The impact of statins on physical activity and exercise capacity: an overview of the evidence, mechanisms, and recommendations.

PURPOSE: Statins are among the most widely prescribed medications worldwide. Considered the 'gold-standard' treatment for cardiovascular disease (CVD), statins inhibit HMG-CoA reductase to ultimately reduce serum LDL-cholesterol levels. Unfortunately, the main adverse event of statin use is the development of muscle-associated problems, referred to as SAMS (statin-associated muscle symptoms). While regular moderate physical activity also decreases CVD risk, there is apprehension that physical activity may induce and/or exacerbate SAMS. While much work has gone into identifying the epidemiology of SAMS, only recent research has focused on the extent to which these muscle symptoms are accompanied by functional declines. The purpose of this review is to provide an overview of possible mechanisms underlying SAMS and summarize current evidence regarding the relationship between statin treatment, physical activity, exercise capacity, and SAMS development. METHODS: PubMed and Google Scholar databases were used to search the most relevant and up-to-date peer-reviewed research on the topic. RESULTS: The mechanism(s) behind SAMS, including altered mitochondrial metabolism, reduced coenzyme Q10 levels, reduced vitamin D levels, impaired calcium homeostasis, elevated extracellular glutamate, and genetic polymorphisms, still lack consensus and remain up for debate. Our summation of the evidence leads us to suggest that the etiology of SAMS development is likely multifactorial. Our review also demonstrates that there is limited evidence for statins impairing exercise adaptations or reducing exercise capacity for the majority of the investigated populations. CONCLUSION: The available evidence indicates that the benefits of engaging in physical activity while on statin medication largely outweigh the risks.

Considering Type 1 Diabetes as a Form of Accelerated Muscle Aging.

Recent evidence reveals impairments to skeletal muscle health in adolescent/young adults with type 1 diabetes (T1D). Interestingly, the observed changes in T1D are not unlike aged muscle, particularly, the alterations to mitochondria. Thus, we put forth the novel hypothesis that T1D may be considered a condition of accelerated muscle aging and that, similar to aging, mitochondrial dysfunction is a primary contributor to this complication.