Those keen to optimise their cardiovascular health and reduce their risk of heart attack and stroke may well, in addition to ‘eating right’, take steps to ‘take exercise’ and be physically fit. Usually, the prescribed exercise here come in the form of ‘cardiovascular’ or ‘aerobic’ forms such as walking, jogging, cycling or rowing. Such activities can increase our ‘fitness’ and capacity for exercise, partly by inducing the production of tiny ‘engines’ in the cells known as mitochondria (my-toe-con-dree-ah). It is in the mitochondria that most of the fuel in our body is converted into energy. The more mitochondria we have (and the more efficiently they work), the fitter and more ‘energised’ we tend to be.
Another quite-common approach to reducing risk of heart attack or stroke is to take a statin. Actually, statins don’t work particularly well for this, and another potential problem is that these drugs deplete levels of the substance coenzyme Q10 (CoQ10) in the body. This is important because CoQ10 performs a vital function in the production of energy in the mitochondria. Low CoQ10 levels could, therefore, stifle energy production and may, theoretically at least, negate some of the benefits one might expect from physical exercise.
Last week, the journal Sports Medicine published a review of the potential impact statins have on effects of regular physical exercise [1]. The authors refer to more than one study in which statins appeared to have no ill-effect on fitness levels (as adjudged by maximum VO2). However, as the authors point out, these studies have generally been done in healthy individuals. This, and other factors such as the short duration of the studies and relatively small sample sizes may mean they do not necessarily tell the whole story.
They refer specifically to one study that provides good evidence, I think, that statins can put a serious brake on the fitness benefits exercise usually offers [2]. In this research, 37 adults underwent 12 weeks of aerobic training. Half of the group just participated in the exercise programme, while the other half took 40 mg of the statin simvastatin (Zocor) each day. Fitness was assessed prior to the study starting, and at the end too.
In those not taking statins, fitness increased by an average of 10 per cent of the 12-week study. However, in those taking simvastatin, fitness increased by only 1.5 per cent.
As part of this study, mitochondrial activity was assessed by measuring activity of the enzyme citrate synthase (a key enzyme involved in energy production in the mitochondria). Citrate synthase activity increased by 13 per cent in those who adopted exercise, but actually fell by 4.5 per cent in those taking the drug.
In the recent review [1], the authors also quote animal research in which statins have been found to reduce endurance and mitochondrial activity.
The evidence suggests, therefore, that statins have the potential to negate at least some of the benefits of exercise. But there is another major problem, too: those who may be fatigued from taking statins or perhaps are suffering from muscle pain (myalgia) as a result of these drugs may be less inclined to take exercise in the first place. The authors of this review cite evidence suggesting that as many as 25 per cent of those taking statins experience muscle symptoms on taking exercise, and that about 40 per cent of people with myalgia avoid even moderate exertion.
Some may say these problems, when they happen, are a small price to pay for the ‘obvious benefits’ of statins. However, it is probably worth bearing in mind that in most people who take statins (those with no history or heart attack or stroke), the research suggests statins have no net health benefit and don’t reduce the risk of death either [3].
References:
1. Murlasits Z, et al. The Effects of Statin Medications on Aerobic Exercise Capacity and Training Adaptations. Sports Medicine epub 11 July 2014
2. Mikus CR, et al. Simvastatin impairs exercise training adaptations. Journal of the American College of Cardiology. Epub 10 April 2013
3. Do statins have a role in primary prevention? An update. Therapeutics Letter Issue 77 Mar-Apr 2010 Therapeutics Initiative University of British Columbia
