724 EFFECTS BLOOD GLUCOSE CONCENTRATION ON PERCEIVED EXERTION DURING PHYSICAL EXERCISE AT

1990 ◽  
Vol 22 (2) ◽  
pp. S121
Author(s):  
I. Tabata ◽  
A. Kawakami ◽  
Y. Ohira
1991 ◽  
Vol 71 (5) ◽  
pp. 1807-1812 ◽  
Author(s):  
I. Tabata ◽  
F. Ogita ◽  
M. Miyachi ◽  
H. Shibayama

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.


1992 ◽  
Vol 2 (4) ◽  
pp. 317-327 ◽  
Author(s):  
Randall L. Wilber ◽  
Robert J. Moffatt

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.


2014 ◽  
Vol 307 (4) ◽  
pp. H587-H597 ◽  
Author(s):  
Mark W. Sims ◽  
James Winter ◽  
Sean Brennan ◽  
Robert I. Norman ◽  
G. André Ng ◽  
...  

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.


2014 ◽  
Vol 19 (3) ◽  
pp. 527-533 ◽  
Author(s):  
Miho Senda ◽  
Susumu Ogawa ◽  
Kazuhiro Nako ◽  
Masashi Okamura ◽  
Takuya Sakamoto ◽  
...  

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