The following article was taken from Ergo-Log
Athletes who do strength sports develop an enlarged heart. This is not a problem in itself, but when combined with anabolic substances this enlargement can result in a fatal abnormality. Taking a Q10 co-enzyme supplement may offer protection, if the results of studies published by American cardiologists in the 1990s are anything to go by.
Under some conditions doing strength sports can cause an enlargement of the left ventricle in the heart. The muscles in this ventricle – in the septal wall and the posterior wall to be precise – that it leads to a reduction in the amount of blood that the ventricle can pump round the body.
Cardiologists observe this phenomenon primarily in people with high blood pressure, but occasionally chemical strength athletes also develop a dangerous form of left ventricular hypertrophy.
According to a 2003 Finnish study, it’s steroids users who also make long-term use of growth hormone that should be worried. The amount of blood that the heart is capable of pumping round the body can reach dangerously low levels in this group.
The American cardiologist Per Langsjoen has been publishing articles regularly since the 1980s on the cardiological effects of Q10. In the 1990s Langsjoen focused on people – not strength athletes – with an enlarged left ventricle. We dug up a small study that he did in 1997, in which he got seven patients to take an average of 200 mg Q10 every day for 3-48 months.
Q10 [chemical formula shown here] is a molecular thumbtack, which functions as a distribution centre for electrons. If the cell pushes enough of these into the mitochondria membranes, they can generate energy faster and cells take longer to reach the point of exhaustion.
Left ventricular hypertrophy is believed to be caused by heart cells becoming chronically fatigued. Langsjoen reasoned that heart cell vitality could be restored through supplementation aimed at reducing the negative effects of left ventricular hypertrophy.
And hey presto: the table below shows that the subjects’ septal wall thickness [SWT] and the posterior wall thickness [PWT] decreased.
EF slope, LVEDD and FS are cardiological variables which indicate how well the heart is pumping blood. The results show an improvement, but it’s not statistically significant. Nevertheless, the patients had less chest pain, were less tired and less short of breath.
“These highly encouraging clinical and echocardiographic findings in hypertrophic cardiomyopathy are in keeping with the working hypothesis that CoQl0 has a beneficial effect on myocardial bioenergetics and ATP production”, the researchers conclude.
Source: Mol Aspects Med. 1997;18 Suppl:S145-51.
Co-Enzyme Q10 Versus Heart Failure
A high daily dose of the co-enzyme Q10 doubles the survival chances of people suffering from heart failure. The Danish cardiologist Svend Aage Mortensen announced this at the annual meeting of the Heart Failure Association of the European Society of Cardiology, held at the end of May in Lisbon.
Q10 is an antioxidant that is naturally present in the body. It plays a role in energy production in the cells. When nutrients are converted into energy molecules Q10 ensures that the electrical charges released don’t cause damage. Scientists believe that a too low concentration of Q10 in brain and heart cells is a contributing factor to the onset of brain diseases, such as Parkinson’s, and heart failure.
Mortensen has been studying the positive effects of Q10 on heart failure since the 1990s. When heart failure occurs the heart is not capable of contracting properly and, as a result, parts of the body don’t get enough oxygen or nutrients. A rare form of heart failure is hypertrophy of the heart muscle, which occurs in strength athletes who use growth hormone and anabolic steroids. In this group the muscle tissue in the heart becomes so enlarged that not enough blood can ‘fit’ into the heart muscle. Q10 supplementation may offer protection against this.
Mortensen and his colleagues performed experiments as part of the Q-SYMBIO study, in which 420 people from nine different countries with serious heart failure took part. Some of them only felt healthy when resting; others were affected by their complaint even when resting. For a period of two years, 202 test subjects were given three doses of 100 mg of the Q10 co-enzyme every day, spread over the day.
The remaining 218 test subjects were given a placebo for two years.
Throughout the experimental period, the heart condition of the Q10 group improved: their complaint became less serious. This did not happen in the placebo group.
During the experimental period, a quarter of those in the placebo group experienced a major adverse cardiovascular event [MACE]. Only 14 percent of the subjects in the Q10 group suffered a similar fate. A major adverse cardiovascular event included hospitalisation as a result of deterioration in the condition, or death.
In the placebo group 17 percent of the subjects died. In Q10 group the figure was 9 percent. This means that Q10 supplementation raised survival chances by a factor 2.1.
“CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy”, said researcher Svend Aage Mortensen of Copenhagen University Hospital in a press release. “Other heart failure medications block rather than enhance cellular processes and may have side effects. Supplementation with CoQ10, which is a natural and safe substance, corrects a deficiency in the body and blocks the vicious metabolic cycle in chronic heart failure called the energy starved heart.”
Mortensen suspects that people on statins may also benefit form Q10 supplementation. Statins block the production of Q10. He recommends that statins users first discuss with their physician or pharmacist before starting to take Q10. Q10 supplementation stimulates blood coagulation, and can therefore reduce the effect of anti-coagulants. Q10 also causes the body to breakdown substances like theophylline more slowly, which can lead to an increased risk of side effects.
Source: European Journal of Heart Failure (2013) 15;(S1):S20.