Blood lactate exchange and removal abilities after relative high-intensity exercise: effects of training in normoxia and hypoxia

2001 ◽  
Vol 84 (5) ◽  
pp. 403-412 ◽  
Author(s):  
Laurent Messonnier ◽  
Hubert Freund ◽  
Léonard Féasson ◽  
Fabrice Prieur ◽  
Josiane Castells ◽  
...  
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Lactate Exchange

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.

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 The Blood Lactate Increase in High Intensity Exercise Is Depressed by Acanthopanax sieboldianus

Nutrients ◽  
2013 ◽  
Vol 5 (10) ◽  
pp. 4134-4144 ◽  
Author(s):  
Morimasa Kato ◽  
Shizue Kurakane ◽  
Atsuyoshi Nishina ◽  
Jaeyoung Park ◽  
Hyukki Chang
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
High Intensity Exercise

scholarly journals Practical approach for the study of metabolic regulation

2004 ◽  
Vol 2 (2) ◽  
pp. 17
Author(s):  
D.V. Macedo ◽  
R. Hohl ◽  
L.S. Tessutti ◽  
F.L. Lazarim ◽  
F.O.C. Silva ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Plasma Glucose ◽  
High Intensity ◽  
Metabolic Regulation ◽  
Ketone Bodies ◽  
Lactate Production ◽  
High Intensity Exercise ◽  
Practical Approach ◽  
Glycogen Depletion ◽  
Low Carbohydrate Diet

First year students in Physical Education must understand metabolic regulation to comprehend thewhole integration of biochemical pathways in attempt to establish the relation with exercise. Thiswhole view is not easy to learn and the task becomes even harder with the lack of time at theend of course, when normally the students think about metabolic integration. Trying to get thestudents attention to this important issue, we developed practical works beginning in the middle ofthe course, in parallel with theory classes. Blood and urine were collected for metabolite analysis ineach practice. The students were divided in groups (10 students) and they created the protocols in formthat they only have been guided and directed by the teacher and monitors. The practical activitiesand biochemical analysis were: six 30m sprints with dierent recovery times (blood lactate and meanvelocities), lactate removal from muscle to blood after high intensity exercise (blood lactate), anaerobicthreshold (blood lactate and heart rate), the eect of glycogen depletion after high and moderateintensity exercises (plasma glucose and urea concentrations) and low carbohydrate diet vs. normaldiet (plasma glucose and urine ketone bodies). After data collection, discussion and interpretation, thestudents presented orally each work in the same order above. Each presentation had the focus on themetabolic pathways involved in each practice. Group 1: phosphocreatine utilization and resynthesis.Group 2: anaerobic glycolysis, lactate production and removal. Group 3: transition between anaerobicglycolysis and oxidative metabolism. In attempt to promote the integration between muscle and liver-Group 4: protein catabolism after high intensity exercise with low muscular glycogen concentration(transamination, Cori Cycle and gluconeogenesis). Group 5: liver ketogenesis in low carbohydratediet. This sequence was intended to promote the comprehension of integrated metabolism. As a nalactivity, the students showed their results in the form of poster. All activities were part of disciplineevaluation. All students approved this practical approach.

scholarly journals Delayed Rebound of Glycemia During Recovery Following Short-Duration High-Intensity Exercise: Are There Lactate and Glucose Metabolism Interactions?

2021 ◽  
Vol 8 ◽  
Author(s):  
Laurent A. Messonnier ◽  
Benjamin Chatel ◽  
Chi-An W. Emhoff ◽  
Léo Blervaque ◽  
Samuel Oyono-Enguéllé
Keyword(s):  
Blood Glucose ◽  
Blood Lactate ◽  
Short Duration ◽  
High Intensity ◽  
Area Under The Curve ◽  
High Intensity Exercise ◽  
Healthy Humans ◽  
Low Intensity Exercise ◽  
Blood Glucose Concentrations ◽  
Peak Value

Lactate constitutes the primary gluconeogenic precursor in healthy humans at rest and during low-intensity exercise. Data on the interactions between lactate and glucose metabolisms during recovery after short-duration high-intensity exercise are sparse. The aim of the present study was to describe blood glucose ([glucose]b) and lactate ([lactate]b) concentration curves during recovery following short-duration high-intensity exercise. Fifteen healthy Cameroonian subjects took part in the study and performed successively (i) an incremental exercise to exhaustion to determine maximal work rate (Pmax) and (ii) a 2-min 110% Pmax exercise after which blood lactate and glucose concentrations were measured during the 80-min passive recovery. In response to the 2-min 110% Pmax exercise, [glucose]b remained stable (from 4.93 ± 1.13 to 4.65 ± 0.74 mmol.L−1, NS) while [lactate]b increased (from 1.35 ± 0.36 to 7.87 ± 1.66 mmol.L−1, p &lt; 0.0001). During recovery, blood lactate concentrations displayed the classic biphasic curve while blood glucose concentrations displayed a singular shape including a delayed and transitory rebound of glycemia. This rebound began at 27.7 ± 6.2 min and peaked at 6.78 ± 0.53 mmol.L−1 at 56.3 ± 9.7 min into recovery. The area under the curve (AUC) of [lactate]b during the rebound of glycemia was positively correlated with the peak value of glycemia and the AUC of [glucose]b during the rebound. In conclusion, the delayed rebound of glycemia observed in the present study was associated with lactate availability during this period.

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