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Post-Meal Resting Energy Expenditure

Food ingestion causes the metabolic rate to rise above the basal level (Jequier 1986; Lusk 1930). This rise in metabolic rate in the non-SCI population is initiated within minutes following meal ingestion, reaches its maximum after approximately one hour, and lasts up to 6 hours after food consumption. The mechanisms whereby nutrients stimulate energy expenditure are not fully understood. The potential role of the central sympathoadrenal system in the stimulation of nutrient-induced thermogenesis requires investigation.

Table 15 Post-Meal Resting Energy Expenditure

Author Year;

PEDro Score
Research Design
Sample Size



Asknes et al. 1993


Prospective Controlled Trial




Population: SCI (N=7): Age range=21-34 yr; Gender: males=7, females=0; Severity of injury: Frankel A=7, complete=7, incomplete=0; Time since injury=1-11 yr; Non-SCI controls (N=6): Age range=18-30 yr; Gender: males=6, females=0.

Intervention: Patients were divided into two groups and received either a liquid form mixed meal (52% carbohydrates, 37% fat, and 11% protein) or water.

Outcome Measures: O2 uptake, respiratory exchange (RE), blood glucose (BG), insulin, catecholamines, heart rate (HR), and energy expenditure (EE).

1.     Basal O2 uptake, EE, BG, insulin and noradrenaline levels was lower in the treatment group compared to controls (p<0.01 for all); HR was high for both groups before ingestion (p<0.05).


2.     Both groups had increased O2 uptake although there were no between group differences.

3.     The treatment group’s RE rate reached a maximum at 90 min (p<0.05) while the controls had an extremely high rate at 15 min which dropped to a rate similar to the treatment group.

4.     Mean EE was higher in the treatment (17 W) versus control (14 W) group.

5.     HR increased 6-7 beats/min in both groups (p<0.05).

6.     The treated group had higher BG and insulin levels compared to controls (p<0.05); noradrenaline levels did not change.


An increase in metabolic rate above basal levels following food ingestion is known as nutrient-induced thermogenesis (Jequier 1986; Lusk 1930). This post-meal rise in metabolic rate is significant to daily heat production and body weight homeostasis and may have a potential role in counteracting the development of obesity. In many obese individuals and in other conditions of insulin resistance, nutrient-induced thermogenesis is reduced below normal levels (Brundin et al. 1992; Pitt et al. 1976; Segal et al. 1985; Segal et al. 1990; Shetty et al. 1981). The rise in resting energy expenditure following food consumption has been generally considered to be mediated by central activation of the sympathoadrenal system. The purpose of a study by Asknes et al. (1993) was to determine the possible role of central sympathoadrenal stimulation for thermogenesis after ingestion of a normal mixed meal, in liquid form, in seven male subjects with chronic complete lesions of the cervical spinal cord (C4-C7). The thermogenic responses were compared to those in healthy males as well as to the responses in a control group of tetraplegic patients who received equal volumes of water instead of the liquid meal. The authors concluded that nutrient-induced thermogenesis in tetraplegic individuals with low sympathoadrenal activity is not diminished compared to healthy controls; efferent sympathoadrenal stimulation from the brain is not necessary for nutrient-induced thermogenesis.


There is level 3 evidence (from one prospective controlled trial; Asknes et al. 1993) that nutrient-induced thermogenesis is not decreased in individuals with tetraplegia with low sympathoadrenal activity; efferent sympathoadrenal stimulation from the brain is not necessary for nutrient-induced thermogenesis.

  • Meal-induced thermogenesis is not decreased in tetraplegic individuals with low sympathoadrenal activity and efferent sympathoadrenal stimulation from the brain is not necessary for nutrient-induced thermogenesis.