Human Energy Expenditure (and semantics)
Even lean individuals store at least two to three months of their energy needs in adipose tissue whereas obese persons can carry a year's worth of their energy needs. It is the cumulative impact of energy imbalance over months and years that results in the development of obesity or under nutrition.

There are three principal components of human energy expenditure (EE), basal metabolic rate (BMR), thermic effect of food (TEF) and activity thermogenesis. There are also other small components of EE that may contribute to the whole, such as the energetic costs of medications and emotion.

BMR is the energy expended when an individual is laying at complete rest, in the morning, after sleep, in the post absorptive state. In individuals with sedentary occupations BMR accounts for approximately 60 percent of total daily EE. Three-quarter's of the variability in BMR is predicted by lean body mass within and across species. TEF is the increase in EE associated with the digestion, absorption, and storage of food and accounts for approximately 10-15 percent of total daily EE.

Activity Thermogenesis has two constituents, exercise-related activity thermogenesis and Non-exercise Activity Thermogenesis (NEAT). For the vast majority of dwellers in the U.S., exercise activity thermogenesis is negligible. NEAT, even in avid exercisers, is the predominant constituent of activity thermogenesis and is the EE associated with all the activities we undertake as vibrant, independent beings. NEAT has an enormous variety of constituents including occupation, leisure and fidgeting. Because of this, NEAT is challenging to study and its role in human energy balance has been difficult to define.

Non-exercise Activity Thermogenesis (NEAT)
NEAT is likely to contribute substantially to the inter- and intra-personal variability in EE. Argue thus; if three-quarters of the variance of BMR is accounted for by variance in lean body mass and, TEF represents 10-15 percent of total EE, then the majority of the variance in total EE that occurs independent of body weight must be accounted for by NEAT. Evidence supports this. NEAT is highly variable and ranges from ~ 15 percent of total daily EE in very sedentary individuals to >50 percent in highly active persons. Even minor changes in physical activity throughout the day can increase daily EE by 20 percent. NEAT is impacted by environment, but is also under biological control.

NEAT and environment
There are many environmental cues that impact NEAT. Broadly, they can be divided into occupational and non-occupational components.

NEAT and occupation
Matched individuals with highly active ambulatory jobs can have NEAT values of 1000 kcal/day greater than sedentary peers. In areas of nutritional need, this has implications for starvation-threatened individuals. In affluent countries, industrialized can convert high-NEAT jobs to lower-NEAT jobs and this has been associated with increased obesity rates.

Non-occupation NEAT

  • Dish washers
  • Cars
  • Remotes
  • Lawnmowers
  • Drive-through
  • Game-boy
  • Elevators
  • Snow blowers

Leisure-time sedentariness has resulted from the availability and volitional use of pervasive mechanization. When the energetic cost of non-work mechanization is estimated experimentally it approximates to, 100-200 kcal/day; a caloric deficit that potentially could account for the entire obesity epidemic.

NEAT and physiology
With experimental overfeeding in humans, NEAT increases. Those who increased their NEAT the most with overfeeding gained the least fat. This suggests that along with self-evident societal slothfulness, NEAT is biologically modulated. Animal data support this. There appear to be central mediators of NEAT. For example, microinjections of orexins into hypothalamic nuclei increase NEAT whereas antagonists decrease it. There may be humeral mediators as experimental hyperthyroidism is associated with increased NEAT. There also be genetic mechanism at play; during overfeeding twinges in part predicts fat gain. Also NEAT is specific for different genetic strains of mice.

Where to from here?

Mechanism: by understanding the neuromodulators and non-central mediators of NEAT; its biological function will become clear.

Physiology: What are the key components of NEAT? What is the role of NEAT in aging, children, gender, and race? How does positive and negative affect NEAT and its components?

Pathology: What is the role of NEAT in obesity and eating disorders?

Intervention: Targeted, evaluated interventions from person to population.

Having read this abstract, please get up and take and short walk down the corridor (or similar). Repeat for each abstract you read.

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