Effects of adenosine, exercise, and moderate acute hypoxia on energy substrate utilization of human skeletal muscle

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.


2013 ◽  
Vol 114 (9) ◽  
pp. 1151-1157 ◽  
Author(s):  
Hayley M. O'Neill ◽  
Rengasamy Palanivel ◽  
David C. Wright ◽  
Tara MacDonald ◽  
James S. Lally ◽  
...  

Interleukin-6 (IL-6) increases glucose uptake in resting skeletal muscle. IL-6 is released from skeletal muscle during exercise; however; it is not known whether this IL-6 response is important for exercise-induced increases in skeletal muscle glucose uptake. We report that IL-6 knockout (KO) mice, 4 mo of age, have similar body weight to wild-type (WT), and, under resting conditions, oxygen consumption, food intake, substrate utilization, glucose tolerance, and insulin sensitivity are not different. Maximal exercise capacity is also similar to WT. We investigated substrate utilization and glucose clearance in vivo during steady-state treadmill running at 70% of maximal running speed and found that WT and IL-6 KO mice had similar rates of substrate utilization, muscle glucose clearance, and phosphorylation of AMP-activated protein kinase T172. These data provide evidence that IL-6 does not play a major role in regulating substrate utilization or skeletal muscle glucose uptake during steady-state endurance exercise.



1990 ◽  
Vol 270 (1) ◽  
pp. 245-249 ◽  
Author(s):  
M J Holness ◽  
M C Sugden

The progressive effects of starvation on muscle glucose utilization were studied in the conscious resting rat. High rates of glucose uptake and phosphorylation in constantly working cardiothoracic (heart, diaphragm) and postural skeletal muscles (soleus, adductor longus) were maintained for at least 9 h of starvation. A rapid decline in cardiac glucose utilization was observed during the period 9-24 h of starvation, but for the other muscles the decline was more gradual. Consequently, even after 24 h, rates of glucose utilization in these muscles remained quantitatively significant. In both cardiothoracic and working (postural) skeletal muscle, glucose uptake and phosphorylation and activity of the active form of pyruvate dehydrogenase exhibited differential sensitivities to starvation and also to acute elevation of fatty acid concentrations during acute (4-9 h) starvation, such that pyruvate oxidation was more rapidly suppressed than glucose uptake and phosphorylation. The results are discussed in relation to the role of the glucose/fatty acid cycle in glucose conservation during the fed-to-starved transition.



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


2014 ◽  
Vol 99 (12) ◽  
pp. 1569-1573 ◽  
Author(s):  
Yet Hoi Hong ◽  
Andrew C. Betik ◽  
Glenn K. McConell


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Sandra Lia Amaral ◽  
Juliana Cavalcante Andrade Louzada ◽  
Thiago José Dionísio ◽  
Bruno Alvares Viscelli ◽  
Evandro José Dionísio ◽  
...  


2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Jeremy L. Theisen ◽  
Stephen M. Ratchford ◽  
Heather L. Clifton ◽  
Kanokwan Bunsawat ◽  
Zachary Barret‐O'keefe ◽  
...  


1999 ◽  
Vol 276 (2) ◽  
pp. H438-H445 ◽  
Author(s):  
Robert C. Roach ◽  
Maria D. Koskolou ◽  
José A. L. Calbet ◽  
Bengt Saltin

A universal O2 sensor presumes that compensation for impaired O2delivery is triggered by low O2tension, but in humans, comparisons of compensatory responses to altered arterial O2 content ([Formula: see text]) or tension ([Formula: see text]) have not been reported. To directly compare cardiac output (Q˙TOT) and leg blood flow (LBF) responses to a range of[Formula: see text] and[Formula: see text], seven healthy young men were studied during two-legged knee extension exercise with control hemoglobin concentration ([Hb] = 144.4 ± 4 g/l) and at least 1 wk later after isovolemic hemodilution ([Hb] = 115 ± 2 g/l). On each study day, subjects exercised twice at 30 W and on to voluntary exhaustion with an[Formula: see text] of 0.21 or 0.11. The interventions resulted in two conditions with matched[Formula: see text] but markedly different [Formula: see text] (hypoxia and anemia) and two conditions with matched[Formula: see text] and different[Formula: see text] (hypoxia and anemia + hypoxia). [Formula: see text] varied from 46 ± 3 Torr in hypoxia to 95 ± 3 Torr (range 37 to >100) in anemia ( P < 0.001), yet LBF at exercise was nearly identical. However, as[Formula: see text] dropped from 190 ± 5 ml/l in control to 132 ± 2 ml/l in anemia + hypoxia ( P < 0.001),Q˙TOT and LBF at 30 W rose to 12.8 ± 0.8 and 7.2 ± 0.3 l/min, respectively, values 23 and 47% above control ( P< 0.01). Thus regulation ofQ˙TOT, LBF, and arterial O2 delivery to contracting intact human skeletal muscle is dependent for signaling primarily on[Formula: see text], not[Formula: see text]. This finding suggests that factors related to [Formula: see text]or [Hb] may play an important role in the regulation of blood flow during exercise in humans.



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.



2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.



2006 ◽  
Vol 99 (2-3) ◽  
pp. 1
Author(s):  
Fabio Ruzzier ◽  
Elena Bandi ◽  
Mihaela Jurdana ◽  
Paola Lorenzon ◽  
Marina Sciancalepore


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