Therapeutic Exercise

Martin D. Hoffman

William J. Kraemer

Daniel A. Judelson

The term therapeutic relates to the treatment of disease or physical disorder, and exercise refers to bodily exertion for the sake of training or improvement of health. This chapter on therapeutic exercise therefore addresses the use of activities requiring physical exertion in the prevention, treatment, and rehabilitation of illness and disabling conditions. The pertinent exercises considered in this chapter include those to develop endurance, strength, flexibility, and proprioception.

The use of therapeutic exercise in the treatment of injuries is not a new concept. Hippocrates (460 to 370 B.C.) reportedly advocated exercise as an important factor in the healing of injured ligaments, and the Hindus and Chinese used therapeutic exercise in the treatment of athletic injuries as early as 1,000 B.C. Today, the various types of exercise probably account for the most commonly used treatments in the field of physical medicine and rehabilitation. Therefore, it is important for clinicians in the field to have a thorough understanding of this area.

The concepts forming the basis for therapeutic exercise come from studies in basic physiologic science and applied exercise physiology. In recent years, epidemiologic investigations have provided additional insight into the importance of exercise in prevention of disease. Consequently, much of this chapter is devoted to this basic information that provides the foundation for the clinical use of exercise.

METABOLIC FUNDAMENTALS

Part of adaptation to regular exercise is the development of the energy systems most involved in the type of training being used. Therefore, to condition an individual optimally for participation in a particular activity or sport, an exercise program should be designed to increase the physiologic capacity of the energy systems most important to that activity. For this reason, it is valuable to have an understanding of how energy is derived for muscular contraction.

The immediate usable form of chemical energy for all muscular contraction is adenosine triphosphate (ATP). ATP is supplied to the muscle through three systems: (a) the adenosine triphosphate-creatine phosphate (ATP-CP) system, (b) the anaerobic glycolysis system, and (c) the aerobic system. The relative utilization of the three systems depends on the intensity and duration of the exercise (Table 61-1) (1).

Anaerobic Metabolism

Anaerobic metabolism refers to a series of chemical reactions that do not require the presence of oxygen. Two of the systems that supply energy for muscular contraction are anaerobic.

The ATP-CP System

ATP and CP are high-energy phosphagen compounds stored within the muscle and ready for immediate use. The breakdown of ATP produces adenosine diphosphate (ADP), inorganic phosphate, and energy used in muscular contraction. CP is broken down to create energy that is used to reform ATP.

This system provides an immediate source of energy for the muscle and has a large power capacity. In other words, a large amount of energy per unit time can be supplied through this system. However, because of the small stores of ATP and CP, the total capacity for work with the ATP-CP system is limited. In fact, the energy resources from the ATP-CP system will be exhausted in 30 seconds or less during an all-out bout of exercise (2,3).

Anaerobic Glycolysis System

Glycolysis refers to a series of reactions resulting in the breakdown of carbohydrate into pyruvate or lactate. Anaerobic glycolysis means that this breakdown of carbohydrate is performed in the absence of oxygen.

During maximal exercise that lasts 1 to 2 minutes, lactic acid produced by the skeletal muscles accumulates in the muscles and blood. This is accompanied by an increase in the proton release causing acidosis. Interestingly, lactate acts as a solid indicator of the changes in the acid-base balance but is not the cause of the acidosis. In fact, lactate acts as a buffer for the acidosis that would otherwise have a more rapid onset and produce fatigue even more quickly (4). At any extent, when the concentration of lactic acid is high enough, nerve endings are stimulated, resulting in the sensation of pain. In addition, the lactic acid within the muscle cell inhibits the production of more ATP (5) and the binding of calcium to troponin (6), which is part of the series of events leading to muscle contraction. Therefore, the amount of energy obtained from the anaerobic glycolysis system is limited by these effects. Nevertheless, the anaerobic glycolysis system is extremely important because it can provide a rapid supply of energy.

TABLE 61.1 Characteristics of the Three Metabolic Systems

Metabolic System		Substrate (Fuel)	Oxygen Required	Speed of ATP Mobilization	Total ATP Production Capacity
Anaerobic metabolism
	ATP—CP system	Stored phosphagens	No	Very fast	Very limited
	Glycolysis	Glycogen/glucose	No	Fast	Limited
Aerobic metabolism		Glycogen/glucose, fats	Yes	Slow	Virtually unlimited
Adapted from Fox EL, Mathews DK. The Physiological Basis of Physical Education and Athletics. Philadelphia, PA: WB Saunders; 1981.

Aerobic Metabolism

In the presence of oxygen, glycolysis produces pyruvate, which is further metabolized through the tricarboxylic acid (TCA) cycle (also known as the Krebs or citric acid cycle) and electron transport system to yield carbon dioxide, water, and energy. Relative to anaerobic glycolysis, the energy produced from a given amount of carbohydrate is about 13 times greater through aerobic metabolism. Furthermore, there are no fatiguing or painful byproducts through aerobic metabolism, and not only carbohydrate but fats and proteins may be metabolized aerobically. Although the ability to metabolize fat means that this system provides a virtually unlimited source of energy, aerobic metabolism provides energy at the slowest rate of the three energy systems.

The Energy Continuum

All three energy systems supply a portion of energy to the body at all times. However, one energy system may predominate during a particular activity. Which energy systems are predominant during a given activity depends on the rate of energy (power) requirement during the activity (Fig. 61-1) (7). In activities performed at maximal intensity for only a few seconds, most of the ATP is supplied by the ATP-CP system. Activities of lower intensity, such as those at a maximal effort that can be sustained for 1 to 2 minutes, primarily rely on the anaerobic glycolysis system. Longer-duration, lower-intensity activities that may last several minutes or hours are supplied almost entirely through aerobic metabolism.

FIGURE 61-1. Relative importance of the different metabolic systems as a function of exercise intensity. (Adapted from Sahlin K. Metabolic changes limiting muscle performance. In: Saltin B, ed. Biochemistry of Exercise VI. Champaign, IL: Human Kinetics; 1986;323-343.)

During a graded exercise test, blood lactate concentration remains relatively constant until a critical exercise intensity is reached, at which time lactate begins to accumulate in the blood (Fig. 61-2) (8). This accumulation does not indicate the onset of anaerobic glycolysis; rather, it is the result of the rate of lactate production exceeding its rate of removal.

Fuel Utilization

The three fuels that may be used to generate ATP for muscular contraction are carbohydrate, fat, and protein. These fuels differ in the amount of oxygen required for metabolization to the end products of carbon dioxide and water (Table 61-2). Thus, the amount of carbon dioxide produced relative to the amount of oxygen used (the respiratory quotient [RQ]) differs among fuels. During exercise, this ratio is referred to as the respiratory exchange ratio (RER) rather than the RQ. This distinction is made because the rate of carbon dioxide exhalation increases out of proportion to metabolism whenever metabolic acidosis exists, as occurs at high exercise intensities. Metabolic acidosis is buffered in the blood by the bicarbonate buffering system with nonmetabolic carbon dioxide produced as a byproduct and in the muscle cell by the phosphate system. Therefore, at maximal exertion during dynamic exercise, an RER greater than 1.1 is expected. In fact, an RER greater than 1.1 is frequently used as a criterion to assess whether maximal exertion was achieved with graded dynamic exercise testing.

Because fat serves as the primary form of stored energy in the body, it is fortunate that it has a caloric density that is much higher than carbohydrate (9.3 kcal/g, compared with 4.1 kcal/g). However, slightly less energy (4.7 kcal/L, compared with 5.0 kcal/L) is produced from every liter of oxygen when fat is used than when carbohydrate is used. Amino acids can also be metabolized to produce energy for muscular actions, although this contribution is generally 10% or less.

The fuel used during exercise is influenced by several factors, including the exercise intensity and duration, pre-exercise
diet, mode of exercise, and level of fitness. As the intensity of the exercise is increased, the predominant fuel source shifts toward carbohydrate. This is partly because ATP production shifts toward anaerobic metabolism during high-intensity exercise and carbohydrate is the only fuel available for anaerobic glycolysis. Carbohydrates are made available to the contracting muscle through mobilization of muscle and liver glycogen stores as well as through ingested carbohydrates that are circulating in the bloodstream.

FIGURE 61-2. Schematic demonstration of the determination of maximal oxygen uptake. Left: Oxygen uptake increases during 5-minute exercise stages on a bicycle ergometer at different workloads (noted within the shadowed area). Right: Oxygen uptake at each workload measured after 5 minutes, plotted in relation to workload. Note that there was no additional increase in oxygen uptake between the 250- and the 300-W workloads. Maximal oxygen uptake is 3.5 L/min. Blood lactic acid concentrations across each workload are also demonstrated. (With permission from Astrand PO, Rodahl K. Textbook of Work Physiology: Physiological Basis of Exercise. 3rd ed. New York: McGraw-Hill; 1986.)

Exercise duration also has an effect on the fuel utilization pattern. Fat usage gradually increases during long bouts of exercise. Free fatty acids are made available to the contracting muscle through lipolysis of triglycerides within extramuscular (e.g., adipose) and muscular stores. The type of diet consumed before exercise affects fuel utilization during exercise. During prolonged exercise, carbohydrate is more likely to be used when one has been eating a diet rich in carbohydrates (Fig. 61-3) (9).

TABLE 61.2 Characteristics of the Different Metabolic Substrates

Fuel	Energy Content (kcal/g)	Oxygen Equivalent (kcal/L)	Respirator Quotient (RQ)
Carbohydrate	4.1	5.0	1.00
Fat	9.3	4.7	0.70
Protein	4.3	4.4	0.80

The mode of exercise can also influence the fuel source used during exercise. Exercise that localizes the work to a small muscle mass will tend to use a greater proportion of carbohydrate as fuel.

Finally, training status can affect the composition of the fuel used during exercise. Adaptations to endurance training increase the ability of muscles to use free fatty acids as a fuel while sparing glycogen (10,11).

FIGURE 61-3. Effect of three different diets on fuel source used during running. Vertical bars represent the points at which exhaustion occurred. (Based on data from Christensen EH, Hansen O. Arbeitsfahigkeit und Ermahrung. Skand Arch Physiol. 1939;8:160-175.)

Oxygen Uptake

Oxygen uptake ([V with dot above]O₂) is a measure of the rate of oxygen utilization for the production of energy. This measure is typically reported in units of liters per minute (L/min) or milliliters per kilogram body mass per minute (mL/kg/min). The latter provides for better comparison among individuals. Another commonly used measurement unit for oxygen uptake is the metabolic equivalent (MET). One MET is equal to 3.5 mL/kg/min, which is approximately the resting metabolic rate. Maximal oxygen uptake ([V with dot above]O_2max) or maximal METs represents the maximal rate at which an individual can use oxygen. Classically, [V with dot above]O_2max is defined as the rate of oxygen uptake at which no further increase occurs despite an increase in dynamic work rate by the individual (see Fig. 61-2). The term peak [V with dot above]O₂ is often referred to when it is recognized that the highest attainable [V with dot above]O₂ is may not have been reached by the individual because of the mode of exercise being used, the testing protocol, physical limitations other than cardiorespiratory, or inadequate motivation. Clinically, assessment of peak or maximal [V with dot above]O₂ (mL/kg/min or MET units) is useful in assessing cardiorespiratory fitness as well as in counseling patients on tolerance for undertaking home, leisure, or vocational activities within a reasonable work intensity.

FIGURE 61-4. Structural and functional subunits of skeletal muscle. (With permission from Lamb DR. Physiology of Exercise: Responses and Adaptations. 2nd ed. New York: Macmillan; 1984.)

MUSCLE PHYSIOLOGY

Structure and Function of Muscle

Morphology

Skeletal muscle is made up of structural and functional subunits as displayed in Figure 61-4 (12). The largest subunit of a muscle, from a morphologic standpoint, is the fascicle. The fascicle contains anywhere from one to hundreds of muscle fibers, the individual muscle cells. At each of these structural levels is a different connective-tissue covering.

Myofibrils are found within the muscle cells. The smallest functional subunit of the myofibril is the sarcomere. Sarcomeres are aligned end to end to form a myofibril. Myofibrils contain two basic protein filaments, a thicker one, called myosin, and a thinner one, called actin. These proteins are arranged in such a way as to give skeletal muscle its striated appearance. Sarcomeres run from one Z-line to the next Z-line.

FIGURE 61-5. Postulated mechanism of crossbridge formation and cycling by actin and myosin filaments. The head of the myosin filament is stippled and forms the crossbridge between the two filaments. Active sites on the actin (thin) filament are outlined by broken circles. 1: No bonds between filaments. 2: Initial attachment of myosin head to one of the active sites on the actin filament. This attachment takes place only in the presence of Ca²⁺ ions. 3: Formation of strong actin-myosin bond. This process causes a conformational change in the angle of the myosin head, which produces a relative movement of actin and myosin filaments across one another. ADP and phosphate ions are lost from the myosin. 4: If ATP is available, the actin-myosin bond can be broken. Subsequent hydrolysis of the ATP by the myosin ATPase returns the cycle to stage 1. If no ATP is available, the actin-myosin bond remains intact, as in muscular rigor. (From Gordon AM. Muscle. In: Ruch T, Patton H, eds. Physiology and Biophysics. Vol. IV. Philadelphia, PA: WB Saunder; 1982:170-260. Reprinted by permission of WB Saunders Co.)

Sliding-Filament Theory

The primary function of muscle is to shorten and develop tension. The sliding-filament theory (Fig. 61-5) (13) provides an explanation of how muscle fibers shorten and so develop tension.

On stimulation from the motor axon, calcium ions are released from storage in the sarcoplasmic reticulum, exposing active binding sites on the actin and allowing actin-myosin cross-bridge formation. Once the actin-myosin bonds are formed, a conformational change in the angle of the myosin head occurs, causing the actin filaments to be pulled over the myosin filaments and to shorten the sarcomere.

For more shortening to occur, ATP is required to break the actin-myosin bond and allow binding of myosin to another actin site closer to the Z-line. The conformation change of the myosin head that is essentially the enzyme myosin ATPase then occurs, resulting in further shortening.

Relaxation of the muscle occurs when stimulation ends. This triggers the active pumping of calcium back into the sarcoplasmic reticulum. The result is a loss of active binding sites on the actin, so that actin-myosin crossbridges are broken, and the muscle relaxes.

Mechanical Model

Figure 61-6 shows a useful model to understand the mechanical properties of muscles (14). This model consists of the
contractile element with both series and parallel elastic elements. The contractile element actively generates force and represents the interaction between actin and myosin filaments. The elastic elements are purely passive components acting as mechanical springs. The series elastic element represents the tendinous insertions of muscle, and the parallel elastic element represents the connective tissue surrounding the various subunits of the muscle.

FIGURE 61-6. Mechanical model of muscle consisting of a contractile element and two elastic elements. (From Roberts TDM. Neurophysiology of Postural Mechanics. London: Butterworth; 1978.)

TABLE 61.3 Muscle Fiber Type Continuum Using the Myosin ATPase Classification System

Type I	IC	IIC	IIAC	IIA	IIAX	Type IIX
Highly oxidative						Least oxidative
High endurance						High force
High mitochondrial density						Lower mitochondrial density
Low contractile speed						High contractile speed

Muscle Fiber Types

Skeletal muscles contain a mixture of muscle fiber types that can be distinguished by their physical and biochemical characteristics. At present, the most often-used classification system is the myosin ATPase histochemical profile for muscle. This array of fiber types allows classification of muscle fibers along a continuum from the most oxidative fiber to the least oxidative phenotype (Table 61-3). Muscle fiber types can be identified using histochemical or gel electrophoresis methods. Histochemical staining of the ATPases is used to separate fibers into type I (slow twitch), type IIA (fast twitch), and type IIB (fast twitch) forms. However, the work of Smerdu et al. (15) indicates that type IIB fibers contain type IIX myosin heavy chain (gel electrophoresis fiber typing). For the sake of continuity, and to decrease confusion on this point, most journals and scientists have now adopted the term IIX to designate IIB fibers. While type IIB muscle fibers are found in humans, they are very rare and are part of the rodent fiber array. Thus, a continuum of muscle fibers exists from the most oxidative type I to the least oxidative type IIX as shown in Table 61-3. A motor unit typically contains type I or type II muscle fibers, thereby giving it specific characteristics important to recruitment order and “size principle” whereby motor units are typically recruited from the low threshold to high threshold motor units that is related to the force production required by the external demands of the task.

Recognition that there may be differences in muscles dates back to observations that fowl has meat that is “red” and “white.” It has since been learned that the different properties of muscles extend beyond the muscle fiber to the level of the motor unit. Based on contraction speed following a stimulus to the nerve axon, two main categories of motor units can be distinguished—fast units and slow units. Peak tension and relaxation are achieved more rapidly for fast units than for slow units (Fig. 61-7). Units with a fast contraction time are composed of muscle fibers with relatively large fiber diameters and are innervated by large, fast-conducting motor neurons. These units also have a larger number of muscle fibers. Compared with the slow units, the fast units produce higher tensions. These fast units are further subdivided into fast-fatiguable (FF) units, which fatigue relatively easily, and fast-fatigue-resistant (FR) units, which have a high resistance to fatigue, similar to the slow units.

Although the number of fibers per unit and the fiber diameter are larger with fast units, these factors do not fully explain the differences in force production of fast and slow units. It is thought that there are also differences in the mechanism of force production within the fibrils (16).

All fibers from a given motor unit have the same histochemical characteristics. Slow units innervate type I slow twitch fibers and these fibers are characterized by high activities of succinic dehydrogenase and nicotinamide adenine dinucleotide dehydrogenase, enzymes involved in the major pathways for oxidative metabolism. The type I fibers are also richly supplied by capillaries. As a result, these fibers are well suited for performance of low-intensity, long-duration activities.

Those fibers innervated by fast motor units (fast-twitch or type II fibers) have a high activity of myofibrillar ATPase, the enzyme that breaks down ATP to release energy for contraction. They also have a high capacity for anaerobic metabolism as demonstrated by the high levels of glycogen and
phosphorylase. Phosphorylase is an enzyme that is involved in the breakdown of glycogen. As a result, these fibers are suited for performance of high-intensity, short-duration work. Hybrid subtypes exist linking the major fibers of I and IA and IX on a continuum from type I to IC to type IIC, IIAC to IIA to IIAX to IIX. With activation of the motor units, a transition of the ATPase isoforms will move from the type IIX to the type IIA subtype (17). The continuum of hybrids fibers goes from the most oxidative isoform type I to the least oxidative isoform type IIX. However, again, when a motor unit is activated, oxidative processes increase and exercise training will even leave type IIX fibers that remain with higher concentrations of oxidative enzymes. Thus, the transition to the primary fiber type as visualized by the histochemical staining is related to the oxidative status of the fiber while it keeps its characteristic size and function. Capillary development also follows this transition to greater density as oxidative needs increase. However, due to the fact that type I motor units are orderly recruited first in almost all activities and are involved for the repetitive endurance activities, their oxidative, mitochondrial, and capillary profiles are always greater than type II or fast motor units.

FIGURE 61-7. Schematic representation of rate of tension generation and force production with different fiber types. The speed of contraction and force are greatest for type II fibers.

Again, there is a continuum of myosin ATPase within muscle fibers ranging from that found in the least oxidative type IIX fibers and extending to the most oxidative fiber, the type I fiber. It has not been shown that any type of voluntary physical training can change fiber types from type II to type I, or vice versa. In reality, a continuum of fibers, including hybrids expressing more than one type of myosin simultaneously, exists in humans, extending through types IIX, IIAX, IIA, IIAC, IIC, IC, and I. The difference in protein composition within human muscle fibers, compared with the less complex situation in animals, appears to be due to a more intricate regulation by the nervous system to achieve functional changes at the level of the contractile unit.

The advantage of having different types of muscle fibers within a muscle is that the characteristics of the muscle are extended beyond that of any single fiber type. It is the proportion of muscle fiber types within a muscle that gives muscles the properties that make them suitable for different functions.

Factors Affecting Muscle Function

A number of factors affect muscle function. It is well recognized that these factors include the state of training and degree of fatigue of the muscle. The specific adaptations of muscle to exercise training and the relationship of fatigue with muscle function are discussed in later sections. In this section, the interaction of other muscular, neural, and mechanical factors affecting muscle function is discussed. The reader is also referred to Chapter 3: Assessment of Human Muscle Function.

Muscular Factors

Cross-Sectional Area

Muscle size is one of the most obvious factors affecting strength. In isolated as well as intact muscles, maximal strength is related to the cross-sectional area of the muscle. This relationship probably is related to the greater quantities of actin and myosin, and therefore greater numbers of crossbridges that can be activated to produce force when the muscle is larger. Muscles can produce 10 to 20 N/cm² of cross-sectional area (18).

Numerous studies have demonstrated changes in muscle cross-sectional area that occur in conjunction with strength changes produced by resistance training or detraining. Nevertheless, strength and muscle cross-sectional area do not change in parallel. It is clear that the cross-sectional area of the muscle does not fully account for differences in strength among individuals.

Muscle Fiber Type

As described earlier, the maximal force and the power generation of a muscle are related to the percentage of fast-twitch fibers. In other words, muscle that has a high percentage of fast-twitch fibers will generate a greater maximal force than the same-size muscle with a lower percentage of these fibers (19).

Neural Factors

Motor Learning and Recruitment

The importance of neural factors in affecting muscular strength has been recognized through the dissociation between changes in strength and muscle size during a strength-training program. The gains in strength during the first few weeks of such training occur without any change in muscle size (20,21). The general consensus is that these early changes reflect neural adaptations that may include improved muscle activation and improved task performance from motor learning and coordination (22).

Inhibitory Reflexes

Neural factors may also play a role in inhibition of muscle contraction. A protective reflex mechanism is thought to operate through the Golgi tendon organs that may be of particular importance when large amounts of force are being generated (23,24). Reflex inhibition of muscle contraction can also result through other sensory nerve endings. For instance, it has been demonstrated that quadriceps muscle inhibition is mediated through afferent activity of intracapsular receptors (25). It is also likely that muscle contraction is inhibited through pain reflexes (26, 27, 28).

Protective reflex mechanisms are also thought to be involved in what has been called the bilateral deficit. The force developed during bilateral contractions of a given muscle group is less than the sum of the forces developed by each limb independently (29,30). Reduced motor unit stimulation is associated with this bilateral deficit (31).

It may be possible to reduce the influence of protective reflexes through strength training. Hypnosis was shown to increase maximal force produced during forearm flexion by 17% among non-resistance-trained individuals, whereas there was no significant change in a strength-trained individual (32). It was concluded that strength training may induce an
inhibition of the protective reflex mechanisms. Furthermore, the bilateral deficit has been shown to be reduced through training with bilateral contractions (33).

FIGURE 61-8. Schematic relationship between maximal muscular force and velocity of movement.

The protective reflexes may be reduced in another way. Strength of a muscle group is increased when its activity is immediately preceded by contraction of the antagonist muscle group (34). The precontraction is thought to reduce the neural protective mechanism, allowing a greater force production.

Mechanical Factors

Force-Velocity Relationship

The maximum force a muscle can exert depends on the speed at which it is contracting. The maximal isometric force of a muscle is always greater than the force that can be exerted during shortening, and the maximal force exerted during lengthening is always greater than that exerted during isometric contraction. This relationship is displayed in Figure 61-8.

It is thought that the shape of the force-velocity curve is explained on the basis of the sliding-filament theory of muscle contraction (16). During a maximal isometric contraction, all crossbridges are formed. However, during shortening, there is an increase in the rate of detachment of crossbridges and an increase in the number of attached crossbridges that exert negative force. The result is a decrease in the total force exerted when the muscle is shortening. During lengthening contractions, the rate of detachment of crossbridges is slower than during a shortening contraction at the same velocity. The effect is that crossbridges are forcibly detached, and so a greater force is produced compared with shortening contractions.

Positive Versus Negative Work

Besides the difference in maximal force production through concentric and eccentric contractions, there is a difference in energy cost for performing work through concentric (positive work) and eccentric (negative work) contractions. The energy cost for negative work is dramatically less than that for performing the same amount of positive work (Fig. 61-9) (35,36). This phenomenon is thought to be linked to the requirement for ATP for the detachment and resetting of the crossbridges in concentric work but not in eccentric work (Fig. 61-10) (37).

FIGURE 61-9. Demonstration of the difference in energy cost between positive and negative work. The two subjects pedaled coupled bicycles with one pedaling forward (performing positive work) and the other providing the resistance as the cranks rotated backward (performing an equal amount of negative work). Graph inset shows the differences in energy costs across the examined power outputs. (From Cavanagh PR, Kram R. Mechanical and muscular factors affecting the efficiency of human movement. Med Sci Sports Exerc. 1985;17:326-331. Reprinted by permission of Williams & Wilkins. Figure based on data from Abbott BC, Bigland B, Ritchie JM. The physiological cost of negative work. J Physiol. 1952;117:380-390.)

Short-Range Stiffness

When a maximally activated muscle is forcibly lengthened, the force produced by the muscle is greater than that produced isometrically (see Fig. 61-8). However, the situation may be different when the muscle is contracting submaximally. Forced lengthening of a partially contracted muscle results in an initial resistance greater than that produced isometrically, but the resistance may then fall below that produced isometrically (38). This phenomenon is referred to as short-range stiffness and is thought to be accounted for as follows. The rapid rise in tension at the beginning of forced lengthening results from the stretch of attached actin-myosin crossbridges. The stiffness of the muscle is very high while the crossbridges are still attached. However, once the crossbridges begin to dissociate, it is thought that the formation of new crossbridges occurs more slowly in a partially activated muscle, and so the number of attached crossbridges and the force produced are diminished.

Short-range stiffness is important in the initial part of the response of a limb to a disturbing force. For instance, partial contraction of agonist and antagonist muscles about a joint
increases the mechanical stiffness of the joint and can provide considerable resistance to perturbating forces such as those that might be encountered while walking across a crowded room with a full glass. This same phenomenon may also play a role in protecting joints from traumatic forces.

FIGURE 61-10. Schematic comparison of the crossbridge formation and cycling during concentric and eccentric work. ATP is required for the detachment and resetting of the crossbridges in concentric work but not in eccentric work. (From Cavanagh PR, Kram R. Mechanical and muscular factors affecting the efficiency of human movement. Med Sci Sports Exerc. 1985;17:326-331. Reprinted by permission of Williams & Wilkins. Figure based on data from White DCS. Muscle mechanics. In: Alexander RMcN, Goldspeak G, eds. Mechanics and Energetics of Animal Locomotion. London: Chapman and Hall; 1977:23-56.)

Muscle Orientation and Attachment

The distance a tendon is inserted from the axis of rotation affects the torque generated by that muscle. For a given tension developed by a muscle, a tendon insertion farther from the center of rotation will allow greater torque production, although angular range will be reduced (Fig. 61-11). This anatomic effect allows some muscles to be more suited for production of large forces than others. Small anatomic variations may also account for some of the performance differences among individuals.

Length-Tension Relationship

The tension produced by a muscle is affected not only by the contractile elements but also by passive stretch of the elastic elements (see Fig. 61-6). When relaxed muscle is passively stretched beyond its resting length, tension progressively develops (Fig. 61-12) (39). Maximal contraction of the muscle at different lengths yields another length-tension curve. Subtraction of the passive tension from the total tension of the contracting muscle yields a closer representation of the actual tension produced by the contractile elements. The greatest tension generated by the contractile mechanism is at the resting length of the muscle, and the greatest total tension is at a length slightly longer than resting length.

FIGURE 61-11. Schematic representation of the effect of tendon insertion site on excursion. The excursion from a more proximally inserted muscle may be double that of a more distally inserted muscle for the same amount of shortening. Whereas a tendon insertion closer to the center of rotation will allow greater excursion, torque production will be reduced for a given tension developed in the muscle.

The influence of length on the force produced by the contractile mechanism is related to the way in which the actin and
myosin filaments interact at the sarcomere level. Figure 61-13 shows the length-tension relationship for a single muscle fiber and the overlap of the actin and myosin filaments in a single sarcomere (40). As the overlap between actin and myosin increases, so does the tension production. Maximal tension is developed at lengths yielding maximal contact of actin and myosin filaments. As the sarcomere length decreases further, the actin filaments begin to overlap. It is believed that this interferes with crossbridge formation and causes a decline in tension development. Variations among sarcomeres and muscle fibers cause the length-tension curve to be more rounded for a whole muscle.

FIGURE 61-12. Length-tension diagram for passive stretch of an unstimulated muscle and total tension when the muscle is maximally stimulated. Active tension resulting solely from muscular contraction is obtained by subtracting the passive-stretch curve from the total-tension curve. Normal resting length is 100%. (Redrawn from Schottelius BA, Senay LC. Effect of stimulation-length sequence on shape of length-tension diagram. Am J Physiol. 1956;186:127-130.)

FIGURE 61-13. Relationship between sarcomere length and tension generation. The amount of overlap between actin and myosin filaments within each sarcomere is shown. The length of each sarcomere is given above, and the tension for each condition is shown below. Maximal tension is produced when there is the greatest overlap between filaments (points 2 and 3). Tension drops if the overlap is less or if the actin filaments contact each other. (Adapted from Gordon AM, Huxley AF, Julian FJ. The variation in isometric tension with sarcomere length in vertebrate muscle fibres. J Physiol. 1966;184:170-192.)

An example of the effect of muscle length on force production is apparent by the position of the wrist during a handgrip. While gripping, the wrist is maintained in extension by contraction of the wrist extensor muscles of the forearm. This allows the finger flexor muscles to be at a more optimal part of the length-tension curve. In this way, a stronger handgrip is produced.

Leverage Effect

The leverage effect relates to the mechanical advantage offered by the angle of tendon insertion. The torque produced by a muscle is dependent on the sine of the insertion angle. When the insertion angle is 90 degrees, the torque production is greatest for a given tension in the muscle.

Torque production is the net result of the length-tension relationship and the leverage effect. As a result of the force-velocity relationship, the torque production for a given movement is also dependent on the velocity of movement. Figure 61-14 displays an isokinetic torque curve for a
movement commonly tested in the clinical setting (41). This figure demonstrates how maximal torque varies across movements when angular velocity is constant.

FIGURE 61-14. Real-time display of gravity-corrected torque and angular position during a knee extension-flexion isokinetic test. (From Baltzopoulos V, Brodie DA. Isokinetic dynamometry: applications and limitations. Sports Med. 1989;8:101-116.)

FIGURE 61-15. Optimal phenomenon in bicycling. Both seat height and pedaling frequency show an optimal point at which energy cost for producing a given power output is minimized. Maximal power output is also related to seat height by a parabolic curve. (From Cavanagh PR, Kram R. Mechanical and muscular factors affecting the efficiency of human movement. Med Sci Sports Exerc. 1985;17:326-331. Reprinted by permission of Williams & Wilkins. Figure based on data from Nordeen-Snyder K. The effect of bicycle seat height variation upon oxygen consumption and lower limb kinematics. Med Sci Sports. 1977;9:113-117; Hamley EJ, Thomas V. Physiological and postural factors in the calibration of the bicycle ergometer. J Physiol. 1967;191:55P-57P; Hagberg JM, Mullin JP, Giese MD, et al. Effect of pedaling rate on submaximal exercise responses of competitive cyclists. J Appl Physiol. 1981;51:447-451.)

Force Transmission

One way in which muscle force transmission is thought to vary without changing the tension developed in the muscle fibers is through a change in the elastic elements described in the mechanical model discussed previously (see Fig. 61-6). A decrease in the elasticity of these elements would allow a greater proportion of the force generated by the sarcomere to be transmitted to the skeletal system. With training, tensile strength of connective tissue is known to increase (42). Such changes may improve force transmission of a muscle.

Elastic Storage and Recovery

Storage and recovery of elastic energy in the muscle-tendon unit occurs when an active prestretch immediately precedes a shortening contraction. This combination of eccentric and concentric contractions is a natural type of movement that has been referred to as the stretch-shortening cycle (43,44) and allows a greater concentric force production or power output than when the prestretch does not occur. In effect, this phenomenon modifies the length-tension curve so that at a given muscle length, the force produced is greater than that without the prestretch. The precise location and mechanism of the elastic storage is not clear, but it has been attributed to compliance of the crossbridges and connective tissue.

The greater force from a concentric contraction when immediately preceded by an eccentric contraction is a common feature of normal movement. An example of the use of elastic storage in this manner is the knee and hip flexion that occurs immediately before jumping. The most dramatic example of the use of elastic storage and recovery to affect the energy cost of movement is seen with the big red kangaroo. This animal actually uses less energy per unit time as its speed increases as a result of greater use of elastic storage and recovery (45).

Optimal Phenomena

The mechanical properties of muscles are important in accounting for what has been referred to as optimal phenomena (35). One such phenomenon is how the aerobic demand of riding a bicycle at a given power output is altered by the seat height. A height can be identified that minimizes aerobic demand and maximizes power output (Fig. 61-15) (46, 47, 48). Another example of optimal phenomena in cycling relates to pedaling rate. There is a pedaling frequency at which the aerobic demand to generate a given power output is minimized (see Fig. 61-15). Individuals also have a stride length that optimizes the aerobic demands of running (Fig. 61-16) (49) and a walking speed
that optimizes the aerobic demands for walking a given distance (Fig. 61-17) (50).

FIGURE 61-16. Optimal phenomena in running. For a given running speed, there is a stride length at which energy cost is minimized. The freely chosen stride length is typically close to optimal. (From Cavanagh PR, Williams KR. The effect of stride length variation on oxygen uptake during distance running. Med Sci Sports Exerc. 1982;14:30-35. Reprinted by permission of Williams & Wilkins.)

FIGURE 61-17. Optimal phenomena during walking. A speed exists at which energy cost per unit distance is minimized. Energy cost is shown here in units of kilocalories per kilogram body mass per meter traveled. (From Cavanagh PR, Kram R. Mechanical and muscular factors affecting the efficiency of human movement. Med Sci Sports Exerc. 1985;17:326-331. Reprinted by permission of Williams & Wilkins. Figure based on data of Ralston JH. Energy-speed relation and optimal speed during level walking. Int Z Angew Physiol. 1958;17:277-283.)

The critical observation to understanding these optimal phenomena has come from the work of Hill (51). He showed that the force-velocity curve could be used to generate a power-velocity curve that shows a point of optimality (Fig. 61-18). Then, by considering the energy cost of developing muscle tension under various conditions, a muscle efficiency-velocity curve was generated that also showed a point of optimality. Thus, the changing of pedaling or stride rate can be considered as moving along the velocity axis of the muscle-efficiency curve. The interaction of the length-tension relationship is also important for some of the optimal phenomena.

FIGURE 61-18. Optimal phenomena can be explained by derivations from the force-velocity relationship. The power-velocity curve is obtained from the product of force and velocity and demonstrates an optimal point. Energetic data allow generation of the efficiencyvelocity curve, which also shows an optimal point. (From Cavanagh PR, Kram R. Mechanical and muscular factors affecting the efficiency of human movement. Med Sci Sports Exerc. 1985;17:326-331. Reprinted by permission of Williams & Wilkins. Figure based on Hill AV. The maximal work and mechanical efficiency of human muscles and their most economical speed. J Physiol. 1922;56:19-41.)

Muscular Fatigue and Endurance

Endurance and exercise intensity are related by hyperbolic functions, as demonstrated in Figures 61-19 and 61-20 (52, 53, 54). At high intensities, exercise can be continued for only short durations, whereas at low intensities, exercise can be continued much longer. The portion of the curve approaching the time axis is predominantly determined by the capacity for aerobic metabolism, whereas the portion of the curve approaching the intensity axis is predominantly determined by the capacity for anaerobic metabolism. The portion with greatest curvilinearity is determined by a combination of aerobic and anaerobic capabilities.

FIGURE 61-19. Isometric endurance as a function of percentage of maximal strength. (Adapted from Rohmert W. Ermittlung von erholungspausen fur statische arbeit des menschen. Int Z Angew Physiol. 1960;18:123-164.)

FIGURE 61-20. Relationship of running speed to exercise duration for world record runs. (From Simonson E. Recovery and fatigue. In: Simonson E, ed. Physiology of Work Capacity and Fatigue. Springfield, IL: Charles C Thomas; 1971:440-458. Reprinted by permission of Charles C Thomas, Publisher, Ltd.; Springfield, Illinois. Figure based on data from Lloyd BB. World running records as maximal performances: oxygen debt and other limiting factors. Circ Res. 1967;20-21(suppl 1):I218-I226.)

Most exercise is performed at submaximal levels. At the onset of exercise, there is little sense of effort, but as the exercise is continued, performance is eventually reduced. This has led to the concept that fatigue is delayed in onset. However, maximal force generation and endurance capacity may begin to decline from the onset of even submaximal work with the same muscle group (Fig. 61-21) (55). Therefore, it may be preferable to think of fatigue as “any reduction in the maximal force-generating capacity” (56).

Another conceptual issue relates to the common belief that fatigue is a failure of normal physiologic function. Perhaps it is more appropriate to consider fatigue as a protective mechanism for survival. Fatigue prevents the onset of irreversible muscle rigor and protects the subsequent recovery process.

The causes of fatigue have received considerable attention but have not been clearly established. It is evident that multiple factors are involved, and the relative importance of each is dependent on the fiber type composition of the contracting muscle; the intensity, type, and duration of the contractile activity; and the individual’s fitness and motivation level. For instance, the fatigue experienced from high-intensity short-duration exercise such as weight lifting is dependent on factors different from those causing fatigue during low-intensity longduration endurance exercise.

In daily life, a reduction in power output is frequently limited by central neural drive. Nevertheless, when motivation is high, the primary sites of muscular fatigue are thought to be within the muscle cell rather than the central nervous system or the neuromuscular junction. Specifically, it is thought that fatigue may result from disturbances in the surface membrane, excitation-contraction coupling, or metabolic events (57).

FIGURE 61-21. Effect of leg cycling at different intensities and durations on maximal isometric knee extension force generation (A) and isometric knee extension endurance at 40% of rested MVC (B). Mean isometric strength and endurance in the rested state are displayed at R. (With permission from Hoffman MD, Williams CA, Lind AR. Changes in isometric function following rhythmic exercise. Eur J Appl Physiol. 1985;54:177-183.)

ACUTE PHYSIOLOGIC RESPONSES TO EXERCISE

Dynamic Exercise

Acute physiologic adjustments occur in most bodily systems with dynamic exercise. Collectively, these adjustments increase the availability of oxygen and nutrients to the active muscle cells, remove exercise-induced metabolic byproducts (e.g., carbon dioxide, lactate, heat), and maintain an appropriate internal milieu (pH, body fluid, etc.) for bodily function.

Dynamic exercise effort is typically expressed in either absolute units (e.g., [V with dot above]O₂ in liters per minute) or relative units (e.g., percentage of an individual’s [V with dot above]O_2max). Absolute units provide a measure of work performed per unit time, whereas relative units reflect the degree of effort or how strenuous the exercise feels. Most physiologic changes with exercise are more proportional to relative than to absolute work units within a certain intensity range (58). This includes heart rate, ventilation, sympathetic/parasympathetic nerve outflow, circulating hormones, and core temperature. The one parameter that increases more in proportion to absolute work performed than relative intensity is cardiac output, which increases about 5 to 6 L/min for each rise in [V with dot above]O₂ of 1 L/min (59). Several factors may influence the magnitude of changes produced by dynamic exercise, such as body posture, age, gender, fitness level, disease state, and mode of exercise (e.g., leg vs. arm).

Many of the cardiovascular adjustments to dynamic exercise are regulated by changes in autonomic nervous activity outflow (60, 61, 62, 63). Parasympathetic tone exists at rest, and its withdrawal at the onset of exercise allows heart rate to rise. When work intensity reaches about 50% [V with dot above]O_2max, parasympathic withdrawal appears to be exhausted, and any further rise in heart rate is totally dependent on increased sympathetic nerve activity. In addition to increasing heart rate, sympathetic nerve activity increases myocardial contractility, mobilizes nutrients, influences several circulating hormone levels, and contributes to blood flow redistribution by vasoconstriction in inactive regions. Although muscle sympathetic nerve activity appears to increase in the active muscles, metabolic byproducts override this vasoconstriction effect to produce vasodilation. Control of the autonomic nervous system during exercise originates from both central and peripheral receptors located in the motor cortex, ergoreceptors, and arterial and cardiopulmonary baroreceptors (63, 64, 65).

FIGURE 61-22. Schematic representation of the blood flow and distribution at rest and during maximal dynamic exercise. Exercise results in increases in blood flow to the exercising muscles and the coronary circulation but in reduced flow to the organs. Blood flow rates are indicated in milliliters per minute. (From Mitchell JH, Bloomqvist G. Maximal oxygen uptake. N Engl J Med. 1971;284:1018-1022. Reprinted by permission of The New England Journal of Medicine.)

The rise in cardiac output (between about four- and sixfold to sevenfold at maximal effort) with upright leg exercise stems from a rise in heart rate (two- to threefold) and stroke volume (about 1.5- to 2-fold) (59,66). The rise in stroke volume results from increased myocardial preload and contractility (59,67,68). Preload increases as a result of enhanced venous return, which is brought on by venoconstriction and muscle contraction. An increase in contractility leads to more complete emptying of the heart (i.e., decreased left ventricular end-systolic volume), whereas an increase in preload increases left ventricular end-diastolic volume. The net effect is increased stroke volume.

Up to 80% of cardiac output can be distributed to the active muscles at maximal effort, compared with only about 20% of cardiac output being distributed to the muscles at rest. As illustrated in Figure 61-22, this marked blood flow redistribution is accomplished by arterial vasodilation in the active muscles and arterial vasoconstriction in other vascular regions (e.g., splanchnic, inactive muscle, renal) (8,59,69,70). Total systemic vascular resistance declines progressively with increasing work intensity. The precise mechanisms leading to vasodilation in the active muscle remain debatable but likely stem from changes in several local factors, including potassium, hydrogen ion, endothelium-relaxing factor, adenosine, osmolarity, and others (71,72).

The oxygen extraction rate is high within the active muscle. This, combined with the increased percentage of blood flow directed to the muscles, leads to an approximately
threefold increase in arteriovenous oxygen difference at maximal exercise (59).

Systolic blood pressure rises progressively with increased dynamic workload, whereas diastolic blood pressure generally remains relatively unchanged. The net effect is a modest increase in mean arterial blood pressure (usually <20 mm Hg).

Ventilation rises linearly with [V with dot above]O₂ up to the anaerobic threshold (73,74). At and above the anaerobic threshold, ventilatory volume and carbon dioxide output ([V with dot above]CO₂) rise out of proportion to metabolism because of the CO₂ produced from the bicarbonate buffering system (73,74). The changes in the relationship among [V with dot above]O₂, ventilation, and [V with dot above]CO₂ with graded exercise testing are used to assess the anaerobic threshold noninvasively (73,74). The significance of determining the anaerobic threshold is that it provides an index of tolerance for sustained work and can be used in prescribing exercise intensity for aerobic training.

Considerable amounts of heat can be produced during exercise, as about 75% of the energy with aerobic metabolism is released as heat. Heat is transported to the skin surface via the cardiovascular system and dissipated via convection, radiation, conduction, and evaporation. Body core temperature rises with exercise, which aids in heat dissipation by increasing the heat flow gradient from the core to the skin (75,76). Reflex and locally mediated arterial vasodilation allow greater blood flow to be directed to the cutaneous vascular bed (63,77,78). This increased blood flow is accomplished in part by blood flow redistribution away from splanchnic and renal arterial vascular beds (63,78). Increased cutaneous venous compliance permits increased cutaneous blood volume and surface flow, which enhance heat dissipation at the skin surface (78,79). Increased cutaneous blood volume may lead to reduced venous return, left ventricular end-diastolic volume, and stroke volume. Heart rate can rise to compensate for the lower stroke volume as long as maximal heart rate is not attained. The sequence of events associated with heat stress during exercise is referred to as cardiovascular drift (77,79,80). Some cardiovascular drift typically occurs with prolonged (e.g., >60 minutes) exercise in a thermoneutral environment, although the magnitude is much greater in hot and/or humid environments because of the greater cutaneous blood flow and blood volume circulatory demands for heat removal. In a hot environment, the skin-to-environment temperature gradient for dissipating heat via convection, radiation, and conduction is reduced or even reversed if air temperature is greater than skin temperature. Similarly, the ability to dissipate heat via evaporation is proportional to the magnitude of the water pressure gradient existing between the skin and environment.

Sustained levels of high work intensity, especially when performed in combination with heat stress, can lead to high rates of sweat loss reaching 2 to 3 L/h. These rates of sweating can lead to dehydration and subsequent sequelae of decreased total blood volume, blunted cardiac output reserve, reduced thermoregulatory capacity, and decreased work tolerance (79,81, 82, 83, 84). To help prevent serious dehydration, fluids should be consumed during sustained exercise. This should occur even in the absence of thirst because a person can lose up to 2% of body water before feeling thirsty (77,81). A number of hormones involved in fluid regulation are altered during exercise, including increases in plasma renin activity, aldosterone, arginine vasopressin, and atrial natriuretic peptide (82,84, 85, 86, 87, 88, 89).

Static Exercise

The hemodynamic responses to static exercise are related to the percentage of maximal voluntary contraction (MVC) and the amount of muscle mass involved in the contraction (90). Increases in [V with dot above]O₂, cardiac output, and heart rate are typically modest during static exercise compared with dynamic exercise (Fig. 61-23) (91). Additionally, total peripheral vascular resistance does not decrease, and stroke volume typically fails to rise as occurs with dynamic exercise (66). Blood flow through the active muscle is dependent on a balance between metabolically induced vasodilation and mechanical restriction of flow associated with contraction of the surrounding muscle. At high static efforts, blood flow through the active muscle is restricted and may be completely occluded (92). Reduced muscle blood flow relative to metabolic demands results in greater reliance on anaerobic metabolism and consequently earlier onset of fatigue than occurs with dynamic exercise. Mechanical and metabolic activation of skeletal muscle afferent nerve fibers during static exercise evokes a pressor response that leads to a significant increase in blood pressure, especially mean and diastolic blood pressures (93). For this reason, static exercise is often viewed as placing primarily a pressure load on the left ventricle, whereas dynamic exercise is viewed as placing more
of a volume load on the left ventricle (94,95). Although initial studies suggested that the magnitude of the presssor response to static exercise was primarily related to the percentage of MVC, most (but not all) subsequent studies suggest that the amount of muscle mass used also impacts positively on the pressor response.

FIGURE 61-23. Schematic comparison of hemodynamic responses to dynamic and isometric exercise. (Adapted from Hanson P, Rueckert P. Hypertension. In: Pollock ML, Schmidt DH, eds. Heart Disease and Rehabilitation. 3rd ed. Champaign, IL: Human Kinetics; 1995: 343-356.)

HEALTH BENEFITS DERIVED FROM A REGULAR PROGRAM OF EXERCISE

Many health benefits have been reported with long-term, regular participation in physical activity. The optimal exercise prescription required for primary and secondary prevention of various disease states and for reducing overall mortality remains under investigation (96, 97, 98, 99). For many years, the primary recommendation was to participate in an aerobic exercise program. More recently, many health organizations have revised their recommendations to acknowledge the benefit of physical activities that may not meet the aerobic criteria (96,100). The new recommendations encourage all people to accumulate a minimum of 30 minutes of at least moderate exercise most, if not all, days of the week (96,100). This 30 minutes can be accumulated from activities performed throughout the day, such as climbing stairs, gardening, and playing with children. This change in recommendations stems from (a) epidemiologic studies showing reduced mortality and/or morbidity in physically active people, including those who were not necessarily participating in an aerobic exercise program; (b) the failure of many people to adopt long-term aerobic exercise programs because of a variety of factors, including discomfort with higher-intensity effort; and (c) the low levels of physical activity required in our normal daily activities (96). Although the magnitude of benefits in terms of prevention is likely to be dose related, benefits are first contingent on long-term compliance with being physically active. As illustrated in the Activity Pyramid in Figure 61-24, the recent recommendations regarding accumulation of at least 30 minutes of moderate intensity of physical activity most, if not all, days of the week and the recommendations for aerobic and strength training provide a continuum of potential health and fitness benefits that can be used in prescribing exercise to people who differ in exercise readiness, health, exercise preferences, and goals. The concept is to individualize the exercise prescription to get more people physically active on a long-term basis to gain health benefits. Some of the health benefits that have been reported with regular participation in physical activity and/or aerobic exercise training are discussed next.

All-Cause Mortality

Several studies indicate a reduction in all-cause mortality (101, 102, 103) with long-term, regular exercise participation. Although the minimal and/or optimal intensity, frequency, and duration for reducing mortality remain uncertain, most studies indicate an inverse linear dose-response relationship between the volume of physical activity and all-cause mortality (104). Some data suggest that the threshold level of physical activity required to have a measurable impact on mortality is an expenditure of 500 to 1,000 kcal/wk (104,105). Expending 1,000 calories per week in physical activity has been reported to reduce all-cause mortality by 20% or more (104,105). An inverse relationship has also been reported between laboratorydetermined cardiorespiratory fitness and all-cause mortality, with an asymptote often reported at the upper level of the fitness distribution.

FIGURE 61-24. The Activity Pyramid is a model to facilitate education of the public about the adoption of a more active lifestyle. (Copyright 1997 Park Nicollet Health Source Institute for Research and Education. Reprinted by permission.)

Primary and Secondary Prevention of Cardiovascular Disease

Physical inactivity is considered a major risk factor for the development of cardiovascular disease (96,106, 107, 108). Many epidemiologic studies (105,109, 110, 111, 112, 113, 114) have shown that people who are physically inactive have a higher incidence of heart disease than those who are physically active. Based on meta-analysis studies, the estimated risk of heart disease is approximately two times greater for inactive than for active people (115,116). In fact, this risk approaches that for hypertension and hypercholesterolemia. Because physical inactivity affects a greater number of people than any other single heart disease risk factor, the significance of physical inactivity is especially noteworthy.

In secondary prevention, meta-analysis of randomized trials of cardiac rehabilitation indicates a 20% to 25% reduction in mortality in those who participated in cardiac rehabilitation versus those who did not (117,118). The independent influence of exercise conditioning on mortality in this population remains uncertain, as several of these programs included education and advice on modifying other risk factors. For additional
information on secondary prevention of cardiovascular disease, the reader is referred to the Chapter, “Cardiac Rehabilitation”.

Reduced incidence of cardiovascular disease through physical activity certainly could have important societal implications. The estimated cost of cardiovascular diseases and stroke in the United States for 2002 was $329 billion (119). If the prevalence rates remain the same, future health care costs could escalate with the projected rise in number of Americans older than 65 years. A regular program of exercise, combined with other healthy lifestyle habits, has tremendous potential in curtailing future health care costs. The nation’s health care goals for the year 2010, published in the Healthy People 2010 Program, are aimed at encouraging Americans to adopt healthier lifestyle habits, including greater participation in a regular program of exercise (120).

The mechanism by which physical activity reduces the risk of heart disease is not entirely clear. Some of the reduced risk stems from its impact on improving other risk factors, such as lipids, blood pressure, obesity, diabetes, and psychological stress (96,121). Physical inactivity remains, however, an independent risk factor for coronary artery disease after statistical adjustment for other risk factors.

Blood Pressure Regulation

Hypertension is a potent risk factor for coronary artery disease, stroke, congestive heart failure, renal disease, and peripheral vascular disease. Both acute and chronic exercise can lower blood pressure (96,104,122, 123, 124, 125). Meta-analysis of aerobic exercise training studies indicates an average decrease in systolic and diastolic blood pressures of 7 and 6 mm Hg, respectively, in those with hypertension and 3 and 2 mm Hg in systolic and diastolic pressures, respectively, in those with normal blood pressure with aerobic training (126). Debate still exists regarding the type of exercise program that produces the best blood pressure-lowering effect (126). Recently, aerobic exercise was reported to be associated with a more favorable blood pressure level than resistance exercise training among 10,000 participants evaluated from 1988 to 1994 in the Third National Health and Nutritional Examination Survey (127). Although there is some suggestion that moderate-intensity dynamic exercise may have a more favorable effect on blood pressure than high-intensity exercise, the data remain inconsistent (126).

Lipid Management

Most studies indicate that aerobic exercise training lowers plasma triglycerides and may raise high-density lipoprotein (HDL) cholesterol (96,128, 129, 130, 131). Elevated triglycerides and low HDL cholesterol are common lipid abnormalities in those with the metabolic syndrome that, in turn, is associated with increased prevalence of diabetes, hypertension, and coronary artery disease. Questions remain regarding the threshold of exercise needed to produce changes in blood lipids (130,132, 133, 134, 135). Some data suggest a dose-dependent relationship (130,133, 134, 135), but Leon and Sanchez (129) stated that there was insufficient evidence to conclusively establish a dose-response relationship. Although lipid changes are associated with long-term participation in an exercise program, a single bout of exercise can also produce acute positive lipid changes (104,136,137).

Weight Control

Percentages of populations within industrialized countries who are considered overweight and obese are rising at epidemic proportions (138, 139, 140). In the U.S. population, more than 30% are considered obese (body mass index [BMI] ≥30 kg/m²) and another nearly 30% of women and 40% of men fall within the overweight category (BMI: 25 to 29.9 kg/m²) (139, 140, 141, 142). Especially disconcerting is the nearly fourfold increase from 1963 to 2004 (<5% to <20%) in the number of obese children. Obesity carries many health risks, including heart disease, type 2 diabetes, hypertension, dyslipidemia, stroke, gallbladder disease, osteoarthritis, and certain types of cancer (139,143). When the BMI increases above 27, mortality increases sharply (143,144).

Most population studies show an inverse relationship between obesity and physical activity (96). Although many overweight and obese people periodically lose significant amounts of weight through diet alone, most regain this weight (145). In fact, many of these individuals undergo a weight loss/weight regain cycle (yo-yo weight pattern) several times in a lifetime. Rather than trying to lose weight through diet alone or exercise alone, a combination of moderate diet restrictions and increased regular exercise results in the best long-term weight management plan (146). Exercise seems to be especially important in long-term maintenance of weight loss (96,139,144). The most appropriate combination of intensity, duration, frequency, and mode of exercise to recommend for weight loss remains uncertain but will likely vary, depending upon percentage of body fat, age, and presence/absence of orthopedic or other medical complications (146, 147, 148). In addition to fat loss, increased physical activity may help maintain or increase lean body tissue during weight loss.

Type 2 Diabetes Mellitus Prevention

Diabetes mellitus (DM) can lead to devastating microvascular complications and is a major risk factor for development of coronary artery disease (149). Morbidity and mortality are also higher in those with coronary artery disease when DM is present. Type 2 DM is increasing at an alarming rate in developed countries and is occurring at younger ages (138). Much of this increased incidence is attributable to lifestyle behaviors such as limited physical activity, excessive food intake, and greater prevalence of obesity.

Many studies have shown that exercise is beneficial for those with type 2 DM. A major benefit of exercise is that it increases insulin sensitivity. This effect is seen after a single bout of exercise as well as with chronic exercise. Exercise may act through several mechanisms to improve glucose regulation (104,150,151). Regular exercise may further benefit those with DM by improving body weight, blood pressure, and lipids.

Because of the devastating potential effects of diabetes, primary prevention of type 2 DM is important. Two recent studies (152,153) found that people with impaired glucose tolerance
(prediabetic state) reduced their incidence of DM during follow-up with a lifestyle diet/exercise intervention program designed to lose weight compared with those receiving normal care. This benefit was even more effective than that resulting from the administration of an oral antihyperglycemic agent.

The optimal intensity, frequency, and duration of exercise to recommend for protection against the development of type 2 DM or improved control of type 2 DM remain uncertain. Most studies showing benefits have used an aerobic exercise program. One study suggested that, for each 500 kcal/d increase in energy expenditure, the age-adjusted risk of type 2 DM could be reduced by 6% (154). Another study found that moderateto-high-intensity exercise (≥5.5 METs) performed more than 40 min/wk reduced the incidence of type 2 DM, whereas lower levels of exercise, regardless of duration, did not provide protection (155). These results suggest that a threshold of exercise must be achieved in terms of intensity and duration.

Improved Psychological Well-being and Quality of Life

Mood state is improved immediately after aerobic exercise among regular exercisers (156). Furthermore, it is well recognized that regular physical activity improves general sense of well-being and quality of life (157, 158, 159, 160, 161, 162). Changes that have been postulated to contribute to this include reduced psychological stress and improved tolerance for activities of daily living. In addition, regular exercise may help improve quality of life by protecting people from development of disabling diseases such as heart disease, diabetes, cancer, and cognitive decline as well as enabling people with diseases to regain functional work tolerance. Freedom from disease and ability to function independently into old age are important factors in quality of life. Shephard (163) estimated that remaining physically active into old age could allow one to maintain functional independence for 10 to 20 years longer than if one is inactive (Fig. 61-25).

Maintenance of Bone Density

Osteoporosis is an important health problem. It causes considerable societal disability among the elderly and is a major contributor to health care costs. Regular physical activity is recommended for enhancing bone density or reducing an age-related decline in bone density (164, 165, 166, 167, 168, 169, 170, 171, 172). Exercise habits during the peak bone-forming years may impact on bone density years later (166,171, 172, 173). The mechanism by which exercise impacts on bone density is incompletely understood, and the optimal intensity or threshold level of exercise for enhancing bone density remains uncertain. An interaction may exist between an adequate intake of calcium and exercise-induced benefits (174). Weight bearing appears to be an important stimulus, although muscle contraction without weight bearing may also promote bone density (164,165,167, 168, 169). In women, very high-intensity training can lead to amenorrhea and reduced bone density (175), an effect believed to be related to decreased estrogen levels.

FIGURE 61-25. Demonstration of the effect of aerobic training on improving aerobic capacity and delaying its drop to a threshold where independent function can no longer be sustained. (Adapted from Shephard RJ. Exercise and aging: extending independence in older adults. Geriatrics. 1993;48:61-64.)

Increased Fibrinolytic Activity

Regular exercise may reduce the risk of thrombotic events by exerting an effect on coagulation and fibrinolytic factors such as lowering fibrinogen, plasminogen activator inhibitor 1, and platelet aggregation while raising tissue plasminogen activation (96,104,176, 177, 178, 179, 180). Most types of chronic exercise appear beneficial. However, acute strenuous exercise may increase platelet adhesiveness and aggregability in some individuals, more so in those who are sedentary than in those who are physically active (104,179,181).

Decreased Inflammatory Marker

Associations have been reported between C-reactive protein and increased risk of cardiovascular disease. Regular exercise may have an anti-inflammatory effect, as evidenced by reduced levels of C-reactive protein with exercise training (180,182) as well as among those who are physically active (183).

Improved Endothelial Function

Improved myocardial perfusion has been reported in patients with known coronary artery disease after a period of exercise training (184). One proposed mechanism is improved endothelial function (184). This may help attenuate a paradoxical
coronary arterial vasoconstrictor response observed in atherosclerotic segments and thereby improve coronary artery blood flow. Aerobic conditioning has been recently reported to help prevent and restore age-related declines in endothelialdependent vasodilation in healthy people (185).

Nonpharmacologic Antiarrhythmic Intervention

By enhancing vagal tone and reducing sympathetic activation, aerobic exercise training may exert an antiarrhythmic effect and thereby reduce the incidence of sudden death (186).

Improved Sleep

Epidemiologic studies indicate that regular physical activity may be beneficial in improving sleep quality and reducing sleepiness during normal waking hours (187). The mechanism(s) by which exercise impacts on sleep remains uncertain.

Possible Enhanced Immune Function

The impact of exercise training on the immune system remains uncertain. Some studies suggest moderate exercise training may enhance the immune system, whereas heavy training or arduous endurance events may depress the immune system. Much of this evidence stems from studies suggesting a protective effect against respiratory illnesses in those participating in regular moderate exercise training compared with sedentary individuals, but increased risk in athletes participating in high-level competitive events compared with sedentary individuals.

Although several studies have reported changes in many components of the immune system (e.g., cytokines, natural killer cell, immunoglobin) with exercise and/or exercise training, further study is required to ascertain whether these changes impact significantly on immunity and, if so, whether they are beneficial or detrimental (188, 189, 190, 191, 192).

Reduced Cancer Risk

A growing number of studies are showing that increased physical activity is associated with reduced risk of colon and perhaps breast, prostate, and lung cancer (110,193, 194, 195). Some of the potential direct and/or indirect pathways by which exercise may be beneficial include reduced bowel lining exposure to mutagens via accelerated movement of food through the intestines, reduced breast tissue exposure to circulating estrogen, lowered circulating concentrations of blood insulin and growth factors, and improved body weight management. Many questions remain regarding the optimal dose of exercise for prevention of cancers, but, in general, exercise guidelines used for prevention of coronary artery disease are recommended (195).

TABLE 61.4 Physiologic Adaptations to Aerobic Exercise Training as Observed in Resting and Exercise States

	Rest	Submaximal Exercise	Maximal Exercise
Aerobic power	No change	No change	Increase
Heart rate	Decrease	Decrease	Decrease
Stroke volume	Increase	Increase	Increase
Cardiac output	No change	No change	Increase
Myocardial O₂ demand	Decrease	Decrease	No change
Ventilation	No change	Decrease	Increase
Arteriovenous O₂ difference	No change	Increase	Increase
Blood lactate concentration	No change	Decrease	Increase
Muscle blood flow	No change	Decrease	Increase
Splanchnic blood flow	No change	No change	Decrease
Systolic blood pressure	Decrease	Decrease	No change
Diastolic blood pressure	Decrease	Decrease	No change

AEROBIC EXERCISE

Physiologic Adaptations to Aerobic Conditioning

Aerobic exercise training produces many physiologic adaptations (Table 61-4). An important adaptation is increased work capacity, or [V with dot above]O_2max. Most studies indicate that sedentary people within diverse populations (age, gender, income, ethnic background, health status) will experience ≥15% improvement in [V with dot above]O_2max within 3 months of starting aerobic training (59,66,96,196,197). This increase is caused about equally by central cardiovascular adaptations that raise maximal cardiac output and peripheral adaptations that enhance oxygen extraction from the circulating blood (66).

Increased oxygen extraction with aerobic training stems from changes within the trained muscle, including increased capillary density, capillary-fiber ratio, tissue myoglobin, size and number of mitochondria per muscle cell, and respiratory enzyme capacity per mitochondrion (198, 199, 200). These muscular adaptations are believed to raise the anaerobic threshold and improve tolerance for sustained work.

The rise in maximal cardiac output with aerobic conditioning resides in increased stroke volume. Maximal heart rate does not rise with aerobic conditioning and may even be lower in well-conditioned endurance athletes than in sedentary individuals. The mechanism by which maximal stroke
volume increases with training is not entirely clear but involves increased cardiac preload and probably enhanced myocardial contractility and relaxation (66,201). Aerobic training causes an increase in total blood volume that partially accounts for the increased cardiac preload. The extent of cardiac adaptations appears to be related to such training factors as the length, intensity, duration, and mode of training and the time of life at which training was initiated.

A characteristic finding among elite male endurance athletes is an increased heart size (“athlete’s heart”) characterized by increased left ventricular end-diastolic volume and a proportional increase in left ventricular mass and normal wall tension (66,202). It is important to note that the enlarged heart of the athlete differs from the enlarged heart in hypertension and congestive heart failure (203). In the elite athlete, left ventricular hypertrophy is eccentric rather than concentric, and ventricular dilation is proportional to wall thickness. Indices of left ventricular diastolic function are typically normal or increased in athletes but impaired in pathologic states (204). The increased heart size in the athlete is believed to be important in permitting high levels of maximal stroke volume and thereby high functional work tolerance. Although highly trained women frequently show cardiac dimensional adaptations, they rarely demonstrate cardiac dimensional changes outside normal limits (205).

Physiologic adaptations to aerobic training may be restricted to the trained muscles when the amount of muscle mass used in the exercise is small (206, 207, 208). For instance, the physiologic benefits of upper-body endurance training appear to be primarily limited to the periphery (206,208). This is attributed to the lower blood flow and cardiac output requirements, which lessen the stimulus for central (i.e., heart) adaptations.

Principles of Aerobic Conditioning

Intensity, duration, and frequency recommendations for aerobic exercise training have been previously provided by various groups. In 1998, the American College of Sports Medicine (ACSM) (209) recommended an exercise intensity range of 55% to 90% of maximal heart rate, or 40% to 85% of maximal reserve or heart rate reserve, with the lower-intensity levels being most applicable to individuals who are quite unfit. This typically translates to rating of perceived exertion (RPE) levels between about 11 to 12 (“fairly light”) and 16 (“hard”) (210,211). The RPE scale on which these values are based is shown in Table 61-5 (212). To achieve these recommended intensities, exercise modes that incorporate a large muscle mass such as walking, running, cycling, swimming, and crosscountry skiing are optimal (211,213). Exercise durations of at least 20 minutes, and exercise frequency of at least three times per week was also recommended.

The ACSM has recently updated and clarified the earlier recommendations (100). This group now indicates that in order to promote and maintain health, all healthy adults need to engage in moderate-intensity aerobic physical activity for a minimum of 30 min/d on 5 d/wk or vigorous-intensity aerobic activity for a minimum of 20 min/d on 3 d/wk. The activity can be accumulated in bouts of at least 10 minutes, and combinations of moderate- and vigorous-intensity activities can be used to meet these guidelines. They also point out that larger amounts of physical activity, including more activity at higher intensities, provide additional health benefits.

TABLE 61.5 Borg RPE 6-20 Scale

6
7	Very, very light
8
9	Very light
10
11	Fairly light
12
13	Somewhat light
14
15	Hard
16
17	Very hard
18
19	Very, very hard
20
Adapted from Borg GAV. Psychological bases of perceived exertion. Med Sci Sports Exerc. 1982;14:377-381.

The optimal rate of progression to follow in implementing an exercise program depends on several factors, including the individual’s current activity levels, physiologic limitations, health, age, and exercise goals (99,209). The primary focus should be on adopting a progression that will result in long-term participation. Attempting to do too much too fast can lead to increased dropout rates as a result of perceived excessive discomfort and/or injuries. The ACSM suggests a progression rate subdivided into three phases, as illustrated in Table 61-6. Exercise programs can be tailored according to personal preferences by selecting various combinations of frequency, duration, intensity, and mode of exercise.

Assessment of Aerobic Capacity

The [V with dot above]O_2max provides a reliable, reproducible measure of dynamic work capacity and cardiovascular fitness. It also provides information regarding medical prognosis in patients with heart disease and can aid in evaluating work resumption after recovery from a cardiac event (95,99,214). Many factors influence [V with dot above]O_2max, including age, gender, chronic levels of exercise, genetics, and disease (95,99). With increasing age, [V with dot above]O_2max declines about 5% to 10% per decade after age 20 (200,215). The age-related loss is attributed to several factors, including a progressive decline in maximal heart rate, body composition changes (e.g., loss of muscle), decreased physical activity, myocardial and vascular stiffening, and disease with increased age (200,215

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