Post-Meal Resting Energy Expenditure
Food ingestion increases the metabolic rate to levels above basal (Jequier 1986; Lusk 1930). This rise in metabolic rate in the able-bodied 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: Post-Meal Resting Energy Expenditure Post SCI
Discussion
The increase in the 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; Segal et al 1990; Segal et al 1985; Shetty et al 1981; Pittet et al 1976). 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 Aksnes 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) (group A). 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 (group B). 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 in man.
Conclusion
- There is level 3 evidence based on one case control study (Asknes et al., 1993) that meal-induced thermogenesis is not decreased in tetraplegic individuals with low sympathoadrenal activity and that 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.
