Wednesday, January 18, 2017

A fitness downside to statin drugs?

Before passing on this article by Gretchen Reynolds and the work of Chung et al. that it points to, I'll start with a personal account of why it immediately caught my attention. I started taking a statin (10 mg simvastatin) over 20 years ago, not because my lipids were high, but because I read that statins had anti-inflammatory effects. Over the past year I have become increasingly alarmed that my hand muscle and grip strength were weakening. For a recital pianist, this can mean the end of performing. Since a known side effect of statins is to do just this, I stopped taking simvastatin, and within days could feel muscle mass and strength returning. (I'm doing a recital on Feb. 19.) It's interesting that this side effect became obvious only after many years, I would guess a function of aging (I'm 74).

Now, getting to the work Reynolds notes , a new study in mice suggest that statin drugs make exercise more difficult and less beneficial. Animals on statins loose grip strength, are more easily fatigued, and do not show the normal exercise-induced increase in muscle fiber size. Here is the technical abstract:
HMG-CoA reductase inhibitors (statins) are the most effective pharmacological means of reducing cardiovascular disease risk. The most common side effect of statin use is skeletal muscle myopathy, which may be exacerbated by exercise. Hypercholesterolemia and training status are factors that are rarely considered in the progression of myopathy. The purpose of this study was to determine the extent to which acute and chronic exercise can influence statin-induced myopathy in hypercholesterolemic (ApoE-/-) mice. Mice either received daily injections of saline or simvastatin (20 mg/kg) while: 1) remaining sedentary (Sed), 2) engaging in daily exercise for two weeks (novel, Nov), or 3) engaging in daily exercise for two weeks after a brief period of training (accustomed, Acct) (2x3 design, n = 60). Cholesterol, activity, strength, and indices of myofiber damage and atrophy were assessed. Running wheel activity declined in both exercise groups receiving statins (statin x time interaction, p less than 0.05). Cholesterol, grip strength, and maximal isometric force were significantly lower in all groups following statin treatment (statin main effect, p less than 0.05). Mitochondrial content and myofiber size were increased and 4-HNE was decreased by exercise (statin x exercise interaction, p less than 0.05), and these beneficial effects were abrogated by statin treatment. Exercise (Acct and Nov) increased atrogin-1 mRNA in combination with statin treatment, yet enhanced fiber damage or atrophy was not observed. The results from this study suggest that exercise (Nov, Acct) does not exacerbate statin-induced myopathy in ApoE-/- mice, yet statin treatment reduces activity in a manner that prevents muscle from mounting a beneficial adaptive response to training.

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