scholarly journals Effects of Blood Glucose Concentration on Ratings of Perceived Exertion during Prolonged Low-Intensity Physical Exercise.

1991 ◽  
Vol 41 (2) ◽  
pp. 203-215
Author(s):  
Izumi TABATA ◽  
Atsushi KAWAKAMI
Keyword(s):  
Blood Glucose ◽  
Physical Exercise ◽  
Glucose Concentration ◽  
Perceived Exertion ◽  
Blood Glucose Concentration ◽  
Ratings Of Perceived Exertion ◽  
Low Intensity

Effect of low blood glucose on plasma CRF, ACTH, and cortisol during prolonged physical exercise

1991 ◽  
Vol 71 (5) ◽  
pp. 1807-1812 ◽  
Author(s):  
I. Tabata ◽  
F. Ogita ◽  
M. Miyachi ◽  
H. Shibayama
Keyword(s):  
Blood Glucose ◽  
Physical Exercise ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Plasma Concentrations ◽  
Bicycle Exercise ◽  
Low Intensity ◽  
Prolonged Physical Exercise ◽  
Blood Glucose Concentrations ◽  
Exercise In Humans

The effects of low blood glucose concentration during low-intensity prolonged physical exercise on the hypothalamus-pituitary-adrenocortical axis were investigated in healthy young men. In experiment 1, six subjects who had fasted for 14 h performed bicycle exercise at 50% of their maximal O2 uptake until exhaustion. At the end of the exercise, adrenocorticotropic hormone (ACTH) and cortisol increased significantly. However, this hormonal response was totally abolished when the same subjects exercised at the same intensity while blood glucose concentrations were maintained at the preexercise level. In experiment 2, in addition to ACTH and cortisol, the possible changes in plasma concentration of corticotropin-releasing factor (CRF) were investigated during exercise of the same intensity performed by six subjects. As suggested by a previous study (Tabata et al. Clin. Physiol. Oxf. 4: 299–307, 1984), when the blood glucose concentrations decreased to less than 3.3 mM, plasma concentrations of CRF, ACTH, and cortisol showed a significant increase. At exhaustion, further increases were observed in plasma CRF, ACTH, and cortisol concentrations. These results demonstrate that decreases in blood glucose concentration trigger the pituitary-adrenocortical axis to enhance secretion of ACTH and cortisol during low-intensity prolonged exercise in humans. The data also might suggest that this activation is due to increased concentration of CRF, which was shown to increase when blood glucose concentration decreased to a critical level of 3.3 mM.

Influence of Carbohydrate Ingestion on Blood Glucose and Performance in Runners

1992 ◽  
Vol 2 (4) ◽  
pp. 317-327 ◽  
Author(s):  
Randall L. Wilber ◽  
Robert J. Moffatt
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Perceived Exertion ◽  
Treadmill Exercise ◽  
Blood Glucose Concentration ◽  
Endurance Performance ◽  
Time To Exhaustion ◽  
Experimental Conditions ◽  
Double Blind ◽  
Carbohydrate Ingestion

Ten trained male runners performed a treadmill exercise test at 80%under two experimental conditions, carbohydrate (CHO, 7% carbohydrate) and placebo (P), to determine the effect of carbohydrate ingestion on endurance performance (treadmill run time), blood glucose concentration, respiratory exchange ratio (RER), and subjective ratings of perceived exertion (RPE). Treatment order was randomized and counterbalanced and test solutions were administered double-blind. Ingestion took place 5 min preexercise (250 ml) and at 15-min intervals during exercise (125 ml). Performance was enhanced by 29.4% (p~ 0.05) during CHO (115 ±25 min) compared to P (92 ± 27 min). Blood glucose concentration was significantly greater during CHO (5.6 ± 0.9 mM) relative to P (5.0 ±0.7 mM). There was a significant increase in mean RER following CHO ingestion (.94±.01) compared to P (.90±.01). Average RPE was significantly less during CHO (14.5±2.3) relative to P (15.4±2.4). These data suggest that time to exhaustion of high-intensity treadmill exercise is delayed as a result of carbohydrate ingestion and that this effect is mediated by favorable alterations in blood glucose concentration and substrate utilization.

Gluconeogenesis in humans with induced hyperlactatemia during low-intensity exercise

2003 ◽  
Vol 284 (6) ◽  
pp. E1162-E1171 ◽  
Author(s):  
Mark J. Roef ◽  
Kees de Meer ◽  
Satish C. Kalhan ◽  
Helma Straver ◽  
Ruud Berger ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Deuterium Oxide ◽  
Lactate Concentration ◽  
Random Order ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Lactate Infusion ◽  
Bicarbonate Infusion

We studied the role of lactate in gluconeogenesis (GNG) during exercise in untrained fasting humans. During the final hour of a 4-h cycle exercise at 33–34% maximal O2 uptake, seven subjects received, in random order, either a sodium lactate infusion (60 μmol · kg−1 · min−1) or an isomolar sodium bicarbonate infusion. The contribution of lactate to gluconeogenic glucose was quantified by measuring 2H incorporation into glucose after body water was labeled with deuterium oxide, and glucose rate of appearance (Ra) was measured by [6,6-2H2]glucose dilution. Infusion of lactate increased lactate concentration to 4.4 ± 0.6 mM (mean ± SE). Exercise induced a decrease in blood glucose concentration from 5.0 ± 0.2 to 4.2 ± 0.3 mM ( P < 0.05); lactate infusion abolished this decrease (5.0 ± 0.3 mM; P < 0.001) and increased glucose Ra compared with bicarbonate infusion ( P < 0.05). Lactate infusion increased both GNG from lactate (29 ± 4 to 46 ± 4% of glucose Ra, P < 0.001) and total GNG. We conclude that lactate infusion during low-intensity exercise in fasting humans 1) increased GNG from lactate and 2) increased glucose production, thus increasing the blood glucose concentration. These results indicate that GNG capacity is available in humans after an overnight fast and can be used to sustain blood glucose levels during low-intensity exercise when lactate, a known precursor of GNG, is available at elevated plasma levels.

PKC-mediated toxicity of elevated glucose concentration on cardiomyocyte function

2014 ◽  
Vol 307 (4) ◽  
pp. H587-H597 ◽  
Author(s):  
Mark W. Sims ◽  
James Winter ◽  
Sean Brennan ◽  
Robert I. Norman ◽  
G. André Ng ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Contractile Function ◽  
Blood Glucose Concentration ◽  
Specific Inhibitor ◽  
Wistar Rat ◽  
Patch Clamp Recording ◽  
Electrical Stability ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose

While it is well established that mortality risk after myocardial infarction (MI) increases in proportion to blood glucose concentration at the time of admission, it is unclear whether there is a direct, causal relationship. We investigated potential mechanisms by which increased blood glucose may exert cardiotoxicity. Using a Wistar rat or guinea-pig isolated cardiomyocyte model, we investigated the effects on cardiomyocyte function and electrical stability of alterations in extracellular glucose concentration. Contractile function studies using electric field stimulation (EFS), patch-clamp recording, and Ca2+ imaging were used to determine the effects of increased extracellular glucose concentration on cardiomyocyte function. Increasing glucose from 5 to 20 mM caused prolongation of the action potential and increased both basal Ca2+ and variability of the Ca2+ transient amplitude. Elevated extracellular glucose concentration also attenuated the protection afforded by ischemic preconditioning (IPC), as assessed using a simulated ischemia and reperfusion model. Inhibition of PKCα and β, using Gö6976 or specific inhibitor peptides, attenuated the detrimental effects of glucose and restored the cardioprotected phenotype to IPC cells. Increased glucose concentration did not attenuate the cardioprotective role of PKCε, but rather activation of PKCα and β masked its beneficial effect. Elevated extracellular glucose concentration exerts acute cardiotoxicity mediated via PKCα and β. Inhibition of these PKC isoenzymes abolishes the cardiotoxic effects and restores IPC-mediated cardioprotection. These data support a direct link between hyperglycemia and adverse outcome after MI. Cardiac-specific PKCα and β inhibition may be of clinical benefit in this setting.

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