Does Q10 offer strength athletes cardiac protection?

Arnold

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Does Q10 offer strength athletes cardiac protection?

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.

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. [Int J Sports Med 2003; 24: 337-343.] 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.

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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.

In 1999 Australian cardiologists published the results of a study which showed that Q10 supplementation had no effect on the left ventricle of patients. [J Am Coll Cardiol. 1999 May; 33(6): 1549-52.] They used a lower dose than the Americans.

Source:
Mol Aspects Med. 1997;18 Suppl:S145-51.
 

Arnold

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Clinicial Studies on CoQ10

Clinicial Studies on CoQ10

Biochemical functions of Coenzyme Q10

Source: Department of Biological Sciences, Purdue University, West Lafayette, Indiana, USA. Abstract

Coenzyme Q is well defined as a crucial component of the oxidative phosphorylation process in mitochondria which converts the energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis. New roles for coenzyme Q in other cellular functions are only becoming recognized. The new aspects have developed from the recognition that coenzyme Q can undergo oxidation/reduction reactions in other cell membranes such as lysosomes. Golgi or plasma membranes. In mitochondria and lysosomes, coenzyme Q undergoes reduction/oxidation cycles during which it transfers protons across the membrane to form a proton gradient. The presence of high concentrations of quinol in all membranes provides a basis for antioxidant action either by direct reaction with radicals or by regeneration of tocopherol and ascorbate. Evidence for a function in redox control of cell signaling and gene expression is developing from studies on coenzyme Q stimulation of cell growth, inhibition of apoptosis, control of thiol groups, formation of hydrogen peroxide and control of membrane channels. Deficiency of coenzyme Q has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase inhibitors (statins) or for unknown reasons in ageing and cancer. Correction of deficiency requires supplementation with higher levels of coenzyme Q than are available in the diet.


Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes.

Hodgson JM, Watts GF, Playford DA, Burke V, Croft KD.

Source: University of Western Australia Department of Medicine and HeartSearch, Royal Perth Hospital, Perth, Western Australia, Australia.

Abstract

OBJECTIVE:

Our objective was to assess effects of dietary supplementation with coenzyme Q10 (CoQ) on blood pressure and glycaemic control in subjects with type 2 diabetes, and to consider oxidative stress as a potential mechanism for any effects.

SUBJECTS AND DESIGN:

Seventy-four subjects with uncomplicated type 2 diabetes and dyslipidaemia were involved in a randomised double blind placebo-controlled 2x2 factorial intervention.

SETTING:

The study was performed at the University of Western Australia, Department of Medicine at Royal Perth Hospital, Australia.

INTERVENTIONS:

Subjects were randomly assigned to receive an oral dose of 100 mg CoQ twice daily (200 mg/day), 200 mg fenofibrate each morning, both or neither for 12 weeks.

MAIN OUTCOME MEASURES:

We report an analysis and discussion of the effects of CoQ on blood pressure, on long-term glycaemic control measured by glycated haemoglobin (HbA(1c)), and on oxidative stress assessed by measurement of plasma F2-isoprostanes.

RESULTS:

Fenofibrate did not alter blood pressure, HbA(1c), or plasma F2-isoprostanes. There was a 3-fold increase in plasma CoQ concentration (3.4+/-0.3 micro mol/l, P<0.001) as a result of CoQ supplementation. The main effect of CoQ was to significantly decrease systolic (-6.1+/-2.6 mmHg, P=0.021) and diastolic (-2.9+/-1.4 mmHg, P=0.048) blood pressure and HbA(1c) (-0.37+/-0.17%, P=0.032). Plasma F2-isoprostane concentrations were not altered by CoQ (0.14+/-0.15 nmol/l, P=0.345).

CONCLUSIONS:

These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes.
 
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