scholarly journals Relationships between rate of increase in post-exercise blood lactate concentration and performance of short-term high-intensity exercise in track athletes

2018 ◽  
Vol 7 (5) ◽  
pp. 253-259
Author(s):  
Naoya Takei ◽  
Kenya Takahashi ◽  
Katsuyuki Kakinoki ◽  
Hideo Hatta
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
High Intensity Exercise ◽  
Short Term ◽  
Post Exercise ◽  
Rate Of Increase ◽  
And Performance ◽  
Track Athletes

Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion

1996 ◽  
Vol 81 (4) ◽  
pp. 1550-1554 ◽  
Author(s):  
K. W. Hinchcliff ◽  
K. H. McKeever ◽  
W. W. Muir ◽  
R. A. Sams
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Specific Rate ◽  
Rate Of Increase ◽  
Accumulated Oxygen Deficit ◽  
Plasma Lactate Concentration

Hinchcliff, K. W., K. H. McKeever, W. W. Muir, and R. A. Sams. Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion. J. Appl. Physiol. 81(4): 1550–1554, 1996.—We theorized that furosemide-induced weight reduction would reduce the contribution of anaerobic metabolism to energy expenditure of horses during intense exertion. The effects of furosemide on accumulated O2 deficit and plasma lactate concentration of horses during high-intensity exercise were examined in a three-way balance randomized crossover study. Nine horses completed each of three trials: 1) a control (C) trial, 2) a furosemide-unloaded (FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded (FL) trial during which the horse received furosemide and carried weight equal to the weight lost after furosemide administration. Horses ran for 2 min at ∼120% maximal O2 consumption. Furosemide (FU) increased O2 consumption (ml ⋅ 2 min−1 ⋅ kg−1) compared with C (268 ± 9 and 257 ± 9, P < 0.05), whereas FL was not different from C (252 ± 8). Accumulated O2 deficit (ml O2 equivalents/kg) was significantly ( P < 0.05) lower during FU (81.2 ± 12.5), but not during FL (96.9 ± 12.4), than during C (91.4 ± 11.5). Rate of increase in blood lactate concentration (mmol ⋅ 2 min−1 ⋅ kg−1) after FU (0.058 ± 0.001), but not after FL (0.061 ± 0.001), was significantly ( P < 0.05) lower than after C (0.061 ± 0.001). Furosemide decreased the accumulated O2 deficit and rate of increase in blood lactate concentration of horses during brief high-intensity exertion. The reduction in accumulated O2 deficit in FU-treated horses was attributable to an increase in the mass-specific rate of O2 consumption during the high-intensity exercise test.

Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise

2003 ◽  
Vol 94 (6) ◽  
pp. 2135-2144 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Blood Lactate ◽  
Plasma Volume ◽  
High Intensity ◽  
Maximal Exercise ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Hydration Status ◽  
Mixed Venous Blood ◽  
Short Term ◽  
Arterial Hypoxemia

It is reported that preexercise hyperhydration caused arterial O2 tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425–429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 ± 1.8% increase in plasma volume was induced with NaCl (0.30–0.45 g/kg dissolved in 1,500 ml H2O) administered via a nasogastric tube, 285–290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant ( P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient.

scholarly journals Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami
Keyword(s):  
Blood Lactate ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Mtdna Copy Number ◽  
Single Bout ◽  
Extracellular Lactate ◽  
Exercise Induced ◽  
The Brain

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

scholarly journals Fetal heart rate short term variation during labor in relation to scalp blood lactate concentration

2018 ◽  
Vol 97 (10) ◽  
pp. 1274-1280 ◽  
Author(s):  
Ke Lu ◽  
Malin Holzmann ◽  
Fahrad Abtahi ◽  
Kaj Lindecrantz ◽  
Pelle G Lindqvist ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Lactate ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Short Term ◽  
Term Variation

Increased clearance of lactate after short-term training in men

1995 ◽  
Vol 79 (6) ◽  
pp. 1862-1869 ◽  
Author(s):  
S. M. Phillips ◽  
H. J. Green ◽  
M. A. Tarnopolsky ◽  
S. M. Grant
Keyword(s):  
Blood Lactate ◽  
Clearance Rate ◽  
Maximal Oxygen Consumption ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Constant Infusion ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Short Term ◽  
Mitochondrial Potential

A short-term training model previously shown to result in a tighter metabolic control in working muscle in the absence of an increase in mitochondrial potential was used to examine changes in lactate turnover. Lactate flux was studied before and after 10 days of cycle training [2 h/day at 59% maximal oxygen consumption (VO2max)] in untrained men [VO2max = 45.5 +/- 2.4 (SE) ml.kg-1.min-1). A primed constant infusion of L-[1–13C]lactate was used to examine lactate kinetics during a prolonged exercise protocol (90 min at 59% VO2max). Rate of appearance of lactate increased with exercise (P < 0.01), both pretraining (rest = 30.3 +/- 4.9 ml.kg-1.min-1, exercise = 115 +/- 14 ml.kg-1.min-1) and posttraining (rest = 28.4 +/- 4.7 ml.kg-1.min-1, exercise = 112 +/- 13 ml.kg-1.min-1). Despite a lower blood lactate concentration (P < 0.05) during exercise after training, there was no difference in the rate of appearance of lactate. Training increased (P < 0.05) the metabolic clearance rate of lactate during exercise from 36.8 +/- 4.8 to 51.4 +/- 6.8 ml.kg-1.min-1. These findings indicate that at least part of the lower exercising blood lactate observed after training is due to an increase in metabolic clearance rate. In addition, the lower intramuscular lactate levels suggest a decreased recruitment of glycolysis particularly early in exercise.

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