The promotion of regular physical activity serves as a sound preventive health strategy. Improvements in habitual activity levels should be expected to reduce the incidence of coronary artery disease, obesity, osteoporosis, and other significant contributors to morbidity and mortality in the population. To succeed in such efforts, an accurate understanding of the determinants of physical activity is essential. Consequently, recent research has focused on identifying those factors that motivate individuals to exercise regularly and influence daily energy expenditure.
These investigations have focused principally on psychological, social, and environmental issues that affect levels of physical activity(14,42). Individuals with fewer years of education and lower socioeconomic status, for example, have less tendency to participate in physical activities. Conversely, those with extrovertive personalities, a greater knowledge of health benefits of exercise, and supportive peers and spouses are more likely to be physically active. Climate, gender, and accessibility to exercise facilities are also important determinants of amount of regular physical activity.
For the most part, these research efforts have failed to consider the potential contribution of biological controls in influencing levels of habitual activity. In fact, abundant evidence supports not only the existence of such intrinsic control of motor behavior but also suggests a significant role of biological control centers in regulating amount of physical activity in both animals and humans. It is the purpose of this review to a) examine the rationale for biological control of physical activity, b) survey the evidence for the existence of such intrinsic regulation, and c) suggest the preventive health and therapeutic implications of biological influences on physical activity.
A biological basis of physical activity implies an inherent control center within the central nervous system that regulates one's daily energy expenditure through motor activity. Such a center is a distinct anatomical-physiological entity, analogous to brain centers that control temperature, hunger, and sexual arousal. And, similar to these other biological regulators, an intrinsic activity center should be expected to regulate amount of daily physical activity to a particular set level.
In this review, physical activity is considered as body movement created by skeletal muscles that results in energy expenditure (11). An intrinsic regulator of level of physical activity within the central nervous system needs to be differentiated from the well recognized motor areas within the cerebral cortex, which initiate purposeful body movement. An activity center controls amount of physical activity over time (i.e., daily energy expenditure) and, in distinction from cortical motor functions, is not under a person's willful control. Like all intrinsic biological controls, it is clear that such an activity regulatory center can be at least temporarily overridden by extrinsic influences. Personal desires, peer influences, and environmental conditions all may act to modify the function of central control in dictating level of physical activity. Nonetheless, there is sufficient evidence for an underlying biological contribution to exercise habits to warrant an understanding of the nature of such control, its response to induced activity programs, and the means it might be beneficially modified to improve level of physical activity.
A RATIONALE FOR BIOLOGICAL CONTROL OF ACTIVITY
Is there any reason to believe a priori that biological mechanisms should exist that control the amount of one's spontaneous physical movement? In fact, the critical necessity for energy homeostasis provides a reasonable scientific rationale upon which to base such a concept.
The human body must be “so perfect,” wrote Claude Bernard in 1865, “that it continually compensates for and counterbalances external variations” (6). This constancy is“established as continually and exactly as if by a very sensitive balance.” Bernard concluded that “all the vital mechanisms, varied as they are, have only one object: that of preserving constant the conditions of life in the `milieu interieur.”'
The human body is replete with critically important regulatory“stats” with their threshold set points, feedback mechanisms, and narrow tolerance limits. Indeed, the stability of the “milieu interieur”-temperature, pH, osmolarity, glucose levels, blood pressure-could not be sustained without precise control of such homeostatic control centers.
As an adequate supply of energy is crucial for sustaining physiological function, it should be expected that a similar control center should exist for maintaining an energy steady state. Such a center would balance “energy in” by affecting appetite with “energy out,” achieved by regulating resting metabolic rate as well as expenditure in the form of physical activity.
There was presumably a survival value in prehistoric times for a controlling mechanism that defended the energy status quo. Early hominids such as Australopithecus afarensis were small individuals who lacked sufficient communication and cooperation skills required for stalking large game (35). Consequently, their diet was obtained from scavenging kills of large carnivores as well as form fruits, grasses, and insects. Obtaining a sufficient caloric intake must have been marginal, and any mechanisms for conserving energy when food was scare would carry significant survival value.
In contemporary times, with easy accessibility to food, the necessity for strategies by the body to conserve energy seems out of place. Indeed, voluntary activity, often with a psychosocial basis (i.e. overeating, sedentary activity) seems to easily override the biological control mechanism. And minor deviations in energy balance is observed to result in pathological energy conservation (i.e., obesity). Still, there is considerable evidence, outlined in this review, that a control center for maintaining a stable energy balance still exists in modern-day humans.
Energy intake is clearly regulated by the hypothalamic appetite center, responding in the short term to input such as blood glucose level and in the long term to body composition (1). A genetic basis for appetite control is supported by the recent identification of leptin, a hormone secreted by adipose tissue that is felt to serve as a satiety signal to hypothalamic appetite centers (38). When animals are restricted in dietary intake, their serum leptin levels fall, and with refeeding the concentrations rise. When leptin is administered to animals they stop eating. The importance of leptin to appetite and derangements of energy balance (i.e., obesity) in humans is not yet clear, but the identification of leptin as a genetic-based regulator of energy intake is illustrative of the strong biological drive for energy homeostasis.
On the energy-out side of the equation, resting and activity metabolic expenditure can strongly influence energy balance. The contribution of resting metabolic rate to total energy expenditure is highly variable but is generally approximately 60% (18). It would be expected that a wise adipostat would “turn down” the rate of resting metabolism as a means of balancing the energy state in times of deficit of energy intake. There is good evidence, in fact, that this occurs. Metabolic rate is usually observed to decline in conditions in which food intake is limited (i.e., dieting obese individuals, patients with anorexia nervosa, experimentally starved subjects). For example, early studies by Keys(25) in men receiving only about one-half their usual daily caloric intake revealed a 30% decrease in basal metabolic rate per unit of body surface area.
Whether such declines simply reflect a diminished amount of metabolically active tissue has not always been clear. However, Liebel et al.(26) clearly demonstrated a reduction of resting metabolic rate (measured by indirect calorimetry) independent of changes in lean body mass in obese subjects who lost 10-20% of their body weight by underfeeding. Resting metabolic rate relative to lean body mass in these individuals declined by approximately 10%. Similar findings were described by Tremblay et al. (53) in subjects whose food intake was maintained constant despite a 3-month exercise program.
Beyond resting metabolic rate, physical activity accounts for most of daily energy expenditure. That regulation of the amount of such activity should serve as a strategy for maintaining a stable energy balance is thus intuitively attractive. The varied evidence supporting this concept will be presented in the remainder of this article. But there are two initial observations that can be made at this point which support the hypothesis that amount of daily activity is related to food intake and resting metabolic rate and that regulation of this activity has a biologic basis.
First, evidence exists that leptin, the hormone that regulates food intake in animals, also influences energy expenditure. Exogenously administered leptin causes mice to increase their level of physical activity, and this may be related to stimulation of the sympathetic nervous system(36). Salbe et al. (41) recently tested the idea that leptin concentrations might be related to resting metabolic rate and habitual physical activity in children. They studied 123 5-yr-old Pima Indian children, using the doubly labeled water technique to assess energy expenditure. Plasma leptin concentrations were directly related to physical activity level (total energy expenditure minus resting metabolic rate) (r = 0.26, P < 0.01) but not to resting metabolic rate. This study supports animal research data suggesting that leptin acts to maintain energy balance not only by controlling hunger but also by regulating energy expenditure in the form of physical activity.
More recently, Nagy et al. (33) demonstrated a significant correlation (r = 0.35, P < 0.01) between activity (by the doubly labeled water technique) and serum leptin concentrations in 76 children. However, this relationship disappeared when leptin concentrations were adjusted for body composition.
The second observation surrounds the temporal changes of physical activity with age, particularly as they parallel resting metabolic rate. In population studies, amount of physical activity declines progressively through life from the time that toddlers first become fully ambulatory(39). This, of course, is verified by everyday observational experience (consider the physical activity levels of a room full of 7-yr olds at a birthday celebration to a group of adults at a cocktail party). That the reason for this “decay” of activity is strongly biological is immediately suggested by the fact that a similar decline in spontaneous activity with aging is seen in animals(17).
In addition, it is observed that the resting or basal metabolic rate(relative to body size) also falls with age. The body's metabolic fires burn less intensely over time: the average resting metabolic rate of a newborn infant, for instance (about 52 cal·m-2·h-1) is 60% greater than that of the typical 70-yr old (21). The patterns of decrease in resting and exercise energy expenditure are quite strikingly similar, suggesting a common mechanism for regulating both resting and activity-generated metabolic expenditure.
To summarize, the concept that a biological control center exists that regulates amount of physical activity is reasonable based on the body's needs for energy homeostasis. First, there is good evidence that biological mechanisms exist for control of other options of maintaining such balance(i.e., energy intake and resting metabolic expenditure). Second, a relationship can be documented between these factors and daily activity levels. Given this reasonable hypothesis, then, the evidence will now be reviewed that supports the concept that central biological centers contribute to the regulation of daily physical activity.
Clues to the existence of biological control of physical activity come from many divergent sources. In this section the evidence will be examined from these various perspectives.
The “activity-stat”. If a biological control center acts as an “activity-stat,” controlling energy expenditure to a particular set point, two features would be expected that are common to the body's other regulatory “stats.” First, we should observe biorhythmicity, a regular temporal variation in spontaneous activity; second, we would expect compensatory decreases in resting or activity energy expenditure (or increases in food intake) in response to imposed periods of physical activity.
Cooper et al. (13) provided data to indicate that the physical activities of children are not random but follow particular temporal patterns. Performing Fourier analysis on activity patterns in 15 children, they found that high intensity activity occurred with significant frequencies of 0.04-0.125 per min. Similarly, Wade et al. (55) described in children at play an oscillation between levels of high and low activity with frequencies of 15 min duration superimposed on a larger cycle of 40 min. These reports support a periodicity of physical activity, at least in children.
There are also research data that document a “compensatory” decline in spontaneous energy expenditure following imposition of physical activity, both in animals (49,50) and humans(16,20). Lore reviewed 11 studies that examined this question from the opposite direction, measuring physical activity in rats immediately after they had been confined for periods ranging from 5 h to 8 d(27). Increases in activity were described in some reports, but most showed no changes.
In humans, Goran and Poehlman (20) studied the effects on total energy expenditure of an 8-wk high intensity (70% ˙VO2max) endurance training program in elderly subjects 56-78 yr old. Total daily energy expenditure, as indicated by the doubly labeled water method, showed no change despite a 10% rise in resting metabolic rate plus the increased energy expenditure from training. The explanation was a 62% reduction in energy expenditure from physical activity outside the training program. In their meta-analysis of 13 studies evaluating exercise for weight loss, Epstein and Wing (16) found that subjects in these studies did not lose as much weight as would be expected from their training energy expenditure. They explained these findings by either a decrease in nonexercise activity or an increase in food intake stimulated by training.
However, others have failed to demonstrate a decline in level of spontaneous physical activity to “balance” energy flux following induced exercise. When Blaak et al. 7 trained obese boys for 4 wk at 50-60% ˙VO2max, total energy expenditure rose by 12%. They concluded that an added hour of physical education per day augments overall energy expenditure with no significant change in spontaneous activity. Similar results have been described in studies of training distance runners(31), healthy adult males (19), and obese females (54).
Shepard et al. (47) found that the addition of 5 h·wk-1 of physical education by Canadian schoolchildren resulted in a small but statistically insignificant reduction in weekday leisure activity. They noted that “the possible existence of hypothalamic biofeedback mechanisms limiting total daily activity is discouraging for those planning physical education curricula. Nevertheless, our data suggest that any such effect is small.”
Such studies of induced activity are confounded by failure to account for possible changes in other components of the energy equation, particularly energy intake. Another difficult issue here is the matter of time. That is, over what period of time might compensatory changes in activity occur? Perhaps looking at days or even weeks is too short. It is not inconceivable that maintenance of a stable degree of energy-out through physical activity might be sustained even over a period of months, well beyond the measurement period of these studies. In addtion, the energetic response to activity may be influenced by both intensity and mode (aerobic or resistance) of the exercise intervention.
The nature of play. Playful physical activity is observed throughout the animal kingdom, particularly in the young. Bear cubs, kittens, and human children alike chase each other, explore, and wrestle. Indeed, this expression of spontaneous motor activity is so pervasive in children that its absence suggests physical or emotional illness. Why do they do this? What are the benefits of play? The answers are unclear, but the ubiquitous nature of playful physical activity throughout the animal kingdom strongly suggests a biological origin. Consequently, insight into the biological control of physical activity might be expected by examining the long-standing struggle to understand the nature of play.
Researchers have long sought an adequate definition of play. In the end, its description remains largely subjective, relying on the visual impressions of the observer. Play, or fun, activities are different from work, or serious, activities, and the definitions suggested for play characteristically include adjectives such as “spontaneous,” “free,”“pleasant,” and “voluntary.”
One of the common themes is that play is nonpurposeful and frivolous(“he is just playing”), but the constant existence of play activity in all healthy animals suggests, to the contrary, that individuals play for some biological reason. That is, researchers have had a difficult time accepting that play is only “the aimless expenditure of exuberant energy” (15). Biological tenets generally hold that such interspecies uniformity of behavior must conform to some“purpose.” But what?
In his book Why People Play, Ellis (15) outlines at least 15 different theories, yet a clear-cut answer remains elusive. Some of the explanations are difficult to accept because they do not readily account for play in small children and animals (such as play representing catharsis-a reduction of stress and anxiety-or serving to act out fantasy, a control over the harshness of reality).
Other explanations for play have bearing on the question of how (and why) biological control centers might direct levels of physical activity. It is not difficult, for instance, to conclude that play in animals reflects a biological instinct, similar to hunger and reproductive activity. Indeed, since at least the 1930s it has been suggested an “autonomous need for activity” could explain much of the daily physical activities of animals(27,52).
The logic is intuitive, but it still begs the question: why would such a drive exist? Early theorists suggested that spontaneous physical activity of play represented a “blowing off” of surplus energy left over from performance of life's more important, survival-related work. That is, given X amount of body energy, and using Y to hunt down the evening's dinner, the body needs to expend X minus Y energy to prevent energy imbalance. This is not too far removed from the activity-stat” idea, but it, again, does not account for play activity in children.
More recent theories with a more scientific foundation surround an explanation of play as means of maintaining optimal arousal of the central nervous system. That is, “the normal state of the organism reflects the state of its nervous system which is in a state of constant activity. The normal organism needs to be in constant receipt of the sensory input from the environment that satisfies its need for stimulation”(15). Schultz (45) proposed the existence of “sensoristasis,” in which sensory stimulation of the central nervous system would be maintained at a constant level.
According to this concept, then, arousal stimulation of the brain is provided in animals and children through locomotor activity. While adults may also engage in playful motor activities, requisite arousal of the central nervous system can be achieved in older individuals via alternate routes such as reading novels, day dreaming, and problem solving. Indeed, providing such stimulation to adults serves as the foundation for the entertainment and communications industries (15).
The strength of this drive for CNS stimulation is evident from the outcomes of experiments in which human volunteers have undergone periods of sensory deprivation (60). Paid subjects who agreed to lie still in a cubicle wearing translucent goggles for extended periods of time experienced visual hallucinations, delusions, distortion of body image, and affective and cognitive disturbances. Other similar studies have documented impaired visual-motor coordination, electroencephalographic changes, and intellectual decrement following perceptual deprivation.
The neurological mechanism proposed for arousal involves the reticular activating system, a network of nerve fibers in the brain stem that receives input from sensory tracts and provides communication to higher centers in the cerebral cortex. The reticular activating system provides an arousal effect, whereas the cerebral cortex is inhibitory. When injury occurs to the reticular activating system in animals, for instance, activity declines and the animal becomes more somnolent.
There is evidence, too, that energy expended as play can be regulated by the brain as a means of maintaining energy homeostasis. A reduction in play activity has been documented in several species after a period of food deprivation (34), and similar findings have been observed in humans (40).
By whatever definition and explanation, it seems reasonable to conclude that play is a reflection of biologically driven physical activity. In this regard, it is of interest to note that amount of play is greater in young as opposed to mature animals and that playful activities become more frequent and complex in higher as opposed to lower animals. The latter observation is consistent with the greater neurological complexity in mammals further up the evolutionary ladder; that is, these animals require more play to elevate central nervous system arousal to optimal levels.
Experimental CNS lesions and pharmacological interventions in animals. Changes in activity that occur in animals following experimentally induced lesions in the central nervous system provide evidence for biological control of physical activity. Moreover, depending on the location of such lesions, activity levels can predictably be augmented or decreased. Such data therefore provide not evidence not only for biological influences on spontaneous motor activity but also indicate that several areas of the brain contribute to this regulatory function.
Panksepp et al. (34) summarized the research experience in which physical activity was assessed in animals following experimentally induced lesions within the central nervous system. Large lesions in the amygdala have consistently diminished spontaneous activity in rats, while septal lesions make animals more hyperactive. Decreased play activity has been described after injury to the dorsomedial thalamus, parafascicular area of the the thalamus, and caudate nucleus. Decorticate rats continue to exhibit play activity but to a lessened extent. Hypophysectomy markedly increases exploratory motor activity in rats.
Animal studies also indicate that a variety of different pharmacological interventions can influence play and motor behavior (51). One of the most consistent, for example, is the action of low-dose morphine in stimulating play activity in rats, an effect that can be blocked with nalaxone(34). Decreases in play fighting have been described in rats given amphetamine or methylphenidate (4). Rats given chlordiazepoxide increase play activities, while those given nicotine become less active (34).
Chemical deficiencies can also affect motor behavior. Iron-deficient rats display less spontaneous activity than those who are iron replete(23). In addition, iron-deficient animals demonstrate a reversal of the normal diurnal variation in activity with greater activity in light rather than dark periods (58). Activity periods revert to their normal pattern with iron treatment. Beard commented that“this reversal in the normal activity pattern with the light:dark cycle is of great interest because it implies a perturbance of a basic hypothalamic and control process” (3). The effect of iron deficiency on activity may be related to alterations in iron-dependent synthesis of CNS neurotransmitters and/or decrease in number of dopamine receptors in the central nervous system (57).
Lead intoxication has been considered responsible for increased motor activity and aggressiveness in children. Silbergeld and Goldberg(48) supported this idea by demonstrating that suckling mice who were fed lead acetate were three times as active as control animals. Amphetamine and methylphenidate caused depression of hyperactivity when administered to the lead-intoxicated mice, while phenobarbital exacerbated their levels of activity.
Specific biochemical and physical influences on the central nervous system, then, clearly act to alter levels of physical activity in animals. The predictability of suppression or exacerbation of activity by particular interventions indicates varying influences on CNS centers that control activity.
Insights from hyperactive children. Children with attention deficit hyperactivity disorder (ADHD) are characterized by high levels of physical activity-often coupled with poor impulse control and learning problems-and offer an excellent model to examine biological determinants of physical activity in humans. A considerable volume of research has provided clues that the excessive physical activity in children with ADHD has an organic basis. By examining these clues, then, one is also provided evidence that biological factors may influence patterns of habitual activity in the general population (2).
The idea that hyperactivity in children is an expression of brain damage initially arose from observations of youngsters who survived bouts of encephalitis in the influenza pandemic of 1916-1917. These restless, hyperactive children were “almost impossible to live with,” demonstrating rapid shifts of attention and destructive tendencies(8). Further evidence that hyperactivity in children has an organic basis came from the report by Bradley in 1937(9) of significant improvement in the hyperkinetic behavior of children after treatment with amphetamine.
It subsequently became apparent that most children in the general population with hyperactivity were not survivors of the influenza epidemic. Moreover, it was recognized that they did not, in fact, demonstrate any evidence by examination, intellectual testing, or laboratory investigations of“brain damage.” It was therefore concluded that they instead had“minimal brain dysfunction,” i.e., subtle brain malfunctioning that was manifest only by hyperactivity, poor impulse control, and inability to concentrate. Several ideas have been proposed to explain the organic basis for these abnormalities, including inadequate inhibition of impulses within the reticular activating system, frontal lobe dysfunction, and CNS neurotransmitter depletion.
It would seem intuitively logical that hyperactive children have excessive arousal of the central nervous system. This conclusion, however, is inconsistent with the observation that most of these children becomeless active after taking amphetamine, a known CNS stimulant. Satterfield et al. (43) suggested, instead, that hyperactive children suffer from a state of depressed CNS arousal. They and others (22) hypothesized a defect in the reticular activating system in these youngsters that results in low arousal, causing an increase in level of physical activity as a stimulus-seeking maneuver.
In support of this idea. Satterfield et al. (22) reported that skin conductance level, an indicator of neurological arousal state, was abnormally low in 50% of a group of ADHD children. Moreover, the severity of their hyperactivity and poor attention span was inversely correlated with the estimated CNS arousal level. However, Hastings and Barkley(22) cautioned against concluding that ADHD children have a malfunctioning reticular activating system, as 7 of 10 studies comparing skin conductance levels of hyperactive and normal children could detect no differences.
Mattes (30) observed that there were similarities in the hyperactive behavior of patients with ADHD and both humans and animals who demonstrate malfunction of the frontal lobe of cerebrum. Such frontal lobe dysfunction could cause increased spontaneous motor activity in ADHD children by lack of inhibition of internal drives, which govern responses to external stimuli (12).
New imaging techniques have provided some support for frontal lobe dysfunction in children with ADHD. Using emission-controlled tomography, Lou et al. (28) showed that, compared with normal subjects, all 11 children with ADHD had diminished perfusion centrally in the frontal lobe white matter. In a second study using the same technique, Lou et al.(29) reported hypoperfusion in the head of the caudate nucleus in ADHD children. They suggested that ADHD might involve a lack of sensorimotor inhibitory function of this structure.
More recently, the role of CNS neurotransmitter depletion in causing increased motor behavior has been suggested by several lines of research evidence. Shaywitz et al. at Yale University (46) demonstrated that 6-hydroxydopamine, a drug that rapidly depletes the brain of dopamine, caused hyperactivity when injected into neonatal rats. Others(10,32) have subsequently duplicated their findings.
Efforts to determine if CNS dopamine levels are low in ADHD patients have been impaired by lack of a direct means of assaying brain tissue in humans. As dopamine does not cross the blood-brain barrier, studies have been limited to quantitating dopamine breakdown products or enzymes related to neurotransmitter function in blood, urine, and cerebrospinal fluid. Studies have demonstrated that levels of 3-methoxy-4-hydroxy-phenoylglycol, a metabolite of norepinephrine, were lower in the urine of ADHD children than healthy controls. But plasma levels of dopamine beta hydroxylase, the enzyme that converts dopamine to norepinephrine, and urine concentrations of vanilylmandelic acid, another norepinephrine metabolite, have been reported to be similar in ADHD and normal children (59).
It remains problematic how these findings can be synthesized into a unified theory for a neurophysiological mechanism of ADHD. Still, the data strongly suggest that such a biological basis for ADHD does exist. Moreover, this information implies that the central nervous system contains centers that can profoundly influence amount of spontaneous physical activity.
Genetics. Demonstration of a genetic influence on habitual physical activity would strongly support the concept of intrinsic regulation of activity. Such evidence does, in fact, exist(24,37,44,56), although the estimated extent of genetic influence has varied. A Finnish study comparing levels of activity in 1537 monozygotic and 3507 dizygotic adult male twins indicated a significant heretability estimate of 0.62 for general physical activity(24).
Perusse et al. (37) found a lower genetic contribution to activity when they studied 1610 subjects from 375 families. Physical activity, estimated by a 3-d activity record, was compared in biologically related individuals (siblings, twins) and unrelated (adopted) siblings. Level of activity was found to be significantly influenced by genetic factors, with an estimated heretability of 29%. The authors concluded that “the results... lead one to speculate that the intrinsic drive to spontaneous physical activity could be partly influenced by the genotype.”
Collectively, the evidence surveyed in this review leaves little doubt that a biological control center exists within the central nervous system that governs, to some extent, how much an individual engages in regular physical activity. There is, to start with, a convincing rationale for the existence of such an “activity-stat”: homeostasis demands a close regulation of energy-in versus energy-out to maintain balance and prevent depletion of energy stores. Altering energy expenditure through physical activity, along with dietary caloric intake and resting metabolic rate, are the principal mechanisms by which this balance can be achieved.
The evidence that such biological control exists is compelling in its diversity. Heredity plays a significant role in activity levels; lesions within specific areas of the central nervous system predictably alter physical activity in animals; the ubiquitous display of play throughout the animal kingdom implies a biological drive for spontaneous motor activity; hyperactivity in humans has been linked to abnormal CNS function; and some studies have shown compensatory decreases in physical activity following imposed exercise programs.
Having accepted an intrinsic biological influence on physical activity, one is then confronted with important questions concerning the strength and malleability of this “activity-stat.” How important is this biological controller in influencing activity compared with environmental and psychosocial determinants? How easy is it to “override” central control of activity? Are there forces that can alter the activity “set point”? Can disturbances in the normal function of the“activity-stat” be held responsible for chronic energy imbalance(i.e., obesity)?
The answers to these questions bear significance to those who are attempting to increase levels of habitual activity in both individuals and in populations as a preventive medicine strategy. Does the existence of biological control of activity imply that the effectiveness of programs of enhanced activity are likely to be minimized by compensatory decreases in nonprogram activity? Not necessarily, as a controller of energy homeostasis has other options for maintaining energy balance (alterations in resting metabolic rate or food intake, for example). Might variations in the pattern of imposed physical activity trigger different responses of an activity-stat? An analogy to the effects of acclimatization in modulating the temperature response to exercise is intriguing.
Likewise, insights into the nature of biological control of activity may prove helpful to those who are attempting to treat diseases such as obesity and ADHD. Pharmacological influences on physiological regulators are well documented (i.e., the effect of aspirin on the set point of body temperature). Do similar responses occur with activity regulation? Might drugs that alter control of activity be helpful therapeutically in patients with recalcitrant obesity or anorexia nervosa?
In considering the extent that biological control centers determine one's overall level of activity, a parallel with appetite may be useful. Unquestionably, food intake is a basic biological drive; yet we seldom interpret our daily eating habits in this light. More often eating seems to be compelled by social and psychological issues: what and when we eat are more often dictated by where we are, whom we are with, and what television commercials we have just viewed rather than a response to hypothalamic control centers. Yet, over an extended period of time such intrinsic mechanisms maintain a close energy balance that outweighs such nonbiological influences. And it is not unreasonable to expect that energy expenditure, controlled by biological regulators, would display the same trend, as noted by Bennett(5). “As with breathing, elimination, and sexual activity, there can be considerable ambiguity about the degree of volition in the timing, frequency, and circumstances of any particular act of eating or exercise. In the moment, snacking may appear to be altogether subject to conscious control; in the aggregate, however, such behavior assumes a certain biologic inevitability.”
These ideas, then, support a consideration of biological influences in the investigation of regulation of physical activity in man. Additional research addressing the nature of such central control may provide dividends in improving the activity levels for both present and future health.
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