Systemic Lactate Elevation Induced by Tobacco Smoking during Rest and Exercise Is Not Associated with Nicotine

Abstract

Lactate is a metabolite produced during anaerobic glycolysis for ATP resynthesis, which accumulates during hypoxia and muscle contraction. Tobacco smoking significantly increases blood lactate. Here we conducted a counter-balanced crossover study to examine whether this effect is associated with inhaling nicotine or burned carbon particles. Fifteen male smokers (aged 23 to 26 years) were randomized into 3 inhalation conditions: tobacco smoking, nicotine vaping, and nicotine-free vaping, conducted two days apart. An electronic thermal evaporator (e-cigarette) was used for vaping. We have observed an increased blood lactate (+62%, main effect: p < 0.01) and a decreased blood glucose (−12%, main effect: p < 0.05) during thermal air inhalations regardless of the content delivered. Exercise-induced lactate accumulation and shuttle run performance were similar for the 3 inhalation conditions. Tobacco smoking slightly increased the resting heart rate above the two vaping conditions (p < 0.05), implicating the role of burned carbon particles on sympathetic stimulation, independent of nicotine and thermal air. The exercise response in the heart rate was similar for the 3 conditions. The results of the study suggest that acute hypoxia was induced by breathing thermal air. This may explain the reciprocal increases in lactate and decreases in glucose. The impaired lung function in oxygen delivery of tobacco smoking is unrelated to nicotine.