Smoking Inhibits Exercise-Induced Mitochondrial Biogenesis in the Brain

Mitochondria in the brain.

Mitochondria are synthesized in the brain in response to training, but this process is hindered by cigarette smoking.

There are numerous studies that discuss the beneficial effects exercise has on the brain. Many of them are featured in this blog and include preventing parkinson's disease, fighting Alzheimer's, and stroke recovery. Many researchers believe that one of the exercise-related factors contributing to these improvements in brain health is exercise's antioxidant effects. Exercise leads to mitochondrial biogenesis (production of new mitochondria) in cerebral neurons.  Mitochondria yield an antioxidant effect because their job is oxidative metabolism, which reduces oxygen thereby preventing free radical oxygen formation. On the other hand, smoking is well-known to have a negative effect on one's health.  With regards to smoking's interaction with exercise, smoking has been shown to generate muscle degradation. In addition, here we'll discuss a study that demonstrated smoking inhibits the production of new mitochondria in the brain in response to exercise (Cigarette Smoke Inhibits Brain Mitochondrial Adaptations of Exercised Mice, 2011 Speck AE, et al.).  

Experimental Design.  Mice were exposed to cigarette smoke for 8 weeks followed by 8 weeks of swimming training.  48 hours post-exercise training brains were removed for mitochondrial analysis.

The study found that exercise increased mitochondria density in the brain, but smoking prior to exercise training dampened the mitochondria biogenesis response. To conduct the experiment, mice were divided into four groups: trained and untrained smokers and trained and untrained nonsmokers. Smoking mice were exposed to high dosages of cigarette smoke for eight weeks. Following the eight weeks of cigarette smoke exposure, the trained mice exercised in a swimming pool for 8 weeks while the untrained mice rested in an empty swimming pool. After, the mice were exercise tested and mitochondrial complex activity measured.

The complexes that make up the electron transport chain were measured using an enzymatic activity assay. The mitochondrial complex activity was significantly elevated in both the hippocampus and frontal cortex in response to exercise.  No effect was observed in the smoking exercise-trained mice. In addition, in the untrained controls no smoking effect was observed. Therefore, exercise alone increases mitochondrial synthesis, but this is negated with the addition of cigarette smoking in the 8 weeks prior to the exercise training. It should be noted that these results do not necessarily signify new mitochondria per se, but at least improved capacity of the mitochondria. The results can be seen in the figure below.

Smoking dampens mitochondrial biogenesis training response.  Smoking protocol was 8 weeks.  Exercise protocol was swimming for the following 8 weeks.  Complex I, an electron transport component in the mitochondria, activity was measured and quantified in nmol/min/mg protein.  Values are expressed as mean ± SEM. * P<0.05 versus untrained/non-smoker control, # P<0.05 versus trained/non-smoker group.

Although mitochondrial biogenesis did not significantly change the mitochondrial count of untrained mice, other studies have shown that an acute bout of smoke inhalation actually protects mitochondrial function in the central nervous system (Nicotine protects rat brain mitochondria against experimental injuries, 2003.  Cormier A, et al.). The effect is apparently mediated through nicotine.  How long the smoking affect lasts on mitochondria biogenesis is not known, but from the results of the Speck paper it must be at least eight weeks.  

In summary, smoking's antioxidant effects are controversial. Studies show that smoking alone may both protect and harm mitochondrial function in the brain. However, it is shown conclusively in the Speck paper that smoking harms mitochondrial brain function.

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