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- Baar, K, et al.
(författare)
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Resistance exercise, muscle loading/unloading and the control of muscle mass
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 61-74
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Tidskriftsartikel (refereegranskat)abstract
- Muscle mass is determined by the difference between the rate of protein synthesis and degradation. If synthesis is greater than degradation, muscle mass will increase (hypertrophy) and when the reverse is true muscle mass will decrease (atrophy). Following resistance exercise/increased loading there is a transient increase in protein synthesis within muscle. This change in protein synthesis correlates with an increase in the activity of protein kinase B/Akt and mTOR (mammalian target of rapamycin). mTOR increases protein synthesis by increasing translation initiation and by inducing ribosomal biogenesis. By contrast, unloading or inactivity results in a decrease in protein synthesis and a significant increase in muscle protein breakdown. The decrease in synthesis is due in part to the inactivation of mTOR and therefore a decrease in translation initiation, but also to a decrease in the rate of translation elongation. The increase in degradation is the result of a co-ordinated response of the calpains, lysosomal proteases and the ATP-dependent ubiquitin-proteosome. Caspase 3 and the calpains act upstream of the ubiquitin–proteosome system to assist in the complete breakdown of the myofibrillar proteins. Two muscle specific E3 ubiquitin ligases, MuRF1 and MAFbx/atrogen-1, have been identified as key regulators of muscle atrophy. In this chapter, these pathways and how the balance between anabolism and catabolism is affected by loading and unloading will be discussed.
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| 2. |
- Frayn, KN, et al.
(författare)
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Fatty acid metabolism in adipose tissue, muscle and liver in health and disease
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 89-103
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Tidskriftsartikel (refereegranskat)abstract
- Fat is the largest energy reserve in mammals. Most tissues are involved in fatty acid metabolism, but three are quantitatively more important than others: adipose tissue, skeletal muscle and liver. Each of these tissues has a store of triacylglycerol that can be hydrolysed (mobilized) in a regulated way to release fatty acids. In the case of adipose tissue, these fatty acids may be released into the circulation for delivery to other tissues, whereas in muscle they are a substrate for oxidation and in liver they are a substrate for re-esterification within the endoplasmic reticulum to make triacylglycerol that will be secreted as very-low-density lipoprotein. These pathways are regulated, most clearly in the case of adipose tissue. Adipose tissue fat storage is stimulated, and fat mobilization suppressed, by insulin, leading to a drive to store energy in the fed state. Muscle fatty acid metabolism is more sensitive to physical activity, during which fatty acid utilization from extracellular and intracellular sources may increase enormously. The uptake of fat by the liver seems to depend mainly upon delivery in the plasma, but the secretion of very-low-density lipoprotein triacylglycerol is suppressed by insulin. There is clearly cooperation amongst the tissues, so that, for instance, adipose tissue fat mobilization increases to meet the demands of skeletal muscle during exercise. When triacylglycerol accumulates excessively in skeletal muscle and liver, sometimes called ectopic fat deposition, then the condition of insulin resistance arises. This may reflect a lack of exercise and an excess of fat intake.
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| 3. |
- Hawley, JA, et al.
(författare)
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Signalling mechanisms in skeletal muscle: role in substrate selection and muscle adaptation
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 1-12
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Tidskriftsartikel (refereegranskat)abstract
- Exercise produces a multitude of time- and intensity-dependent physiological, biochemical and molecular changes within skeletal muscle. With the onset of contractile activity, cytosolic and mitochondrial [Ca2+] levels are rapidly increased and, depending on the relative intensity of the exercise, metabolite concentrations change (i.e. increases in [ADP] and [AMP], decreases in muscle creatine phosphate and glycogen). These contraction-induced metabolic disturbances activate several key kinases and phosphatases involved in signal transduction. Important among these are the calcium dependent signalling pathways that respond to elevated Ca2+ concentrations (including Ca2+/calmodulin-dependent kinase, Ca2+-dependent protein kinase C and the Ca2+/calmodulin-dependent phosphatase calcineurin), the 5′-adenosine monophosphate-activated protein kinase, several of the mitogen-activated protein kinases and protein kinase B/Akt. The role of these signal transducers in the regulation of carbohydrate and fat metabolism in response to increased contractile activity has been the focus of intense research efforts during the past decade.
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