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; Country PEDro Score Research Design Sample Size	Methods	Outcomes
Asknes et al. 1993 Sweden Prospective Controlled Trial N=13	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). Post-meal: 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.

Author Year;

Country
PEDro Score
Research Design
Sample Size

Methods

Outcomes

Asknes et al. 1993

Sweden

Prospective Controlled Trial

N=13

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).

Post-meal:

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.

Discussion

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.

Conclusion

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.

Post-Meal Resting Energy Expenditure

Table 15 Post-Meal Resting Energy Expenditure

Discussion

Conclusion

Effects of Nutrient Intake on Ambulation Performance

Cardiovascular, Endocrine and Renal Responses to Dietary Sodium Restriction in Persons with Paraplegia and Tetraplegia

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