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Can Endurance Exercise Promote Cancer? Steve replied: Paul, you said “. How confident are you that she died “from” running marathons?
Of course, not confident at all. Maybe if she’d been a sprinter she would have died at 5. Maybe if Lance Armstrong had been a couch potato he would still have had testicular cancer metastasized to his brain and lung at age 2.
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A few days ago I got an email. Two highly fit endurance athletes, both of whom have always tended to their health and been careful to eat “healthy” (i. My correspondent asked, “Why?”Let’s look into this. Is it possible that endurance exercise, especially if combined with a high- carb diet, may promote cancer? Oxidative Damage to DNA and Cancer.
Human DNA is constantly being damaged and repaired. It’s been estimated that over the course of a cell cycle – that is, from the time a cell is formed to the time it divides into two daughter cells – a human cell develops 5,0. DNA breaks due to oxidative damage from reactive oxygen species (ROS). The vast majority are repaired by the body’s DNA repair machinery.
In people with Bloom syndrome, an inherited condition which creates a strong predisposition to cancer, fully 1% or 5. Usually, this does not break the coding region for a protein, but it does break non- coding regions resulting in changes to gene expression. These sorts of genetic changes are observed both in cancer and in aging. And diets and activities that minimize oxidative stress can minimize cancer risk and facilitate recovery. Endurance exercise generates oxidative stress. Marathon running “caused a large increase in the tissue content of oxidized glutathione (1. Besides oxidative stress, other factors such as metabolic, hormonal and thermal stress in addition to the ultra- structural damage of muscle tissue are characteristic responses to prolonged strenuous exercise, that can lead to the release of cytokines, acute phase proteins and to the activation or inhibition of certain lines of the cellular immune system .
Moderate exercise actually protects DNA by upregulating DNA repair: Sato et al. An Ironman triathlon has significant effects on hormones and inflammatory markers, some of which persist for more than 1. Briefly, as described in details elsewhere . Except for cortisol, which decreased below pre- race values (P< 0. P< 0. 0. 01, P< 0. IL- 1. 0). Five days post- race CK activity, myoglobin, IL- 6 and hs- CRP had decreased, but were still significantly (P< 0.
Nineteen days post- race most parameters had returned to pre- race values, with the exception of MPO and PMN elastase, which had both significantly (P< 0. CRP, which were slightly, but significantly higher than pre- race . DNA damage in peripheral immuno- competent cells, indeed, most likely resulted from an increased generation of RONS due to initial systemic inflammatory responses or the delayed inflammatory processes in response to muscle damage (Fig. Quantitatively, glucose metabolism produces 5 NADH molecules (entering at complex I) for every one succinate molecule (entering at complex II), while fatty acid metabolism produces only 2 NADH for every one succinate. High- carb dieting tends to habituate the body to metabolism of glucose. Therefore, it increases utilization of complex I. This is significant because complex I is vulnerable to production of excess oxidative stress under some circumstances.
In principle, every mitochondrial complex has the potential to operate cleanly with minimal production of superoxide. However, if mitochondrial function is in any way impaired, so that operation of a complex is inhibited, then ROS production can rise substantially. If for some reason electrons cannot flow properly through the electron transport chain, then they leave as superoxide: One factor which may sensitise cells to increased DNA damage is impaired mitochondrial function . Reduced electron flow through the mitochondrial respiratory chain, particularly through the inhibition of complex I or complex III, favours the enhanced production of superoxide and H2.
O2. Together, with the age- dependent increase in oxidative stress and decline in NAD+ and ATP content, we found a tendency to the reduction in the activity of the respiratory complexes with age in all organs. Similarly, threshold inhibition of complex IV caused an accelerated ROS production. By contrast, inactivation of complex I to a small extent (1. ROS formation, and no clear threshold inhibition could be determined. However, in complexes III and IV, there is a high threshold of inhibition of electron transport before any superoxide is produced.
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In complex I, there is no threshold: even very slight inhibition will generate ROS. This means that during practical living, the great majority of excess ROS is produced from complex I. This means that high- carb dieting, which increases utilization of complex I, will tend to generate oxidative stress if there is any inhibition of complex I. But in endurance exercise, there is inhibition of complex I.
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To name just one pathway, exercise increases levels of the hormone DHEA, and DHEA inhibits complex I. For instance, wheat germ agglutinin, a wheat toxin that is very effective at distributing itself through the body through transcytosis, is able to damage mitochondria: WGA induced a loss of transmembrane potential, disruption of the inner mitochondria membrane, and release of cytochrome c and caspase- 9 activation after 3. It’s conceivable that at physiological levels WGA damage to mitochondria might mildly inhibit complex I and increase oxidative stress. Of course, any deficiency in antioxidant minerals zinc and copper, which dismutate superoxide to hydrogen peroxide which is then disposed of by glutathione peroxidase (a selenium containing enzyme), would increase oxidative stress. Wheat contains phytic acid which chelates minerals and reliance on wheat as a calorie source may impair antioxidant status. Conclusion. I don’t want to exaggerate the risks of endurance sports. With the exception of melanoma .
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And if this post seemed a bit tortuous, it’s because there’s no simple “smoking gun” pathway connecting endurance exercise to cancer. On the other hand, endurance exercise is probably not as healthy, in terms of cancer risk, as shorter- duration activities. Also, the risk may rise substantially on high- carb or wheat- based diets. There are at least a few plausible mechanisms, not all of which I’ve discussed here, that might connect endurance exercise on grain- based high- carb low- fat diets to cancer. References. Endogenous DNA double- strand breaks: production, fidelity of repair, and induction of cancer. Proc Natl Acad Sci U S A. Oct 2. 8; 1. 00(2.
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Lots of endurance athletes now promote a gluten-free diet. What's all the fuss about?
The effect of marathon running on carnitine metabolism and on some aspects of muscle mitochondrial activities and antioxidant mechanisms. Autumn; 4(2): 7. 9- 8. Exercise- induced DNA damage: is there a relationship with inflammatory responses?
Age related changes in NAD+ metabolism oxidative stress and sirt. Apr 2. 6; 6(4): e. Quantitative relationship between inhibition of respiratory complexes and formation of reactive oxygen species in isolated nerve terminals. Dehydroepiandrosterone inhibits complex I of the mitochondrial respiratory chain and is neurotoxic in vitro and in vivo at high concentrations. Oct; 9. 3(2): 3. 48- 5. A novel apoptotic pathway as defined by lectin cellular initiation. Biochem Biophys Res Commun.
Mar 2. 6; 3. 16(1): 2. Malignant melanoma in marathon runners. Nov; 1. 42(1. 1): 1.
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