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

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 < 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.

1998 ◽  
Vol 23 (6) ◽  
pp. 583-593 ◽  
Author(s):  
Arend Bonen ◽  
Margaret Ball-Burnett ◽  
Caryl Russel

We compared the effects of low- and high-intensity exercise on oral glucose tolerance immediately and 24 hr after each exercise bout. Participants were 5 male and 5 female individuals (age 40-48). A fasted, oral glucose tolerance test (OGTT) was conducted several days before the first exercise bout. Glucose and insulin concentrations were determined every 15 min throughout a 2 hr, 75 g OGTT. Immediately after low-intensity exercise, the incremental glucose area under the curve was reduced by 16%, compared to the fasting OGTT (p < .05). This was reduced further (−30%) 24 hr postexercise (p < .05). After high-intensity exercise, similar results were observed, with the incremental glucose area reduced by 14 and 35% immediately and 24 hr postexercise, respectively (p < .05). In conclusion, exercise improves glucose tolerance, this effect is more pronounced 24 hr postexercise, and low-and high-intensity exercise provide similar beneficial effects on glucose tolerance. Key words: cycle ergometry, insulin


1989 ◽  
Vol 257 (3) ◽  
pp. E405-E412 ◽  
Author(s):  
D. M. Cooper ◽  
T. J. Barstow ◽  
A. Bergner ◽  
W. N. Lee

We hypothesized that whole body glucose uptake (Rd) during exercise is not related in a simple, linear manner to O2 uptake (VO2). To test this, seven healthy male subjects (age range 23-34 yr) were studied in the postabsorptive but not glycogen-depleted state. Three conditions were examined: 1) rest, 2) 40 min of constant exercise in which the work rates were carefully chosen to consist of low-intensity exercise (no elevated blood lactate, a mean of 40% maximal VO2), and 3) 40 min of high-intensity exercise (markedly elevated blood lactate, 79% maximal VO2). Gas exchange was measured breath by breath, and glucose uptake and production were measured using [6,6-2H2]glucose. Low-intensity exercise (n = 7) resulted in a small but not statistically significant increase in mean Rd [3.06 +/- 0.37 (SE) mg.min-1.kg-1] compared with resting values (2.87 +/- 0.39 mg.min-1.kg-1) despite a fourfold increase in the production of CO2 and VO2. By contrast, the high-intensity exercise Rd (n = 5, 6.98 +/- 0.67 mg.min-1.kg-1) was significantly greater than the resting value (3.03 +/- 0.56 mg.min-1.kg-1). Results of glucose production were virtually the same. Similarly, mean levels of epinephrine and norepinephrine increased significantly above resting values during high- but not low-intensity exercise. Our data demonstrate that whole body glucose dynamics and regulation during 40 min of exercise do not change in a simple linear manner with respect to metabolic rate.


2010 ◽  
Vol 108 (6) ◽  
pp. 1472-1478 ◽  
Author(s):  
Patrice Brassard ◽  
Thomas Seifert ◽  
Mads Wissenberg ◽  
Peter M. Jensen ◽  
Christian K. Hansen ◽  
...  

Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity ( Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2, and arterial Pco2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. In randomized order, a bolus of saline or 0.3 mg of phenylephrine was then injected during semisupine cycling, eliciting a low (∼110 beats/min) or a high (∼150 beats/min) heart rate. At rest, MAP and MCA Vmean increased ∼20% ( P < 0.001) and ∼10% ( P < 0.001 for 0.25 mg of phenylephrine and P < 0.05 for 0.4 mg of phenylephrine), respectively. ScO2 then decreased ∼7% ( P < 0.001). Phenylephrine had no effect on SjvO2, PaCO2, or CMRO2. MAP increased after the administration of phenylephrine during low-intensity exercise (∼15%), but this was attenuated (∼10%) during high-intensity exercise ( P < 0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (−5%, P < 0.001) and abolished during high-intensity exercise (−3%, P = not significant), where PaCO2 decreased 7% ( P < 0.05) and CMRO2 increased 17% ( P < 0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.


2018 ◽  
Vol 247 ◽  
pp. 57-60 ◽  
Author(s):  
Reid A. Mitchell ◽  
Michele R. Schaeffer ◽  
Andrew H. Ramsook ◽  
Sabrina S. Wilkie ◽  
Jordan A. Guenette

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami

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.


2020 ◽  
Vol 66 (4) ◽  
pp. 414-418
Author(s):  
Tingting Li ◽  
Xu Zhang ◽  
Mingming Chen ◽  
Rui Wang ◽  
Lianping He ◽  
...  

SUMMARY OBJECTIVE Psychological distress is an important mental health problem among university students. The goal of this study was to determine psychological distress and its associated risk factors among students in the Anhui province. METHODS A cross-sectional study was conducted in a sample of 1304 students. In this study, a self-administered questionnaire consisting of the general demography and General Health Questionnaire (GHQ-12) was completed. Psychological distress was assessed using the GHQ-12-item questionnaire. A dichotomous category split was imposed on the GHQ-12 for the purpose of analysis. A GHQ-12 score of 4 or higher indicated psychological distress. The data were analyzed by SPSS 20.0 system. RESULTS A total of 1304 samples were analyzed in this study. The results indicated that the education level of the father and mother was associated with the students’ psychological distress (P<0.001). A significant association was found between high-intensity exercise and low-intensity exercise and psychological distress. However, no significant difference was identified between gender and psychological distress (P=0.173). CONCLUSION The education level of parents, high-intensity exercise, and low-intensity exercise were associated with psychological distress. Our results suggest that it is indispensable to raise awareness of psychological disorders and its associated risk factors among university students. Further studies are required to develop appropriate interventions for high-risk groups.


2018 ◽  
Vol 50 (5S) ◽  
pp. 792 ◽  
Author(s):  
Emily M. Miele ◽  
Steven Vitti ◽  
Laura Christoph ◽  
Elizabeth C. O’Neill ◽  
Tracey D. Matthews ◽  
...  

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