Relationship Among Recovery Oxygen, Oxygen Missed, Lactate Production and Lactate Removal During and Following Severe Hypoxia in the Unanesthetized Dog

1958 ◽  
Vol 192 (3) ◽  
pp. 585-591 ◽  
Author(s):  
Norman R. Alpert ◽  
Herbert Kayne ◽  
Winona Haslett

An experiment was designed to test the ‘O2debt’ hypothesis. Oxygen consumption and plasma lactate were measured before, during and following hypoixa in unanesthetized spinally transected dogs. The O2 consumption was depressed during hypoxia and returned toward control levels during recovery. Lactate levels increased during the hypoxia and returned to the control during recovery. Oxygen missed was correlated with the excess consumption of recovery. A highly significant relationship was found which indicated that the larger the depression in O2 consumption during hypoxia, the greater was the depression during the recovery period and the more prolonged the return to control levels. Oxygen missed during hypoxia was compared to lactate production. A significant relationship was found. Lactate removal was compared to excess consumption of recovery. No correlation existed between lactate removal and recovery O2 consumption. The authors postulate the presence of a metabolic governor which controls the rate of O2 uptake.

1989 ◽  
Vol 257 (5) ◽  
pp. E782-E789 ◽  
Author(s):  
C. M. Donovan ◽  
M. J. Pagliassotti

Constant infusions of cold molar lactate (178.0 +/- 1.6 mumol.kg-1.min-1), [U-14C]lactate (0.50 muCi/min), and [6-3H]glucose (0.5 muCi/min) were employed to study the effects of endurance training (running 1 h/day, at 38 m/min, 10% grade) on lactate clearance in resting, hyperlactatemic rats. Before infusion, resting blood lactate levels were not significantly different between controls, 1.10 +/- 0.04 mM, and trained animals, 1.16 +/- 0.04 mM. Lactate levels increased significantly during the infusion period, attaining steady-state mixed venous concentrations of 11.32 +/- 0.24 mM and 5.44 +/- 0.09 mM, respectively, for controls and trained animals. Lactate clearance rates, based on net lactate removal (i.e., not tracer-estimated lactate removal), were twofold greater in trained animals vs. controls, 33.0 +/- 0.7 and 15.4 +/- 0.4 ml.kg-1. min-1, respectively. Lactate specific activity values during the infusion period were not significantly different between controls, 22,243 +/- 236 dpm/mumol, and trained animals, 21,270 +/- 374 dpm/mumol, indicating similar endogenous dilution of the pyruvate-lactate pool. For both control and trained animals, essentially 100% of the 14C infused as lactate was recovered as either glucose or CO2; however, trained animals demonstrated a 25% greater rate of gluconeogenesis. At a given lactate production rate, trained animals maintain lower lactate levels through enhanced clearance via gluconeogenesis and oxidation.


1978 ◽  
Vol 56 (4) ◽  
pp. 578-584 ◽  
Author(s):  
E. Hohtola ◽  
H. Rintamäki ◽  
R. Hissa

A dose-controlled chemical sympathectomy with 6-hydroxydopamine (6-OHDA) did not disrupt thermostasis in the pigeon at +38 °C. At +6 °C, thermogenesis was impaired, but the lower body temperature and oxygen consumption were stable and vasoconstriction was normal. The stability may partly be explained by a massive release of adrenaline from the adrenals (50% in 20 min). Despite a deficit in heat production both after sympathectomy and after acute 6-OHDA, no change in muscle electrical activity was observed. Plasma free fatty acid (FFA) concentration was significantly elevated after sympathectomy, but no changes occurred in blood glucose or plasma lactate levels. The results indicate a major compensatory role for the adrenals in avian thermogenesis. They also suggest a sympathetically mediated auxiliary thermogenic mechanism independent of muscle electrical activity and coupled to FFA metabolism.


2000 ◽  
Vol 203 (12) ◽  
pp. 1809-1815
Author(s):  
D.A. Scholnick ◽  
T.T. Gleeson

During recovery from even a brief period of exercise, metabolic rate remains elevated above resting levels for extended periods. The intensity and duration of exercise as well as body temperature and hormone levels can influence this excess post-exercise oxygen consumption (EPOC). We examined the influence of activity before exercise (ABE), commonly termed warm-up in endotherms, on EPOC in the desert iguana Dipsosaurus dorsalis. The rate of oxygen consumption and blood lactate levels were measured in 11 female D. dorsalis (mass 41.1 +/− 3.0 g; mean +/− s.e.m.) during rest, after two types of ABE and after 5 min of exhaustive exercise followed by 60 min of recovery. ABE was either single (15 s of maximal activity followed by a 27 min pause) or intermittent (twelve 15 s periods of exercise separated by 2 min pauses). Our results indicate that both single and intermittent ABE reduced recovery metabolic rate. EPOC volumes decreased from 0.261 to 0.156 ml of oxygen consumed during 60 min of recovery when lizards were subjected to intermittent ABE. The average cost of activity (net V(O2) during exercise and 60 min of recovery per distance traveled) was almost 40 % greater in lizards that exercised without any prior activity than in lizards that underwent ABE. Blood lactate levels and removal rates were greatest in animals that underwent ABE. These findings may be of particular importance for terrestrial ectotherms that typically use burst locomotion and have a small aerobic scope and a long recovery period.


1993 ◽  
Vol 74 (1) ◽  
pp. 435-443 ◽  
Author(s):  
P. G. Catcheside ◽  
G. C. Scroop

Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P < 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.


1989 ◽  
Vol 144 (1) ◽  
pp. 377-393 ◽  
Author(s):  
TODD T. GLEESON ◽  
PAULA M. DALESSIO

We evaluated the metabolic mechanisms by which the iguanid lizard Dipsosaurus dorsalis deals with the lactate which accumulates during vigorous exercise. Fasted, cannulated lizards were run for 5 min on a treadmill at 40°C, which elevated whole-body lactate to 24 mmol l−1 and depleted hindlimb glycogen to 70% of resting levels. Oxygen consumption increased fivefold and respiratory exchange ratios approached 2.0. Exhausted animals were then injected intravenously with either [U-14C]lactate or [U-14C]glucose, and allowed to recover quietly on the treadmill at 40°C. After 2h, 79% of the accumulated lactate had been removed and hindlimb muscle glycogen stores had returned to pre-exercise levels. Although blood glucose remained unchanged at 8.6 ± 0.27 mmol l−1 throughout the recovery period, whole-body glucose increased significantly from 1.6 ± 0.23 to 5.5 ± 0.38 mmol l−1 (P&lt;0.05). Based on isotope distribution, 50% of the lactate removed was used to synthesize glucose and glycogen, but only 16% of the lactate was oxidized. Lactate oxidation accounted for about 40% of the post-exercise oxygen consumption. Lactate rather than glucose appeared to be the prevalent substrate for muscle glycogen synthesis under these conditions. These animals appear to employ a strategy of lactate removal which is different from that in mammals; favoring lactate-supported gluco- and glyconeogenesis and rapid muscle glycogen replenishment instead of rapid lactate removal via oxidative pathways.


1998 ◽  
Vol 201 (14) ◽  
pp. 2183-2193 ◽  
Author(s):  
A P Farrell ◽  
A K Gamperl ◽  
I K Birtwell

Mature, wild sockeye salmon (Oncorhynchus nerka) demonstrated their remarkable stamina and recovery abilities by performing three consecutive critical swimming speed tests with only a 45 min interval for recovery between subsequent tests. Although the repeated swimming challenges were performed without a full recovery, normoxic fish swam just as well on the second swim, and the majority of fish swam only marginally more poorly on the third swim. In addition, metabolic loading in these fish, as measured by the rate of oxygen consumption, ventilation rate and plasma lactate levels during recovery, did not appear to be cumulative with successive swims. Fish, however, did not recover as well after a similar level of initial swimming performance under moderately hypoxic conditions (water PO2&gt;100 mmHg; 1 mmHg=0.1333 kPa). Four out of the five fish did not swim again and their high plasma lactate levels indicated a greater anaerobic effort. In another group of fish, metabolic loading (elevated control rates of oxygen consumption) was induced with an overnight sublethal exposure to pentachlorophenol, but these fish swam as well as normoxic fish on the first swim, and five of the six fish swam for a third time at a marginally lower critical swimming speed. In contrast to expectations, pentachlorophenol pretreatment and moderate hypoxia were not additive in their effects. Instead, the effects resembled those of pentachlorophenol pretreatment alone. The results are discussed in terms of what aspects of fatigue might impair the repeat swimming performance of sockeye salmon.


PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5719 ◽  
Author(s):  
Marcio S. Ferreira ◽  
Paulo H.R. Aride ◽  
Adalberto L. Val

Background In the wild, matrinchã (Brycon amazonicus) and tambaqui (Colossoma macropomum) rely strongly on their swimming capacity to perform feeding, migration and reproductive activities. Sustained swimming speed in fishes is performed almost exclusively by aerobic red muscles. The white muscle has high contraction power, but fatigue quickly, being used mainly in sprints and bursts, with a maximum duration of few seconds. The Ucrit test, an incremental velocity procedure, is mainly a measure of the aerobic capacity of a fish, but with a high participation of anaerobic metabolism close to the velocity of fatigue. Our previous study has indicated a high swimming performance of matrinchã (Ucrit) after hypoxia exposure, despite increased levels of lactate in plasma. In contrast, tambaqui with high lactate levels in plasma presented very low swimming performance. Therefore, we aimed to study the resistance of matrinchã and tambaqui to the increased lactate levels in muscle over an incremental velocity test (Ucrit). As a secondary aim, we analyzed the differences in anaerobic metabolism in response to environmental hypoxia, which could also support the better swimming performance of matrinchã, compared to tambaqui. Methods We measured, over incremented velocities in both species, the metabolic rate (the oxygen consumption by the fish; MO2), and the concentrations of lactate and nitrites and nitrates (NOx) in muscles. NOx was measured as an indicator of nitric oxide and its possible role in improving cardiorespiratory capacity in these fishes, which could postpone the use of anaerobic metabolism and lactate production during the swimming test. Also, we submitted fishes until fatigue and hypoxia (0.5 mg L−1) and measured, in addition to the previous parameters, lactate dehydrogenase activity (LDH; the enzyme responsible for lactate production), since that swimming performance could also be explained by the anaerobic capacity of producing ATP. Results Matrinchã exhibited a better swimming performance and higher oxygen consumption rates. Lactate levels were higher in matrinchã only at the moment of fatigue. Under hypoxia, LDH activity increased in the white muscle only in tambaqui, but averages were always higher in matrinchã. Discussion and conclusions The results suggest that matrinchã is more resistant than tambaqui regarding lactate accumulation in muscle at the Ucrit test, but it is not clear how much it contributes to postpone fatigue. The higher metabolic rate possibly allows the accumulated lactate to be used as aerobic fuel by the matrinchã, improving swimming performance. More studies are needed regarding matrinchã’s ability to oxidize lactate, the effects of exercise on muscle acidification, and the hydrodynamics of these species, to clarify why matrinchã is a better swimmer than tambaqui.


1966 ◽  
Vol 23 (1) ◽  
pp. 65-83 ◽  
Author(s):  
Brian R. Hammond ◽  
Cleveland P. Hickman Jr.

Physiological effects of physical conditioning to water current were studied on three groups of [Formula: see text]-year-old rainbow trout, Salmo gairdneri, acclimated to 4 C. Group one (control) was raised in still water. Groups two and three were conditioned to water velocities of 20 cm/sec and 40 cm/sec, respectively, for 16 days before sampling. Muscle and plasma samples were collected before exercise and four times during subjection to 15 min of forced swimming at 53.4 cm/sec and eight times during a 24-hr recovery period. Conditioning significantly delayed the point of fatigue during forced exercise: the unconditioned fish were fatigued after about 5 min swimming, group two after about 10 min swimming, and group three at about 15 min.Physically conditioned trout showed significantly higher muscle and plasma lactate levels when fatigued, and more rapid removal of lactate from muscle and plasma during recovery from fatigue, than unconditioned trout. Exercise resulted in parallel oscillating concentration fluctuations of tissue phosphate and significant increases in concentrations of plasma phosphate in both conditioned and unconditioned fish. Plasma glucose showed no significant change during exercise but rose slightly during the recovery of all groups.


1984 ◽  
Vol 247 (6) ◽  
pp. E747-E755 ◽  
Author(s):  
J. M. Naylor ◽  
D. S. Kronfeld ◽  
D. E. Freeman ◽  
D. Richardson

Hepatic lactate metabolism was studied in five sheep receiving infusions of either lactic acid or sodium lactate using an arteriovenous difference technique. Hepatic uptake of lactate was a saturable process with second order (Michaelis-Menten) kinetics. Although lactic acid infusion decreased blood pH, hepatic saturation of lactate uptake occurred before changes in pH could influence hepatic lactate metabolism. The Vmax for hepatic lactate metabolism is 5.72 mmol X kg-0.75 X h-1 and the Km 3.06 mmol/l. These findings have therapeutic relevance. In acidosis, the hepatic response to therapeutic administration of sodium lactate during fluid therapy will be variable. If plasma lactate is low, lactated fluids may increase hepatic uptake and produce an alkalizing effect. If plasma lactate is already high, hepatic lactate metabolism is nearly saturated, and additional lactate will not produce a hepatic alkalizing response. Extrahepatic tissues switch from lactate production to lactate utilization under conditions of lactate loading. They remove more lactate than liver at high plasma lactate concentrations. Muscle may be important in lactate removal in certain types of exercise.


2003 ◽  
Vol 284 (3) ◽  
pp. H1028-H1034 ◽  
Author(s):  
Henning Bundgaard ◽  
Keld Kjeldsen ◽  
Karen Suarez Krabbe ◽  
Gerrit van Hall ◽  
Lene Simonsen ◽  
...  

We assessed the hypothesis that the epinephrine surge present during sepsis accelerates aerobic glycolysis and lactate production by increasing activity of skeletal muscle Na+-K+-ATPase. Healthy volunteers received an intravenous bolus of endotoxin or placebo in a randomized order on two different days. Endotoxemia induced a response resembling sepsis. Endotoxemia increased plasma epinephrine to a maximum at t = 2 h of 0.7 ± 0.1 vs. 0.3 ± 0.1 nmol/l ( P < 0.05, n = 6–7). Endotoxemia reduced plasma K+reaching a nadir at t = 5 h of 3.3 ± 0.1 vs. 3.8 ± 0.1 mmol/l ( P < 0.01, n = 6–7), followed by an increase to placebo level at t = 7–8 h. During the declining plasma K+, a relative accumulation of K+was seen reaching a maximum at t = 6 h of 8.7 ± 3.8 mmol/leg ( P < 0.05). Plasma lactate increased to a maximum at t = 1 h of 2.5 ± 0.5 vs. 0.9 ± 0.1 mmol/l ( P < 0.05, n = 8) in association with increased release of lactate from the legs. These changes were not associated with hypoperfusion or hypoxia. During the first 24 h after endotoxin infusion, renal K+excretion was 27 ± 7 mmol, i.e., 58% higher than after placebo. Combination of the well-known stimulatory effect of catecholamines on skeletal muscle Na+-K+-ATPase activity, with the present confirmation of an expected Na+-K+- ATPase-induced decline in plasma K+, suggests that the increased lactate release was due to increased Na+-K+-ATPase activity, supporting our hypothesis. Thus increased lactate levels in acutely and severely ill patients should not be managed only from the point of view that it reflects hypoxia.


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