Factors influencing hydrogen ion concentration in muscle after intense exercise

1988 ◽  
Vol 65 (5) ◽  
pp. 2080-2089 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
M. I. Lindinger ◽  
J. R. Sutton ◽  
N. L. Jones

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)

1988 ◽  
Vol 65 (5) ◽  
pp. 2090-2096 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
M. I. Lindinger ◽  
G. Obminski ◽  
J. R. Sutton ◽  
...  

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)


1984 ◽  
Vol 57 (5) ◽  
pp. 1558-1563 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
N. L. Jones

Six healthy male subjects performed three exercise tests in which the power output was increased by 100 kpm/min each minute until exhaustion. The studies were carried out after oral administration of CaCO3 (control), NH4Cl (metabolic acidosis), and NaHCO3 (metabolic alkalosis). Ventilation (VE), O2 intake (VO2), and CO2 output (VCO2) were monitored continuously. Arterialized-venous blood samples were drawn at specific times and analyzed for pH, PCO2, and lactate concentration. Resting pH (mean +/- SE) was lowest in acidosis (7.29 +/- 0.01) and highest in alkalosis (7.46 +/- 0.02). A lower peak power output (kpm/min) was achieved in acidosis (1,717 +/- 95) compared with control (1,867 +/- 120) alkalosis (1,867 +/- 125). Submaximal VO2 and VCO2 were similar, but peak VO2 and VCO2 were lower in acidosis. Plasma lactate concentration was lower at rest and during exercise in acidosis. Although lactate accumulation was reduced in acidosis, increases in hydrogen ion concentration were similar in the three conditions. We conclude that acid-base changes influence the maximum power output that may be sustained in incremental dynamic exercise and modify plasma lactate appearance, but have little effect on hydrogen ion appearance in plasma.


Perfusion ◽  
2004 ◽  
Vol 19 (3) ◽  
pp. 145-152 ◽  
Author(s):  
R Peter Alston ◽  
Laura Cormack ◽  
Catherine Collinson

Metabolic acidosis is a frequent complication of cardio-pulmonary bypass (CPB). Commonly, its cause is ascribed to hypoperfusion; however, iatrogenic causes, related to the composition and volume of intravascular fluids that are administered, are increasingly being recognized. The aim of this study was to determine if metabolic acidosis during CPB was associated with hypoperfusion, change in strong ion difference (SID) or haemodilution. Forty-nine patients undergoing cardiac surgery using CPB in the Royal Infirmary of Edinburgh (RIE) or the HCI, Clydebank were included in the study. Arterial blood samples were aspirated before induction of anaesthesia and the end of CPB. Samples were subjected to blood gas analysis and measurement of electrolytes and lactate. Changes in concentrations were then calculated. Change variables that were found to be significant (p B-0.1) univariate correlates of the change in hydrogen ion concentration were identified and entered into a multivariate regression model with hydrogen ion concentra tion at the end of CPB as the outcome variable (r2=0.65, p<0.001). Change variance in hydrogen ion concentration was created by first entering the baseline hydrogen ion concentration into the model. Next, any variance resulting from the respiratory component of acidosis was removed by entering the change in arterial carbon dioxide tension (regression coefficient (β)=0.67, p<0.01). Change in SID (β=-0.34, p<0.01) and surgical institution (β=-0.40, p<0.01) were then found to be predictors of the remaining variance whilst change in concentration of lactate (β in=0.16, p=0.07) and volume of intravascular fluid that was administered (β=-0.07, p=0.52) were rejected from the model. These findings suggest that the metabolic acidosis developing during CPB is partially the result of iatrogenic decrease in SID rather than hypoperfusion, as estimated by lactate concentration, or haemodilution.


2001 ◽  
Vol 280 (2) ◽  
pp. R481-R487 ◽  
Author(s):  
Robert J. Preston ◽  
Aaron P. Heenan ◽  
Larry A. Wolfe

In accordance with Stewart's physicochemical approach, the three independent determinants of plasma hydrogen ion concentration ([H+]) were measured at rest and during exercise in the follicular (FP) and luteal phase (LP) of the human menstrual cycle. Healthy, physically active women with similar physical characteristics were tested during either the FP ( n = 14) or LP ( n = 14). Arterialized blood samples were obtained at rest and after 5 min of upright cycling at both 70 and 110% of the ventilatory threshold (TVent). Measurements included plasma [H+], arterial carbon dioxide tension (PaCO2 ), total weak acid ([ATot]) as reflected by total protein, and the strong-ion difference ([SID]). The transition from rest to exercise in both groups resulted in a significant increase in [H+] at 70% TVentversus rest and at 110% TVent versus both rest and 70% TVent. No significant between-group differences were observed for [H+] at rest or in response to exercise. At rest in the LP, [ATot] and PaCO2 were significantly lower (acts to decrease [H+]) compared with the FP. This effect was offset by a reduction in [SID] (acts to increase [H+]). After the transition from rest to exercise, significantly lower [ATot] during the LP was again observed. Although the [SID] and PaCO2 were not significantly different between groups, trends for changes in these two variables were similar to changes in the resting state. In conclusion, mechanisms regulating [H+] exhibit phase-related differences to ensure [H+] is relatively constant regardless of progesterone-mediated ventilatory changes during the LP.


1962 ◽  
Vol 17 (4) ◽  
pp. 656-660 ◽  
Author(s):  
Ronald L. Wathen ◽  
Howard H. Rostorfer ◽  
Sid Robinson ◽  
Jerry L. Newton ◽  
Michael D. Bailie

Effects of varying rates of treadmill work on blood gases and hydrogen ion concentrations of four healthy young dogs were determined by analyses of blood for O2 and CO2 contents, Po2, Pco2, and pH. Changes in these parameters were also observed during 30-min recovery periods from hard work. Arterial and mixed venous blood samples were obtained simultaneously during work through a polyethylene catheter in the right ventricle and an indwelling needle in an exteriorized carotid artery. Mixed venous O2 content, Po2 and O2 saturation fell with increased work, whereas arterial values showed little or no change. Mixed venous CO2 content, Pco2, and hydrogen ion concentration exhibited little change from resting levels in two dogs but increased significantly in two others during exercise. These values always decreased in the arterial blood during exercise, indicating the presence of respiratory alkalosis. On cessation of exercise, hyperventilation increased the degree of respiratory alkalosis, causing it to be reflected on the venous side of the circulation. Submitted on January 8, 1962


1976 ◽  
Vol 50 (4) ◽  
pp. 241-247 ◽  
Author(s):  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. Seven healthy males were studied during cycle ergometer exercise at 33%, 66% and 90% of V̇o2 max. on three occasions when NH4Cl, NaHCO3 or CaCO3 (as a control substance) were administered in gelatin capsules double blind and in randomized order. Plasma growth hormone (HGH), lactic acid and hydrogen ion concentration ([H+])weremeasured at frequent intervals. 2. Ammonium chloride produced highest blood [H+] and NaHCO3 the lowest. These differences were maintained during exercise and in recovery. Plasma lactic acid concentrations were similar at rest. At 66%, 90% V̇o2 max. and recovery lactic acid was highest with NaHCO3 and lowest with NH4Cl. 3. Exercise stimulated HGH secretion in all studies and the elevation was proportional to the intensity of the exercise. NH4Cl caused a variable elevation of HGH at rest and 33% V̇o2 max. At 66% V̇o2 max., plasma HGH was significantly elevated to similar concentrations in all studies and, at 90% V̇o2 max., HGH was highest with NaHCO3. 4. An infusion of sodium l(+)-lactate producing plasma lactate concentrations of 3–5 mmol/l did not influence HGH secretion. 5. Exercise is a physiological stimulus to HGH secretion and the mechanism is independent of blood [H+] and lactate concentrations.


1977 ◽  
Vol 42 (2) ◽  
pp. 129-132 ◽  
Author(s):  
J. D. MacDougall ◽  
G. R. Ward ◽  
J. R. Sutton

Six subjects exercised to exhaustion on a cycle ergometer at intensities corresponding to approximately 140% of their maximal aerobic power. Subjects attempted to pedal for 1-min intervals with 3-min rest periods between, and continued until 30 s of exercise could no longer be maintained. Venous blood was sampled for lactate and glucose analysis. Muscle biopsies were extracted from the quadriceps before and immediately after exercise and at 2-, 5-, 12-, and 24-h intervals thereafter for total glycogen analysis. Three subjects consumed a mixed controlled diet (approx. 3,100 kcal) during the 24 h after exercise, and three consumed the same diet plus an additional 2,500/kcal carbohydrate. Following exercise, glycogen concentration had dropped to a mean value of approximately 28% of its preexercise value. After 2 h, it had recovered to 39%, at 5 h to 53%, at 12 h to 67%, and at 24 h to 102% of its preexercise value, with no difference in resynthesis rate between the two groups. It was concluded that, following glycogen depletion through intense intermittent exercise, complete recovery to preexercise values may be accomplished within 24 h; and that within this time period, the rate of resynthesis cannot be accelerated by a higher than normal carbohydrate intake.


1981 ◽  
Vol 61 (3) ◽  
pp. 331-338 ◽  
Author(s):  
J. R. Sutton ◽  
N. L. Jones ◽  
C. J. Toews

1. Five males were studied on three occasions, after oral administration of CaCO3 (control), NH4Cl (acidosis) and NaHCO3 (alkalosis), in a dose of 0.3 g/kg, taken over a 3 h period at rest. The subjects then exercised on a cycle ergometer for 20 min at 33% maximal oxygen uptake (Vo2 max.), followed by 20 min at 66% and at 95% Vo2 max. until exhaustion. 2. Endurance at 95% Vo2 max. was longest with alkalosis (5.44 ± 1.05 min), shortest with acidosis (3.13 ± 0.97 min) and intermediate in the control study (4.56 ± 1.31 min); venous blood pH at exhaustion was 7.33 ± 0.02 (mean ±1 sem), 7.13 ± 0.02 and 7.26 ± 0.02 respectively. 3. Concentrations of plasma lactate at exhaustion were 7.10 ± 0.8 mmol/l 4.0 ± 0.5 and 7.9 ± 0.9 mmol/l in the control, acidosis and alkalosis studies respectively. 4. Muscle lactate increased most from rest to exhaustion with alkalosis to 17.1 ± 2.5 μmol/g and least with acidosis to 12.2 ± 1.4 μmol/g. Muscle glycogen depletion was comparable in control and alkalosis studies. 5. The lower plasma lactate concentration during exercise in acidosis compared with control and alkalosis appears to be due to an inhibition of muscle glycolysis combined with a reduction in lactate efflux from muscle.


1992 ◽  
Vol 70 (12) ◽  
pp. 1625-1633 ◽  
Author(s):  
R. S. McKelvie ◽  
M. I. Lindinger ◽  
N. L. Jones ◽  
G. J. F. Heigenhauser

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.Key words: isokinetic cycle ergometer, potassium, lactate, red cell volume, arteriovenous difference.


1998 ◽  
Vol 85 (4) ◽  
pp. 1384-1393 ◽  
Author(s):  
Barry W. Scheuermann ◽  
John M. Kowalchuk ◽  
Donald H. Paterson ◽  
David A. Cunningham

Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La−]pl) during fatiguing exercise. We hypothesized that a lower [La−]plmay be associated with faster O2uptake (V˙o 2) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, <V˙eT) or to a V˙o 2 corresponding to ∼50% of the difference between the work rate atV˙eT and peakV˙o 2(>V˙eT). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (<V˙eT) or a three-component exponential model (>V˙eT). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La−]pl. MRT was similar during Con (31.2 ± 2.6 and 32.7 ± 1.2 s for on and off, respectively) and Acz (30.9 ± 3.0 and 31.4 ± 1.5 s for on and off, respectively) for work rates <V˙eT. At work rates >V˙eT, MRT was similar between Con (69.1 ± 6.1 and 50.4 ± 3.5 s for on and off, respectively) and Acz (69.7 ± 5.9 and 53.8 ± 3.8 s for on and off, respectively). On- and off-MRTs were slower for >V˙eT than for <V˙eT exercise. [La−]plincreased above 0-W cycling values during <V˙eT and >V˙eT exercise but was lower at the end of the transition during Acz (1.4 ± 0.2 and 7.1 ± 0.5 mmol/l for <V˙eT and >V˙eT, respectively) than during Con (2.0 ± 0.2 and 9.8 ± 0.9 mmol/l for <V˙eT and >V˙eT, respectively). CA inhibition does not affect O2 utilization at the onset of <V˙eT or >V˙eT exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.


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