Tidal volume (TV)	The amount of air inspired or expired in a normal breath at rest (0.5 L)
Inspiratory reserve volume (IRV)	The maximal amount of air that can be inspired beyond the TV (3 L)
Expiratory reserve volume (ERV)	The maximal amount of air that can be expired beyond the normal TV expiration (1L)
Residual volume (RV)	The volume of air that remains in the lungs after a forced, maximal expiration (1.2 L)
Inspiratory capacity (IC)	The maximal amount of air that can be inspired; equivalent to TV + IRV
Functional residual capacity (FRC)	The amount of air remaining in the lungs after normal exhalation; equivalent to ERV + RV
Vital capacity (VC)	The volume of air exhaled during a forced exhalation; IRV + TV + ERV
Total lung capacity (TLC)	TV + IRV + ERV + RV (4 L in females; 5.7 L in males)

AEROBIC METABOLISM

Aerobic metabolism is the most efficient mechanism used by the body to convert food energy into energy easily used by the body for fuel. ATP is the primary energy source at rest and during low-intensity exercise. It is composed of a ribose sugar backbone, a nitrogen and carbon chain, adenine, and three phosphate molecules. Aerobic metabolic pathways are also referred to as oxidative because of their dependence on O₂ to generate ATP. Aerobic metabolism is therefore limited by the function of the cardiovascular, respiratory, and musculoskeletal systems, in addition to readily available supplies of O₂. If one of these systems is deficient or unable to generate enough ATP rapidly through oxidative means, the body must rely on less efficient anaerobic systems. Although submaximal activity performed for an extended period primarily taxes the aerobic system, greater-intensity activity performed for a shorter period taxes both aerobic and anaerobic pathways, and near-maximal activity for an even shorter period relies almost solely on anaerobic means for fuel.

The primary sources of fuel driving the aerobic system are carbohydrates and fats. Fat molecules, or triglycerides, are composed of one glycerol molecule and three fatty acid chains. Because the body cannot store triglycerides in their ingested form, they are broken down during a process known as lipolysis into glycerol and fatty acid chains. Fatty acid chains, composed predominantly of hydrogen and carbon atoms, are stored either in fat cells or released into the bloodstream to be oxidized for energy. When taken up by mitochondria, free fatty acid chains undergo beta oxidation, a process that produces acetyl CoA and hydrogen. Acetyl CoA enters the Krebs cycle, and H⁺ is carried by nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH₂) to the electron transport chain (ETC). For every two carbons in a fatty acid, oxidation yields five ATPs generating acetyl CoA and 12 more ATPs oxidizing the coenzyme, producing a net 17 ATP (Figure 4-1).

Figure 4-1 Energy stores.

Carbohydrates are composed of carbon, hydrogen, and oxygen and classified on the basis of the number of sugar molecules that compose the compound (monosaccharide, disaccharide, or polysaccharide). Aerobic glycolysis is the process by which glucose is broken down into pyruvate. The Krebs cycle begins with pyruvate, the end product of glycolysis. The Krebs cycle produces two ATP molecules from guanine triphosphate (GTP) per molecule of glucose consumed. In addition, six molecules of NADH and two molecules of FADH₂ are produced and enter the ETC. The ETC uses these molecules to produce ATP from ADP. The process ATP formation from aerobic pathways is referred to as oxidative phosphorylation. The resultant energy production in a net of 38 ATP0 molecules generated from one molecule of glucose is shown in Figures 4-2 and 4-3).

Figure 4-2 Krebs cycle.

Figure 4-3 Fuel source as a function of exercise intensity.

Efficiency is the proportion of total available energy that is used for work or is stored for future use. Fat is a more efficient fuel source during low-level activities because it is more readily available through fat stores and lipolysis. Energy produced from 1 g of fatty acids is 9 kcal compared with 4 kcal/g from carbohydrate or protein. The individual’s nutritional intake, as well as the intensity and duration of exercise performed, dictates whether fats or carbohydrates are the primary or secondary fuel source in aerobic metabolic pathways. Fats are primarily used during lower-intensity activities over a long duration. Carbohydrates are primarily used during more intense activities of shorter duration activities. At rest, more fats than carbohydrates are typically burned for fuel. As activity level increases, a shift from the utilization of fats to more carbohydrates occurs to meet the increasing energy demands (Figure 4-4).

Figure 4-4 A and B, Maximal oxygen consumption (O₂max) testing.

ACUTE CHANGES IN AEROBIC METABOLISM WITH EXERCISE

Exercise-imposed demands on the cardiovascular and respiratory systems alter O₂ availability via circulation, respiration, ventilation, and aerobic metabolic pathways while maintaining O₂ saturation. If the CV system is not up-regulated with the initiation of exercise, adequate O₂ supplies will not reach working muscles and CO₂ will accumulate in the blood. In addition, if the respiratory system fails to increase ventilation rate, inadequate O₂ supplies will cause a shift to less efficient anaerobic metabolic pathways for energy.

Cardiovascular System

Exercise rapidly increases the energy demands of the body. The CV system matches these energy requirements through the regulation of blood flow to working muscles. Increasing circulation ensures adequate O₂ supplies for aerobic energy pathways and removal of waste products to prevent the accumulation of CO₂, lactic acid, and heat. Changes in both central and peripheral centers aid in the regulation of O₂ delivery and CO₂ removal.

HR is one of the most commonly used means to determine exercise intensity. As mentioned earlier, the number of times the heart contracts per minute in a resting state is referred to as the RHR. With the onset of both aerobic and resistance exercise, RHR rapidly rises.² The rapid increase in HR is a function of parasympathetic stimulation by the ANS. Older, sedentary adults may have a more rapid increase in HR in response to low-intensity exercise compared with more active older adults or even sedentary, younger adults. HR continues to rise in a positive, linear fashion with an increase in exercise intensity. Maximal heart rate (MHR) is the maximum number of times the heart can beat in 1 minute. Prediction models have generated simple mathematical equations that easily predict MHR from age.

For example, a 29-year-old male, based on age-adjusted equations, would have an MHR of 191 beats/min. The heart’s response to exercise depends on age, gender, body mass, fitness level of the individual, and disease presence. More sophisticated means of determining MHR, such as treadmill stress testing, are more accurate determinants of MHR; however, these tests must be performed by trained health care professionals and are expensive to perform.

Stroke volume (SV) is the volume of blood ejected from the left ventricle with each beat. SV is the difference in volumes between the end diastolic volume (EDV), or amount of blood available in the left ventricle after diastole, and end systolic volume (ESV), or volume of blood available after systole. Initiation of aerobic exercise results in increased SV ² explained by the Frank-Starling mechanism. The Frank-Starling mechanism is a mechanical property of cardiac muscle stating that muscle contraction force is directly proportional to a muscle’s length. With exercise, there is an increase in left ventricular filling during diastole. The rise in circulatory blood volume increases the stretch, or length, on ventricular myocardial muscle. The greater muscle stretch yields a more forceful contraction during systole, ejecting a greater volume of blood with each heart beat. The volume of blood or fraction of EDV ejected from the heart with each beat is called the ejection fraction.

Evidence-Based Clinical Application: Assessing Aerobic Capacity

Aerobic capacity is the ability of the cardiovascular system to deliver and use O₂. Assessment of aerobic capacity can be determined via direct, maximal test measures or indirect, submaximal testing. The “gold standard” for determining aerobic capacity is O₂maxtesting. O₂max testing measures the amount of O₂ consumed per unit of time. These values are derived from inspiratory and expiratory volume measures, as well as inspired O₂ and expired CO₂ concentrations. Treadmills, stationary bicycles, and upper body ergometers are the main methods used to determine aerobic capacity. During O₂max testing individuals are asked to perform an activity while workload is progressively increased until an increase in workload does not elicit a further increase in O₂ consumption (Figure 4-5).

Figure 4-5 Bicycle ergometer.

Gold standard methods are not always easy to administer and are often time consuming, making them impractical clinical tests. Submaximal tests, although less accurate, have been validated through correlation of O₂max and physiological measures of submaximal exercise such as HR. Predictive equations have been derived on the basis of the linear relationships between HR and O₂ consumption. Examples of submaximal assessments of aerobic capacity include the YMCA cycle ergometer test, 3-minute Step Test, Cooper 12-minute walk/run test, and the Rockport One-Mile Fitness Test (Figure 4-6).

Figure 4-6 Borg Rate of Perceived Exertion Scale.

Older adults have reduced exercise capacity; therefore when measuring O₂ uptake, a longer warm-up, smaller increments of speed/slope per stage, and lower work peak rate should be used. As a result of reduced exercise capacity with age, some health care professionals prefer to predict aerobic capacity on the basis of submaximal exercise intensity.

Although SV rapidly rises with the onset of aerobic exercise,^2,³ it reaches a plateau at which SV remains at a specific volume despite increasing exercise intensity. At 40% of maximal oxygen consumption (O₂max), SV approaches near maximum levels.³ The early increase in SV is a function of increased venous return. Heavy resistance training does not induce similar changes in SV. SV does not change or changes little in response to resistance exercise. During resistance training, individuals often hold their breath to generate greater force. This results in increased intra-abdominal and intrathoracic pressures, which limits venous return and subsequently does not significantly alter EDV. This mechanism of enhancing force-generating capacity is referred to as the Valsalva maneuver.

Cardiac output (CO) is the amount of blood ejected from the heart per minute. CO is directly related to HR and SV and is expressed in liters or milliliters per minute. This is demonstrated in the following equation:

At rest, SV is approximately 80 ml and resting HR is about 70 beats/min, giving rise to a CO of approximately 5.6 L/min at rest.

At the onset of aerobic exercise there is a concomitant rapid increase in CO as a function of increased HR and SV.^2,³ As exercise intensity and exertion increase continue to rise, HR and SV and therefore CO continue to increase. As O₂ uptake values approach maximum, CO reaches a steady-state or plateau at which CO remains constant despite increasing intensity.³ Increased myocardial contractility, increased blood flow to working muscles, constriction of venous blood vessels, and decreased total peripheral resistance also influence CO during exercise. CO can increase from 5.6 L/min at rest to 35 to 40 L/min with strenuous exercise in young adults. This represents a sevenfold to eightfold increase in CO.

Heavy resistance training does not appear to significantly alter CO. Small increases may be visible secondary to a rise in HR with heavy resistance training. Modification of resistance training parameters to stress more aerobic energy pathways may produce more substantial changes in CO. This can be achieved by increasing the number of repetitions and lowering the resistance.

Evidence-Based Clinical Application: The Valsalva Maneuver

The Valsalva maneuver, a natural response to lifting heavy loads, is characterized by a forced exhalation against a closed glottis. During forced exhalation, a sudden increase in intra-abdominal and intrathoracic pressures is produced by the contractions of the abdominal and respiratory muscles. Elevated pressures compress the blood vessels within the chest cavity, leading to a decrease in venous return and CO. In addition, compression of the aorta leads to stimulation of the baroreceptors, producing a reflex-induced bradycardia to compensate for the increased pressures. Aortic pressure subsequently rises, stimulating sympathetic activity. HR and BP rise in response to maintain CO and perfusion. At the cessation of the forced exhalation, venous return rapidly increases, intra-abdominal pressures drop, and CO is increased, dramatically increasing the mechanical load on the heart.⁴

The Valsalva maneuver can be dangerous due to the sudden and abrupt changes in BP. These dramatic changes in HR, BP, and CO may produce symptoms including dizziness, lightheadedness, and syncope. However, the Valsalva technique can help protect against injury during heavy weight lifting. The supporting ligaments of the spine can only support 4 to 5 lb of pressure before failing.⁵ Therefore performing the Valsalva maneuver during heavy lifts, such as the Roman dead lift, squats, bench press, and clean and jerk, assists core musculature in supporting the spine and decreases the compressive load on the intervertebral disks.⁶

Strength and conditioning coaches often recommend the Valsalva maneuver during weight-lifting exercises requiring a stable core. Individuals are coached to perform the maneuver during the work phase of the lift. Individuals should inhale before the exercise, hold their breath through the most difficult phase of the lift, and exhale to complete the lift. Because the consequences of improper breathing with weight lifting can be severe, proper education is essential.

BP is a function of CO and resistance to blood flow or total peripheral resistance (TPR). Increases in systolic blood pressure (SBP) are also evident at the onset of aerobic exercise, whereas small decreases, if any, are noted in diastolic blood pressure (DBP).² SBP continues to increase in a positive, linear fashion as exercise intensity progressively increases. A 10- to 20-mmHg increase in SBP can be expected during dynamic exercise. DBP, on the other hand, has been observed to slightly decrease during dynamic treadmill exercise. Resistance training results in increased central/carotid SBP, although BP returns to preexercise levels within 30 minutes of the exercise bout.⁷

O₂max is a measure of the body’s utilization of O₂ and is the greatest amount of O₂consumed per minute at maximum effort. O₂max is a major determinant of cardiopulmonary fitness and is often expressed relative to body weight (ml/kg/min). The rate of extraction of O₂ in the tissues of an individual at rest is 4 to 5 ml of O₂ per 100 ml of blood. The amount of O₂ consumed and the percent of O₂max used depend on body mass, exercise intensity, and mode of exercise. At the onset of aerobic exercise, O₂ uptake increases progressively. As intensity increases and nears O₂max, O₂ extraction rate increases to approximately 13 to 16 ml of blood during maximal aerobic exercise intensity. As a general rule, the greater the percentage of muscle mass used during aerobic exercise, the greater the rate of O₂extraction. Activities such as running, swimming, and cycling use a large percentage of O₂max because larger muscle groups (i.e., quadriceps femoris, gluteal muscles, latissimus dorsi) are the prime workers.