Oxygen Debt & Recovery | Energy Systems | Anatomy & Physiology Oxygen Debt & Recovery Oxygen Debt & Recovery What is it all about then? When you have a short intense burst of exercise such as sprinting you generate energy for this anaerobically or without oxygen. When you stop exercising you are still breathing heavily. This is your body taking in extra oxygen to 'repay' the oxygen debt. Well, that is the simple solution but there is a little more to it if you want to look a bit deeper. True, your body has worked anaerobically and will have produced energy without some of the oxygen it would normally have used performing low intensity exercise such as slow steady running. The difference between the oxygen the body required and what it actually managed to take in during the sudden sprint is called oxygen deficit. When you stop sprinting and start to recover you will actually need more oxygen to recover than your body would have liked to use had enough been available. This is called Excess Post Exercise Oxygen Consumption. So why does it take more oxygen to recover then? You needed to replace the oxygen the body needed but couldnt get (oxygen deficit). Breathing rate and heart rate are elevated (to remove CO2) and this needs more oxygen.

Body temperature and metabolic rate is increased and this needs more oxygen. Adrenaline and Noradrenaline are increased which increases oxygen consumption. So after exercise there are other factors causing an increase in oxygen needs as well as repaying the lack of oxygen during exercise. The chart below is often seen and shows how the amount of oxygen used by the body changes over time. At the beginning the body works anaerobically leaving an oxygen deficit. Over time the oxygen consumption levels out to a steady state. After exercise the oxygen is pain back (oxygen debt). Notice the area of oxygen debt is greater than the area of oxygen deficit for the reasons stated above. What has Lactic Acid got to do with it? Lactic acid is a by product of exercising without using oxygen (anaerobially). It is essential this is removed but it is not necessarily a waste product. It is recycled into other useful chemicals: During prolonged intensive exercise (e.g. 800m race) the heart may get half its energy from lactic acid. It is converted back to pyruvic acid and used as energy by the heart and other muscles.

It is thought that 70% of lactic acid produced is oxidised, 20% is converted to glucose (energy) in the liver. 10% is converted to protein. How long does it take to remove lactic acid? About 1 hour if cooling down with gentle exercise. It can take 2 hours or more if you dont warm down with gentle exercise. More Anatomy & Physiology Oxygen Debt Oxygen Debt During muscular exercise, blood vessels in muscles dilate and blood flow is increased in order to increase the available oxygen supply. Up to a point, the available oxygen is sufficient to meet the energy needs of the body. However, when muscular exertion is very great, oxygen cannot be supplied to muscle fibres fast enough, and the aerobic breakdown of pyruvic acid cannot produce all the ATP required for further muscle contraction. Lactic Acid During such periods, additional ATP is generated by anaerobic glycolysis. In the process, most of the pyruvic acid produced is converted to lactic acid . Although about 80% of the lactic acid diffuses from the skeletal muscles and is transported to the liver for conversion back to glucose or glycogen.

Oxygen Ultimately, once adequate oxygen is available, lactic acid must be catabolized completely into carbon dioxide and water. After exercise has stopped, extra oxygen is required to metabolize lactic acid; to replenish ATP, phosphocreatine, and glycogen; and to pay back any oxygen that has been borrowed from hemoglobin, myoglobin (an iron-containing substance similar to hemoglobin that is found in muscle fibres), air in the lungs, and body fluids. The additional oxygen that must be taken into the body after vigorous exercise to restore all systems to their normal states is called oxygen debt (Hill 1928) [1] . Eventually, muscle glycogen must also be restored. This is accomplished through diet and may take several days, depending on the intensity of exercise. The maximum rate of oxygen consumption during the aerobic catabolism of pyruvic acid is called "maximal oxygen uptake". It is determined by sex (higher in males), age (highest at about age 20) and size (increases with body size). Highly trained athletes can have maximal oxygen uptakes that are twice that of average people, probably owing to a combination of genetics and training.

As a result, they are capable of greater muscular activity without increasing their lactic acid production, and their oxygen debts are less. It is for these reasons that they do not become short of breath as readily as untrained individuals. Oxygen consumption following exercise After a strenuous exercise there are four tasks that need to be completed: Replenishment of ATP Replenishment of myoglobin with oxygen Replenishment of glycogen The need for oxygen to replenish ATP and remove lactic acid is referred to as the "Oxygen Debit" or "Excess Post-exercise Oxygen Consumption" (EPOC) - the total oxygen consumed after exercise in excess of a pre-exercise baseline level. In low intensity, primarily aerobic exercise, about one half of the total EPOC takes place within 30 seconds of stopping the exercise and complete recovery can be achieved within several minutes (oxygen uptake returns to the pre-exercise level). Recovery from more strenuous exercise, which is often accompanied by increase in blood lactate and body temperature, may require 24 hours or more before re-establishing the pre-exercise oxygen uptake. The amount of time will depend on the exercise intensity and duration.

The two major components of oxygen recovery are: Alactacid oxygen debit (fast component) the portion of oxygen required to synthesise and restore muscle phosphagen stores (ATP and PC) Lactacid oxygen debit (slow component) the portion of oxygen required to remove lactic acid from the muscle cells and blood The replenishment of muscle myoglobin with oxygen is normally completed within the time required to recover the Alactacid oxygen debit component. The replenishment of muscle and liver glycogen stores depends on the type of exercise: short distance, high intensity exercise (e.g. 800 metres) may take up to 2 or 3 hours and long endurance activities (e.g. marathon) may take several days. Replenishment of glycogen stores is most rapid during the first few hours following training and then can take several days to complete. Complete restoration of glycogen stores is accelerated with a high carbohydrate diet . References HILL, A.V (1928) The diffusion of oxygen and lactic acid through tissues. Proceedings of the Royal Society of London, 104 (728) DAVIS, B. et al. (2000) Physical Education and the Study of Sport. Fourth Edition.

London: Harcourt Publishers. p. 102 Related References The following references provide additional information on this topic: GAESSER, G. A. and BROOKS, G. A. (1983) Metabolic bases of excess post-exercise oxygen consumption: a review. Medicine and Science in Sports and Exercise, 16 (1), p. 29-43 VERMA, G. M. et al. (2014) Oxygen Debt and Rise of Blood Lactate During Submaximal Exercise in Relation to Physical Fitness and Endurance. Defence Science Journal, 19 (2), p. 115-120 DIMRI, G. P. and ARORA, B. S. (2014) Recovery Ventilation and Oxygen Debt-A Mathematical Model for the Prediction of Recovery Ventilation. Defence Science Journal, 32 (4), p. 285-292 Page Reference If you quote information from this page in your work then the reference for this page is: MACKENZIE, B. (2000) Oxygen Debt [WWW] Available from: [Accessed Understanding Aerobic Fitness. The Science Behind Aerobics.

THE SCIENCE BEHIND AEROBIC FITNESS VO2 MAX AND AEROBIC TRAINING The science of aerobic fitness is not difficult to understand, and it can help both trainers and exercisers make workout decisions. Muscles involved in exercise produce a significant amount of energy by combining foodstuffs with oxygen. As the oxygen needs of an individual’s exercising muscles increase, the lungs supply more oxygen to the blood. The heart, in turn, pumps more oxygenated blood to the working muscles. If a steady supply of oxygen is not produced to meet the energy demands of an activity, then an energy imbalance develops, blood lactate (LA) levels rise, blood pH levels decrease and fatigue occurs. An individual’s ability to engage in sustained high levels of physical activity without significant fatigue is determined by the body’s ability to deliver oxygenated blood to the muscles, and the ability of the muscles to extract the oxygen from the blood and utilize it for the production of energy in the form of adenosine triphosphate (ATP). A fundamental knowledge of how the body works during different types of exercise is necessary for understanding both the basic concepts of energy production and the physiological adjustments made by the body to meet the energy requirements of exercising skeletal muscles.

Basic concepts of energy and its sources The energy that is required for the normal functioning (muscle contraction, conduction of nervous impulses, hormone synthesis, etc.) of all living cells in the human body is produced by chemical reactions. These chemical reactions are either aerobic (occurring in the presence of oxygen) or anaerobic (without oxygen). An individual must continually produce energy or the various tissues and organs in the body will cease to function. It would be akin to pulling the plug of an appliance from the electrical outlet. To clarify the relationship between food consumption and energy production, individuals should think of the human body as a factory. The body must process different raw materials to make its final product — energy. This energy is used by every cell of the body. The three basic raw materials the body uses to produce energy are oxygen, carbohydrates (sugar and starches) and fat. These materials essentially are available in an unlimited supply. Since humans live in a veritable sea of oxygen, an adequate supply is generally not a problem. When individuals eat food, carbohydrates and fat are replenished. It is important to note that of the three calorie-providing nutrients, protein is the only one that the body does not usually use to produce energy under normal circumstances.

Proteins provide much of the structural basis for cells and are a major component of enzymes (substances responsible for controlling various chemical reactions at the cellular level). If more protein is consumed than the body needs, the excess will be converted into either fat or carbohydrate. Since the amount of energy required at rest is so small, the human body does not consume much oxygen. Accordingly, the resting energy needs are easily met by the aerobic system. During the initial stages of exercise, however, the situation changes. When the work demands placed on an individual’s body increase, the body needs extra energy immediately. Unfortunately, the rate of aerobic energy production is sluggish (i.e., oxygen must be breathed in, transferred from the lungs to the blood, carried to the heart and then pumped to the muscles where it actually is needed). Thus, a delay exists in the delivery of oxygen from the outside. If a sudden demand for more energy arises, an emergency back-up system must exist that will permit the body to function until the aerobic “assembly line” speeds up its production. The anaerobic energy system serves this function. Since a specific amount of work requires a given amount of energy, the body must always have an appropriate level of energy available to meet the demands placed on it.

The following descriptive timetable illustrates how energy is produced during the initial stages of exercise and during moderate intensity exercise: Since a specific amount of work requires a given amount of energy, the body must always have an appropriate level of energy available to meet the demands placed on it. The following descriptive timetable illustrates how energy is produced during the initial stages of exercise and during moderate intensity exercise: * When exercise first starts, only a limited supply of energy is present in the muscles for immediate use. During this phase, oxygen is not required. * Either glycogen stored in the muscle or glucose transported by the blood from the liver can be used without oxygen to provide a limited supply of energy. Lactic acid is the by-product of this anaerobic reaction. * Most of the lactic acid formed during an anaerobic reaction is released into the blood and transported to the liver, where it is converted back to glycogen and stored. * As additional oxygen becomes available, the aerobic system is used more and more. After a few minutes, the aerobic system is able to supply all the energy needed for relatively mild exercise. * At this time, liver glycogen is converted to glucose and released into the blood to provide fuel for both systems (aerobic and anaerobic).

* Finally, adipocytes (fat cells) release more and more fat, the preferred fuel for the aerobic system. If the exercise bout is relatively intense, other events take place to ensure that adequate amounts of energy are provided for the working skeletal muscles. The production of energy during exercise at relatively high levels of intensity occurs as follows: * The speed of the aerobic reactions increases to provide more energy. More carbon dioxide is also produced. * The faster anaerobic system supplies increasing amounts of energy as the exercise becomes more intense. The intensity of the muscle contractions causes a compression of the small arteries and, in effect, prevents oxygen, glucose or fat from entering the muscle cell. Thus, the majority of the carbohydrate needed comes from that which is already stored within the muscle itself. * Eventually, more lactic acid is formed, and increased amounts of lactic acid are released into the bloodstream. As lactic acid levels within the muscles increase, the efficiency of the aerobic chemical reactions are inhibited. When this occurs, inadequate amounts of energy can be produced aerobically. Accordingly, an individual has to either decrease the intensity level of the exercise bout (thereby reducing the amount of energy needed) or rely more heavily on the anaerobic system.

* Only a small percentage of lactic acid is transformed back into glycogen in the liver; the majority remains in the blood and the muscles. An individual’s body can accumulate and tolerate a limited amount of lactic acid. In all likelihood, it is the presence of lactic acid that causes excessive breathing while exercising, and causes feelings of fatigue and heaviness in the muscles, eventually forcing an individual to stop exercising. To better comprehend how the body works during different types of exercising, an individual should understand the relative importance of the anaerobic and aerobic systems for energy production. Figure 1 provides an approximate idea of the maximal amount of energy a well-trained individual can produce over time, and how that energy is produced. For comparison purposes, the energy required at rest is given a value of one. Although the stored energy can be used to perform a lot of work very rapidly, these stockpiles are essentially exhausted after 10 to 20 seconds. This factor partially explains why individuals cannot run 400 meters as fast as they can run 100 meters, or why weightlifters can lift more in one lift than they can in three lifts without a pause.

The production of energy anaerobically is relatively high (peaking in approximately 40 to 50 seconds), but it doesn’t last long because individuals are limited by the body’s relative intolerance of lactic acid. After 10 minutes, the amount of energy produced is very small. After five to six minutes of continuous exercise, the majority of energy the body requires has to be produced aerobically. The longer the duration of exercise, the greater the importance of the aerobic system. Anything over 10 minutes has to be performed aerobically, except for the occasional and brief increases in work output. Maximal oxygen uptake. If an individual increases the intensity level of exercise, a number of things will happen. Increases occur in heart rate, respiration and oxygen intake, as well as in the activity levels of other parts of the aerobic systems. A point occurs, however, beyond which oxygen intake cannot increase even though more work is being performed. At this point, the individual has reached a level that is commonly referred to as maximal oxygen uptake (VO2 max).

This measure is considered to be the best single indicator of aerobic fitness, since it involves the optimal ability of three major systems of the body (pulmonary, cardiovascular and muscular) to take in, transport and utilize oxygen. Thus, the higher an individual’s level of maximal oxygen uptake, the greater the level of physical work that can be performed. Energy production and exercise intensity. If the amount of work being performed is progressively increased along the continuum to levels of maximum capacity, the ability to produce energy aerobically will not be able to completely match the energy demands. For most sedentary individuals, this point occurs at a work output requiring approximately half of their VO2 max. In other words, below 50 percent of VO2 max, the “slower” aerobic system can provide all the energy a person needs. Of course, the human body does not switch over to the anaerobic system all at once, but gradually shifts gears to produce energy at a faster rate. A level between 50 and 70 percent of VO2 max represents a transition phase for most people.

Above 70 percent of VO2 max, the aerobic system does not produce energy fast enough, thereby causing individuals to rely more and more on their anaerobic systems. Another important factor that must be considered when examining the relationship between the production of energy and exercise intensity is lactic acid. Figure 2 presents a schematic diagram of the level of lactic acid in the blood relative to the intensity of exercise. The level of lactic acid is a rough indictor of the degree to which the anaerobic mechanism is being used. As Figure 2 illustrates, lactic acid will begin to rise slowly around 50 percent of VO2 max. Because the increase is not too great, an individual’s body can compensate up to 70 percent of maximum with little trouble. Beyond 70 percent of VO2 max, however, as the buildup of lactic acid becomes progressively more dramatic, an individual will start to get “winded.” This explains why a person can run at a certain pace (50 to 60 percent of VO2 max) with no problem, but will become exhausted relatively quickly after trying to run faster (80 to 90 percent of VO2 max).

Depending on the intensity and duration levels of the activity, it is important to note that many physical activities require both aerobic and anaerobic production of energy. For example, soccer players who often are required to run for extended periods (i.e., 20 to 30 minutes nonstop) perform aerobic exercise. Obviously, if the activity did not depend on the aerobic system for energy, they would not be able to run for nearly as long. However, when a game situation requires players to sprint after the ball (high-intensity intervals which exceed 70 percent of VO2 max), these athletes are forced to draw upon their emergency (anaerobic) sources. In other words, whether an activity involves the body’s aerobic system or its anaerobic system depends on the demands placed on it by the activity at a particular point in time. Anaerobic chemical reactions are primarily used in high-intensity exercise of relatively brief duration (e.g., sprinting short distances or heavy weight lifting), while aerobic chemical reactions are primarily involved in low-intensity, long-duration exercise activities such as walking, cycling, stair climbing, etc. Physiological adjustments to exercise The aerobic metabolism of fats and carbohydrates is the preferred and more efficient mode of energy production.

This method, however, is limited by the body’s ability to transport and deliver oxygen to, and the utilization of oxygen by, the working muscles. Several physiological adjustments are made during exercise. The primary objective of these adjustments is to provide an exercising muscle with oxygenated blood that can be used for the production of energy. An individual’s endurance capabilities will be greatly influenced by the magnitude and direction of these changes. Academy Of Art University. Cardiac output. The amount of blood pumped per minute by the heart is explained by the term cardiac output (Q). This measure is indicative of the rate of oxygen delivery to the peripheral tissues (e.g., exercising skeletal muscles). Cardiac output, which is the product of heart rate (HR) and stroke volume (SV), increases linearly as a function of work rate. At rest, Q is roughly four to five liters per minute, but can rise to 20 to 25 liters per minute during exercise in young, healthy adults. This exercise-induced increase of Q is due to alterations in both HR and SV. Heart rate. Heart rate, one of the two primary determinants of Q, also rises linearly with work rate.

The gradual withdrawal of vagal (parasympathetic nervous system) influences and the progressive increases in sympathetic nerve activity which occur during exercise, are largely responsible for the observed increases in HR. At or near VO2 max, HR begins to level off and is referred to as maximal heart rate. The equation “220 minus your age” (expressed in whole years) provides a rough estimate of an individual’s maximal heart rate (with a standard deviation of 10 to 12 beats per minute). As the equation implies, an individual’s maximal heart rate declines with age. Stroke volume. Stroke volume (SV) is the other primary determinant of Q, and represents the amount of blood ejected from the heart during each beat. Unlike HR, SV does not increase linearly with work rate. SV increases progressively until a work rate equivalent to approximately 50 to 75 percent VO2 max is reached. Thereafter, continued increases in work rate cause little or no increase in SV. Exercise-induced increases in SV are believed to be the result of factors that are both intrinsic and extrinsic to the heart.

According to the Frank-Starling law, a greater stretch is placed on the muscle fibers of the heart (due to a greater venous return of blood to the heart during physical activity or exercise), resulting in a more forceful contraction of those fibers and, consequently, a greater SV. Extrinsic factors such as increased nervous (sympathetic) or endocrine (release of adrenal hormones epinephrine and norepinephrine) stimulation to the myocardium can also contribute to the increased SV that occurs during exercise. Blood pressure. Systolic blood pressure (SBP) represents the force developed by the heart during ventricular contraction. SBP increases linearly with work rate. In healthy adults, SBP tends not to exceed 220 mm Hg at maximal exercise levels. Diastolic blood pressure (DBP), on the other hand, is indicative of the pressure in the arterial system during ventricular relaxation and reflects peripheral resistance to blood flow. DBP changes little from rest to maximal levels of exercise. Therefore, an individual’s pulse pressure (the algebraic difference between SBP and DBP) increases in direct proportion to the intensity of exercise. Pulse pressure is important because it reflects the driving force for blood flow in the arteries.

Total peripheral resistance. The sum of all the forces that oppose blood flow in the systemic circulation is expressed by the term total peripheral resistance (TPR). Numerous factors can affect TPR, including blood viscosity, vessel length, hydrostatic pressure and vessel diameter. Vessel diameter is by far the most important of these factors, since TPR is inversely proportional to the fourth power of the radius of the vessel. If one vessel has half the radius of another, and if all other factors are equal, the larger vessel would have 16 times (24) less resistance than the smaller vessel. As a result, 16 times more blood would flow through the larger vessel at the same pressure. This factor has important implications for exercise, since certain organs require more blood flow than others during physical activity. During exercise, resistance in the vessels supplying the muscles and skin is decreased. As a result, blood flow to these parts of the body is enhanced. On the other hand, resistance in those vessels that supply the visceral organs of the body (e.g., the liver, gastrointestinal tract, kidneys) is increased, thereby reducing the level of blood flow to those areas of the body.

These changes are almost entirely due to intrinsic factors (i.e., the increased metabolic demands of the muscles and the requirement of blood flow to the skin to facilitate heat dissipation). The TPR tends to decrease during progressive dynamic exercise because vasodilation occurring in the muscles and skin seem to override the vasoconstriction that is occurring in the visceral organs. Arteriovenous oxygen difference. The arteriovenous oxygen difference is the difference between the oxygen contents of the arterial blood and mixed venous blood. It is a reflection of the amount of oxygen extracted from the blood by the muscles. Obviously, the more oxygen that is actually extracted from the blood, the more oxygen there is for aerobic energy production. The oxygen content of venous blood can be reduced to one-half to one-third of an individual’s resting levels by the exercising muscles. Such a reduction indicates that the muscles are extracting a much higher proportion of the oxygen delivered to them in the arterial blood.

(It should be noted that approximately 85 percent of the oxygen in arterial blood can be extracted during maximal exercise.) Aerobic conditioning results in alterations (e.g., increased capillary density, increased mitochodrial size and density, increased myoglobin content and enhanced activity of oxidative enzymes) that can enhance the ability of skeletal muscle to extract oxygen. A matter of chemistry By definition, all physical activity involves movement. In turn, sound exercise is often defined as purposeful movement. Because exercise involves the body’s muscular system, energy is required. The source of this energy for muscular actions is a series of chemical reactions which involve varying amounts of oxygen and foodstuffs. Knowing how the body responds to the energy demands attendant to exercise — particularly how the cardiovascular and muscular systems adjust to supply oxygen to exercising muscles — can affect exercisers in a variety of positive ways. For example, such an understanding can enable an individual to be better prepared to select an appropriate exercise mode or to manipulate a particular exercise prescription to achieve a specific personal goal. At the least, such knowledge will provide a clearer insight into why a given exercise bout may vary (i.e., more challenging, less challenging, etc.) from another.

Ultimately, a potential byproduct of such insight will be to provide a better exercise environment for individuals. REFERENCES Astrand, P.O., & K. Rodahl. Textbook of Work Physiology, 3rd ed. New York, NY: McGraw-Hill, 1986. Brooks, G.A., & T.D. Fahey. Exercise Physiology: Human Bioenergetics and Its Applications. New York, NY: John Wiley & Sons, 1984. Fox, E.L., R.D. Bowers & M.L. Foss. The Physiological Basis of Physical Education and Athletics, 4th ed. Philadelphia, Penn.: W. B. Saunders Company, 1988. Kenneth W. L., R.H. Humphrey & C.X. Bryant. ACSM’s Guidelines for Exercise Testing and Prescription, 5th ed. Philadelphia, Penn.: Williams & Wilkins, 1995. Lamb, D.R. Physiology of Exercise: Responses & Adaptations, 2nd ed. New York, NY: Macmillan, 1984. Peterson, J.A., & C.X. Bryant.

The Fitness Handbook, 2nd ed. Champaign, Ill.: Sagamore Publishing Co. Inc., 1995. Skinner, J.S. Functional effects of physical activity. In Zeigler, E.F. (Ed.), Physical Education and Sport: An Introduction. Philadelphia, Penn.: Lea & Febiger, 1982. Skinner, J.S., S.P. Noeldner & J.S. O’Connor. The development and maintenance of physical fitness. In Ryan, A.J., & F.D. Allman (Eds.), Sports Medicine, 2nd ed. New York, NY: Academic Press 1989. Wilmore, J.H., & D.L. Costill. Training for Sport and Activity, 3rd ed. Dubuque, IA: Wm. C. Brown Publishers, 1988. Figure 1. Relative importance of various energy-producing systems over time. Used with permission from Body Energy by James S. Skinner, 1981 (Anderson World Inc., Mountain View, Calif.). Figure 2. Blood lactic acid related to exercise intensity. Used with permission from Body Energy by James S.

Skinner, 1981 (Anderson World Inc., Mountain View, Calif.). James Peterson, Ph.D., FACSM, is a sports medicine consultant, fellow of the American College of Sports Medicine, a former faculty member at the United States Military Academy and a former director of sports medicine for StairMaster Sports/Medical Products Inc. A&#38P-Chapter 9 - Muscles and Muscle Tissur Types of Muscle Tissue Skeletal muscle is associated with the bony skeleton, and consists of large cells that bear striations and are controlled voluntarily. Cardiac muscle occurs only in the heart, and consists of small cells that are striated and under involuntary control. Smooth muscle is found in the walls of hollow organs, and consists of small elongated cells that are not striated and are under involuntary control. Functions of Muscles Muscles produce movement by acting on the bones of the skeleton, pumping blood, or propelling substances throughout hollow organ systems. Muscles aid in maintaining posture by adjusting the position of the body with respect to gravity. Muscles stabilize joints by exerting tension around the joint. Muscles generate heat as a function of their cellular metabolic processes.

Functional Characteristics of Muscle Tissue Excitability, or irritability, is the ability to receive and respond to a stimulus. Contractility is the ability to contract forcibly when stimulated. Extensibility is the ability to be stretched. Elasticity is the ability to resume the cells' original length once stretched.

Skeletal Muscle Anatomy - Gross Anatomy of Muscle Organ Origin, belly and insertion endomysium surrounds each muscle fiber The deep fascia is interconnected to the subcutaneous fascia and the subserous fascia The deep fascia connects to bones via tendons & aponeuroses Fasica surrounds of muscles forming compartments Muscles attach: Directly - epimysium of the muscle is fused to the periosteum of a bone Indirectly - connective tissue wrappings extend beyond the muscle as a tendon or aponeurosis Muscle Classification: Functional Groups Skeletal muscles work together or in opposition Muscles only pull (never push) As muscles shorten, the insertion generally moves toward the origin Whatever a muscle (or group of muscles) does, another muscle (or group) &#34undoes" Prime movers - provide the major force for producing a specific movement Antagonists - oppose or reverse a particular movement Synergists - add force to a movement or reduce undesirable or unnecessary movement Fixators - synergists that immobilize a bone or muscle&#39s origin Parallel - fascicles run parallel to the long axis of the muscle Fusiform - spindle-shaped muscles Pennate - short fascicles that attach obliquely to a central tendon running the

 length of the muscle Convergent - fascicles converge from a broad origin to a single tendon insertion Circular - fascicles are arranged in concentric rings Location of muscle - bone or body region associated with the muscle Shape of muscle - e.g., the deltoid muscle (deltoid = triangle) Relative size - e.g., maximus (largest), minimus (smallest), longus (long) Direction of fibers - e.g., rectus (fibers run straight), transversus, and oblique (fibers run at angles to an imaginary defined axis) Number of origins - e.g., biceps (two origins) and triceps (three origins) Location of attachments - named according to point of origin or insertion Action - e.g., flexor or extensor, as in the names of muscles that flex or extend, respectively Microscopic Anatomy of a Muscle Fiber Each fiber is a long, cylindrical cell with multiple nuclei just beneath the sarcolemma (plasma membrane - supported by dystrophin) Sarcoplasma - specialties Where is the binding site for the cross bridge?

How is covered up during relaxation ? How is it exposed for contraction? When does myosin bind to actin? Binding sites exposed (Ca++ present) Crossbridges form when myosin heads attach using ATP energy Myosin crossbridges bends pulling on actin using energy from ATP Crossbridges detach when ATPase hydrolyses new ATP Relaxation : Ca++ are pumped back into _______. 1. At the axon ending a nerve impulse causes the release of ____________ from the synaptic _________. (Acetylcholine is a _______________) 2. Acetylcholine crosses the _______ _____ and binds to ___ _________ of the _____ ___ _____ on the sarcolemma. 3. This opens _____ channels and ____ enter the muscle cell. 4. Na+ enters the cell and the membrane becomes __________ generating an ______ _________ 5. The __- _______ carries the action potential through out the cell causing the release of ______from the _________ ___________. 6. Which then stimulates the _______ _______ action. Meanwhile back at the junction............................. 7. The membrane is repolarized to accept another stimulus (refractory period) K+ leaves the cel lfor a quick repoarlization.

Cholinesterase decomposes ________and removes it from _________ Na+-K+ pump returns ions to _______ membrane potential conditions. 8. In this process where are the 3 places ATP is necessary? Why does the nerve impulse cross the synapse? Outside of the cell membrane the electrical charge is positive Inside the the cell the membrane has a negative charge.

The predominant extracellular ion is Na+ The predominant intracellular ion is K+ The sarcolemma is relatively impermeable to both ions All the above facts establish a - mV resting membrane potential Initially, this is a local electrical event called end plate potential (synapse) Later, it ignites an action potential that spreads in all directions across the sarcolemma and down the T-Tubules Motor Unit : Nerve-Muscle Functional Unit A motor unit is a motor neuron and all the muscle fibers it supplies The number of muscle fibers per motor unit can vary from four to several hundred Muscle fibers from a motor unit are spread throughout the muscle; therefore, contraction of a single motor unit causes weak contraction of the entire muscle Muscles that control fine movements (fingers, eyes) have small motor units Large weight-bearing muscles (thighs, hips) have large motor units Muscle Twitch A muscle twitch is the response of a muscle to a single, brief threshold stimulus The three phases of a muscle twitch are: Latent period - first few milliseconds after stimulation when excitation-contraction coupling is taking place Period of contraction - cross bridges actively form and the muscle shortens Period of relaxation - Ca++ is reabsorbed into the SR, and muscle tension goes

 to zero Variations in the degree of muscle contraction Required for proper control of skeletal movement Responses are graded by: More rapidly delivered stimuli result in incomplete tetanus If stimuli are given quickly enough, complete tetanus results Changing the strength of the stimulus Threshold stimulus - the stimulus strength at which the first observable muscle contraction occurs Beyond threshold, muscle contracts more vigorously as stimulus strength is increased Force of contraction is precisely controlled by multiple motor unit summation This phenomenon, called recruitment, brings more and more muscle fibers into play Starting length of the muscle - optimal length-tension relationship The relative size of the muscle - the bulkier the muscle, the greater its strength Contraction of Skeletal Muscle (Organ Level) The two types of muscle contractions are: Isometric contraction - Tension increases to the muscle&#39s capacity, but the muscle neither shortens nor lengthens Isotonic contraction - the muscle changes in length (decreasing the angle of the joint) and moves the load Muscle tone: Is the constant, slightly contracted state of all muscles, which does not produce active movements Keeps the muscles firm, healthy, and ready to respond to stimulus Spinal reflexes account for muscle tone by: Activating one motor unit and then another Responding to activation of stretch receptors in muscles and

 tendons Treppe: The Staircase Effect Increased contraction in response to multiple stimuli of the same strength Contractions increase because: There is increasing availability of Ca2+ in the sarcoplasm Muscle enzyme systems become more efficient because heat is increased as muscle contracts Muscle Metabolism: Energy for Contraction The partial catabolism of glucose to generate ATP occurs in anaerobic cellular respiration.

This system can provide enough energy for about 30-40 seconds of maximal muscle activity (e.g., 300-meter race). Muscular activity lasting more than 30 seconds depends increasingly on aerobic cellular respiration (reactions requiring oxygen). This system of ATP production involves the complete oxidation of glucose via cellular respiration (biological oxidation). Heat Production Only 40% of the energy released in muscle activity is useful as work The remaining 60% is given off as heat Dangerous heat levels are prevented by radiation of heat from the skin and sweating Excess ATP within resting muscle used to form creatine phosphate Creatine phosphate 3-6 times more plentiful than ATP within muscle Its quick breakdown provides energy for creation of ATP Sustains maximal contraction for 15 sec (used for 100 meter dash).

Athletes tried creatine supplementation gain muscle mass but shut down bodies own synthesis (safety?) ATP produced from glucose breakdown into pyruvic acid during glycolysis if no O2 present pyruvic converted to lactic acid which diffuses into the blood Glycolysis can continue anaerobically to provide ATP for 30 to 40 seconds of maximal activity (200 meter race) Aerobic Respiration ATP for any activity lasting over 30 seconds if sufficient oxygen is available, pyruvic acid enters the mitochondria to generate ATP, water and heat fatty acids and amino acids can also be used by the mitochondria Provides 90% of ATP energy if activity lasts more than 10 minutes Muscle Fatigue - Inability to contract after prolonged activity Factors that contribute to fatigue central fatigue is feeling of tiredness and a desire to stop (protective mechanism) insufficient release of acetylcholine from motor neurons depletion of creatine phosphate decline of Ca+2 within the sarcoplasm insufficient oxygen or glycogen buildup of lactic acid and ADP Oxygen Debt - the extra amount of O2 needed for a muscle to return to a resting state: Oxygen reserves must be replenished Lactic acid must be converted to pyruvic acid

 Glycogen stores must be replaced Muscle Fatigue and Oxygen Debt Muscle fatigue - the muscle is in a state of physiological inability to contract Muscle fatigue occurs when: ATP production fails to keep pace with ATP use There is a relative deficit of ATP, causing contractures Lactic acid accumulates in the muscle Ionic imbalances are present - Na+-K+ pumps cannot restore ionic balances quickly enough SR is damaged and Ca2+ regulation is disrupted Intense exercise produces rapid muscle fatigue (with rapid recovery) Low-intensity exercise produces slow-developing fatigue Oxygen Debt - the extra amount of O2 needed for a muscle to return to a resting state: Oxygen reserves must be replenished Lactic acid must be converted to pyruvic acid Glycogen stores must be replaced Determined by the two following factors: Contraction rate depends on speed in which ATPases split ATP Anaerobic (Glycolytic) or Aerobic (oxidative) Slow Twitch Oxidative Fibers Lack coarse connective tissue sheaths of skeletal muscle, but have endomysium Organized into two layers (longitudinal and circular) of closely apposed fibers Found in walls of hollow organs (except the heart) When longitudinal layer contracts, the organ dilates & contracts When the circular layer

 contracts, the organ elongates Peristalsis - alternating contractions and relaxations of smooth muscles that mix and squeeze substances through the lumen of hollow organs Innervation of Smooth Muscle Smooth muscle lacks neuromuscular junctions Innervating nerves have bulbous swellings called varicosities Varicosities release neurotransmitters into wide synaptic clefts called diffuse junctions They contract in unison, reflecting their electrical coupling with gap junctions Action potentials are transmitted from cell to cell Characteristics of Smooth Muscle Unique characteristics of smooth muscle include: Smooth muscle tone Smooth muscle exhibits stress-relaxation response in which: Smooth muscle responds to stretch only briefly, and then adapts to its new length The new length, however, retains its ability to contract This enables organs such as the stomach and bladder to temporarily store contents Smooth muscle has good regenerative ability This is shown by estrogen&#39s effect on the uterus At puberty, estrogen stimulates the synthesis of more smooth muscle, causing the uterus to grow to adult size During pregnancy, estrogen stimulates uterine growth to accommodate the increasing size of the growing fetus Autonomic nervous system and endocrine systems are major controls Neurotransmitters and hormones?

Spasm = involuntary contraction of single muscle Cramp = a painful spasm Tic = involuntary twitching of muscles normally under voluntary control--eyelid or facial muscles Tremor = rhythmic, involuntary contraction of opposing muscle groups Fasciculation = involuntary, brief twitch of a motor unit visible under the skin Atrophy caused by disuse (disuse atrophy) or severing of the nerve supply (denervation atrophy) the transition to connective tissue can not be reversed Hypertrophy increase in the diameter of muscle fibers resulting from very forceful, repetitive muscular activity and an increase in myofibrils, SR & mitochondria Exercise-Induced Muscle Damage Intense exercise can cause muscle damage electron micrographs reveal torn sarcolemmas, damaged myofibrils an disrupted Z discs increased blood levels of myoglobin & creatine phosphate found only inside muscle cells Delayed onset muscle soreness 12 to 48 Hours after strenuous exercise stiffness, tenderness and swelling due to microscopic cell damage Rigor mortis is a state of muscular rigidity that begins 3-4 hours after death and lasts about 24 hours After death, Ca+2 ions leak out of the SR and allow myosin heads to bind to actin Since ATP

 synthesis has ceased, crossbridges cannot detach from actin until proteolytic enzymes begin to digest the decomposing cells.

Regeneration of Muscle Skeletal muscle fibers cannot divide after 1st year growth is enlargement of existing cells repair satellite cells & bone marrow produce some new cells if not enough numbers---fibrosis occurs most often Cardiac muscle fibers cannot divide or regenerate all healing is done by fibrosis (scar formation) Smooth muscle fibers (regeneration is possible) cells can grow in size (hypertrophy) some cells (uterus) can divide (hyperplasia) new fibers can form from stem cells in BV walls Aging and Muscle Tissue Skeletal muscle starts to be replaced by fat beginning at 30 &#34use it or lose it" Why does lactic acid build up in muscles? And why does it cause soreness? - Scientific American Scientific American Advertisement | Report Ad Stephen M. Roth, a professor in the department of kinesiology at the University of Maryland, explains. As our bodies perform strenuous exercise, we begin to breathe faster as we attempt to shuttle more oxygen to our working muscles. The body prefers to generate most of its energy using aerobic methods, meaning with oxygen. Some circumstances, however, --such as evading the historical saber tooth tiger or lifting heavy weights--require energy production faster than our bodies can adequately deliver oxygen.

In those cases, the working muscles generate energy anaerobically. This energy comes from glucose through a process called glycolysis, in which glucose is broken down or metabolized into a substance called pyruvate through a series of steps. When the body has plenty of oxygen, pyruvate is shuttled to an aerobic pathway to be further broken down for more energy. But when oxygen is limited, the body temporarily converts pyruvate into a substance called lactate, which allows glucose breakdown--and thus energy production--to continue. The working muscle cells can continue this type of anaerobic energy production at high rates for one to three minutes, during which time lactate can accumulate to high levels. A side effect of high lactate levels is an increase in the acidity of the muscle cells, along with disruptions of other metabolites. The same metabolic pathways that permit the breakdown of glucose to energy perform poorly in this acidic environment. On the surface, it seems counterproductive that a working muscle would produce something that would slow its capacity for more work. In reality, this is a natural defense mechanism for the body; it prevents permanent damage during extreme exertion by slowing the key systems needed to maintain muscle contraction.

Once the body slows down, oxygen becomes available and lactate reverts back to pyruvate, allowing continued aerobic metabolism and energy for the body¿s recovery from the strenuous event. Contrary to popular opinion, lactate or, as it is often called, lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise. Rather, the production of lactate and other metabolites during extreme exertion results in the burning sensation often felt in active muscles, though which exact metabolites are involved remains unclear. This often painful sensation also gets us to stop overworking the body, thus forcing a recovery period in which the body clears the lactate and other metabolites. Researchers who have examined lactate levels right after exercise found little correlation with the level of muscle soreness felt a few days later. This delayed-onset muscle soreness, or DOMS as it is called by exercise physiologists, is characterized by sometimes severe muscle tenderness as well as loss of strength and range of motion, usually reaching a peak 24 to 72 hours after the extreme exercise event.

Though the precise cause of DOMS is still unknown, most research points to actual muscle cell damage and an elevated release of various metabolites into the tissue surrounding the muscle cells. These responses to extreme exercise result in an inflammatory-repair response, leading to swelling and soreness that peaks a day or two after the event and resolves a few days later, depending on the severity of the damage. In fact, the type of muscle contraction appears to be a key factor in the development of DOMS. When a muscle lengthens against a load--imagine your flexed arms attempting to catch a thousand pound weight--the muscle contraction is said to be eccentric. In other words, the muscle is actively contracting, attempting to shorten its length, but it is failing. These eccentric contractions have been shown to result in more muscle cell damage than is seen with typical concentric contractions, in which a muscle successfully shortens during contraction against a load. Thus, exercises that involve many eccentric contractions, such as downhill running, will result in the most severe DOMS, even without any noticeable burning sensations in the muscles during the event.

Given that delayed-onset muscle soreness in response to extreme exercise is so common, exercise physiologists are actively researching the potential role for anti-inflammatory drugs and other supplements in the prevention and treatment of such muscle soreness, but no conclusive recommendations are currently available. Although anti-inflammatory drugs do appear to reduce the muscle soreness--a good thing--they may slow the ability of the muscle to repair the damage, which may have negative consequences for muscle function in the weeks following the strenuous event.

Question: What is the substance produced by hard exercise and oxygen debt, causing stiffness in the muscles?
Answer: Lactic acid