scholarly journals Role of Tissue-Specific Blood Flow and Tissue Recruitment in Insulin-Mediated Glucose Uptake of Human Skeletal Muscle

Circulation ◽  
1998 ◽  
Vol 98 (3) ◽  
pp. 234-241 ◽  
Author(s):  
Riccardo C. Bonadonna ◽  
Maria Pia Saccomani ◽  
Stefano Del Prato ◽  
Enzo Bonora ◽  
Ralph A. DeFronzo ◽  
...  

2012 ◽  
Vol 302 (3) ◽  
pp. R385-R390 ◽  
Author(s):  
Ilkka Heinonen ◽  
Jukka Kemppainen ◽  
Kimmo Kaskinoro ◽  
Juha E. Peltonen ◽  
Hannu T. Sipilä ◽  
...  

Glucose metabolism increases in hypoxia and can be influenced by endogenous adenosine, but the role of adenosine for regulating glucose metabolism at rest or during exercise in hypoxia has not been elucidated in humans. We studied the effects of exogenous adenosine on human skeletal muscle glucose uptake and other blood energy substrates [free fatty acid (FFA) and lactate] by infusing adenosine into the femoral artery in nine healthy young men. The role of endogenous adenosine was studied by intra-arterial adenosine receptor inhibition (aminophylline) during dynamic one-leg knee extension exercise in normoxia and acute hypoxia corresponding to ∼3,400 m of altitude. Extraction and release of energy substrates were studied by arterial-to-venous (A-V) blood samples, and total uptake or release was determined by the product of A-V differences and muscle nutritive perfusion measured by positron emission tomography. The results showed that glucose uptake increased from a baseline value of 0.2 ± 0.2 to 2.0 ± 2.2 μmol·100 g−1·min−1 during adenosine infusion ( P < 0.05) at rest. Although acute hypoxia enhanced arterial FFA levels, it did not affect muscle substrate utilization at rest. During exercise, glucose uptake was higher (195%) during acute hypoxia compared with normoxia ( P = 0.058), and aminophylline had no effect on energy substrate utilization during exercise, despite that arterial FFA levels were increased. In conclusion, exogenous adenosine at rest and acute moderate hypoxia during low-intensity knee-extension exercise increases skeletal muscle glucose uptake, but the increase in hypoxia appears not to be mediated by adenosine.



2015 ◽  
Vol 69 (6) ◽  
pp. 734-739 ◽  
Author(s):  
P Mitrou ◽  
E Petsiou ◽  
E Papakonstantinou ◽  
E Maratou ◽  
V Lambadiari ◽  
...  


2006 ◽  
Vol 572 (1) ◽  
pp. 295-305 ◽  
Author(s):  
José González-Alonso ◽  
Stefan P. Mortensen ◽  
Ellen A. Dawson ◽  
Niels H. Secher ◽  
Rasmus Damsgaard


1999 ◽  
Vol 276 (6) ◽  
pp. H1951-H1960 ◽  
Author(s):  
G. Rådegran ◽  
B. Saltin

The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of N G-monomethyl-l-arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 ± 0.08 to 0.18 ± 0.03 l/min ( P < 0.01), i.e., by ∼52%, and increased leg O2 extraction from 62.1 ± 9.8 to 100.9 ± 4.5 ml/l ( P < 0.004); thus leg O2 uptake (V˙o 2, 22 ± 4 ml/min, ∼0.75 ml ⋅ min−1 ⋅ 100 g−1) was unaltered [not significant ( P = NS)]. Mean arterial pressure (MAP) increased by 8 ± 2 mmHg ( P < 0.01). Heart rate (HR, 53 ± 3 beats/min) was unaltered ( P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 ± 0.4 l/min, ∼163 ml ⋅ min−1 ⋅ 100 g−1), MAP (117 ± 3 mmHg), HR (98 ± 5 beats/min), or legV˙o 2 (704 ± 55 ml/min, ∼24 ml ⋅ min−1 ⋅ 100 g−1, P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 ± 1.0 l/min, ∼258 ml ⋅ min−1 ⋅ 100 g−1), MAP (140 ± 8 mmHg), and leg V˙o 2(1,173 ± 139 ml/min, ∼40 ml ⋅ min−1 ⋅ 100 g−1) were unaffected at termination of peak effort ( P = NS). Peak HR (137 ± 3 beats/min) was, however, lowered by 10% ( P < 0.01). During recovery, NOS inhibition reduced FABF by ∼34% ( P< 0.04), which was compensated for by an increase in the leg O2 extraction by ∼41% ( P < 0.04); thus legV˙o 2 was unaltered ( P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O2 extraction, and thusV˙o 2 is maintained.



1999 ◽  
Vol 521 (3) ◽  
pp. 729-737 ◽  
Author(s):  
Olli-Pekka Pitkänen ◽  
Hanna Laine ◽  
Jukka Kemppainen ◽  
Esa Eronen ◽  
Anu Alanen ◽  
...  


1992 ◽  
Vol 263 (2) ◽  
pp. E199-E204 ◽  
Author(s):  
M. Laakso ◽  
S. V. Edelman ◽  
G. Brechtel ◽  
A. D. Baron

In vivo insulin-mediated glucose uptake (IMGU) occurs chiefly in skeletal muscle, where it is determined by the product of arteriovenous glucose difference (delta AVG) and blood flow (BF) rate into muscle. Epinephrine (Epi) reduces the rate of IMGU in whole body. To examine whether this is due to a reduction in delta AVG across or BF into skeletal muscle we constructed insulin dose-response curves for whole body IMGU and leg muscle IMGU- using euglycemic clamp ((+)[3-3H]glucose infusion) and leg balance techniques during insulin infusions ranging from 10 to 1,200 mU.m-2.min-1. We studied six subjects [wt 70 +/- 2 (SE) kg] during an Epi infusion at a single rate of 0.002 mg.kg-1.min-1 and six subjects (70 +/- 3 kg) during a saline infusion alone. Maximum whole body glucose uptake (WBGU) was similar during Epi and saline infusions [71.4 vs. 73.6 mmol.kg-1.min-1, P = not significant (NS)]. Compared with saline, maximum delta AVG was decreased during Epi infusion (1.04 vs. 1.31 mM, P less than 0.01). Compared with saline alone maximum leg BF was increased (5.3 vs. 4.3 dl/min, P less than 0.01) during Epi infusion. Thus maximum leg glucose uptake (LGU) was similar (696 vs. 821 pmol.leg-1.min-1, P = NS) during infusion of Epi and saline, respectively. Half-maximal effective dose for insulin's effect to stimulate WBGU, delta AVG, BF, and LGU was increased two- to threefold during Epi vs. saline infusions (P less than 0.01 for all values).(ABSTRACT TRUNCATED AT 250 WORDS)



1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.



Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3721
Author(s):  
Chun-Ching Huang ◽  
Chia-Chen Liu ◽  
Jung-Piao Tsao ◽  
Chin-Lin Hsu ◽  
I-Shiung Cheng

The present study aimed to investigate the effect of oral resveratrol supplementation on the key molecular gene expressions involved in mitochondria biogenesis and glycogen resynthesis in human skeletal muscle. Nine young male athletes participated in the single-blind and crossover designed study. All subjects completed a 4-day resveratrol and placebo supplement in a randomized order while performing a single bout of cycling exercise. Immediately after the exercise challenge, the subjects consumed a carbohydrate (CHO) meal (2 g CHO/Kg body mass) with either resveratrol or placebo capsules. Biopsied muscle samples, blood samples and expired gas samples were obtained at 0 h and 3 h after exercise. The muscle samples were measured for gene transcription factor expression by real-time PCR for glucose uptake and mitochondria biogenesis. Plasma glucose, insulin, glycerol, non-esterified fatty acid concentrations and respiratory exchange ratio were analyzed during post-exercise recovery periods. The results showed that the muscle glycogen concentrations were higher at 3 h than at 0 h; however, there were no difference between resveratrol trial and placebo trial. There were no significantly different concentrations in plasma parameters between the two trials. Similarly, no measured gene expressions were significant between the two trials. The evidence concluded that the 4-day oral resveratrol supplementation did not improve post-exercise muscle glycogen resynthesis and related glucose uptake and mitochondrial biosynthesis gene expression in men.



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