The more cholesterol elderly people consume in their diet, the more muscle mass they build up with strength training, American sports scientists discovered. A high intake of cholesterol has an even more hypertrophic effect if the same people also take cholesterol-reducing statins.
The researchers are looking for a way to halt sarcopenia [breakdown of muscles as a result of ageing]. Sarcopenia is likely to be a huge problem in the future. Population experts forecast that by 2040, 21 percent of the American population will be over 65.
The researchers got fifty men and women aged between sixty and seventy to do strength training three times a week. The subjects did their sets at 75 percent of their 1RM. The subjects were also advised to eat a diet consisting of fifty percent carbs, twenty percent protein and thirty percent fat.
After twelve weeks the researchers measured the amount of lean body mass the subjects had acquired. The subjects kept a diary of their food intake during the same period. From these the researchers were able to deduce that the cholesterol intake was the most important dietary factor influencing the lean body mass increase.
Protein intake was not a factor, and neither was the amount of kilocalories consumed.
The subjects who ate a lot of cholesterol became stronger more quickly than the subjects whose diet contained small amounts of cholesterol. For example, the people who consumed 7.2 to 10.2 mg cholesterol per kg lean body mass were 88 percent stronger in the chest and leg press. The subjects who consumed 2.2 to 3.5 mg cholesterol per kg lean body mass only showed a 41 percent improvement in strength.
Cholesterol makes cell membranes stiffer. Studies suggest that, as a result, cells are more sensitive to nitrogen monoxide, protein kinase C-alpha, nuclear factor-kappa B, phosphoinositide kinase-3, protein kinase C, epidermal growth factor receptor, platelet-derived growth factor receptor, interleukin-6 and AKT1. These are all factors that cause hypertrophy in muscle cells. Another possibility is that cholesterol enables muscle cells to repair micro traumas caused by strength training more easily.
It was noticeable that a high HDL level seemed to inhibit muscle growth progression. HDL keeps cholesterol out of the body, and carries it off to the liver. And the other way round, a high level of LDL – the ‘bad’ cholesterol that keeps cholesterol in the body – promotes muscle growth.
When the elderly subjects took statins as well, they made even better progress.
The researchers were surprised that the statins had a stimulatory effect, “given the well-established effects of cholesterol on health and effects of statins on skeletal muscle”.
Statins inhibit the work of the enzyme HMG-CoA in the liver. Statins make the LDL receptors more sensitive, and as a result, LDL disappears from the blood more quickly. The statin that had the biggest muscle growth effect in the study is lovastatin.
The researchers come up with a complex theory about how statins promote the growth of muscle tissue. Statins reduce the amount of cholesterol in the body, they reason. Less cholesterol means less isopentenylpyrophosphate, a compound the cell needs to make seleno-proteins. Genetically modified mice that make less of the seleno-proteins have more muscle. Voila!
Impressive theory, but it doesn’t explain why people who a) eat high amounts of cholesterol and b) take statins as well show the most progress in strength training. We, unhindered by an overdose of knowledge, have another theory. Statins not only make the liver absorb more cholesterol, but have the same effect on muscle cells.
The researchers are cautious. “It is necessary to examine changes in cardiovascular risk due to dietary cholesterol consumption (within the context of exercise training) so that reduction in sarcopenia and disability is not at the price of elevated cardio vascular disease”, they conclude.
The most important sources of cholesterol in our diet are egg yolks [a whole egg contains 200 mg cholesterol], beef, chicken, turkey and shrimps. A diet consisting of lots of chicken, fish and shellfish easily provides 600 mg cholesterol per day.
The health effects of cholesterol in our diet are still not clear. Ten to twenty years ago cardiologists and nutritional scientists regarded dietary cholesterol as an important negative factor for heart health. This is no longer the case.
Statins and dietary and serum cholesterol are associated with increased lean mass following resistance training.
Age-related muscle loss (sarcopenia) is a prevalent condition associated with disability and mortality. Exercise and optimal nutrition are interventions to prevent and treat sarcopenia, yet little is known, outside of protein, of the effect of common nutrition recommendations and medication use on exercise-related muscle gain.
Forty-nine community-dwelling, 60- to 69-year-old men and women completed 2 weeks of nutrition education (American Dietetic Association recommendations) followed by 12 weeks of high intensity resistance exercise training (RET) with postexercise protein supplementation and 3x/wk dietary logs.
We observed a dose-response relationship between dietary cholesterol (from food logs) and gains in lean mass that was not affected by variability in protein intake. Serum cholesterol and the serum cholesterol lowering agent statin were also independently associated with greater increases in lean mass. Dietary cholesterol was not associated with serum cholesterol or the significant reduction in blood pressure observed, but trends were observed for altered plasma C-reactive protein.
These data suggest that dietary and serum cholesterol contribute to the skeletal muscles’ response to RET in this generally healthy older population and that some statins may improve this response.
PMID: 17921432 [PubMed – indexed for MEDLINE]