Terminology in Mobilization and Exercise

Before moving into the physiology of mobilization and exercise, a few definitions are necessary to clarify the discussion. Strict definitions are important when discussing the following concepts:

Exercise has been the basis for physical therapy for more than 100 years, but exercise science has only emerged as a discipline within the past 60 years. Over this time, typical responses of various organ systems to both short- and long-term exercise stress have been detailed by researchers. The main question being addressed pertains to what physiological changes can be expected when an individual initiates exercise (particularly in a test with a standardized protocol). Changes in breathing, heart rate, blood pressure arterial saturation, , and , as well as subjective responses of exertion and fatigue, are all aspects of this study. An understanding of these responses has enabled physical therapists to use exercise as a tool in the assessment, evaluation, and training of patients.

Physiological response can vary in deconditioned people where a given work rate is perceived as highly strenuous, yet the absolute work rate is relatively low. These responses can be markedly altered in people with a range of pathologies (depending on their types and severities) and these differences need to be anticipated and considered (see Chapters 24 and 25) in the assessment of a patient.

For evaluation, exercise tests can serve as standardized outcome measures. As evaluation tools, tests are repeated periodically (e.g., every few weeks) in order to progress the exercise or training prescription until the target conditioning goal is achieved. Special attention is paid in these cases to pre-exercise conditions and the standardization of both exercise procedures and measurement procedures (Chapter 19).

Clinically, physical therapists select which test outcomes are relevant based on the patient’s needs and goals. In some patients, objective responses such as HR or SpO₂ may be primarily of interest, whereas subjective responses such as breathlessness, fatigue, or pain may be of particular interest. Some pathologies can limit the level of conditioning that is achievable with training; thus a comprehensive multisystem assessment is needed to establish realistic goals for the training, along with parameters to maximize its benefits and limit potential adverse effects.

Often for people with chronic conditions, many of whom may be older, submaximal tests can be used to compare responses from one time to another for given work rates. In other cases, the physical therapist may wish to estimate by conducting a test, which can be done directly or indirectly. Direct measurement of requires metabolic measurement with a cart and capacity for expired gas analysis for O₂ and CO₂ (Figure 18-1). Such carts require pretest gas calibration in addition to calibration of the exercise modality (treadmill or ergometer). The patient needs to be familiarized and habituated to the tester(s) and testing situation, and practice beforehand, to ensure the results are valid. Indirect assessment of is imprecise but can provide an index of general conditioning if methods are tightly standardized; this is particularly important when test results are used as outcome measures. Practices related to exercise testing and training prescription are detailed in Chapter 19.

 Mobilization

 Exercise

 Body positioning

 Arousal

 Breathing control maneuvers

 Coughing

 Postural drainage

 Manual techniques

 Bagging

 Suctioning

 Range-of-motion (ROM) exercises

Cellular Energetics in Response to Acute Mobilization and Exercise

The integrity of the cardiopulmonary unit is fundamental to maximize oxygen transport and cellular respiration. Oxygen is continuously being used by every cell in the body for oxidative phosphorylation and the synthesis of adenosine triphosphate (ATP). The splitting of a phosphate bond from ATP to form adenosine diphosphate yields a considerable amount of energy for metabolism. The energy for this process comes from the reduction of hydrogen in the formation of water and carbon dioxide, which are the end products of the Krebs cycle and the electron transfer chain (i.e., cellular respiration). These metabolic processes, which make up oxidative phosphorylation, take place in the mitochondria of the cells (see Chapter 2).

The balance between oxygen consumption and oxygen delivery is precisely regulated to ensure not only that there is an adequate supply of oxygen but also that, under typical resting conditions, approximately four times as much oxygen is delivered to the tissues as is used. This safety margin permits the immediate availability of oxygen when the system is perturbed by physical, gravitational, or psychological challenges (see Chapter 2).

Anaerobic metabolism is prevalent at the initiation of all movement/activity/exercise and also during intense, short, sprint-type activities (i.e., sports such as hockey, soccer, and volleyball or functional activities such as stair climbing, heavy lifting/carrying, and vigorous walking/running). Physical therapists tend to focus on aerobic rather than anaerobic exercise; however, in situations where tasks to be improved involve high levels of intensity, training programs may be designed to elicit anaerobic adaptations. In conditions for which DO₂ is compromised, patients may rely on anaerobic metabolism to sustain ATP production and breakdown to provide energy. Anaerobic capacity and, specifically, the anaerobic threshold can increase with training; however, anaerobic training effects are less than aerobic training effects achieved with aerobic training.

Although the term anaerobic implies that the exercise is performed in the absence of oxygen, anaerobic metabolism provides a short-term means of supporting phosphorylation, using substrates other than oxygen to generate and split ATP. If insufficient oxygen is available, the amount of ATP that can be generated anaerobically is limited; thus this process can be sustained for only a short period.

Lactic acid accumulates in the blood during anaerobic metabolism. In healthy, untrained individuals lactic acid increases exponentially at an exercise intensity of about 55% of maximal aerobic power.⁶

Anaerobic metabolism is thought to be triggered by tissue hypoxia, though the term anaerobic is somewhat a misnomer: oxygen is still needed to pay the oxygen debt. In healthy patients the need for oxygen is delayed rather than eliminated; in patients with disease, anaerobic metabolism occurs when a patient’s oxygen transport system cannot meet the metabolic demand required (i.e., patients with sepsis and multisystem organ dysfunction). Serum lactate levels are elevated in these patients, resulting in metabolic acidosis, which is unfavorable to the maintenance of homeostasis.

During exercise, the cellular PO₂ is lower than the surrounding interstitial fluid PO₂ and oxygen diffuses rapidly through cell membranes. At the onset of physical exercise, the increased metabolic demand of the muscle and supporting tissues increases the oxygen diffusion gradient. Feedback mechanisms are triggered to increase DO₂, which depends primarily on arterial oxygen content and CO.

The first line of defense is the response to an increase in pericellular pH. The concentration of carbon dioxide is increased, and this, as a result of the decrease in pH, facilitates the dissociation of oxygen from hemoglobin (i.e., it shifts the oxyhemoglobin dissociation curve to the right). CO, the product of stroke volume and heart rate (SV × HR), increases commensurate with metabolic demand. The immediate response to oxygen utilization and lowered tissue oxygen is an increase in CO to increase DO₂. This averts arterial desaturation that is not typically observed in health, even with extreme exertion. With progressive exercise intensity, SV increases disproportionately at lower intensities to increase CO, with HR contributing to a greater extent at moderate and high exercise intensities. However, older individuals exercising at high intensity in upright positions rely more on the Frank-Starling effect than on HR.⁷ In health, exercise-induced cardiac fatigue has been proposed as a limiter to prolonged exercise.⁸ The mechanisms of the associated reduced left ventricular systolic and diastolic function are unclear.

The increase in systemic CO results in increased venous return and pulmonary CO. The SV plateaus at 40% of , and thereafter CO is augmented by increases in HR (Figure 18-2). One exception in health is in elite athletes, whose SV may continue to increase commensurate with exercise intensity.⁹ To oxygenate a greater volume of blood in the lungs, an increased volume of air must be inspired. To increase , tidal volume (V_T) and respiratory rate (RR) increase. At low intensities of exercise, V_T increases disproportionately to RR, whereas at moderate to high intensities, V_T plateaus and further increases in are effected by an increase in RR (Figure 18-3).¹⁰ Exercise is associated with a small increase in airway diameter and length of pulmonary structures, hence, a reduction in airway resistance. Zone 2, the zone of greatest alveolar ventilation to perfusion () matching in the lungs, is increased as a result of pulmonary capillary dilation and recruitment. Diaphragmatic excursion is enhanced, and the distributions of ventilation and perfusion become more uniform throughout the lungs, which minimizes airway closure and atelectasis. Exercise increases diaphragmatic excursion, which leads to inflation of the lungs in three planes (anteroposterior, transverse, and cephalocaudal, particularly in the upright position).

Rhythmic inflation and deflation of the lungs associated with physical activity has several clinically important effects:

Circulation to the heart and periphery is primed and responds to the increased demands of acute exercise. Hemodynamic adjustments occur immediately with the onset of exercise stress and in fact may precede it due to a typical anticipatory response. To maximize the availability of CO to working muscle (e.g., the legs), blood shifts from the venous capacitance reservoirs, such as the venous compartments of the gut and extremities. At rest, most of the circulation (70%) is contained within the highly compliant venous circulation. The Starling law of the heart regulates the forward movement of blood commensurate with the volume of blood that is received. The heart chambers are normally distensible; they adjust to changing volumes of blood returning to the heart and pump more forcefully when stretched than at rest, in order to eject blood through the pulmonary and peripheral circulations. Muscle enzymes that extract oxygen at the cellular level are also primed and are synthesized commensurate with chronic metabolic demand.

Effects of Mobilization and Exercise on Oxygen Transport

In health, optimal oxygen transport depends on the integrity of each step in the oxygen transport pathway and the interdependency of these steps. Cardiovascular and pulmonary dysfunction can lead to dysfunction in one or more steps in the oxygen transport pathway. Because of the interdependence of these steps and the ability of functional steps to compensate for dysfunctional steps, gross measures of gas exchange and oxygenation can be normal. The number of steps in the pathway that are affected by pathology and its severity determine the impairment of oxygen transport overall and the degree to which this impairment is reflected in gross measures of oxygen transport.

To maximize the capacity of the steps in the oxygen transport pathway, the oxygen transport system must be exposed to two principal stressors: (1) gravitational stress and (2) exercise stress. These stressors are essential to life in that they enhance the biochemical, physical, and mechanical efficiency of the steps in the oxygen transport pathway and the patient’s capacity to respond rapidly to changes in the physical environment.

Conversely, the absence of gravitational stress and exercise stress are the two primary factors contributing to impaired oxygen transport secondary to bed rest deconditioning. Exploiting both gravitational and exercise stress to prevent cardiovascular and pulmonary dysfunction is thus indicated. Further, mobilization and exercise are the two most vital physiological interventions available to the physical therapist for remediating cardiovascular and pulmonary dysfunction. Body position has marked effects on pulmonary and cardiovascular function (Chapter 20) and thus on exercise performance. The more acutely ill a patient is, the more important it is that upright body positioning be coupled with mobilization to increase aerobic capacity and tolerance to exercise stress. The degree to which this is done, however, depends on the patient’s status and ongoing monitoring (see Chapters 16, 34, and 35).

The Prescription of Mobilization and Exercise

The prescription of exercise is fundamental to the management of primary and secondary cardiovascular and pulmonary dysfunction. Guidelines have been well developed for prescribing exercise to maximize functional work capacity or aerobic power for healthy people and individuals with chronic heart and lung conditions.14–21

As clinical exercise specialists, physical therapists strive to take advantage of the effects of exercise in most patients and adapt the prescription based on the patient’s clinical presentation and needs. Exercise training is typically based on a person’s responses to a maximum graded exercise test. Although somewhat less precise, exercise training intensity can be prescribed based on a proportion of the individual’s age-predicted maximum heart rate provided there is no significant medical history. Submaximal exercise testing is often indicated for patients with severely impaired functional work capacity because of the inherent risks associated with maximal testing and the potential for invalid test results.²² Submaximal exercise testing has had a greater role in patient assessment and evaluation than as a basis for exercise prescription. Because of the greater utility of submaximal exercise testing in patient populations, guidelines for the latter warrant being better elucidated.

The prescription of mobilization for the patient with acute cardiovascular and pulmonary dysfunction has been a relatively neglected research priority when compared with the number of studies concerning the prescription of exercise. This is surprising, given that early mobilization is generally a key component of cardiovascular and pulmonary physical therapy for patients who are acutely ill. Orlava (1959)²³ was among the first to report the beneficial use of mobilization to manage acute cardiovascular and pulmonary compromise; specifically, bronchopulmonary pneumonia. In addition, the physiological literature has long supported an unequivocal role for therapeutic mobilization to maximize oxygen transport in patients with acute cardiovascular and pulmonary dysfunction.²⁴ Even for patients who are critically ill, the goal of mobilization is to evaluate the patient’s responses with respect to oxygen transport reserve capacity and use this as a basis for estimating the limits of a patient’s physiological capacity to be mobilized, with a view to returning the patient to living within the community. The more critically ill the patient, the greater the need to assess the relationship between the patient’s and oxygen delivery (DO₂) (see Chapter 2);²⁵ this ensures that the patient’s capacity for oxygen transport is not exceeded.

Unlike exercise testing and prescription for the patient with chronic cardiovascular and pulmonary conditions, the patient with acute dysfunction is not exercise-tested in the conventional manner because of understandable risk and the patient’s incapacity to perform such a test. Given the profound and direct effects of mobilization and exercise on cardiovascular and pulmonary function, the physical therapist needs to identify the specific effects of exercise required and define the optimal therapeutic stimulus (i.e., the stimulus that yields the maximal benefit to oxygen transport with the least risk). The parameters for the mobilization prescription are based on factors other than a maximal or peak effort (see Chapters 16, 34, and 35).

Acute and chronic cardiovascular and pulmonary pathology have the additional challenges of compromising functional capacity in two ways. First, in acute illness, the patient tends to be recumbent in bed a great proportion of the time; second, in both acute and chronic illnesses, the patient’s physical activity is reduced. Recumbency and restricted mobility have physiologically distinct effects on oxygen transport that contribute jointly to bed rest deconditioning; recumbency, however, has been considered to be the primary determinant of bed rest deconditioning.26–28 The impact of these factors is exaggerated in smokers, young people, older adults, obese individuals, and patients who are mechanically ventilated.

The goals of mobilization and exercise are directed at correcting impairments and enhancing the patient’s capacity for activity and participation (see overview of the WHO International Classification of Function, Disability and Health in Chapters 1 and 17). Outcomes related to improving abilities and participation include self-care, home management, return to work, and resumption of avocational activities. Return to work warrants special mention. Return to work is often related to oxygen transport capacity in terms of aerobic and muscle power. However, there are economic, psychosocial, and environmental factors that need to be considered. These factors, too, should be part of the overall assessment and incorporated when setting overall goals and establishing the appropriate outcomes for a given patient.

Cardiovascular and Pulmonary Effects

A primary effect of mobilization and exercise on the cardiovascular and pulmonary systems is enhanced mucociliary transport and airway clearance.¹² Frequent changes in body position augment airway clearance and minimize the pooling and stagnation of bronchial secretions, hence reducing airway obstruction and airflow resistance (Chapter 20). The benefits of frequent body position changes to prevent the accumulation of secretions or resolve them can be augmented when combined with mobilization.

The cardiovascular deconditioning resulting from bed rest includes the loss of fluid-volume and pressure regulating mechanisms, the loss of plasma volume, and diuresis.67–70 In turn, the hematocrit is increased, and the risk for developing deep vein thromboses and thromboemboli is increased. This is exacerbated by increases in blood viscosity, platelet count, platelet stickiness, plasma fibrinogen,⁷¹ and stasis of venous blood flow.

Venous thromboembolic disease is preventable with conservative management, including prophylactic anticoagulation in some instances.⁷² In addition to restricted mobility, other risk factors include being older, undergoing venous catheterization, and hormone replacement therapy. Conditions that are associated with risk include previous thromboembolus, myocardial infarction, heart failure, severe lung disease, cancer, obesity, and paralytic conditions such as stroke. After acute stroke, patients are particularly at risk due to paresis, recumbency, restricted mobility, and circulatory stasis.⁷³ The work of the heart is increased in a patient who is immobile and recumbent, as is the work of breathing. The work of the heart is greater as a result of the increased filling pressures and heart rate associated with chronic recumbency and the increased blood viscosity. The work of breathing is increased because of reduced lung volumes secondary to visceral encroachment on the underside of the diaphragm, increased intrathoracic blood volume, and restricted chest wall motion.

Pulmonary sequelae of recumbency include reduced lung volumes and capacities, particularly functional residual capacity (FRC), residual volumes (RV), and forced expiratory volumes.74–78 A reduction in FRC in the supine position compared with the sitting position has been attributed to both a decrease in thoracic volume and an increase in thoracic blood volume, thereby increasing pulmonary venous engorgement.⁷⁹ Thus alveolar-arterial oxygen difference and arterial oxygen tension are reduced during bed rest.^80–82 Closing volumes are increased, precipitating arterial desaturation in recumbent positions and subsequent complications.

With bed rest, the blood vessels of the muscles and splanchnic circulation dilate. With prolonged bed rest, they may lose their ability to constrict. The ability of these vessels to constrict is essential for preventing the pooling of blood and maintaining circulating blood volume when the patient assumes the upright position. Following bed rest, a patient may feel lightheaded or dizzy and may faint. Individual differences in terms of orthostatic intolerance have been reported and need to be assessed.67,68,83,84 Individuals with greater venous compliance in the legs recruit mechanisms to compensate, such as activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, and inhibition of the parasympathetic nervous system, so they tolerate orthostatic challenges better.

Musculoskeletal Effects

With only a few days of bed rest, muscle atrophy is initiated, leading to weakness, discoordination, and balance difficulty.57,85 With severe weakness, excessive strain may be placed on ligaments and joints. Muscles and their inert structures are differentially affected. In the knee extensors, for example, tendon stiffness is reduced and their hysteresis characteristics become exaggerated, whereas this does not occur in the plantar flexors.⁸⁶ Muscle mass and strength may be lost, and muscle and ligament shortening may occur along with joint contractures, skin lesions, and decubitus ulcers.^87,88

At the cellular level, disuse atrophy begins within 4 hours of bed rest. Compared with type IIa muscle fibers in vastus lateralis, type I fibers have been reported to be more seriously affected by bed rest, and they respond less favorably to muscle-resistance training.⁸⁹ Differences in fiber type may explain why muscles in the lower limbs are differentially affected; for example, the plantar flexors are particularly affected.⁹⁰ Also, sex differences in muscle strength loss with bed rest have been reported.⁹¹ Muscle imbalance may result from poor postural alignment.

Skeletal muscle protein synthesis is compromised by bed rest, aging, nutritional deficit, uncontrolled diabetes mellitus, and sepsis.⁹² Disuse osteoporosis results from reduction of the mechanical stress caused by gravity and from lack of active muscle contraction across joints. Prevention is a primary goal because recovery of mineral loss in bone is prolonged and its loss is largely irreversible.⁹³ Bone mass is restored later than muscle mass and function after a period of restricted mobility, which contributes to fracture risk.⁹⁴

The limited positioning alternatives in bed may contribute to poor postural alignment, stiffness, and soreness. Bed rest allocates weight bearing to various body parts not adapted for weight bearing. Skin breakdown most commonly occurs over bony prominences, such as the sacrum, trochanters, elbows, scapulae, and heels. Risk factors for pressure ulcers include age, prolonged hospitalization, restricted mobility and general debility, low body weight, low diastolic BP, and surgical intervention.⁹⁵

Immobile patients are at risk for bone demineralization. An issue of particular importance in older populations, patients with disabilities, postmenopausal women, and patients on steroids is calcium loss. Prevention of disuse osteoporosis is the primary aim because remineralization of bone, even with aggressive exercise, body positioning, electrical stimulation, and possible pharmaceutical agents, is unlikely.⁹³ In patients who are critically ill, cytokines have been implicated in inactivity-related inflammation and muscle injury and atrophy. Activity has been proposed as a countermeasure.⁹⁶

Renal Effects

Bed rest–induced diuresis increases renal load. Patients with renal insufficiency are particularly seriously affected by this effect, as well as by other sequelae of bed rest.⁹⁷ As a result, they may exhibit dysrhythmias, muscle wasting, weakness, neuropathy, glucose intolerance, and reduced bone density.

Central Nervous System Effects

With bed rest and recumbency, orthostatic intolerance in combination with resting tachycardia and reduced exercise capacity occur, reflecting diminished reflex activity of the sympathetic nervous system. Baroreceptor-mediated activity is blunted and appears to involve abnormal processing in the central nervous system at the level of the ventrolateral medulla.⁹⁸ CNS changes include slowed electrical activity of the brain, emotional and behavioral changes, slowed reaction times, sleep disturbances, and impaired psychomotor performance.^88,99 Diminished sympathetic activity is the primary factor responsible for orthostatic intolerance along with hypovolemia; the net result is bed rest deconditioning.¹⁰⁰

Metabolic Effects

Metabolic changes that occur during periods of bed rest and the relative absence of muscle contraction include glucose intolerance and reduced insulin sensitivity;¹⁰¹ increased calcium excretion due to bone loss; and increased nitrogen excretion secondary to protein loss from atrophying muscle.^102,103 In sedentary people, plasma lipids are elevated and skeletal muscle becomes insulin resistant.¹⁰⁴ Insulin sensitivity and triglyceride levels are highly responsive to changes in diet, activity level, and thermogenic state. Fit people are highly insulin sensitive, whereas unfit sedentary people tend to be insulin insensitive. Reversal and the normalizing of insulin sensitivity are dependent on increasing muscle contraction.

Immunological Effects

Bed rest has been associated with reduced cytokine function and antibody counts, hence, reduced immunity and an increased risk for infection.105,106 Lymph flow is reduced with bed rest, which may predispose patients to further risk for infection.¹⁰⁷

Psychological Effects

Bed rest also affects psychological status. Patients may become depressed or sensorily deprived or may develop a psychoneurosis.¹⁰⁸

Alternatives to the Nonspecific Use of Bed Rest

The evidence supports the following:

Given this evidence, alternatives need to be exploited within and outside physical therapy treatment. Physical therapists, for example, need to become active in designing furniture and devices that are better suited to patients’ normal physiological functioning and to the needs of patients’ courses of recovery. Such appliances would include the presence in ICUs of a greater number of stretcher chairs that enable easy transfer of patients from bed to chair and upright positioning and a greater availability of patient-lifting devices. Greater attention needs to be given to chair design in settings where patients may be immobile; effective chair design could augment the mobilization process in addition to promoting body position changes.

Kinetic and rotating beds are electromechanical beds that turn the patient through an arc of about 30 degrees to both sides from the supine position over several minutes.109,110 These beds are used for heavy-care patients who are critically ill and are unable or difficult to turn. Even though studies have shown these beds can enhance oxygenation in severely compromised patients such as those with acute respiratory distress syndrome,^111,112 they need to be used selectively judiciously.¹¹³ Reliance on passive positioning by the bed should not substitute for more active and active-assisted patient positioning. Such interventions constitute the initial stages of mobilization and ambulation.

The use of tilt tables to promote mobilization may be hazardous because the muscle pumping action when the legs are dependent is minimal. Passive standing on a tilt table constitutes a greater hemodynamic stress than does active standing. Upright sitting postures with the legs dependent may elicit greater physiological benefit than passive standing and with less risk because of the resulting increased hemodynamic stress. Leg movement elicited by stepping in place, however, can counter the marked fluid shifts associated with the upright position.

Even in patients who are seriously acutely ill (e.g., those in the ICU), body positioning and mobilization are essential to offset the deleterious effects of loss of gravitational stimulation from being upright and loss of exercise stimulation from restricted mobility (Chapters 33, 34, 35, and 36).¹¹⁴

Indications for Bed Rest

Despite the universal acceptance of bed rest as a medically therapeutic intervention, indications for its therapeutic use have not been well documented, and its effectiveness continues to be questioned.³⁹ Further, much more is known about the adverse and potentially life-threatening hazards of bed rest than about its benefits. Bed rest should clearly be used as selectively and prescriptively as other medical interventions to ensure that specific benefits are being derived and that the multisystemic negative sequelae are minimized.

Many procedures such as surgery are associated with considerable pain, so being relatively immobile and recumbent in bed is believed to minimize postsurgical discomfort. Minimizing the effects of gravity and the need to bear weight is commonly indicated in patients after orthopedic surgery. Likewise, the bed enables a patient with multiple wounds and fractures to be immobilized and supported in a fixed position that is believed to promote healing.

Conditions that are associated with edema require minimizing the effect of gravity on the affected limbs. Whether edema can be controlled by localized elevation rather than bed rest must be established. Certain conditions may require some activity restriction, particularly in their acute stages in order to reduce the work of the heart, as in cases of myocardial infarction. However, 50 years ago, restriction to a chair was reported to be more beneficial than restriction to bed in patients with heart disease.¹¹⁵ Despite this finding, many patients continue to recline in beds rather than sit upright in chairs and initiate ambulation. Mobilizing patients and permitting bathroom privileges has also been reported to be less stressful than having to use a bedpan.¹¹⁶

A comprehensive list of the physiological benefits of acute exercise is presented in Table 18-3. The principal benefits include:

The particular benefits of acute mobilization and exercise can be directed at each patient’s specific pathophysiological deficits.

After decades of research in exercise science, based in particular on college-aged male students, an increasing number of studies have identified sex differences in exercise responses. Higher peak and muscle strength are found in men compared with women even when adjusted for body weight. These are explained primarily by hormonal differences, specifically estrogen and progesterone in women and testosterone and androgen in men. Differences in autonomic function contribute to the reduced risk by women for heart disease and to their increased longevity.¹¹⁷ Women have greater parasympathetic control of the heart and less sympathetic activity.

Prescribing Exercise and Mobilization

The clinical decision-making process involved in defining the optimal mobilization and exercise stimulus for a given patient is multifactorial. The integrity of each step in the oxygen transport pathway and the overall integrity of the system in preserving arterial oxygenation and pH, are determined based on the:

Once the necessary specific effects of acute mobilization or exercise are identified and matched to the patient’s underlying pathophysiology (Box 18-1), the mobilization or exercise stimulus can be prescribed. Rather than a rigidly structured regimen, the prescription must evolve as the patient progresses in order to maximize its benefits (Table 18-4).

1. Establishing a stable baseline founded on standardizing the preexercise conditions; and

2. Determining the appropriateness of the quantitative and qualitative changes in the objective and subjective responses during the onset of activity, the steady-state phase of activity, cool-down, and recovery.

  reflects the sum of the conductances of an integrated system of oxygen transport from the inspired air to the mitochondria.

 CO is in part passively regulated by the elastic characteristics of the peripheral circulation,¹⁵⁷ so its anatomic and physiological integrity is essential to DO₂.

Mobilization Testing for Progression

Evaluating a patient’s response to a mobilization stimulus can be assessed in two ways: through challenges or through observation.

If stable, the patient can be exposed to a mobilization challenge test. The patient is monitored before, during, and after mobilization activities comparable to monitoring for a graded exercise test. Box 18-2 outlines levels of mobilization and devices that can be used (by the physical therapist or the patient) to augment the patient’s performance; these are factors included in the overall prescription and are likely to be revised frequently from one treatment session to the next, or even within a session. Relatively low-intensity activities, such as bed exercises, moving in bed, changing body position, sitting up, dangling over the bed’s side, transferring to a chair, doing chair exercises, and taking short walks with assistance, constitute a sufficient stimulus to elicit the acute effects of exercise, as well as gravitational stimulus. The degree of assistance required to perform the activity should be noted because it demonstrates the patient’s individual effort.

Monitoring for Progression

Patients for whom mobilization is prescribed require monitoring. Because of the stress to the oxygen transport system that mobilization elicits, the following variables, in addition to oxygen transport variables, are useful:

The RPP is an index of myocardial during exercise and an indicator of the work of the heart.¹⁶⁷ In individuals with ischemic heart disease, the anginal threshold often can be defined by the RPP. After bed rest, healthy individuals have blunted sympathetic responses to isometric exercise in the antigravity muscles;¹⁶⁸ thus patients who have had periods of recumbency and restricted activity may show similar abnormal responses to exercise. Subjective responses, including discomfort and pain, fatigue, exertion, and breathlessness, can be recorded as needed. Visual analog scales are commonly used, as are modified Borg scales: 0 (nothing at all) to 10 (maximal exertion).¹⁶⁹ Subjective responses are more inherently variable and unreliable, therefore potentially less valid.¹⁷⁰ Nonetheless, intrasubject reliability may be acceptable if measures are conducted in a standardized manner and thus can serve as supplementary outcome measures.

Prescription of a Mobilization Stimulus

Prescribing a mobilization stimulus for its acute effects parallels the prescription of exercise for its long-term effects but with some important differences. In patients with acute disease, a mobilization stimulus often results in a greater response gain than is found with such a stimulus in patients with subacute or chronic illness. In addition to the rapid favorable response an acutely ill patient may have to acute exercise, the patient may exhibit a negative response just as quickly. Thus judicious monitoring of treatment responses in these patients is essential; the prescription is driven by patient response.

Patients for whom mobilization is indicated have had variable periods of recumbency that can alter their hemodynamics and autonomic function, as well as their capacity to respond normally to mobilization.¹⁷¹ Hemodynamic responses even to static exercise can be blunted, and this may vary from day to day. Further, such responses can vary from hour to hour in acutely ill patients, and day to day in patients with chronic dysfunction. In patients who are severely and acutely ill, passive rather than active exercise may be the only feasible option. Little research has been done to examine the acute and chronic effects of such exercise, although when passive cycling is compared with active cycling (10% of ) in healthy people, , HR, exertion, and electromyographic (EMG) activity are predictably lower.¹⁷² The shortening of the duration of the preejection period and the length of this period in relation to ejection time, however, is similar. Plasma catecholamines remain at resting levels for both types of exercise, but blood lactates increase in both, with higher levels occurring in active cycling. Thus the inotropic response to exercise probably depends on both skeletal muscle mechanoreceptors and the Frank-Starling effect (preload and shortening in the preejection period).

The optimal therapeutic dose of the acute mobilization stimulus, particularly the initial dose, is based on the patient’s presentation and history; the specific parameters are determined by the goals of the treatment and the acute effects of exercise that are indicated. The intensity of mobilization necessary for many patients will be the intensity that elicits the reactions outlined in Box 18-3.

Over time, exposure to an acute exercise stimulus of an appropriate intensity, for an appropriate duration and at an appropriate frequency, will stimulate long-term aerobic adaptation to that stimulus. Underprescribing the exercise stimulus results in less potent effects; overprescribing results in excessive, deleterious effects. Although the latter may be tolerated in the short run, the patient’s well-being may be jeopardized by suboptimal treatment responses, overtraining signs and symptoms, and risk.

The duration of each mobilization session and the frequency of sessions are response-dependent rather than time-dependent. The optimal mobilization threshold, in which physiological variables increase but not in excess of predetermined acceptable and safe limits, should be maintained for as long as possible within the patient’s fatigue and comfort levels and in the absence of adverse responses (determined by ongoing monitoring). The mobilization sessions should be repeated as often as the patient can tolerate them (i.e., as often as the patient exhibits beneficial responses or no deterioration and adequately recovers between treatments). Treatment sessions for acute cardiovascular and pulmonary dysfunction are usually shorter and more frequent than for patients with chronic cardiovascular and pulmonary dysfunction. The patient’s condition changes rapidly with respect to both improvement and deterioration. Progression of mobilization for its immediate acute effects is usually rapid. Progression of exercise for its long-term effects may occur every several weeks, whereas progression of mobilization for its acute effects may occur as frequently as every treatment to every few days. Over time, exposure to a progressive mobilization stimulus leads to long-term physiological adaptations throughout the oxygen transport pathway. The goal is to achieve the oxygen transport status that is consistent with being able to discharge the patient from care to home or from one level of care to the next lowest level of care (e.g., from critical care to the ward).

The Mobilization Session

The scheduling of and preparation for a mobilization session is crucial to the response that can be expected. The conditions outlined in Table 18-6 should be adhered to as closely as possible, and their details should be recorded so that any factor that influences the response to treatment can be identified.

Circadian rhythms refer to physiological changes that occur in response to the fluctuating synthesis and secretion of hormones and other endocrine regulators over time (usually over 24 hours). These have a profound effect on physiological function. Circadian rhythms can be exploited in optimizing functional performance. Younger people may want to exercise later in the day, whereas older people might optimize their activity and exercise in the morning.¹⁷⁴ These differences are important to the physical therapist concerned with optimizing performance in patient populations whose response to activity and functional capacities may be dependent on time of day. Growth hormone production is determined by circadian fluctuations, sleep, and exercise.¹⁷⁵ Growth hormone is implicated in metabolism and physical performance throughout life. Thus exercise-induced growth hormone is an important effect of exercise that can optimize levels of growth hormone for general health, well-being, and successful aging. Circadian rhythms can be desynchronized during illness and, in particular, during hospitalization. That is why normal day and night cycles should be maintained, even in critical care units, so as to augment patients’ recovery.

The basic components of a mobilization session should approximate the components of an exercise session described by the American College of Sports Medicine for long-term training effects¹⁴ (Figure 18-5). Wherever possible, the session should include warm-up, steady-rate, cool-down, and recovery. These components are less distinct when a patient has minimal functional capacity or is being mobilized to remediate acute cardiovascular and pulmonary dysfunction. The rhythmic movement of large muscle groups is still ideal. Prolonged static maneuvers are usually avoided, particularly if the patient is severely ill, because of their disproportionate hemodynamic response. The movements that are usually considered when mobilizing a patient include turning, sitting up, shifting, transferring, standing, and taking some steps. The progression of the levels of mobilization and exercise for medical and surgical patients, based on a consideration of metabolic cost (up to light to moderate activity), is illustrated in Figure 18-6. This schema represents the low end of the incremental staircase of activities based on the MET level shown in Figure 18-7 for a broader range of physical activities (up to very heavy activity).

Patients progress from one level to the next on the basis of their objective and subjective responses. Mobilization can be metabolically demanding for patients with acute cardiovascular and pulmonary dysfunction. Thus pacing the mobilization session allows the patient to rest between stages. The patient is reassured and encouraged to relax and coordinate deep breathing and coughing with the activity. Throughout the session, attention is given to the patient’s biomechanical alignment, postural erectness, and stability. Back extension or body positioning minimizes the slumping of the chest wall and compromised ventilation. In this way, chest wall expansion is maximized in three dimensions. The erect position is efficient and requires the least amount of energy to maintain. Less demand is placed on the accessory muscles of respiration in erect sitting, and this effect is enhanced further by leaning forward and supporting the arms.

This chapter emphasizes the principles of mobilization and progression for the patient who is acutely ill but medically stable. Patients who are medically unstable, including those in the ICU, warrant special consideration, which is addressed in Chapters 33, 34, 35, and 36. Regardless of the clinical setting, however, the rate at which progression occurs typically depends on a patient’s response rather than a structured protocol.

Adaptation to an Acute Mobilization Stimulus

When an individual is exposed to repeated exercise stress of a specific threshold intensity and for a response-dependent duration and frequency, there is a cumulative adaptive response to that repeated stimulation, or a long-term training response. The goal is to adapt the patient to multiple short mobilization sessions per day, as frequently as once per hour as indicated and as tolerated, and progressively increase the intensity of these sessions, reduce the duration, and correspondingly reduce the frequency of sessions. Table 18-7 illustrates the inverse relationship between exercise duration and frequency of the sessions.

Mobilization activities prescribed to enhance oxygen transport can be coupled with resistive muscle work to increase muscle strength and endurance (e.g., weights, use of a monkey bar for moving in bed and sitting up, manual resistive exercise, the use of wrist or ankle weights, ergometry, and walking). Coordinating postural changes, thoracic mobility, and upper-extremity exercises with inspiratory and expiratory efforts can be effective in stimulating increased V_T and improving ventilation-perfusion matching. Chapters 22 and 23 illustrate how such movement and breathing patterns can be combined in order to maximize oxygen transport in patients with neurological conditions. Such coordinated exercise, however, can also be used in patients with acute cardiovascular and pulmonary conditions. Isometric exercises, postures that require increased muscle work for stabilization, and activities that elicit the Valsalva maneuver produce disproportionate hemodynamic responses, which could be detrimental. The capacity of the patient to respond appropriately to these loads must be assessed beforehand to minimize risk.

In deconditioned individuals and in those whose oxygen transport system has been pathologically compromised, the exercise intensity associated with relatively low-intensity mobilizing activities (such as bed exercises, moving in bed, sitting up, dangling over bedside, transferring to chair, chair exercises, and short walks with assistance) constitute sufficient progressive gravitational and exercise stimuli to initiate adaptation to being upright and moving. However, it is important to stress that optimal adaptation occurs only if these activities are prescribed at the requisite intensity, duration, and frequency, and the exercise prescription progresses commensurate with the individual’s adaptation. Mechanical ventilation is not a contraindication to mobilization; new generations of mechanical ventilators are portable and perform comparably to conventional ventilation. They are associated with minimal adverse effects on hemodynamic variables and oxygen transport¹⁷³ and can facilitate mobilization and ambulation.

In the management of acute cardiovascular and pulmonary dysfunction, the parameters of mobilization stimuli include a relatively low intensity (although it is often perceived as intense by the patient), short duration, and high frequency of sessions. If the patient is severely compromised, as in end-stage heart or lung disease, interrupted or interval training is indicated. This type of training is characterized by either on-off exercise, which allows for rest in between bouts of exercise, or high-low intensities of activity. The volume of work that can be achieved in an interrupted protocol by a severely compromised patient is greater than that achievable during continuous activity. With physiological adaptation over time, the exercise period can be increased and the rest period decreased and possibly eliminated. When high- and low-intensity exercises are alternated, the workload can be progressed by increasing the respective loads in each phase or by increasing the duration of the higher load period. If the patient has a low functional work capacity but sufficient physiological reserve, adaptation can be rapid, necessitating small, frequent progressions. As the patient’s aerobic capacity increases, the response gains are correspondingly smaller. If the patient has both poor functional capacity and poor physiological reserve capacity, progress would be correspondingly slower.

When mobilization is prescribed to remediate acute cardiovascular and pulmonary dysfunction, particularly in patients in the ICU, extensive and often invasive monitoring is required. This permits detailed assessment and ongoing metabolic assessment of the patient’s treatment responses and recovery. With these supports, mobilization and exercise can be prescribed effectively for these patients. Judicious monitoring minimizes inherent risks for either under- or overprescribing the intensity of the exercise stimulus (see Part II). Monitoring leads, lines, and catheters may restrict body positions and activities. Such encumbrances, however, do not preclude most activities, including ambulation. Moving relatively immobile patients who are confined to their beds with lines and leads is crucial, because it is these patients who benefit significantly from exercise stress and succumb most severely to its removal.

Long-Term Effects of Mobilization and Exercise

In health, the long-term effects of exercise occur in response to a specific and sufficient exercise stimulus to which the individual is exposed for a finite period. With respect to aerobic training or adaptation, the essential training parameters for generally healthy people are shown in Table 18-5. As central and peripheral adaptation to the exercise stimulus occurs, each step in the oxygen transport system becomes more efficient in facilitating DO₂, , and extraction at the cellular level.^6,15,19 The long-term effects of aerobic exercise are summarized in Table 18-8.

Cardiovascular and Pulmonary Effects

In addition to an increase in , training results in exercise-induced bradycardia and increased SV at rest and in reduction in the physiological demands of submaximal work rates. Specifically, ventilation and hemodynamic responses to submaximal exercise are decreased. Endurance training increases parasympathetic activity and decreases sympathetic activity at rest.¹⁷⁷ Arterial stiffness is decreased,¹⁷⁸ and microcirculatory function and tissue perfusion are improved.¹⁷⁹ The subjective experience of exercise stress is also reduced. These training effects are commensurate with increases in the efficiency of oxygen transport at each step in the pathway. Unlike the effects in patients with low functional work capacity, however, exercise does not improve ventilatory performance, as is evidenced by the relationship between ventilation and the production of carbon dioxide:¹⁸⁰

and

Because of the marked ventilatory reserve in health, it is normally CO, rather than ventilation, that limits exercise. However, there is some evidence that the respiratory system can limit endurance in healthy sedentary people, in athletes (especially women) with a higher fitness level, and in patients with chronic respiratory disease.181–183

Although change in is the gold standard for aerobic conditioning, theoretically, submaximal values for given work rates do not change with training¹⁸⁴ unless improvement in movement efficiency and economy has occurred. With training, an individual reduces the physiological responses to each exercise load on an incremental exercise test and so is able to achieve a higher work load, thus a higher with training.

The theory that maximum HR (HR_max) is genetically determined and does not change with training has been challenged.¹⁸⁵ Factors that down-regulate HR have been implicated in resetting maximum heart rate. Such factors include the baroreceptors, autonomic function, electrophysiology of the sinoatrial node, and a reduction in the number and density of beta-adrenergic receptors.

The rheology of blood plays an important role in cardiovascular disease. Platelet adhesiveness and aggregation are reduced with regular aerobic exercise.⁷¹ Optimal platelet adhesiveness along with blood volume maintain optimal blood viscosity, which is important for blood flow through the heart and blood vessels and for perfusion of peripheral tissue. Increased plasma viscosity and hematocrit have been attributed to exercise-induced hemoconcentration as a result of the shift of fluid from the blood to the interstitium.¹⁸⁶ With long-term endurance training, the plasma volume expands, which may reduce the resistance of blood flow to working muscle.

Exercise is a powerful controller of normal BP and an effective intervention to control high BP in patients with hypertension. The antihypertensive effects of long-term aerobic exercise are mediated through a reduction in total peripheral resistance and altered blood rheology. In addition, exercise may lead to weight loss, which contributes to lower BP. Individuals who are normotensive experience no changes in BP with an aerobic exercise program, even though peripheral resistance is reduced.¹⁸⁷

Aerobic exercise improves the hemodynamic responses and lipid profiles of individuals with cardiac disease (see Chapter 24). Walking, cycling, and running are common types of aerobic exercise. However, patients from other cultures and those who do not enjoy these types of exercise may prefer tai chi, which also has been shown to have beneficial effects on BP, lipid profiles, and relaxation.^188,189

Hemoglobin concentration and the number of circulating red blood cells are essential to effecting optimal oxygen transport (see Chapters 2 and 13). A single bout of exercise, as well as long-term exercise, can influence the erythropoietin processes in bone marrow.¹⁹⁰ In the extreme, exercise can interfere with these processes and result in “sports anemia.” This condition can reflect postexercise plasma expansion, increased hemolysis with intense exercise, iron deficiency, bleeding into the digestive and urinary systems, and abnormal erythropoiesis.

Changes in cardiac structure and function after prolonged exercise by healthy people have been of interest to researchers in their attempt to understand changes during ill health. Questions such as “Does the heart muscle show signs of fatigue and impaired function with such exercise?” have been posed. One study of highly trained male athletes showed some cardiac damage, along with reduced diastolic filling and contractility of the left ventricle, after completion of a half-ironman triathlon.¹⁹¹

Central Nervous System Effects

The responses of the CNS to training include autonomic nervous system conditioning that is associated with BP control and thermoregulation.¹⁹² Training is associated with a more sensitive vascular response to stress, which may reflect greater alpha-adrenergic sensitivity.¹⁹³ The capacity to sweat is primed in response to exercise, which ensures that the muscle and internal organs remain at a temperature that is metabolically and energetically optimal for a given workload.

As the body adapts to the exercise training stimulus (overload principle), the intensity is increased to elicit further training benefit. This is the basis for the physiological adaptation to a training stimulus. Depending on the goals of the exercise prescription, a decision is made after several weeks about whether the exercise intensity should be raised to further increase aerobic capacity or whether a maintenance program is indicated. The training program is progressed by establishing a new exercise intensity, which usually is based on 40% to 85% of the HRR achieved in a repeat of the initial exercise test.

Metabolic Effects

The effect of exercise on glucose kinetics is clinically important for several reasons. First, illness creates metabolic stress on glucose metabolism; second, bed rest reduces insulin sensitivity; third, sedentary lifestyle and high-glycemic diets contribute to hyperglycemia and insulin insensitivity; and fourth, physical therapy’s primary drug, exercise, places stress on energy substrates, including glucose metabolism, commensurate with the type, intensity, and duration of exercise. The time course of changes in glucose metabolism is important to the physical therapist because the patient must be protected from hypoglycemia and the effects of training on the muscles’ sensitivity to insulin must be optimized. Even though these changes are well known to occur with multiple weeks of aerobic training, serial measures over the training period show that after 10 days there are benefits to glucose kinetics.¹⁹⁴

Effects in Special Populations

Aggressive mobilization/exercise has been reported to have significant functional impact in the management of patients in the ICU. Prolonged intensive physical training, for example, has been reported to result in the regeneration of skeletal muscle after prolonged catabolism and weight loss.¹⁹⁵ Despite studies supporting aggressive mobilization, the physical therapist needs to establish the optimal dose at any given time and to monitor to ensure the best response and the least risk.

Aerobic power declines with age. The capacity to train, however, is not age-limited; training effects have been reported in octogenarians.¹⁹⁶ Often older people show greater gains in response to training because of their reduced levels of baseline conditioning. Oxygen kinetics may be slowed with aging. Training responses reflect an increasing contribution to aerobic training by peripheral as opposed to central adaptations.¹⁹⁷ Furthermore, based on a 30-year follow-up study, age-related decline in aerobic power over the course of 30 years was reversible with aerobic training.¹⁹⁷ Tasks and exercises that involve various physiological systems are differentially affected by aging as well as by training. Training profiles of young and middle-aged adults show an age-related performance decline in cardiorespiratory endurance but not in muscle endurance.¹⁹⁸ This finding has implications for norms of fitness and prognosis for recovery. Finally, lack of exercise has been implicated in the incidence of cognitive impairment in older adults.¹⁹⁹ Physiological changes associated with aging, particularly those related to exercise capacity, are often confounded by deconditioning and related physical deterioration in older adults rather than being an immutable consequence of aging.²⁰⁰

Summary

Physical therapists are clinical exercise physiologists whose primary interventions include mobilization and exercise to address limitations in participation and activity irrespective of whether these limitations result from primary or secondary cardiovascular/pulmonary dysfunction. This chapter first distinguishes mobilization, physical activity, and exercise. The role of mobilization and exercise in assessment and evaluation is addressed. Next, the chapter describes three distinct goals associated with the prescription of mobilization and exercise in the management of impaired oxygen transport: to exploit the preventive effects, acute effects, and long-term effects of mobilization and exercise so as to maximize an individual’s oxygen transport capacity and his or her capacity for activity and participation in life when that person is limited by impairment of oxygen transport at the structural and functional levels. Special attention is given to prolonged sedentary behavior and to bed rest, focusing on how their injurious effects can be prevented.

The physical therapist needs a comprehensive and detailed understanding of the potent and direct effects of mobilization and exercise on oxygen transport preventively, acutely, and in the long term, as well as their multisystem effects. The specific mobilization or exercise prescription is based on a comprehensive multisystem assessment, an analysis of oxygen transport dysfunction or failure, and the treatment goals for a given patient. Ongoing monitoring is essential for defining the starting point of a mobilization or exercise program, progressing it over time, and evaluating time for discontinuation. Progression is response-dependent rather than protocol-dependent; thus patients will progress at varying rates.