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The Effects of Statin Medications on Aerobic Exercise Capacity and Training Adaptations

Abstract

The incidence of myopathy increases dramatically in statin users who also exercise, likely limiting the positive impact of this lifesaving medication. New evidence also indicates that statin use can directly compromise aerobic exercise capacity; however, we are just beginning to understand the interactions of statins with exercise training and adaptations. This review focuses on the interactions of statins with aerobic exercise capacity and training adaptations to summarize the available information and draw attention to the gaps in our current knowledge in this area. PubMed, Web of knowledge, and Google scholar databases were searched between January 2000 and December 2013 using the following terms and their combinations: statins, exercise, aerobic capacity, endurance training, adaptations. The reference lists of the relevant articles were also scanned for additional information. Considering the widespread use of statins and the need for exercise for cardiovascular health, a better understanding of the interactions of these interventions as well as practical solutions are needed to reduce statin adverse effects associated with exercise.

Full-text

Alex’s Notes: This is just pathetic,

“Statins are the best-selling drugs in history and as of 2010, they remain among the most prescribed medications worldwide [1]; in the USA, approximately a quarter of the population aged 45 years and older had used some type of statin in the preceding years [2]. Moreover, as predicted, new updated guidelines will most likely increase statin prescription by physicians [3].”

It is also surprising given the number of adverse side-effects statins have that reduce quality of life to a point of compromising medication compliance. The most notable side-effects are myopathies, which are believed to occur in about 25% of patients in clinical practice. The largest issue with these muscle diseases is that they discourage statin users from engaging in physical activity because of pain, weakness, and fatigue. It is well known that exercise is a general health promoter, and as little as 3 hours of exercise per week is associated with a 22% reduced risk of heart attack among men. Isn’t reducing that risk the point of statins in the first place? But exercise also improves psychological well-being, body composition, and muscle strength, endurance, and function; all things that statins may work against. The review at hand acknowledges this, and aims to focus on the direct effects statins may have on endurance exercise performance and overall training adaptations.

Starting with the obvious, muscle pain and weakness caused by statins can decrease endurance performance, but statins can also directly affect long-term adaptations. This was demonstrated by a study in which previously sedentary overweight and obese subjects with metabolic syndrome underwent 12 weeks of supervised treadmill training or a combined exercise training and daily simvastatin treatment (40 mg). While endurance training alone increased aerobic capacity, as indicated by a 10 % increase in VO2max, the combined group failed to improve this measure significantly, showing only a 1.5 % change. Additionally, in contrast to a 4.5 % decrease in the statin-exercise group, skeletal muscle citrate synthase activity was also elevated by 13 % in the training group without simvastatin, demonstrating that statin treatment eliminates adaptations in aerobic capacity/cardiovascular fitness.

In addition to the above, it has been shown that only 20% of professional athletes were able to tolerate any of the available statins without adverse effects or a decrease in performance, and it has been observed that 38% of statin-treated patients with myalgia avoid even moderate physical exertion during everyday life and as many as 25% of the patients who exercise experience muscle symptoms.

The authors speculate that statin’s impact on exercise capacity is likely the result of structural and metabolic alteration in the skeletal muscles, and conclude that,

“The statin (HMG-CoA reductase inhibitor)-mediated depletion of the cholesterol synthesis pathway intermediates, such as CoQ10, isoprenoids, and dolichol, is the most likely candidate responsible for the adverse effects of these medications. In turn, the reduced level of these metabolites can manifest in mitochondrial dysfunction and functional deficits in the affected skeletal muscle cells. The mitochondria are the vital structures for energy production and cellular viability and play a central role in adaptations to exercise training. Thus, it is not surprising that the mechanisms of statin-exercise interaction converge on the mitochondria.”

For us Super Humans, all this is moot anyways. I shake my head at the idea of using statins, as they act against a more beneficial health promoter. I speak of exercise. Exercise to improve health should always start before medication, and sedentary individuals need to get off their couches and go do something.

 
 

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