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Chang Woock Lee, Teak V Lee, Vincent CW Chen, Steve Bui, and Steven E Riechman. Dietary Cholesterol Affects Skeletal Muscle Protein Synthesis Following Acute Resistance Exercise. FASEB Vol. 25, No. 1_supplement April 2011
Abstract
We have previously shown that high cholesterol (CL) intake resulted in greater lean mass gains in elderly men and women after 12 weeks of resistance training. However, little is known about the effects of CL on protein synthesis rates in skeletal muscle. We examined the effects of CL consumption on muscle protein synthesis in response to acute bouts of high intensity resistance exercise (RE).
Two groups of 20–28 year old, healthy, untrained adults underwent 10 days of either high CL (HC: 14mg/kg lean/day, ~800mg/day, n=8) or low CL (LC: 3.5mg/kg lean/day, <200mg/day, n=7) diet followed by acute bouts of high intensity unilateral leg exercises (leg press & extension: 5 sets, reps to failure, 85% of max strength, emphasis on eccentric contraction) where one leg was exercised while the other leg served as the non-exercise control. Biopsies were taken from vastus lateralis muscle 22h after exercise and cumulative myofibrillar protein synthesis (FSR) was measured using 2H2O as a tracer.
A significant difference in FSR (relative to control) was observed between the groups (HC: 94.6±23% vs. LC: −65.4±25%, p<0.01) with ANCOVA analysis (covariates: exercise history, lean mass, & degree of muscle soreness after RE). Our data suggest that CL may affect the anabolic response to RE possibly through its effect on membrane stability, inflammatory response, and lipid rafts/cell signaling.
*****Researchers compared a high (~800 mg/d) and a low (< 200 mg/d) cholesterol diet in young, healthy adults. The high cholesterol group had a nearly 3 times higher myofibrillar protein synthesis rate 22 hours after intense resistance exercise than the low cholesterol group. Myofibrillar protein synthesis is a measure of muscle growth, specifically how quickly your muscles are creating new proteins, so these findings again suggest a high cholesterol diet is beneficial for muscle growth.
So what does cholesterol do?
* Cholesterol increases membrane viscosity, which may influence membrane stability. This may have an influence on the extent to which muscle cells are damaged during exercise and the magnitude of the inflammatory response.
* Cholesterol seems to play a role in the muscle repair process by controlling inflammation (Omega 3 has a similar effect). Muscle damage creates inflammation, which leads to the recruitment of immune cells to assist with the recovery process.
* Cholesterol is essential for lipid raft formation. Lipid rafts assemble the components for signaling pathways and enhance signaling between pathways that play an important role for muscle hypertrophy, such as the growth factors IGF-I and mTOR. Cholesterol depletion can lead to protein mis-sorting, which reduces the signal transduction. Activation of mTOR corresponds with the found increase in myofibrillar protein synthesis after cholesterol consumption. Vegans will not have this effect.
Just as important, cholesterol is the precursor for anabolic hormones and is crucial for their production although the limiting factor seems to be the transportation of cholesterol in to the mitochondria.
There is also lots of evidence that eating a diet low in saturated fats, which are loaded with cholesterol will in turn cause a drastic reduction in the amount of total and free testosterone produced in the body.
Abstract
We have previously shown that high cholesterol (CL) intake resulted in greater lean mass gains in elderly men and women after 12 weeks of resistance training. However, little is known about the effects of CL on protein synthesis rates in skeletal muscle. We examined the effects of CL consumption on muscle protein synthesis in response to acute bouts of high intensity resistance exercise (RE).
Two groups of 20–28 year old, healthy, untrained adults underwent 10 days of either high CL (HC: 14mg/kg lean/day, ~800mg/day, n=8) or low CL (LC: 3.5mg/kg lean/day, <200mg/day, n=7) diet followed by acute bouts of high intensity unilateral leg exercises (leg press & extension: 5 sets, reps to failure, 85% of max strength, emphasis on eccentric contraction) where one leg was exercised while the other leg served as the non-exercise control. Biopsies were taken from vastus lateralis muscle 22h after exercise and cumulative myofibrillar protein synthesis (FSR) was measured using 2H2O as a tracer.
A significant difference in FSR (relative to control) was observed between the groups (HC: 94.6±23% vs. LC: −65.4±25%, p<0.01) with ANCOVA analysis (covariates: exercise history, lean mass, & degree of muscle soreness after RE). Our data suggest that CL may affect the anabolic response to RE possibly through its effect on membrane stability, inflammatory response, and lipid rafts/cell signaling.
*****Researchers compared a high (~800 mg/d) and a low (< 200 mg/d) cholesterol diet in young, healthy adults. The high cholesterol group had a nearly 3 times higher myofibrillar protein synthesis rate 22 hours after intense resistance exercise than the low cholesterol group. Myofibrillar protein synthesis is a measure of muscle growth, specifically how quickly your muscles are creating new proteins, so these findings again suggest a high cholesterol diet is beneficial for muscle growth.
So what does cholesterol do?
* Cholesterol increases membrane viscosity, which may influence membrane stability. This may have an influence on the extent to which muscle cells are damaged during exercise and the magnitude of the inflammatory response.
* Cholesterol seems to play a role in the muscle repair process by controlling inflammation (Omega 3 has a similar effect). Muscle damage creates inflammation, which leads to the recruitment of immune cells to assist with the recovery process.
* Cholesterol is essential for lipid raft formation. Lipid rafts assemble the components for signaling pathways and enhance signaling between pathways that play an important role for muscle hypertrophy, such as the growth factors IGF-I and mTOR. Cholesterol depletion can lead to protein mis-sorting, which reduces the signal transduction. Activation of mTOR corresponds with the found increase in myofibrillar protein synthesis after cholesterol consumption. Vegans will not have this effect.
Just as important, cholesterol is the precursor for anabolic hormones and is crucial for their production although the limiting factor seems to be the transportation of cholesterol in to the mitochondria.
There is also lots of evidence that eating a diet low in saturated fats, which are loaded with cholesterol will in turn cause a drastic reduction in the amount of total and free testosterone produced in the body.
