scholarly journals Aerobic capacity and telomere length in human skeletal muscle and leukocytes across the lifespan

Aging ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 359-369 ◽  
Author(s):  
Danielle Hiam ◽  
Cassandra Smith ◽  
Sarah Voisin ◽  
Josh Denham ◽  
Xu Yan ◽  
...  
2011 ◽  
Vol 111 (2) ◽  
pp. 427-434 ◽  
Author(s):  
Lorenzo K. Love ◽  
Paul J. LeBlanc ◽  
J. Greig Inglis ◽  
Nicolette S. Bradley ◽  
Jon Choptiany ◽  
...  

Pyruvate dehydrogenase (PDH) is a mitochondrial enzyme responsible for regulating the conversion of pyruvate to acetyl-CoA for use in the tricarboxylic acid cycle. PDH is regulated through phosphorylation and inactivation by PDH kinase (PDK) and dephosphorylation and activation by PDH phosphatase (PDP). The effect of endurance training on PDK in humans has been investigated; however, to date no study has examined the effect of endurance training on PDP in humans. Therefore, the purpose of this study was to examine differences in PDP activity and PDP1 protein content in human skeletal muscle across a range of muscle aerobic capacities. This association is important as higher PDP activity and protein content will allow for increased activation of PDH, and carbohydrate oxidation. The main findings of this study were that 1) PDP activity ( r2 = 0.399, P = 0.001) and PDP1 protein expression ( r2 = 0.153, P = 0.039) were positively correlated with citrate synthase (CS) activity as a marker for muscle aerobic capacity; 2) E1α ( r2 = 0.310, P = 0.002) and PDK2 protein ( r2 = 0.229, P =0.012) are positively correlated with muscle CS activity; and 3) although it is the most abundant isoform, PDP1 protein content only explained ∼18% of the variance in PDP activity ( r2 = 0.184, P = 0.033). In addition, PDP1 in combination with E1α explained ∼38% of the variance in PDP activity ( r2 = 0.383, P = 0.005), suggesting that there may be alternative regulatory mechanisms of this enzyme other than protein content. These data suggest that with higher muscle aerobic capacity (CS activity) there is a greater capacity for carbohydrate oxidation (E1α), in concert with higher potential for PDH activation (PDP activity).


2012 ◽  
Vol 97 (6) ◽  
pp. 774-784 ◽  
Author(s):  
Elodie Ponsot ◽  
Andoni Echaniz-Laguna ◽  
Anna-Maria Delis ◽  
Fawzi Kadi

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Adam Konopka ◽  
Paul Reidy ◽  
Bozena Jemiolo ◽  
Leonard Kaminsky ◽  
Todd Trappe ◽  
...  

1997 ◽  
Vol 8 (12) ◽  
pp. 1429-1438 ◽  
Author(s):  
S. Decary ◽  
V. Mouly ◽  
C. Ben Hamida ◽  
A. Sautet ◽  
J. P. Barbet ◽  
...  

2008 ◽  
Vol 40 (1) ◽  
pp. 82-87 ◽  
Author(s):  
FAWZI KADI ◽  
ELODIE PONSOT ◽  
KARIN PIEHL-AULIN ◽  
ABIGAIL MACKEY ◽  
MICHAEL KJAER ◽  
...  

2006 ◽  
Vol 31 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Mark A Tarnopolsky

Exercise physiologists are interested in metabolic myopathies because they demonstrate how knocking out a component of a specific biochemical pathway can alter cellular metabolism. McArdle's disease (myophosphorylase deficiency) has often been studied in exercise physiology to demonstrate the influence of removing the major anaerobic energy supply to skeletal muscle. Studies of patients with McArdle's disease have shown the increased reliance on blood-borne fuels, the importance of glycogen to maximal aerobic capacity, and the use of nutritional strategies to bypass metabolic defects. Myoadenylate deaminase deficiency is the most common metabolic enzyme deficiency in human skeletal muscle. It is usually compensated for endogenously and does not have a major influence on high-energy power output. Nutritional interventions such as carbohydrate loading and carbohydrate supplementation during exercise are essential components of therapy for patients with fatty acid oxidation defects. Cases of mitochondrial myopathies illustrate the importance of peripheral oxygen extraction for maximal aerobic capacity and show how both exercise and nutritional interventions can partially compensate for these mutations. In summary, metabolic myopathies provide important insights into regulatory and nutritional aspects of the major biochemical pathways of intermediary metabolism in human skeletal muscle. Key words: myoadenylate deaminase deficiency, MELAS syndrome, McArdle's disease, mitochondrial disease, inborn errors of metabolism.


2018 ◽  
Author(s):  
S Höckele ◽  
P Huypens ◽  
C Hoffmann ◽  
T Jeske ◽  
M Hastreiter ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 159-OR
Author(s):  
THEODORE P. CIARALDI ◽  
SUNDER MUDALIAR ◽  
LIWU LI ◽  
ROSARIO SCALIA ◽  
XIAO JIAN SUN ◽  
...  

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