Exercise has a positive and significant impact on the human body by improving physiological function, physical fitness, and health. Physical activity can lead to numerous physiological changes that may lower the prevalence of chronic disease and cause significant adaptions in many physiological systems of the body. There are potential benefits of exercise on the cardiovascular, pulmonary, and neuroendocrine systems. Increased physical activity can directly affect energy expenditure, metabolic change, neurobiological effects, and neuroendocrine changes.

Skeletal muscle fibers are responsible for the generation of force in order to produce movement. Myofibrils are organized to compose skeletal muscle fibers. These myofibrils are surrounded by portions of the sarcoplasmic reticulum and have deep channels (T tubules) (Fig. 25–1).

Muscle fibers vary in terms of their mechanical, physiological, and biochemical properties, making skeletal muscle a heterogeneous tissue. Skeletal muscle fibers have been classified by using histochemical techniques (ATPase and oxidative enzymes stains), measurements of contraction (twitch) or fiber shortening velocity, and the identification of myosin heavy chain isoform with use of protein electrophoresis. Skeletal muscle may contain up to three types of fibers in varying proportion: fiber types I, IIa, and IIx.¹ It is important to note that skeletal muscle fibers can express more than one type of myosin heavy chain isoform simultaneously.¹ Type I myosin heavy chain isoform muscle fibers are the slow, oxidative, fatigue-resistant fibers. Type IIx are very fast contracting, glycolytic, and fatigable fibers. Type IIa have intermediate properties. These fibers are fast contracting but with an oxidative metabolic profile. Fibers that express more than one type of myosin heavy chain isoform are known as hybrid fibers; various combinations (I/IIa, IIa/IIx, I, IIa, IIx) have been reported.¹

Force can be generated while skeletal muscle remains static, shortens, or increases in length.² During most types of movement or exercise, muscles alternate between static and dynamic muscle actions.³

The generation of force by muscle fibers is dependent on a complex series of well-orchestrated events initiated by a nerve impulse, which triggers the release of acetylcholine (ACH) into the synaptic cleft. The ACH initiates muscle contraction by binding to the ACH receptors in the neuromuscular junction. This impulse quickly spreads from the sarcolemma as calcium ions are released into the sarcoplasm. The calcium ions eventually bind to troponin, which causes a change in the morphology of the thin filament. Tropomyosin, which is located on actin (on the thin filament) is shifted, and the shift exposes active sites on the thin filament. Concomitantly, myosin heads located on the thick filaments are also exposed to the active sites, and cross-bridges are formed.

Myosin heads shift and thin filaments are moved toward the sarcomere center. Subsequently, ATP binds to the myosin heads and is broken down into ADP and P. At this point, the myosin heads detach from the thin filaments and return to the original position. With the cessation of the nerve impulse, calcium ions are transported into the sarcoplasmic reticulum, and filaments slide to their relaxed state. This cycle of shortening of the sarcomere and muscle contraction is propagated as long as calcium ions remain bound to troponin (Fig. 25–2).

Static (isometric) muscle actions occur when the muscles generate force without changing length or have any associated joint movement. In this case, the force generated by myosin and actin cross-bridges is less than the force of the external resistance. Although there is energy expenditure, no work has been done (work = force × distance) as there is no displacement (Fig. 25–3). An example of isometric activity is if one were carrying an object with their shoulder flexed to 90º and elbow fully extended. The gravitational weight of the object would be pulling downward, but the arms would be opposing the motion with equal force upwards. Since the arms are neither raising nor lowering and there is no joint movement, the biceps will contract isometrically.

Dynamic (isotonic) muscle actions can be divided into concentric and eccentric muscle actions. During concentric actions, the muscles produce enough force to overcome the external resistance. This occurs when myosin and actin myofilaments form cross-bridges, the filaments slide past each other, the muscle shortens, and joint movement occurs (Fig. 25–4).

Since displacement occurs by means of force production, energy expenditure results in muscle contraction and joint movement. An example of this would be a concentric contraction of the bicep, causing the arm to flex at the elbow and lift a weight up towards the shoulder (e.g., a bicep curl).

During eccentric actions, the muscle lengthens while it generates force. The lengthening occurs because the external resistance moves in the direction opposite of the shortening.³ An example of this would be the lowering of the weight after a bicep curl, or a person resisting the drop of a heavy object. Eccentric muscle actions are important in the training of muscles because of the high force generated by the contractile elements. These exercises can be associated with muscle damage and soreness, and should be limited when a person first begins to exercise.

Dynamic (isokinetic) muscle actions are characterized by constant velocity. The velocity of the muscle shortening or lengthening and the velocity of the movement of the limb is predetermined and held constant by a rate-limiting device known as an isokinetic dynamometer. This action does not occur in nature. This device can be used for training or testing purposes. Athletes may use them to perform exercises that simulate the actual speeds of their sport-specific activity.³

Multiple factors can determine the capacity for prolonged exercise. These factors include muscle buffering capacity, gender, age, and genetics.^4–8 The acid-base state of the muscle is important when it comes to the accumulation of lactic acid (metabolic by-product of anaerobic glycolysis). The lactic acid increases the intracellular acidity of the muscle, which impairs muscle actions. Eventually, the lactic acid is converted into glucose, but the process takes time—over strenuous exercise can cause an abundance of lactic acid. Thus, this lactate threshold, or the exercise intensity at which lactate begins to accumulate, is a good indicator of the individual’s performance in endurance events³ (Fig. 25–5).

Gender is a factor, as women have smaller hearts, lower hemoglobin concentrations, and lower blood volumes, which all result in lower stroke volume and lower blood oxygen carrying capacity. Age will also be a factor, as with increasing age there is a decline in aerobic capacity. A reduction in habitual physical activity increases with age, and this may in part explain a portion of the decline in aerobic capacity. Aerobic capacity decreases by approximately 10% per decade in men and women^9,10 (Fig. 25–6).

However, in athletes who maintain a high level of endurance training, the decline in VO₂ max can be up to half that of the sedentary. The most important factor that causes a decrease in VO₂ max over time is the reduction in cardiac output secondary to increased peripheral resistance and lower stroke volume. Genetics can also play a crucial role in the development of exercise capacity. It appears elite endurance athletes are born with an exceptional genetic potential for the development of very high levels of cardio respiratory fitness.³ Studies on identical and fraternal twins have suggested that genetics account for 20% to 30% of VO₂ max values.^4,11

Delayed-onset muscle soreness (DOMS) is the soreness experienced by an athlete, which is felt most strongly 24 to 72 hours after the exercise.¹² Symptoms can range from muscle tenderness to severe debilitating pain. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity, or when they are first introduced to a certain type of activity, regardless of the time of the year.¹³ DOMS is seen the most with eccentric muscle activity, as this induces micro-injuries at a greater frequency and severity than other types of muscle actions.¹³

Six hypothesized theories have been proposed for the mechanism of DOMS: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation, and the enzyme efflux theories. However, an integration of two or more theories is more likely to explain muscle soreness.¹³ DOMS can cause reduction in joint range of motion, shock attenuation, and peak torque, which can affect athletic performance. DOMS can also cause unaccustomed stress to be placed on muscle ligaments and tendons due to alterations in muscle sequencing and recruitment patterns.¹³

Treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated positive effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used.¹³ Exercise is the most effective temporary means of alleviating pain during DOMS.¹⁴ Athletes should reduce intensity and duration of exercise for 1 to 2 days after the onset of DOMS. Eccentric exercises should be introduced progressively over the period of 1 to 2 weeks at the beginning of the season to prevent DOMS-related physical impairment.¹³

Exercise is a form of stress that can affect the physiological response of the neuroendocrine system. In terms of the neuroendocrine system, stress can affect the physiological or psychological integrity (i.e., homeostasis) of an individual.¹⁵ Exercise can play a dual role of being a stressor and/or being a modifier of stress within the neuroendocrine system.¹⁶

Physical exercise serves as a robust activator of the neuroendocrine system. However, the magnitude of the neuroendocrine stress response seems to be directly proportional to the volume of exercise exposure. The volume (intensity and/or duration) of exercise must be sufficient in order to illicit a response.¹⁶ The measurement of hormones associated with the sympathetic nervous system and the hypthalamo–pituitary–adrenocortical–adrenomedullary systems are helpful in quantifying the neuroendocrine stress response. The key hormones of those systems are typically identified as norepinephrine, epinephrine, adrenocorticotropic hormone (ACTH), and cortisol.^16,17 The stress hormone responses are typically transient in nature and only last a few minutes to hours into recovery (Fig. 25–7).

Chronic exposure to exercise training results in adaptations in the neuroendocrine system. This is noted as a reduction in hormonal stress response to submaximal exercise and, in many cases, reduced circulating basal stress hormone levels.^16,18 This means that chronic exposure to exercise training allows adaptation and accommodation within the neuroendocrine system, such that stress response to subsequent exercise is lessened.¹⁶ However, excessive exercise training can force the neuroendocrine exercise stress response to become inappropriate. This results in the development of overtraining syndrome, in which the physiological response to exercise-induced stress becomes harmful. This may induce maladaptation in the athlete and compromise the subsequent ability to perform.¹⁹ Overtraining syndrome occurs when the training stimulus is too much or adequate rest is not allowed between exercise sessions. The athlete is unable to adapt to drastic increases in training overload (an exercise volume stimulus not previously experienced). This can result in decreased competitive performance, decreased muscular strength, increased muscular soreness, and chronic fatigue, as well as psychological functions such as increased feelings of depression, lethargy and apathy, or emotional abnormalities.¹⁹

The Fick equation is used to determine oxygen consumption. It is as follows: VO₂ = CO × (CaO₂ – CVO₂), where VO₂ is oxygen consumption, CO is cardiac output, and CaO₂ – CVO₂ is the difference between arterial and venous blood (also known as the a – VO₂ difference).²⁰ This equation demonstrates that the two major determinants that can limit VO₂ max are cardiac output and the capacity of active muscle to extract oxygen from arterial blood.³

CO is defined as the product of stroke volume and heart rate, and is equivalent to the amount of blood pumped by the heart in 1 minute. In general it has an approximate resting value of 5 L/min and has the potential to increase in a linear fashion with regard to exercise intensity between 20 and 40 L/min. The amount that it increases depends on the conditioning of the athlete. Stroke volume increases up to 40% to 60% of the VO₂ max and then levels off.^3,21