Lactate Transport and Exchange During Exercise

Gladden, L. Bruce

doi:10.1002/cphy.cp120114

Cited by 28 publications

(35 citation statements)

References 180 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lactate generation by muscle during exercise has been attributed to intracellular hypoxia (see Gladden, 1996). The assumption has been that flux of substrates in glycolysis in excess of that oxidized by the mitochondria must reflect an oxygen limitation to oxidative phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo

Conley

Kushmerick

Jubrias

1998

The Journal of Physiology

View full text Add to dashboard Cite

1. We tested the hypothesis that the cytoplasmic control mechanism for glycolysis is affected by the presence of oxygen during exercise. We used a comparison of maximal twitch stimulation under ischaemic and intact circulation in human wrist flexor and ankle dorsiflexor muscles. 31P magnetic resonance spectroscopy followed the phosphocreatine (PCr), Pi and pH dynamics at 6-9 s intervals. Glycolytic PCr synthesis was determined during stimulation from pH and tissue buffer capacity, as well as the oxidative phosphorylation rate. 2. Ischaemic vs. aerobic stimulation resulted in similar glycolytic fluxes in the two muscles. The onset of glycolysis occured after fifty to seventy stimulations and the extent of glycolytic PCr synthesis was directly proportional to the number of stimulations thereafter. 3. Two-fold differences in the putative feedback regulators of glycolysis, [Pi] and [ADP], were found between aerobic and ischaemic stimulation. The similar glycolytic fluxes in the face of these differences in metabolite levels eliminates feedback as a control mechanism in glycolysis. 4. These results demonstrate that glycolytic flux is independent of oxygenation state and metabolic feedback, but proportional to muscle activation. These results show a key role for muscle stimulation in the activation and maintenance of glycolysis. Further, this glycolytic control mechanism is independent of the feedback control mechanism that governs oxidative phosphorylation.

show abstract

Section: Discussionmentioning

confidence: 99%

Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo

Conley

Kushmerick

Jubrias

1998

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…They are well summarized by Gladden (1996). One possibility is that lactate levels are in part determined by sympathoadrenal activity Mazzeo et al, 1991;Young et al, 1991;Brooks et al, 1992;Reeves et al, 1992;Mazzeo et al, 1994;Hamann et al, 2001).…”

Section: Relationship Between Arterial Lactate Levels and Circulatingmentioning

confidence: 96%

Persistence of the Lactate Paradox over 8 Weeks at 3800 m

Pronk

Tiemessen²,

Hupperets³

et al. 2003

High Altitude Medicine & Biology

View full text Add to dashboard Cite

The arterial blood lactate [La] response to exercise increases in acute hypoxia, but returns to near the normoxic (sea level, SL) response after 2 to 5 weeks of altitude acclimatization. Recently, it has been suggested that this gradual return to the SL response in [La], known as the lactate paradox (LP), unexpectedly disappears after 8 to 9 weeks at altitude. We tested this idea by recording the [La] response to exercise every 2 weeks over 8 weeks at altitude. Five normal, fit SL-residents were studied at SL and 3,800 m (Pbar = 485 torr) in both normoxia (PIO2 = 150 torr) and hypoxia (PIO2 = 91 torr approximately air at 3,800 m). Arterial [La] and blood gas values were determined at rest and during cycle exercise at the same absolute workloads (0, 25, 50, 75, 90, and 100% of initial SL-VO2Max) and exercise duration (4, 4, 4, 2, 1.5, and 0.75 min, respectively) at each time point. [La] curves were elevated in acute hypoxia at SL (p < 0.01) and at 3,800 m fell progressively toward the SL-normoxic curve (p < 0.01). On the same days, [La] responses in acute normoxia showed essentially no changes over time and were similar to initial SL normoxic responses. We also measured arterial catecholamine levels at each load and found a close relationship to [La] over time, supporting a role for adrenergic influence on [La]. In summary, extending the time at this altitude to 8 weeks produced no evidence for reversal of the LP, consistent with prior data obtained over shorter periods of altitude residence.

show abstract

“…The discrepancies between DABE and D[La] blood can be clarified if additionally La -and Cl -shifts from plasma into the red cells are considered (see below). It is important to state that during the experiment, especially during recovery, H + and La -are not only leaving but also entering muscle fibers and other cells (reviewed by Gladden 1996Gladden , 2004 Gladden 1996Gladden , 2004. A delay for the [La] ery increase has been observed in experiments with short all-out exercise (Juel et al 1990;Lindinger et al 1992) and sometimes but not always in incremental tests (e.g.…”

Section: Generalmentioning

confidence: 98%

Causes of differences in exercise-induced changes of base excess and blood lactate

et al. 2006

View full text Add to dashboard Cite

It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H+ than La- leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid-base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (-deltaABE) was 2.2 +/- 0.5 (SEM) mmol l(-1) larger than the increase of [La]blood at exhaustion, and the difference rose to 4.8 +/- 0.5 mmol l(-1) during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (delta[La](if+blood)) during exercise and only slightly larger during recovery. The discrepancy between -deltaABE and delta[La]blood mainly results from the Donnan effect hindering the rise of [La]erythrocyte to equal values like [La]plasma. The changing Donnan effect during acidosis causes that Cl- from the interstitial fluid enter plasma and erythrocytes in exchange for HCO3(-). A corresponding amount of La- remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to delta[La]blood instead to delta[La](if+blood). When performing correct comparisons and considering Cl-/HCO3(-) exchange between erythrocytes and extracellular fluid, neither the use of deltaABE nor of deltaSBE provides evidence for differences in H+ and La- transport across the tissue cell membranes.

show abstract

Lactate Transport and Exchange During Exercise

Abstract: The sections in this article are: Why Does [La] Increase During Exercise? Muscle Hypoxia: The Traditional Hypothesis Evidence Against Muscle Hypoxia Multiple Factors Criticism of Evidence Against O 2 ‐limitation Near‐Equilibrium Steady State… Show more

Cited by 28 publications

References 180 publications

Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo

Glycolysis is independent of oxygenation state in stimulated human skeletal muscle in vivo

Persistence of the Lactate Paradox over 8 Weeks at 3800 m

Causes of differences in exercise-induced changes of base excess and blood lactate

Contact Info

Product

Resources

About