Meal-induced rise in resting energy expenditure in patients with complete cervical spinal cord lesions

Central activation of the sympathoadrenal system is generally considered to be an essential component of the mechanisms whereby food ingestion stimulates resting energy expenditure. The functional importance of such sympathoadrenal stimulation has been demonstrated primarily in animals. To the extent that central sympathoadrenal stimulation is required for normal human nutrient-induced thermogenesis, this process should be defective in patients with complete cervical spinal cord lesion and severed connection between the central nervous system and the peripheral sympathetic nerves. Consequently, respiratory gas exchange was measured by indirect calorimetry in 9 tetraplegic patients and in 6 healthy individuals. Measurements were performed before and 2 hours after ingestion of a standardised mixed meal (40% of basal 24 h energy requirements). The basal energy expenditure was 64 +/- 4 watts in the tetraplegic patients and 79 +/- 6 watts in the controls. After the meal, energy expenditure increased on average by 17 +/- 2 watts or 26 +/- 3% of the basal values in the patients and by 14 +/- 2 watts or 19 +/- 3% in the healthy controls (NS). The thermic effect of the meal, ie the rise in energy expenditure expressed in percent of the meal's energy content, was 5.5 +/- 0.7% in the patients and 3.8 +/- 0.6% in the controls (NS). Plasma concentrations of noradrenaline were low in the tetraplegic patients (0.3-0.4 nmol/l) compared to the healthy controls (1.1-1.4 nmol/l), p < 0.02. It is concluded that nutrient-induced thermogenesis in tetraplegic patients with low sympathoadrenal activity is not diminished compared to healthy controls. The findings indicate that efferent sympathoadrenal stimulation from the brain is not a causal necessity for nutrient-induced thermogenesis in man.