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.
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.