Understanding Metabolism and Skeletal Muscle Function

Introduction

Physical activity means any physical motion that originates from the skeletal muscles and leads to energy consuming that override its consuming in rest. Metabolism includes 2 different types of processes, 'Constructional' processes include cell building and energy storage, 'Destructive' processes involving breaking energy molecules. The plurality of calories used by the body are burned during physical activity, In fact, 65% to 75% of calories burned in one day are burned through metabolism to preserve the continuity of the body's vital processes. Physical activity contributes up to 30% of the total calories burned daily and is still considered one of the best ways to enhance the metabolic rate.

As age increases, the metabolic rate slows and muscles weaken, and the metabolic rate begins to decline as early as the 20s. The severe diet may be counterproductive, affecting both metabolic rate and severity. Studies have shown that people who eat less than 1200 calories per day are likely to become metabolized at a slower rate over time making burning calories and losing weight more difficult for them.

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Even periods between meals can slow the metabolic rate.The thyroid regulates metabolism and hormone production, thyroid disorders cause metabolic problems. If the hypothalamic gland (hypothyroidism) produces less than normal hormones, slowing down metabolism, this leads to weight gain. If the gland is overactive (hyperthyroidism), it accelerates metabolism, often leading to weight loss. in general, there are 3 stages of metabolism :

1. hydrolysis: polysaccharides, lipid, protein is broken down to glucose, amino acid, FA and glycerol
2. preparatory stage: monosaccharides , FA, glycerol AA inter in the metabolic pathway to form energy and stored as ATP
3. oxiditve stage: carb , lipid, protein from acetyl CoA and in presence of oxygen acetyl co A is oxidized to co2 and h2o by TCA cycle ( Randle, 1998) (1)

Importance of Skeletal Muscle

Provides system shape, support, stability, and movement to the body.

For example, bones protect the internal organs of the body and support body weight, which serves as the main repository of calcium and phosphorus, and contains ingredients for the production of blood cells. Muscles of the musculoskeletal system keep bones in place and play a role in the movement of bones, allowing for various movements such as standing, walking, and running. To allow movement, the joints and muscle connect the various bones by the connective tissue such as ligaments and ligaments. The presence of cartilage prevents bones from direct contact with each other (Skeletal muscle can use fatty acids, ketone bodies, or glucose as fuel, according to the degree of the activity of a muscle ) .(Noland, 2009) (2)

Skeletal muscle metabolism during rest and fed state

Depended on levels of glucose, which is provide the energy to muscle. The excess glucose converted to glycogen by glycogenesis the main fuel is fatty acid which is come from adipose tissue and ketone bodies from the liver These are oxidized to produce acetyl-CoA, which enters the citric acid cycle for oxidation and produce CO2 and the electron transfer to O2 and ATP formed by oxidative phosphorylation, cause increase in protein synthesis and During the fed state, the adipose tissue can mutate glucose (through pyruvate and acetyl-CoA) to fatty acids, then convert the fatty acids to Triglycerides and store them (Koves, 2005) (3)

Metabolism during Starvation

In fasting state, The low blood-sugar level cause decreased secretion of insulin and increased secretion of glucagon. -the glycogen store exhausted and the glycogenolysis decreased. So, gluconeogenesis in the liver increases for a synthesis of glucose from amino acids that come from protein breakdown

After hours, Due to low blood glucose level, as we said before, the pancreas secretes glucagon to stimulate. Glycogen is broken down (glycogenolysis), so glucose released into the bloodstream to maintain the blood glucose level then The protein breakdown to amino acids

Due to the decreasing of gluconeogenesis from amino acids, the stored TGs in adipose tissues are hydrolyzed by lipolysis to glycerol and fatty acids and released to the bloodstream

Free fatty acids enter the skeletal muscles and use as energy source.

The excess acetyl CoA from β-oxidation in liver mutated to ketone bodies to use it as fuel. (Muoio, 2010) (4)

Metabolism of skeletal muscle During Exercise

• The first source of ATP will be Anaerobic glycolysis (lactate) --> generates AMP --> Glycogenolysis and glycolysis are activated together because of a sensitivity to AMP
• For Short duration exercise: ATP stored ATP is formed from creatine phosphate and ADP (direct phosphorylation )then glycogen stored in muscle is breakdown to glucose which is oxidized to generate ATP (anaerobic pathway ) (called Cori cycle).
• And for Prolonged duration exercise: ATP is generated by the breakdown of several nutrient energy fuels by the aerobic pathway. uses blood glucose and fatty acids with ketone bodies. The glucose is phosphorylated, then degraded by glycolysis to pyruvate, which is converted to acetyl-CoA
• Epinephrine stimulates the release of glucose from liver glycogen to blood and the breakdown of glycogen in muscle tissue.
• Also, alanine is formed in active muscle by the transamination of pyruvate and converted into glucose by the liver. (Dube, 2008) (5)(6)

References:

1. Randle, P. J. (1998) Regulatory Interactions Between Lipids and Carbohydrates: The Glucose-Fatty Acid Cycle After 35 Years. Diabetes Metab. Rev. 14, 263 – 283
2. Noland, R. C., etal. (2009) Carnitine Insufficiency Caused by Aging and Overnutrition Compromises 5. Mitochondrial Performance and Metabolic Control. J. Biol. Chem. 284, 22840 – 22852.
3. Koves, T. R., etal. (2005). PeroxisomeProliferator-activated Receptor-gamma Co-activator 1alpha-mediated Metabolic Remodeling of Skeletal Myocytes Mimics Exercise Training and Reverses Lipid-induced Mitochondrial Inefficiency. J. Biol. Chem. 280, 33588 – 33598.
4. Muoio, D. M. (2010) Intramuscular Triacylglycerol and Insulin Resistance: Guilty as Charged or Wrongly Accused? Biochim. Biophys. Acta 1801, 281 – 288.
5. Dube, J. J., etal. (2008) Exercise-induced Alterations in Intramyocellular Lipids and Insulin Resistance: The Athlete’s Paradox Revisited. Am. J. Physiol. Endocrinol. Metab. 294, E882 – E888.
6. Koves, T. R., etal. (2008) Mitochondrial Overload and Incomplete Fatty Acid Oxidation Contribute to Skeletal Muscle Insulin Resistance. Cell. Metab. 7, 45 – 56.
7. Thyfault, J. P., etal. (2010) Metabolic Profiling of Muscle Contraction in Lean Compared to Obese Rodents. Am. J. Physiol. Regul. Integr. Comp. Physiol. Epub ahead of print.