Even though several mathematical methods can be used to calculate PvCO2, the most precise is an iterative statistical analysis to obtain the best-fit curve for PETCO2 with time, from which PvCO2 is obtained from PETCO2 at 20 seconds after the start of rebreathing. In the Collier or equilibrium method, a bag having CO2 concentration higher than PvCO2 is rebreathed. If an appropriate initial bag volume CO2 has been selected, equilibration will occur in the lung-bag system, recognized as a plateau in the PCO2 rebreathing record. If a plateau is not obtained, PvCO2 can be estimated by extrapolating the line joining the points of expired PCO2 during the 8th and 12th seconds of rebreathing to that of the 20th second. With the equilibrium method, the plateau PCO2 is systematically higher than PvCO2 (downstream effect) and a correction is applied to obtain PvCO2. PaCO2 can be estimated from PETCO2 or from the mixed-expired PCO2 and an assumed physiologic dead space, except in patients with abnormal lung function, in whom PaCO2 must be measured directly. The content of CO2 in blood may be calculated from PCO2 by the equation: In(CCO2) = [0.396 X In(PCO2)] + 2.38 More complex algorithms are available to calculate CCO2 if the pH, hemoglobin, and arterial O2 saturation are widely divergent from resting values. The indirect Fick method applied to CO2 during exercise can be used to obtain a valid and reproducible measurement of Q comparable to that obtained by invasive methods.

Carbon Dioxide↗
PubMed1988

Ion fluxes during tetanic stimulation in isolated perfused rat hindlimb.

The present study examined the relationships between changes in intra- and extracellular concentrations of strong ions, the appearance of nonvolatile acid (NVA) in venous perfusate, and skeletal muscle fatigue during intense electrical stimulation. A one-pass system was used to perfuse an isolated rat hindlimb during 5 min of intermittent tetanic contractions. Initial isometric tensions averaged 2.85 kg/hindlimb and declined by 45% during 5 min. During stimulation, intracellular lactate concentration ([La-]i) increased by 2, 13, 15, and 21 meq/l of intracellular fluid in the soleus, plantaris, and red and white gastrocnemius. This was associated with a proportionate decrease in intracellular K+ ([K+]i) and Mg2+([Mg2+]i) concentrations and increased intracellular Na+ ([Na+]i) and Cl-([Cl-]i) concentrations. A stoichiometrically equivalent uptake of Na+ and Cl- from the perfusate peaked at 8.5 mu eq.min-1.g-1 at the end of the 5th min. The increase in plasma [K+] during the last 4 min of stimulation was constant at 0.5 mu eq.min-1.g-1. A significant reduction in intracellular strong ion difference of all muscles contributed directly to an increase in [H+] during stimulation. After the 1st min of stimulation the rate of appearance of NVA in venous perfusate exceeded that of the increase in venous plasma [La-] by 12-fold; this decreased to 2.7-fold at the end of 5 min. La- release and NVA appearance in venous perfusate was maximal at 3.1 and 9.7 mu eq.min-1.g wet wt-1 during the 4th min of stimulation. It is concluded that the changes in the intracellular concentrations of strong ions during intense contractile activity are the primary factors contributing to skeletal muscle fatigue.

Action Potentials↗
PubMed1988

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)

Acid-Base Equilibrium↗
PubMed1988

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)

Acid-Base Equilibrium↗