Studies of Substrate Metabolism in Isolated Myocytes

1983 ◽  
pp. 217-230 ◽  
Author(s):  
John J. Spitzer
Keyword(s):  
Substrate Metabolism

scholarly journals Fasting-induced changes in the expression of genes controlling substrate metabolism in the rat heart

2001 ◽  
Vol 42 (11) ◽  
pp. 1752-1758
Author(s):  
Karin A.J.M. Van der Lee ◽  
Peter H.M. Willemsen ◽  
Sonia Samec ◽  
Josiane Seydoux ◽  
Abdul G. Dulloo ◽  
...  
Keyword(s):  
Rat Heart ◽  
Substrate Metabolism ◽  
Expression Of Genes ◽  
Induced Changes

scholarly journals Regulation of Energy Substrate Metabolism in Endurance Exercise

2021 ◽  
Vol 18 (9) ◽  
pp. 4963
Author(s):  
Abdullah F. Alghannam ◽  
Mazen M. Ghaith ◽  
Maha H. Alhussain
Keyword(s):  
Fatty Acids ◽  
Exercise Intensity ◽  
Fat Metabolism ◽  
Glycogen Storage ◽  
Regulatory Mechanisms ◽  
Critical Importance ◽  
Energy Substrate ◽  
Substrate Metabolism ◽  
Atp Turnover ◽  
Energy Demands

The human body requires energy to function. Adenosine triphosphate (ATP) is the cellular currency for energy-requiring processes including mechanical work (i.e., exercise). ATP used by the cells is ultimately derived from the catabolism of energy substrate molecules—carbohydrates, fat, and protein. In prolonged moderate to high-intensity exercise, there is a delicate interplay between carbohydrate and fat metabolism, and this bioenergetic process is tightly regulated by numerous physiological, nutritional, and environmental factors such as exercise intensity and duration, body mass and feeding state. Carbohydrate metabolism is of critical importance during prolonged endurance-type exercise, reflecting the physiological need to regulate glucose homeostasis, assuring optimal glycogen storage, proper muscle fuelling, and delaying the onset of fatigue. Fat metabolism represents a sustainable source of energy to meet energy demands and preserve the ‘limited’ carbohydrate stores. Coordinated neural, hormonal and circulatory events occur during prolonged endurance-type exercise, facilitating the delivery of fatty acids from adipose tissue to the working muscle for oxidation. However, with increasing exercise intensity, fat oxidation declines and is unable to supply ATP at the rate of the exercise demand. Protein is considered a subsidiary source of energy supporting carbohydrates and fat metabolism, contributing to approximately 10% of total ATP turnover during prolonged endurance-type exercise. In this review we present an overview of substrate metabolism during prolonged endurance-type exercise and the regulatory mechanisms involved in ATP turnover to meet the energetic demands of exercise.

scholarly journals Neuromuscular Electrical Stimulation Improves Energy Substrate Metabolism and Survival in Mice With Acute Endotoxic Shock

Shock ◽  
2020 ◽  
Vol 53 (2) ◽  
pp. 236-241
Author(s):  
Takayuki Irahara ◽  
Norio Sato ◽  
Kosuke Otake ◽  
Satoru Murata ◽  
Kazuo Inoue ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Endotoxic Shock ◽  
Neuromuscular Electrical Stimulation ◽  
Energy Substrate ◽  
Substrate Metabolism

The Effect Of Taurine Supplementation On Substrate Metabolism During Fasting And Endurance Running In Mice

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 589-590
Author(s):  
Yumiko Takahashi ◽  
Tatsuya Hanawa ◽  
Eiki Urushibata ◽  
Hiroyuki Masuda ◽  
Tsuyoshi Masuda ◽  
...  
Keyword(s):  
Endurance Running ◽  
Taurine Supplementation ◽  
Substrate Metabolism

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Mapk Signaling ◽  
Redox Signaling ◽  
Defense System ◽  
High Fat ◽  
Substrate Metabolism ◽  
Endogenous Antioxidant

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.

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