Intramuscular triacylglycerol utilization in human skeletal muscle during exercise: is there a controversy?

2002 ◽  
Vol 93 (4) ◽  
pp. 1185-1195 ◽  
Author(s):  
Matthew J. Watt ◽  
George J. F. Heigenhauser ◽  
Lawrence L. Spriet

Intramuscular triacylglyerols (IMTGs) represent a potentially important energy source for contracting human skeletal muscle. Although the majority of evidence from isotope tracer and 1H-magnetic resonance spectroscopy (MRS) studies demonstrate IMTG utilization during exercise, controversy regarding the importance of IMTG as a metabolic substrate persists. The controversy stems from studies that measure IMTG in skeletal muscle biopsy samples and report no significant net IMTG degradation during prolonged moderate-intensity (55–70% maximal O2 consumption) exercise lasting 90–120 min. Although postexercise decrements in IMTG levels are often reported from direct muscle measurements, the marked between-biopsy variability (∼23%) that has been reported with this technique in untrained subjects is larger than the expected decrease in IMTG content, effectively precluding significant findings. In contrast, recent data obtained in endurance-trained subjects demonstrated reduced variability between duplicate biopsies (∼12%), and significant changes in IMTG were detected after 120 min of moderate-intensity exercise. Therefore, it is our contention that the muscle biopsy, isotope tracer, and 1H-MRS techniques report significant and energetically important oxidation of free fatty acids derived from IMTGs during prolonged moderate exercise.

2002 ◽  
Vol 282 (3) ◽  
pp. E688-E694 ◽  
Author(s):  
T. J. Stephens ◽  
Z.-P. Chen ◽  
B. J. Canny ◽  
B. J. Michell ◽  
B. E. Kemp ◽  
...  

The effect of prolonged moderate-intensity exercise on human skeletal muscle AMP-activated protein kinase (AMPK)α1 and -α2 activity and acetyl-CoA carboxylase (ACCβ) and neuronal nitric oxide synthase (nNOSμ) phosphorylation was investigated. Seven active healthy individuals cycled for 30 min at a workload requiring 62.8 ± 1.3% of peak O2consumption (V˙o 2 peak) with muscle biopsies obtained from the vastus lateralis at rest and at 5 and 30 min of exercise. AMPKα1 activity was not altered by exercise; however, AMPKα2 activity was significantly ( P < 0.05) elevated after 5 min (∼2-fold), and further elevated ( P < 0.05) after 30 min (∼3-fold) of exercise. ACCβ phosphorylation was increased ( P < 0.05) after 5 min (∼18-fold compared with rest) and increased ( P< 0.05) further after 30 min of exercise (∼36-fold compared with rest). Increases in AMPKα2 activity were significantly correlated with both increases in ACCβ phosphorylation and reductions in muscle glycogen content. Fat oxidation tended ( P = 0.058) to increase progressively during exercise. Muscle creatine phosphate was lower ( P < 0.05), and muscle creatine, calculated free AMP, and free AMP-to-ATP ratio were higher ( P < 0.05) at both 5 and 30 min of exercise compared with those at rest. At 30 min of exercise, the values of these metabolites were not significantly different from those at 5 min of exercise. Phosphorylation of nNOSμ was variable, and despite the mean doubling with exercise, statistically significance was not achieved ( P = 0.304). Western blots indicated that AMPKα2 was associated with both nNOSμ and ACCβ consistent with them both being substrates of AMPKα2 in vivo. In conclusion, AMPKα2 activity and ACCβ phosphorylation increase progressively during moderate exercise at ∼60% of V˙o 2 peak in humans, with these responses more closely coupled to muscle glycogen content than muscle AMP/ATP ratio.


1981 ◽  
Vol 60 (3) ◽  
pp. 19P-19P
Author(s):  
F. Martin ◽  
J. Levi ◽  
G. Slavin ◽  
T. J. Peters

2001 ◽  
Vol 280 (4) ◽  
pp. E669-E675 ◽  
Author(s):  
Mark Bruce ◽  
Dumitru Constantin-Teodosiu ◽  
Paul L. Greenhaff ◽  
Leslie H. Boobis ◽  
Clyde Williams ◽  
...  

The aims of the present study were twofold: first to investigate whether TCA cycle intermediate (TCAI) pool expansion at the onset of moderate-intensity exercise in human skeletal muscle could be enhanced independently of pyruvate availability by ingestion of glutamine or ornithine α-ketoglutarate, and second, if it was, whether this modification of TCAI pool expansion had any effect on oxidative energy status during subsequent exercise. Seven males cycled for 10 min at ∼70% maximal O2 uptake 1 h after consuming either an artificially sweetened placebo (5 ml/kg body wt solution, CON), 0.125 g/kg body wtl-(+)-ornithine α-ketoglutarate dissolved in 5 ml/kg body wt solution (OKG), or 0.125 g/kg body wt l-glutamine dissolved in 5 ml/kg body wt solution (GLN). Vastus lateralis muscle was biopsied 1 h postsupplement and after 10 min of exercise. The sum of four measured TCAI (ΣTCAI; citrate, malate, fumarate, and succinate, ∼85% of total TCAI pool) was not different between conditions 1 h postsupplement. However, after 10 min of exercise, ΣTCAI (mmol/kg dry muscle) was greater in the GLN condition (4.90 ± 0.61) than in the CON condition (3.74 ± 0.38, P < 0.05) and the OKG condition (3.85 ± 0.28). After 10 min of exercise, muscle phosphocreatine (PCr) content was significantly reduced ( P < 0.05) in all conditions, but there was no significant difference between conditions. We conclude that the ingestion of glutamine increased TCAI pool size after 10 min of exercise most probably because of the entry of glutamine carbon at the level of α-ketoglutarate. However, this increased expansion in the TCAI pool did not appear to increase oxidative energy production, because there was no sparing of PCr during exercise.


1999 ◽  
Vol 87 (1) ◽  
pp. 325-331 ◽  
Author(s):  
R. S. Richardson ◽  
J. S. Leigh ◽  
P. D. Wagner ◽  
E. A. Noyszewski

Previously, by measuring myoglobin-associated [Formula: see text](PMb o 2) during maximal exercise, we have demonstrated that 1) intracellular[Formula: see text] is 10-fold less than calculated mean capillary [Formula: see text] and 2) intracellular[Formula: see text] and maximum O2 uptake (V˙o 2 max) fall proportionately in hypoxia. To further elucidate this relationship, five trained subjects performed maximum knee-extensor exercise under conditions of normoxia (21% O2), hypoxia (12% O2), and hyperoxia (100% O2) in balanced order. Quadriceps O2 uptake (V˙o 2) was calculated from arterial and venous blood O2concentrations and thermodilution blood flow measurements. Magnetic resonance spectroscopy was used to determine myoglobin desaturation, and an O2 half-saturation pressure of 3.2 Torr was used to calculate PMb o 2from saturation. Skeletal muscleV˙o 2 max at 12, 21, and 100% O2 was 0.86 ± 0.1, 1.08 ± 0.2, and 1.28 ± 0.2 ml ⋅ min−1 ⋅ ml−1, respectively. The 100% O2 values approached twice that previously reported in human skeletal muscle. PMb o 2values were 2.3 ± 0.5, 3.0 ± 0.7, and 4.1 ± 0.7 Torr while the subjects breathed 12, 21, and 100% O2, respectively. From 12 to 21% O2,V˙o 2 and PMb o 2were again proportionately related. However, 100% O2 increasedV˙o 2 max relatively less than PMb o 2, suggesting an approach to maximal mitochondrial capacity with 100% O2. These data 1) again demonstrate very low cytoplasmic [Formula: see text] atV˙o 2 max, 2) are consistent with supply limitation of V˙o 2 maxof trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular [Formula: see text] in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscleV˙o 2 are being approached.


2009 ◽  
Vol 8 (7) ◽  
pp. 3265-3277 ◽  
Author(s):  
Kenneth C. Parker ◽  
Ronan J. Walsh ◽  
Mohammad Salajegheh ◽  
Anthony A. Amato ◽  
Bryan Krastins ◽  
...  

1986 ◽  
Vol 61 (3) ◽  
pp. 832-835 ◽  
Author(s):  
K. Soderlund ◽  
E. Hultman

The concentrations of ATP, phosphocreatine (PCr), creatine, and lactate were determined in muscle biopsy samples frozen immediately or after a delay of 1–6 min. During the delay the samples were exposed to normal air or a gas mixture of 6.5% CO2-93.5% O2. The ATP content was unchanged, but PCr increased significantly from 72 mmol after rapid freezing to 85 mmol X kg dry muscle-1 during the 1st min in air. The lactate concentration increased (2.8 to 5.2 mmol X kg-1). If muscles were made anoxic by circulatory occlusion for 4–6 min before sampling, no increase in PCr was observed. Direct homogenization of fresh tissue in perchloric acid gave the same ATP, PCr, and lactate contents as frozen samples. It is concluded that the ATP and PCr contents in muscle are unaffected by freezing but that the biopsy procedure activates the energy utilization processes resulting in PCr decrease. It is suggested that the muscle PCr content after a 1-min delay in tissue freezing corresponds to the level in resting fresh muscle.


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