A number of readers have asked me about the recent article in the NY Times which quoted an online article in the Journal of the American College of Cardiology which discussed the adverse effects of statin use on skeletal muscle.
To begin with, there is a molecule called Co-enzyme Q (or Q-10) which lines the inside of the membrane of mitochondria. A mitochondrion is an organelle inside a cell where ATP, the source of the cell's energy is generated. There are many mitochondria in muscle cells, for obvious reasons. The electron chain to create ATP must pass through Co-Q, so that in the absence of Co-Q the cell can generate no energy. Finally, one side effect of the use of statins is the reduction of the amount of Co-Q in the body. Another side effect of statins is muscle aches and occasionally elevation of CPK, which indicates muscle damage.
The study involved a study of overweight men and women, who did no exercise, and satisfied the criteria for the metabolic syndrome. They first did a stress test and underwent a muscle biopsy. Then one-half of the subjects were given a daily dose of a statin, and both groups underwent supervised exercise for 45 minutes five times a week. After 12 weeks, repeat stress testing and muscle biopsies were done.
Now we already have evidence that exercise and statins lower cholesterol, and lower the death rate in patients with dyslipidemia. There also was an article in this year's Lancet (Feb. 2, p. 394) that showed that in veterans with dyslipidemia both exercise and statins lower cholesterol levels and reduce mortality, and the effect of exercise plus statin was greater than either modality alone.
After the 12 weeks, the non-medicated group had increased their physical fitness, but the medicated group did not. The energy enzyme levels in muscle mitochondria increased in the non-drug group and decreased in the drug group.
What does this all mean? Since we do not know the precise mechanism(s) by which exercise lowers the death rate, the study cannot be interpreted. One would have to look at the death rate or heart attack rate of both groups, and since this is a group with no history of a heart attack, we would probably have to wait five years to detect a possible difference in outcomes. In other words, we know that exercise is beneficial for cardiac health, and the fact that statin use apparently prevents an increase in aerobic fitness does not mean that exercise plus statin use is no better than either treatment alone.
Just as lack of exercise and elevated cholesterol are separate risk factors for heart attacks, and together they are synergistic in increasing one's risk, so are statin use and exercise synergistic in preventing such an event.