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 High-intensity exercise and recovery during short-term supplementation with creatine plus a protein-carbohydrate formula

2006 ◽  
Vol 18 (4) ◽  
pp. 136
Author(s):  
JR Clark
Keyword(s):  
Creatine Kinase ◽  
Exercise Training ◽  
Blood Lactate ◽  
High Intensity ◽  
Muscle Pain ◽  
Repeated Measures ◽  
Creatine Supplementation ◽  
High Intensity Exercise ◽  
Fatigue Index ◽  
Short Term

Objective. To determine the effect of short-term creatine supplementation plus a protein-carbohydrate formula on high-intensity exercise performance and recovery. Design. A repeated-measures, experimental study, employing a randomised, double-blind, placebo-controlled, group comparison design was used. Interventions. Thirty active but not sprint-trained male subjects were randomly assigned to 1 of 3 groups: creatine plus protein-carbohydrate formula (CRF); creatine only (CRE); and control (CON). All groups were exposed to the same high-intensity sprint exercise programme, 3 times per week for 30 days. Main outcome measures. Dependant variables included total repeat sprint distance, fatigue index, perceived muscle pain, and blood lactate, urea, creatine kinase, and cortisol concentrations. Results. All groups significantly (p ≤ 0.05) increased total sprint distance and decreased blood urea concentrations. There were no significant changes in blood lactate or cortisol concentrations in any group. CRF showed significant decreases (p ≤ 0.05) in fatigue index, muscle pain, and creatine kinase concentration. However, no significant differences were found between groups. Conclusion. Short-term creatine supplementation with or without protein-carbohydrate supplementation does not appear to enhance performance or recovery significantly over high-intensity exercise training alone in non-sprint-trained individuals. A longer trial period may be required to evaluate effect on recovery more conclusively. In addition, the prime importance of physical conditioning, and in particular task-specific exercise training, in stimulating performance and recovery adaptations is highlighted. South African Journal of Sports Medicine Vol. 18 (4) 2006: pp. 136-140

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.

Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease

1990 ◽  
Vol 68 (4) ◽  
pp. 1393-1398 ◽  
Author(s):  
J. M. Hagberg ◽  
D. S. King ◽  
M. A. Rogers ◽  
S. J. Montain ◽  
S. M. Jilka ◽  
...  
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
Maximal Exercise ◽  
Matched Control ◽  
Slow Component ◽  
High Intensity Exercise ◽  
O2 Consumption ◽  
Control Subjects ◽  
Mcardle's Disease ◽  
Mcardle’S Disease

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow “lactacid” component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.

scholarly journals Nasal strips do not affect pulmonary gas exchange, anaerobic metabolism, or EIPH in exercising Thoroughbreds

2001 ◽  
Vol 90 (6) ◽  
pp. 2378-2385 ◽  
Author(s):  
Thomas E. Goetz ◽  
Murli Manohar ◽  
Aslam S. Hassan ◽  
Gordon J. Baker
Keyword(s):  
Blood Lactate ◽  
Anaerobic Metabolism ◽  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Mixed Venous Blood ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Exercise Induced ◽  
Mixed Venous

The present study was carried out to examine whether nasal strip application would improve the exercise-induced arterial hypoxemia and hypercapnia, diminish anaerobic metabolism, and modify the incidence of exercise-induced pulmonary hemorrhage (EIPH) in horses. Two sets of experiments, control and nasal strip experiments, were carried out on seven healthy, sound, exercise-trained Thoroughbred horses in random order, 7 days apart. Simultaneous measurements of core temperature, arterial and mixed venous blood gases/pH, and blood lactate and ammonia concentrations were made at rest, during submaximal and near-maximal exercise, and during recovery. In both treatments, whereas submaximal exercise caused hyperventilation, near-maximal exercise induced significant arterial hypoxemia, desaturation of Hb, hypercapnia, and acidosis. However, O2 content increased significantly with exercise in both treatments, while the mixed venous blood O2 content decreased as O2 extraction increased. In both treatments, plasma ammonia and blood lactate concentrations increased significantly with exercise. Statistically significant differences between the control and the nasal strip experiments could not be discerned, however. Also, all horses experienced EIPH in both treatments. Thus our data indicated that application of an external nasal dilator strip neither improved the exercise-induced arterial hypoxemia and hypercapnia nor diminished anaerobic metabolism or the incidence of EIPH in Thoroughbred horses performing strenuous exercise.

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