CHAPTER 111 Deconditioning

INTRODUCTION

Most patients with an episode of low back pain will improve significantly in a relatively short period of time, while others with seemingly minor injuries and often times minimal imaging abnormalities go on to develop chronic low back pain and significant disability. It is believed that there is a reduced level of physical activity associated with their pain leading to a decreased level of fitness or deconditioning. In recent years there has been great interest in why some develop chronic pain and subsequent disability and deconditioning. There is also great interest in what is occurring from a physical as well as a psychological perspective. Deconditioning, or its related terms detraining and disuse, is a multifactorial process that occurs in multiple body systems and is often secondary to an inciting event. Medline lists more than 2.6 million articles published since 1996 related to deconditioning of the heart, vessels, cardiovascular set-points, bone, cognition, affect, and muscles. The common factor for the pathologic change to these varied systems revolves around exercise or, more precisely, a lack of exercise exacerbating pathology. Though deconditioning is a common search term, it is not an entity defined in Steadman’s Medical Dictionary. Moreover, existing literature has used the term in various related manners, depending upon whether the investigator is a physiologist, neurologist, physiatrist, or orthopedic surgeon. The favorite terms in the literature associated with deconditioning are: decreased exercise tolerance, decreased VO₂ max, decreased ability of adaptation to functional demands, and general decreased performance in occupation and/or activities of daily living. With such an array of connotations and denotations, is it any wonder that the literature is conflicting at times?

Since most of those who become disabled are of working age, the costs of their lost productivity and treatment is shouldered by all of society. It now appears evident that chronic low back pain (CLBP) is not merely a function of incomplete healing after an injury. While there certainly may be residual pain, most recover sufficiently to continue working and functioning in daily life. Understanding the reasons behind the development of chronic pain, deconditioning, and disability as well as the physical, psychosocial, and socioeconomic consequences holds significant promise for improved treatment, reduced pain, suffering and disability, and potentially enormous cost savings. A pure physical or anatomic model fails to adequately explain chronic pain and the associated disability and deconditioning. As a result, chronic pain is now conceptualized as a multifactorial phenomenon with biological, psychological, and socioeconomic variables interplaying. Our discussion here will include a review of deconditioning-related physiologic changes such as muscle atrophy, osteoporosis, and obesity as well as deconditioning-related functional changes such as a reduced cardiovascular capacity, a decrease in muscle strength and impaired coordination or motor control in the presence of CLBP. Psychological variables such as fear-avoidance beliefs and depression and their relationship with CLBP and deconditioning are also reviewed.

Chronic low back pain is one of the most costly as well as the one of the most common diseases affecting industrialized societies today. While the incidence of lower back injuries has not changed over time, disability rates have increased sharply over the past 20 years.¹ It has been estimated that a percentage as small as 20% of low back pain patients account for 90% of the costs.² The enormous costs for the treatment including lost productivity and worker replacement has been estimated as high as US$837 billion^3,⁴ secondary to chronic spinal disorders.

It has been proposed that with chronic pain there comes inactivity, disuse, and deconditioning. Kottke ⁵ in 1966 stated, ‘The functional capacity of any organ is dependent within physiologic limits upon the intensity and frequency of its activity. Although rest may be protective for a damaged organ it results in progressive loss of functional capacity for normal organs.’ The decrease in function will be proportional to the duration, degree, and type of limitation of activity. Hasenbring et al.⁶ proposed physical disuse as a risk factor for chronicity in lumbar disc patients. Disuse or disuse syndrome and deconditioning are terms associated with this loss of functional capacity.

The disuse syndrome was first described by Bortz in 1984.⁷ He pointed out how our society had become progressively more sedentary, adhering to an anthropologic law called the Principle of Least Effort. This, stated simply, says when an organism has a task to perform it will seek that method of performance that demands the least effort. Focusing on the long-term adverse consequences of inactivity, he described the identifying characteristics of the syndrome as cardiovascular vulnerability, obesity, musculoskeletal fragility, depression, and premature aging. He did not consider the reasons for inactivity but observed that disuse is physically, mentally, and spiritually debilitating.

Mayer and Gatchel ⁸ introduced the term ‘deconditioning syndrome’ in 1988. They felt deconditioning may be a response mediated physically by the injury as well as psychologically by a variety of secondary factors. Some of these include injury-imposed inactivity, neurologically mediated spinal reflexes, iatrogenic medication dependence, nutritional disturbance, and psychologically mediated responses to prior psychiatric distress, vocational adjustment problems, and/or limited social coping resources.⁹ As a result of inactivity, physical deconditioning represented by muscle inhibition/atrophy, decreased cardiovascular conditioning, decreased neuromuscular coordination, decreased ability to perform complicated repetitive tasks, and musculotendinous contractures ensues. They use the term ‘deconditioning syndrome’ to represent the cumulative disuse changes, physical and psychological, produced in the chronically disabled patient suffering from spinal and other chronic musculoskeletal disorders.

We will review the physical and psychological consequences of inactivity or disuse in patients with CLBP. Physical measurements have addressed muscle function or strength and endurance isometrically, isokinetically, and isotonically. Methods such as magnetic resonance imaging (MRI), computed tomography (CT) scanning, and electromyography have been utilized to measure changes in muscle composition and function. Cardiovascular capacity and motor control or coordination have also been measured in CLBP patients. Psychosocial issues or variables such as distress, depression, anxiety, and fear-avoidance beliefs and their relationship with CLBP will be reviewed.

DECONDITIONING: A HISTORICAL PERSPECTIVE

Original interest in a deconditioning syndrome was prompted primarily by two things. First, as part of the practice of medicine at one time, bed rest was often a prescribed treatment. However, physicians began to realize a multitude of adverse consequences secondary to this imposed immobility. Second, as the space program evolved, astronauts spent longer periods of time in a weightless environment, stimulating further interest on the affects of immobilization. Sixty years ago Dietrick et al.¹⁰ studied the effects of immobilization by placing four normal men in plaster casts from the umbilicus to the toes for 6 weeks and then followed them through a 4–6 week recovery period. They and other investigators observed a multitude of physiologic and metabolic changes. While our patients with CLBP certainly have not been immobilized to such a degree, a short review of that literature is enlightening.

During exercise, cardiac output, heart rate, and left ventricular function all increase. Even with moderate exercise cardiac output may triple, heart rate may double, and left ventricular effort may more than triple. Oxygen uptake with heavy exercise rises six times higher than that seen at rest. With inactivity, physical fitness decreases rapidly. Resting heart rate was reported to increase by 0.4 beats per minute during an immobilization period.¹¹ Stroke volume decreased by as much as 30% during maximal exercise following a period of immobilization.¹¹ The maximal oxygen uptake (VO₂ max) is felt to be the most sensitive measure of physical fitness. A decrease in VO₂ max of 21% after 30 days of bed rest was observed by Greenleaf.¹² Pulmonary function as measured by total lung capacity, forced vital capacity, forced expiratory volume, alveolar–arterial oxygen tension difference, and membrane diffusing capacity remained unchanged or showed decreases only in proportion to decreases in cardiovascular output and maximal oxygen uptake.^10,¹¹ In these studies the immobilization was virtually absolute and cognitive, emotional, and social effects were observed as well as the physiologic and metabolic effects. With immobilization, skeletal muscle obviously undergoes atrophy as well as decreased strength, endurance, and coordination. Muller¹³ reported strength loss of approximately 3% per day for the first 7 days in the muscle of the upper extremity immobilized in a cast. Little further strength loss was observed with further immobilization. Bone marrow content is lost during immobilization, resulting in osteopenia or osteoporosis.¹⁴ This skeletal calcium loss is associated with increased urinary calcium excretion which begins to rise on the second or third day of immobilization.^10,¹⁴ Decreased physical activity alone without actual confinement to bed may result in skeletal calcium loss.¹⁵ Gaber et al.¹⁶ have shown that patients with CLBP have an increased incidence of osteopenia and osteoporosis. Another metabolic consequence is a negative nitrogen balance with losses of 29–83 grams during 6–7 weeks of immobilization. This loss reflects the equivalent of 1.7 kilograms of muscle protoplasm.¹⁰

Before beginning our discussion of a deconditioning syndrome as it relates specifically to patients with CLBP, there are several terms should be defined. Verbunt et al.¹⁷ defined ‘disuse’ as performing at a reduced level of physical activity in daily life. They described ‘physical deconditioning’ as a decreased level of physical fitness with an emphasis on the physical consequences of inactivity for the human body, whereas Mayer and Gatchel⁸ included the psychological effects secondary to inactivity or disuse along with the physical consequences as part of their definition of the deconditioning syndrome. Verbunt chose to include the term ‘disuse syndrome’ in their discussion as well. The ‘disuse syndrome’ is defined as a result of long-term disuse, which is characterized by both physical and psychosocial effects of inactivity. Our discussion here will include a review of the literature on disuse or what is actually known about the level of physical activity in daily life of patients with CLBP. We have chosen to utilize the term deconditioning syndrome as defined by Mayer and Gatchel to represent the cumulative changes secondary to disuse, both physiological and psychological, produced in the patient suffering from CLBP. Thus, we can see how disuse leads to the deconditioning syndrome. The assumption is that we can show a significantly reduced level of physical activity resulting in deconditioning in patients with CLBP.

DISUSE

In 1946, Young ¹⁸ described the effects of use and disuse on nerve and muscle. Introducing the term disuse into the medical literature, he described it as not using the musculoskeletal system during periods of immobility. Then Bortz in 1984 referred to the disuse syndrome and included many of the adverse consequences of inactivity in his definition beyond those affecting muscle and nerve. For purposes of this discussion we will define disuse as performing at a reduced level of physical activity.¹⁷ We are sure many of us hold the belief that our patients with CLBP are leading a very sedentary existence with an activity level significantly below that of the norm. But, in actuality, what is known about the activity level of these patients? In a group of patients with chronic pain (but not specifically low back pain) the Baecke Total Physical Activity Score was significantly higher in female than in male patients, a finding not observed in healthy controls.¹⁹ This study also revealed a statistically significant reduction in a physical work capacity index of 34% in males and only a 17% reduction in found in women, which hardly reached the significance level. The authors concluded that chronic pain may have a greater impact on activity level in male patients than in female patients, whereas Protas²⁰ and Verbunt et al.²¹ found that physical activity in the daily life of patients with CLBP did not differ significantly from healthy age- and gender-matched controls. The physical activity in daily life expressed as whole-body acceleration measured with a triaxial accelerometer and as the ratio between average daily metabolic rate, measured by the doubly labeled water technique, and resting metabolic rate, measured by ventilated hood, was reported by Verbunt et al.²¹ Both techniques were used simultaneously for 14 days. They noted that the mean level of physical activity did not differ in CLBP patients when compared with healthy controls. Thus, they could not confirm the presence of disuse in this group of patients. Given that 77% of the patients in this study were employed despite their back problems, it is possible that the patients participating in this study were in relatively better physical condition than other patients with CLBP. Further measurements revealed no difference in percentage of body fat and body mass between patients and controls. They found it remarkable that although patients felt disabled because of their back pain as shown in their Rowland Disability Questionnaire scores, their level of physical activity as actually measured was not decreased in comparison with controls. They also noted there was no correlation between pain intensity and physical activity levels.

Several theories as to the reasons for the differing results with regards to the presence or absence of disuse have been offered. Work status may indeed have a significant impact on physical activity levels. On the one hand, in the study by Verbunt et al.²¹ 77% of the CLBP subjects were working, whereas in Neilens and Plaghki’s studies^19,^22,²³ only 20–34% of subjects had a paying job. Different methods for assessment of the degree of inactivity have also been employed. While Verbunt utilized physiologic measurements, others used self-reporting to assess physical activity levels. A discrepancy in reported functioning by patients and actual functioning has been reported.^24,²⁵ Physical activity levels as reported by patients with CLBP and as reported by their physical therapists revealed that the patients significantly underestimated their level of activity.²⁵ It also has been shown that patients with CLBP have greater difficulty actually estimating their level of exertion during a performance test.²⁴ From these studies, it would appear that self-reporting of activity levels in patients with CLBP is unreliable.

In summary, it is surprising that so few studies have been performed on the level of physical activities in daily life or disuse in patients with CLBP. The results have been equivocal and thus, despite what our beliefs may be about the activity level of these CLBP patients, the literature does not support the definitive presence of a reduced activity level. This lack of a decreased activity level particularly seems to be the case, at least in patients with CLBP, who continue to work. The study by Verbunt et al.²¹ is the most scientifically well designed of these and they were unable to confirm the presence of disuse in a group of CLBP patients. The work status and/or varying methods of reporting activity level may offer some explanation for the inconclusive results reported here.

DECONDITIONING IN CHRONIC LOW BACK PAIN

The presence of disuse or a reduced level of physical activity in daily life has not been definitively supported by the literature. However, since deconditioning is felt to be a result of disuse, the presence of deconditioning in CLBP may be used as supportive evidence of a low level of activity. There may be both physiological as well as psychosocial changes associated with the deconditioning syndrome. Physical consequences of inactivity may include decreased cardiovascular endurance, decreased strength and muscular atrophy, impaired coordination, osteoporosis, metabolic changes and obesity. Psychosocial changes may include distress, depression, anxiety, or behaviors consistent with the fear-avoidance model.

Cardiovascular capacity

Endurance or cardiovascular capacity in patients with CLBP has been measured utilizing various methods. The most widely accepted measure of cardiovascular fitness is maximal oxygen uptake (VO₂ max). The various methods of measurement have included measurement of VO₂ max as well as utilizing submaximal exercise testing. Interestingly, the results have not led to a definitive conclusion about the cardiovascular capacity of patients with CLBP. In measuring parameters such as predicted VO₂ max utilizing a symptom-limited treadmill test or bicycle ergometer some studies have shown significantly lower levels of cardiovascular fitness in patients ^24,²⁶^–²⁸ whereas Wittink et al.²⁹ and several others have failed to demonstrate a significantly reduced level of aerobic fitness in patients with CLBP.³⁰^–³² A lower cardiovascular capacity was shown for men compared with controls but not for women in some studies.^19,^22,²³

Wittink et al.²⁹ tested a sample of 50 patients with CLBP with a mean duration of symptoms of 40 months. Oxygen consumption (VO₂) was measured during a symptom-limited modified treadmill test. Prediction equations were employed to estimate VO₂ max. The mean observed VO₂ max values for men and women with CLBP were consistent with those found in earlier studies that tested normal subjects. Given these results, they concluded that rather than being a group of significantly deconditioned subjects, at least from an aerobic standpoint, this group of patients with CLBP represented a sample of moderately fit individuals. Furthermore, their data suggest that aerobic fitness levels are independent of diagnosis, duration of pain, pain intensity, work status, or smoking. Previously, Wittink et al.³³ had subjects with CLBP perform three symptom-limited maximal exercise tests: a treadmill, an upper extremity ergometer, and a bicycle ergometer test. The treadmill test was found to be by far the best test for measuring aerobic fitness in these patients. Wittink et al.³⁴ went on to show that there is no significant relation between aerobic fitness and pain intensity in patients with CLBP and that a lack of cardiovascular fitness therefore does not contribute to pain intensity in patients with CLBP. In a follow-up sample, patients reported significantly less pain before and after treadmill testing at the end of a functional restoration program compared with their pain intensity with testing before the program. Since their predicted VO₂ max had not changed, the authors noted that there had been a decreased pain intensity independent of aerobic fitness levels.

Hurri et al.³² measured VO₂ max in 245 subjects with CLBP, 81 who were treated as inpatients, 88 treated as outpatients, and 76 controls with a history of CLBP but who were still working. They performed bicycle ergometer tests four times over a 30-month period. The estimated VO₂ max of their patients was not significantly different than reference values of healthy persons. Battie et al.³⁰ noted that aerobic fitness did not affect the risk of back injury in a prospective study. He did observe that it might affect the response to the problem and subsequent recovery. Cady et al.,³⁵ in his oft quoted study from 1979 on a group of firefighters, showed a graded and statistically significant protective effect for increasing levels of fitness and conditioning. A criticism of Cady’s study was that fitness level included both cardiovascular or endurance parameters as well as strength measures, making it impossible to isolate the benefits of these individually.

On the other hand, some investigators have shown what most of us would believe to be true, that indeed there is a significantly decreased level of cardiovascular fitness in CLBP patients. Brennan et al.²⁶ used bicycle ergometry to determine a predicted VO₂ max in 40 patients with herniated discs with an average duration of symptoms of 87 days. Comparing these results with those of a matched control group revealed a significantly reduced predicted VO₂ max for the patients. Others,^24,²⁷ in addition to van der Velde and Meirau,²⁸ have also shown diminished cardiovascular capacity in patients with CLBP. Their original experimental objective was to determine the effects of 6 weeks of exercise on aerobic capacity and on measures of pain and disability in patients with CLBP.²⁸ Baseline measurements determined that the percentile rank of aerobic capacity for the patients with CLBP was statistically significantly lower than those measures for the controls. Patients who completed a 6-week program of aerobic, muscular endurance, and flexibility exercises showed a statistically significant improvement in the mean percentile rank for aerobic capacity. In addition, they showed significant decreases in pain and disability after completion of the exercise program.

We can see that despite what our preconceived ideas may be regarding a decreased aerobic capacity in patients with CLBP, the literature is inconclusive. Instead, it reveals that a decreased aerobic capacity may or may not actually be present in these individuals. Work status again has been offered as a possible reason why the results have varied so, the thought being that even in the presence of CLBP those individuals continuing to work are more likely to possess a fitness level equal to the norm. Unfortunately, information pertaining to work status is not available for all of the studies considered here. It is notable that in most studies where no difference in cardiovascular capacity was reported, most of the subjects being studied were still working. The cardiovascular capacity was better for CLBP patients who were working compared with those who were not in one study.³⁶ In several studies^19,^22,²³ male subjects had decreased cardiovascular capacity when compared with controls, whereas females did not. Speculation as to why this may be so centered on the idea that when men lose their job there is a greater degree of inactivity, whereas in the case of women they remain more active at home with tasks such as cooking, cleaning, and childcare. This keeps them at an activity level equivalent to that of healthy females.

Muscle changes: composition and performance

Skeletal muscle has incredible plasticity associated with it. It can adapt to almost any array of functional demands we place upon it. The level by which muscle function declines with inactivity depends upon the level of training before inactivity began and the duration of inactivity. In discussing muscle, it is important to understand the function of muscle subtypes. Type II (predominantly subtypes a and b) fibers are generally ‘fast twitch.’ They can track fast and are maximally powered by glycolysis, and therefore fatigue quickly. They are usually recruited late when the body needs to exert ‘maximal effort.’ Type I fibers are generally ‘slow twitch.’ They contrast slowly and are metabolically inexpensive, utilizing aerobic metabolism. In the acute period (14–30 days), fiber type is preserved even with activity reduction greater than 75% given the absence of an associated neuromuscular injury (i.e. foot drop such as from an L4 nerve root impingement).^37,³⁸ In the subacute period (30–90 days), large progressive shifts of type IIa fibers to type IIb fibers (both fast twitch fibers) occur at a rate of 5–19%.³⁹ This shift can precede fatty replacement of muscle (apoptosis) in animal models. There is also a 15% decrease in the number as well as the size of type I (efficient slow twitch muscle fibers).⁴⁰ In chronic detraining (90 days to 9 months), power lifters showed oxidative muscle (type I) fibers increased by 1.4 times,⁴¹ while type II fibers (fast twitch) decreased by 60% in axial muscles.^42,⁴³ It has been noted that the very young (less than 20 years old) may exhibit a certain immunity to fiber-type change in the face of detraining.^44,⁴⁵

A changed fiber cross-sectional area (atrophy) also occurs with deconditioning and detraining. In athletes both type I and type II fibers decreased in size by 9–23% in as little as 6 weeks of detraining.⁴⁶ In a chronic period (7 months) there can be as much as 37% atrophy across all muscle fiber types.⁴¹ Mayer et al.⁴⁷ noted in CT that CLBP patients (in both operative and nonoperative segments) had significantly decreased muscle bulk with evidence of fatty replacement of muscle. The authors further correlated this observational qualitative finding of atrophy with a quantitative finding of greater than 50% mean reduction in strength testing for the atrophied spinal muscle group compared to age- and gender-matched controls. Several other studies have shown smaller cross-sectional areas of the paraspinal muscles by CT or MRI scanning in subjects with CLBP.⁴⁸^–⁵⁰ It remains debatable, but some papers have shown that larger muscles (postural muscles of the back and lower extremities) become atrophic at a faster rate than extremity muscles.

Few authors have actually correlated strength performance to atrophy, but generally strength is largely preserved during short periods of convalescence although eccentric strength decreases earlier than other aspects of neuromuscular performance (7–21 days). In the subacute period (4–12 weeks) there are declines in strength, measured by both force and power, of 7–15%.^51,⁵²

For chronic periods, decreases in power were 40–60% for trained muscles in the arms and legs, but less dramatic decreases of 15–37% were noted in the contralateral untrained arm.^37,⁵³ Muscle endurance times are also decreased with deconditioning. Decreased strength as well as decreased endurance for trunk/spinal musculature was seen in patients with chronic low back pain despite having similar physical activity levels as age- and gender-matched controls.^49,⁵⁴ Mayer et al.⁵⁵ demonstrated significant strength deficits for both trunk flexors and extensors for a group of CLBP patients utilizing a Cybex prototype sagittal trunk strength tester. Using a dynamic isokinetic lifting device, Kishino et al.⁵⁶ show significantly decreased isokinetic as well as isometric lifting capabilities for patients with CLBP. Houston et al.³⁷ have noted a capillary density diminution in as few as 15 days after training cessation. However, other authors have noted that even after 90 days of detraining, capillarization remained largely unchanged with only minor decreases in VO₂ max.⁵⁷ Mujika and Padilla, who have analyzed much of the existing data, surmise that capillaries and muscles are preserved in trained athletes and may account for their greater speed to reach previous training levels than in sedentary individuals.^58,⁵⁹

Rapid and progressive reduction in mitochondrial oxidative enzymes creates a rapid decrease in the efficiency of muscle cells to manufacture APT.⁵⁹ Further, ‘run-time exhaustion’ or subthreshold muscle failure is associated with decreased mitochondrial density and/or efficiency.⁶⁰ Deconditioned, formerly trained individuals retain higher enzymatic and mitochondrial numbers than sedentary individuals and will reach peak performance levels faster when they resume activity.⁶¹

Motor control is also adversely affected in the presence of CLBP. Performing a standardized reach task, postural control in patients with CLBP was more affected in those with severe low back pain compared with moderate pain.⁶² Patients with CLBP showed a delayed-onset contraction of abdominal muscles during motion of the upper extremities.^63,⁶⁴ Patients with low back pain were shown to have decreased trunk motion patterns while performing a repetitive wheel rotation task.⁶⁵ Haines⁶⁶ showed immobility, as well as decreased coordination and balance. Several surface EMG studies have shown reduced recruitment patterns and lower maximum integrated electromyography in paraspinal muscles in CLBP patients.^67,⁶⁸ Moreover, studies of movement patterns have shown the delayed onset of contraction of the transversus abdominis indicating a deficit of motor control, hypothesized to result in inefficient muscular stabilization of the spine.⁶⁹

Thus, it appears that in the presence of CLBP there is muscular atrophy with a subsequent decrease in strength and endurance. In addition, altered recruitment patterns may affect muscular stabilization of the spine.

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