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Muscle Metabolism
thick filament consisting of 300 separate but attached myosin molecules. Interestingly, rigor mortis after death is the result of “running out of ATP molecules,” which are necessary to have actin and myosin separate from each other. This leads to permanent contraction of the muscles.
MUSCLE METABOLISM
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ATP is necessary for muscle contraction and must be available in large numbers for the muscle to function. ATP is necessary for both the actin-myosin contraction and for the active transport of calcium across the sarcoplasmic reticulum. There isn’t much ATP stored in muscle cells—only enough for about one second of a muscle contraction. For this reason, there are multiple mitochondria inside the muscle cell—each of which is a powerhouse for making new ATP molecules.
These are essentially three mechanisms for ATP synthesis in the muscle cell. These are creatine phosphate metabolism, anaerobic metabolism (called glycolysis), and aerobic respiration (in the mitochondria).
Creatine phosphate is a molecule that stores energy inside its phosphate bonds. When the muscle is resting, ATP transfers its energy to creatine in order to make creatine phosphate and ADP. This is the immediate muscle reserve for ATP. It’s the front line for making ATP molecules when the muscle contracts. The creatine phosphate transfers its stored energy back to ADP to make creatine and ATP through the action of the enzyme called creatine kinase. This gives only about 15 seconds of muscle energy.
When ATP is depleted, the muscles will undergo glycolysis, which is an anerobic process, meaning it is independent of oxygen. It is not as quick as creatine phosphate metabolism and involves glucose metabolizing into two pyruvate molecules, leading to the production of two ATP molecules. When oxygen levels are low, the pyruvate becomes lactic acid as an end-product.
If oxygen is available, the pyruvate will go on to the mitochondria to make many more molecules of ATP. Glycolysis can be sustained for one minute so it is useful in facilitating short bursts of energy output. About 95 percent of ATP for the exercising muscle is provided through the activity of aerobic respiration in mitochondria. This is
much more efficient and produces 36 ATP molecules per molecule of glucose. It requires a steady input of oxygen, stored in the myoglobin in the muscle cell, allowing for the greatest efficiency of muscle contractions. Figure 4 shows the sources of ATP in the muscle cell:
Aerobic training will increase the efficiency of the circulatory system so that oxygen can be supplied to muscle for longer periods of time. Muscle fatigue happens when the muscle can no longer contract, even after receiving the proper signals from the central nervous system. No one knows exactly what happens to induce muscle fatigue. It probably has something to do with ATP reserves being low as well as increased lactic acid buildup, which may lower the pH of the inside of the cell, affecting the ability of enzymes to function in the muscle cells. Long periods of time in which there is sustained exercise may result in damage to the sarcoplasmic reticulum so that it cannot properly regulate calcium release as would be necessary for muscle contraction.
Because muscles need to function effectively for a period of time, there is a lot of phosphocreatine and a large amount of muscle glycogen in order to fuel the muscle cells so they can participate in ATP synthesis. As mentioned, ATP energy can come from phosphocreatine. Other sources of ATP energy are muscle glycogen (which is the storage form of glucose), nutrients from the circulation, such as fatty acids and glucose, and amino acids (which can come from the circulation as well as inside the muscle fibers themselves).
Intense activity of muscle tissue results in an oxygen debt, which involves the amount of oxygen necessary to compensate for ATP produced without oxygen during exercise. Oxygen is required to restore ATP and creatine phosphate levels, to convert lactic acid
back into pyruvate, and to convert lactic acid into glucose or glycogen in the liver. This leads to increased breath rate before and immediately after exercise. This increase in oxygen intake by the body will persist until the oxygen debt has been paid.
Ultimately, the motor neuron will stop releasing acetylcholine into the synaptic cleft at the neuromuscular junction. This results in repolarization of the muscle, which closes the calcium ion gates in the sarcoplasmic reticulum; ATP-dependent pumps will move the calcium back into the sarcoplasmic reticulum. Actin-binding sites on the actin molecule get reshielded and the muscle is allowed to relax again.
The number of actual skeletal muscle fibers in a given muscle is determined genetically and will not change over a person’s lifetime. This means that muscle strength is related specifically to the number of sarcomeres and myofibrils in each muscle fiber. Hormones and anabolic steroids acting on the muscle can increase the production of sarcomeres and myofibrils per muscle fiber, leading to hypertrophy of the muscles. Atrophy of the muscles happens when the number of sarcomeres and myofibrils decreases, while the actual number of muscle fibers remains the same.
The relaxation of muscle so that it can return to its original length is referred to as the muscle’s elasticity. Muscle also has extensibility, which is the ability to stretch and extend when provoked. Finally, it can have contractility, which is what allows the muscle to shorten from its relaxed state.
There are differences between skeletal muscle and the other muscle types in the human body. Skeletal muscle involves regular arrangement of myofibrils and muscle cells with muscle cells being long and multinucleated. Cardiac muscle fibers have one to two nuclei per muscle fiber cell and there is electrical connection between these muscle cells so that they contract as a unit by forming a syncytium.
Smooth muscle cells are irregularly-aligned and there is just one nucleus per cell. Smooth muscle is called “smooth” because it is not striated. It is the smooth muscles that control the blood pressure and contractility of the blood vessels. Central smooth muscle cells in the major blood vessels will contract to increase the blood pressure, while peripheral blood vessel smooth muscle will relax in order to increase the blood
