Blood Lactate Predicts Resting Energy Expenditure in Non-Obese Caucasian Females

Abstract

Background: Obesity and Type 2 Diabetes are both global epidemics that continue to skyrocket. High basal plasma lactate levels, reduced oxidative capacity, and insulin resistance are co-morbidities with these metabolic disorders. However, it is unknown if those co-morbid traits are also displayed in the non-obese who may be predisposed to obesity. A higher plasma lactate concentration is the product of the shift to anaerobic glycolysis due to the reduction of oxidative capacity. With aerobic respiration being limited, we believed it would reduce the resting energy expenditure (REE), and potentially propel an individual toward obesity and related metabolic disease(s). Purpose: The purpose of the study was to investigate if plasma lactate can be used to predict resting energy expenditure in non-obese humans. Methods: Non-obese subjects (n=40) with body mass index (BMI) between 18.5-26.0 kg/m2 were screened for plasma lactate concentration. Subjects with the highest (n=10) and lowest (n=11) plasma lactate were selected and grouped into a High Lactate (High) and a Low Lactate (Low) Group. Both groups had their body composition, REE, resting respiratory exchange ratio (RER), and aerobic capacity (VO2 peak) assessed on the first testing day. Blood measurements, and oxidative capacity were assessed using near infrared spectroscopy (NIRS), and submaximal exercise RER (low intensity at 50% VO2 peak) were assessed on the second testing day. Results: Lactate and REE were negatively correlated (R=-0.6093) in the High Lactate Group. This correlation was stronger when REE was adjusted for fat free mass (FFM) (R=-0.6823, P<0.05). Aerobic capacity adjusted for FFM was significantly lower in the High Lactate Group (P<0.05). Lactate and aerobic capacity adjusted for FFM also revealed a strong relationship (R=-0.7232, P<0.001). Lactate and oxidative capacity demonstrated a negative relationship (R=-0.364) in the High Lactate Group. Lactate and substrate change ([delta]RER) from resting to submaximal exercise were strongly correlated (R=0.6393, P<0.05). Laboratory blood analysis showed no difference in plasma lactate, insulin or glucose. Conclusion: Lactate is associated with resting energy expenditure in non-obese Caucasian females. The inability for higher lactate individuals to match more fat substrates utilized as the lower lactate subjects may be an indication of a lesser mitochondrial and capillary density. The implication of early signs of elevated lactate concentrations may be an indicator of a compromised energy transduction capacity, which may be a contributor to obesity. Further research is needed to look at the plasma lactate concentration, and oxidative capacity affecting energy expenditure.