BACKGROUND: Motion sickness can influence energy homeostasis by enhancing thermolysis. This study tested the hypothesis that resting energy expenditure (REE), as the major component of thermogenesis, might also play a role during motion sickness. METHODS: The effect of seasickness on REE at sea was examined in 71 healthy Chinese male volunteers. Change in REE, heart rate variability (HRV), blood ghrelin levels, and leptin levels were observed across baseline, voyage, and recovery stages. Seasickness severity was assessed using the Graybiel motion sickness questionnaire (GMSQ), and the nausea syndrome rating (NSR) of each participant was also evaluated. REE was examined by indirect calorimetry. HRV was derived from the electrocardiogram to analyze cardiac sympathovagal activity. Blood ghrelin and leptin levels were tested by radioimmunoassay. RESULTS: In subjects with severe seasickness during the voyage, the GMSQ and NSR scores were higher than in subjects with slight and moderate seasickness. The REE declined significantly compared to baseline and recovery levels and was lower than in subjects with slight and moderate seasickness. Cardiac sympathetic activity was significantly decreased, while vagal activity was increased. Plasma ghrelin levels were also significantly increased and were negatively correlated with the measured REE levels and positively correlated with NSR as well as change of HRV LF/HF ratio from baseline. DISCUSSION: Severe motion sickness induces REE suppression, which may be attributed to dramatic alteration of sympathovagal activity and plasma ghrelin levels in humans.
BACKGROUND: Motion sickness can influence energy homeostasis by enhancing thermolysis. This study tested the hypothesis that resting energy expenditure (REE), as the major component of thermogenesis, might also play a role during motion sickness. METHODS: The effect of seasickness on REE at sea was examined in 71 healthy Chinese male volunteers. Change in REE, heart rate variability (HRV), blood ghrelin levels, and leptin levels were observed across baseline, voyage, and recovery stages. Seasickness severity was assessed using the Graybiel motion sickness questionnaire (GMSQ), and the nausea syndrome rating (NSR) of each participant was also evaluated. REE was examined by indirect calorimetry. HRV was derived from the electrocardiogram to analyze cardiac sympathovagal activity. Blood ghrelin and leptin levels were tested by radioimmunoassay. RESULTS: In subjects with severe seasickness during the voyage, the GMSQ and NSR scores were higher than in subjects with slight and moderate seasickness. The REE declined significantly compared to baseline and recovery levels and was lower than in subjects with slight and moderate seasickness. Cardiac sympathetic activity was significantly decreased, while vagal activity was increased. Plasma ghrelin levels were also significantly increased and were negatively correlated with the measured REE levels and positively correlated with NSR as well as change of HRV LF/HF ratio from baseline. DISCUSSION: Severe motion sickness induces REE suppression, which may be attributed to dramatic alteration of sympathovagal activity and plasma ghrelin levels in humans.