Blood Lactate Levels in Free-Swimming Rainbow Trout (Salmo gairdneri) Before and After Strenuous Exercise Resulting in Fatigue

1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.

2019 ◽  
Vol 15 (2) ◽  
pp. 85-93
Author(s):  
D. Singla ◽  
M.Y. Shareef ◽  
M.E. Hussain

Previous studies commonly examined the acute effect of plyometric exercise on blood lactate. To the best of our knowledge, no study has examined the effect of short-term plyometric training on blood lactate levels of cricket players. To investigate the effect of an 8 week plyometric training program on blood lactate concentration in cricket players of different maturity level. 55 healthy male cricket players (aged 14-35 years) were categorised into 14-17, 18-25 and 26-35 groups. Blood lactate concentration (BLAC) was assessed before and after 8 weeks of the intervention period. Regardless of the maturity level, a significant reduction in BLAC was observed in the experimental cricketers (P<0.05) in response to 8 weeks of training. Blood lactate responses did not vary significantly in 14-17, 18-25 and 26-35 groups of cricket players following plyometric training. Plyometric training significantly reduced BLAC in cricket players despite non-significant differences amongst 14-17, 18-25 and 26-35 groups. Plyometric training could be recommended for adolescent (14-17) and adult cricketers (18-25 and 26-35) for improving their physiological capacities so as to develop optimal performance.


Author(s):  
Giovanni Carpenè ◽  
Diletta Onorato ◽  
Riccardo Nocini ◽  
Gianmarco Fortunato ◽  
John G. Rizk ◽  
...  

Abstract Coronavirus disease 2019 (COVID-19) is an infectious respiratory condition sustained by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which manifests prevalently as mild to moderate respiratory tract infection. Nevertheless, in a number of cases the clinical course may deteriorate, with onset of end organ injury, systemic dysfunction, thrombosis and ischemia. Given the clinical picture, baseline assessment and serial monitoring of blood lactate concentration may be conceivably useful in COVID-19. We hence performed a systematic literature review to explore the possible association between increased blood lactate levels, disease severity and mortality in COVID-19 patients, including comparison of lactate values between COVID-19 and non-COVID-19 patients. We carried out an electronic search in Medline and Scopus, using the keywords “COVID-19” OR “SARS-CoV-2” AND “lactate” OR “lactic acid” OR “hyperlactatemia”, between 2019 and present time (i.e. October 10, 2021), which allowed to identify 19 studies, totalling 6,459 patients. Overall, we found that COVID-19 patients with worse outcome tend to display higher lactate values than those with better outcome, although most COVID-19 patients in the studies included in our analysis did not have sustained baseline hyperlactatemia. Substantially elevated lactate values were neither consistently present in all COVID-19 patients who developed unfavourable clinical outcomes. These findings suggest that blood lactate monitoring upon admission and throughout hospitalization may be useful for early identification of higher risk of unfavourable COVID-19 illness progression, though therapeutic decisions based on using conventional hyperlactatemia cut-off values (i.e., 2.0 mmol/L) upon first evaluation may be inappropriate in patients with SARS-CoV-2 infection.


1986 ◽  
Vol 60 (1) ◽  
pp. 232-241 ◽  
Author(s):  
R. S. Mazzeo ◽  
G. A. Brooks ◽  
D. A. Schoeller ◽  
T. F. Budinger

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1–13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.


1996 ◽  
Vol 4 (3) ◽  
pp. 286-296
Author(s):  
Fiona Iredale ◽  
Frank Bell ◽  
Myra Nimmo

Fourteen sedentary 50- to 55-year-old men were exercised to exhaustion using an incremental treadmill protocol. Mean (±SEM) peak oxygen uptake (V̇O2peak) was 40.5 ± 1.19 ml · kg1· min−1, and maximum heart rate was 161 ± 4 beats · min−1. Blood lactate concentration was measured regularly to identify the lactate threshold (oxygen consumption at which blood lactate concentration begins to systematically increase). Threshold occurred at 84 ± 2% of V̇O2peak. The absolute lactate value at threshold was 2.9 ± 0.2 mmol · L−1. On a separate occasion, 6 subjects exercised continuously just below their individual lactate thresholds for 25 min without significantly raising their blood lactate levels from the 10th minute to the 25th. The absolute blood lactate level over the last 20 min of the steady-state test averaged 3.7 ± 1.2 mmol · L−1. This value is higher than that elicited at the threshold in the incremental test because of the differing nature of the protocols. It was concluded that although the lactate threshold occurs at a high percentage of V̇O2peak, subjects are still able to sustain exercise at that intensity for 25 min.


1983 ◽  
Vol 104 (1) ◽  
pp. 247-268 ◽  
Author(s):  
JEFFREY D. TURNER ◽  
CHRIS M. WOOD ◽  
DONNA CLARK

Chronically cannulated rainbow trout were subjected to 6 min of severe burst exercise and monitored over a 12 h recovery period. There were short-lived increases in haematocrit, haemoglobin, plasma protein, Na+ and Cl− levels. Plasma [Cl−] later declined below normal as organic anions accumulated. A much larger and more prolonged elevation in plasma [K+] probably resulted from intracellular acidosis. An intense extracellular acidosis was initially of equal respiratory (i.e. Pa,COa,CO2) a nd metabolic (i.e. ΔH+m) origin. However Pa,COa,CO2 was rapidly corrected while the metabolic component persisted. Plasma ammonia increases had negligible influence on acid-base status. Elevations in blood lactate (ΔLa−) were equal to ΔH+m immediately post-exercise but later rose to twice the latter. Simultaneous white muscle biopsies and blood samples demonstrated that muscle to blood gradients of lactate and pyruvate were maximal immediately post-exercise. As blood levels rose and muscle levels declined, an approximate equilibrium was reached after 4 h of recovery. Intra-arterial infusions of lactic acid in resting trout produced a severe but rapidly corrected metabolic acidosis. The rates of disappearance of ΔH+m and ΔLa− from the blood were equal. Infusions of similar amounts of sodium lactate produced a small, prolonged metabolic alkalosis with a much slower ΔLa− disappearance rate. It is suggested that the excess of ΔLa− over ΔH+m in the blood after exercise is associated with differential release rates of the two species from white muscle rather than differential removal rates from the bloodstream, and that the majority of the lactic acid load in muscle is removed by metabolism in situ.


1994 ◽  
Vol 76 (2) ◽  
pp. 846-852 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.


2015 ◽  
Vol 10 (3) ◽  
pp. 388-395 ◽  
Author(s):  
Nuttaset Manimmanakorn ◽  
Jenny J. Ross ◽  
Apiwan Manimmanakorn ◽  
Samuel J.E. Lucas ◽  
Michael J. Hamlin

Purpose:To compare whole-body vibration (WBV) with traditional recovery protocols after a high-intensity training bout.Methods:In a randomized crossover study, 16 athletes performed 6 × 30-s Wingate sprints before completing either an active recovery (10 min of cycling and stretching) or WBV for 10 min in a series of exercises on a vibration platform. Muscle hemodynamics (assessed via near-infrared spectroscopy) were measured before and during exercise and into the 10-min recovery period. Blood lactate concentration, vertical jump, quadriceps strength, flexibility, rating of perceived exertion (RPE), muscle soreness, and performance during a single 30-s Wingate test were assessed at baseline and 30 and 60 min postexercise. A subset of participants (n = 6) completed a 3rd identical trial (1 wk later) using a passive 10-min recovery period (sitting).Results:There were no clear effects between the recovery protocols for blood lactate concentration, quadriceps strength, jump height, flexibility, RPE, muscle soreness, or single Wingate performance across all measured recovery time points. However, the WBV recovery protocol substantially increased the tissue-oxygenation index compared with the active (11.2% ± 2.4% [mean ± 95% CI], effect size [ES] = 3.1, and –7.3% ± 4.1%, ES = –2.1 for the 10 min postexercise and postrecovery, respectively) and passive recovery conditions (4.1% ± 2.2%, ES = 1.3, 10 min postexercise only).Conclusion:Although WBV during recovery increased muscle oxygenation, it had little effect in improving subsequent performance compared with a normal active recovery.


1960 ◽  
Vol 17 (4) ◽  
pp. 487-500 ◽  
Author(s):  
Edgar C. Black ◽  
Anne C. Robertson ◽  
Arthur R. Hanslip ◽  
Wing-Gay Chiu

Rainbow trout [Formula: see text] years old (fall spawners) raised in the hatchery at Summerland, B.C., and 2-year-old mature spawning Kamloops trout (spring spawners) captured from Lake Okanagan, were subjected to 15 minutes strenuous exercise. Muscle glycogen was depleted in both groups. Following 30 minutes of moderate activity, muscle glycogen remained high in the [Formula: see text]-year-old trout. Liver glycogen levels were not significantly lowered during either strenuous or moderate exercise. Blood lactate levels were markedly elevated during 15 min of strenuous exercise and continued to rise for 2 hours of post-exercise recovery in both groups of fish. In the [Formula: see text]-year-old trout, blood lactate declined to resting levels at about the 8th hour of recovery, and was increased 3-fold following 30 min of moderate activity. Blood glucose and hemoglobin were not significantly altered during either strenuous or moderate activity.In the [Formula: see text]-year-old trout, starvation of up to 7 days duration resulted in a marked depletion of liver glycogen. There was little change in muscle glycogen, blood lactate, glucose or hemoglobin, regardless of whether or not the fish had been exercised at the beginning of the starvation period. Feeding during the period of recovery from 15 min of strenuous exercise resulted in increases in both muscle and liver glycogen levels.


1983 ◽  
Vol 105 (1) ◽  
pp. 1-14
Author(s):  
PETER NEUMANN ◽  
GEORGE F. HOLETON ◽  
NORBERT HEISLER

Rainbow trout (Salmo gairdneri) were electrically stimulated to exhausting activity and the changes in cardiac output and blood flow distribution to gills and systemic tissues resulting from the developing severe lactacidosis were repeatedly measured by the microsphere method (15 μm). Determination of cardiac output by application of the Fick principle resulted in values not significantly different from cardiac output measured by the indicator dilution technique, suggesting that cutaneous respiration, oxygen consumption, and arterio-venous shunting were insignificant under these conditions. Following muscular activity, cardiac output was elevated by up to 60%. In the gills, the blood flow distribution in the gill arches showed a consistent pattern, even during lactacidosis, with a higher perfusion in gill arches II and III, and in the middle sections of individual gills. Blood flow to white and red muscle was increased much more than cardiac output (+230 and +490%, respectively) such that blood flow to other tissues was actually reduced. We conclude that the elimination of lactate from muscle cells during the recovery period from strenuous exercise is delayed, not as a result of an impaired post-exercise muscle blood flow, but probably as a result of a high diffusion resistance in the cell membrane. Note: Deceased.


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