Statins are drugs that play a key role in the prevention of cardiovascular disease. Their effects are not limited to a pure reduction in plasma cholesterol levels but exert a strong protective effect at vascular level, which is clinically expressed in a reduction in cardiovascular events, such as stroke and myocardial infarction.
Unfortunately, however, these drugs are burdened with a negative reputation for the possible negative effects they can exert on the muscles. In truth, this adverse effect is not as common as one can believe, but a climate of distrust established towards these drugs, so much to favour what is called the ‘nocebo effect’. An adverse effect induced by a drug that are not justifiable on a clinical level. It is essentially the opposite of what happens for the placebo effect, when an inert substance induces health benefits, without actually being able to exert any real organic effect.
The constant intake of statins, when indicated, is extremely important for cardiovascular health, so much so that it is preferable to continue treatment even when mild muscle symptoms occur or there are minimal changes in blood chemistry parameters.
Muscle mitochondrial function and capillarization of muscle fibres
A recent study, published in the Journal of the American College of Cardiology, seeks to analyse the relationship between exercise and muscle symptoms in statin users.
Assuming that physical activity is a pivotal process for the prevention of cardiovascular disease, the researchers analysed whether it was able to improve muscle and physical performance, muscle mitochondrial function and capillarization of muscle fibres in patients taking statins, with or without muscle disorders.
Three groups of subjects were created: asymptomatic statin users, symptomatic statin users, and statin non-users. All of them started a moderate strength and endurance physical activity program for 12 weeks.
The strengthening exercise was performed once a week for 60 minutes and included a series of exercises that targeted the muscles of the legs, torso, arms, and shoulders. Each exercise consisted of 3 sets of 12 repetitions, with 1 minute of rest between sets. Workloads were then progressively increased as participants were able to perform more than 12 repetitions in 2 of 3 sets.
Endurance training included bi-weekly exercises on a cycle-ergometer and consisted of a 10-minute warm-up, followed by 40 minutes at 70% -80% of maximum heart rate and a subsequent 5-minute recovery.
Before starting the training and after it was carried out, the following were assessed: the maximum oxygen consumption, expression of the intensity of performance, muscle performance and muscle symptoms. In addition, muscle biopsies were collected to assess any alterations in the muscle fibres, in its various components. On these samples the activity of citrate synthase, the production capacity of adenosine triphosphate (ATP), the distribution of the type of muscle fibre, the size of the fibre and its capillarization were evaluated.
Improving the quality of life
At baseline, then before starting the training program, type I muscle fibres were less prevalent in symptomatic statin users than in control subjects. These muscle fibres, also called red fibres, are those responsible for slow muscle contraction, those that guarantee resistance. On the other hand, the white muscle fibres, are those responsible for rapid contraction, those that guarantees the speed of action.
After completing the training program, it was seen how the subjects of all three groups, without differences between them, had improved muscle strength, resistance to fatigue and capillarization of muscle fibres. In addition, a higher prevalence of type I muscle fibres has been documented in all of them.
Citrate synthase activity also improved in all subjects, but asymptomatic patients receiving statins showed less improvement than control subjects. Peak oxygen consumption, ATP production capacity, fibre size and muscle symptoms remained unchanged in all groups after the training period.
The resistance of the muscles to fatigue in patients treated with statins and symptomatic, was associated with a prevalence of type I muscle fibres. It is important to emphasize that in this group of subjects, physical exercise did not cause a worsening of symptoms.
The scores obtained from the questionnaires that assessed the quality of life, as perceived by the individual, improved only in symptomatic statin users, after the period of exercise.
Muscle fibres in statin users
Therefore, the results obtained in this study seem to demonstrate that a regular exercise program, in addition to other well-known positive effects, can improve muscle performance, capillarization and the mitochondrial content of muscle fibres in statin users, asymptomatic and symptomatic, without exacerbating muscle disorders.
Hence, even in patients on statin treatment who present with muscle disorders, exercise not only does not increase symptoms, but brings a series of benefits, at a muscular level, to health and, as evidenced by the questionnaires, can even improve the quality of life.
The authors conclude by stating that the use of statins is unlikely to alter the response to exercise and therefore their use should not be a factor that limits doctors from prescribing physical activity.
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