To the Editor Moheimani et al1 suggested that electronic cigarettes (e-cigarettes) are associated with increased cardiovascular risk. To reach this conclusion, the authors measured the heart rate variability, an index of sympathovagal modulation, and 3 parameters of oxidative stress, ie, low-density lipoprotein oxidizability, high-density lipoprotein antioxidant/anti-inflammatory capacity, and paraoxonase-1 activity, in the plasma of e-cigarettes smokers and nonsmokers.1 Notably, physical activity, or exercise training (both terms are usually used interchangeably), has important effects on sympathovagal activity and oxidative stress, 2 mechanisms analyzed by the authors. Most importantly, the changes induced by short-term or long-term exercise training on these parameters are substantially different. The reduction of parasympathetic influence after short-term exercise has been demonstrated using heart rate variability, showing a gradual reduction in high-frequency power paralleling increased exercise intensity,2 while long-term exercise–trained individuals have increased heart rate variability as well as improved baroreflex responsiveness.3 On the other hand, short-term exercise bouts considerably increase oxidative stress, wherein trained individuals show an enhanced endogenous antioxidant enzyme capacity and an increased tolerance to exercise-induced oxidative stress.4 Likewise, sedentary lifestyle is also associated with increased oxidative stress5 and negatively affects heart rate variability. In fact, it has been reported that a sedentary lifestyle is as hazardous as smoking in terms of cardiovascular risk.