Long Term Calorie Restriction in Rats Slows Muscle Fiber Atrophy with Aging
Muscle mass and strength declines with age, leading to sarcopenia and contributing to frailty. Many distinct mechanisms are thought to be involved, from stem cell inactivity to chronic inflammation. Most of these mechanisms are favorably impacted by the sweeping metabolic changes induced by the practice of calorie restriction. The study here adds to past evidence for calorie restriction to slow the onset of sarcopenia, yet another of the many reasons to consider it as a lifestyle choice.
Aging causes loss of skeletal muscle mass and function, which is called sarcopenia. While sarcopenia impairs the quality of life of older adults and is a major factor in long-term hospitalization, its detailed pathogenic mechanism and preventive measures remain to be identified. Caloric restriction (CR) suppresses age-related physiological and pathological changes in many species and prolongs the average and healthy life expectancy. It has recently been reported that CR suppresses the onset of sarcopenia; however, few studies have analyzed the effects of long-term CR on age-related skeletal muscle atrophy. Thus, we investigated the aging and CR effects on soleus (SOL) muscles of 9-, 24-, and 29-month-old ad libitum-fed rats (9AL, 24AL, and 29AL, respectively) and of 29-month-old CR (29CR) rats.
The total muscle cross sectional area (mCSA) of the entire SOL muscle significantly decreased in the 29AL rats, but not in the 24AL rats, compared with the 9AL rats. SOL muscle of the 29AL rats exhibited marked muscle fiber atrophy and increases in the number of muscle fibers with a central nucleus, in fibrosis, and in adipocyte infiltration. Additionally, although the decrease in the single muscle fiber cross-sectional area (fCSA) and the muscle fibers' number occurred in both slow-type and fast-type muscle fibers, the degree of atrophy was more remarkable in the fast-type fibers.
However, CR suppressed the muscle fiber atrophy observed in the 29AL rats' SOL muscle by preserving the mCSA and the number of muscle fibers that declined with aging, and by decreasing the number of muscle fibers with a central nucleus, fibrosis, and denervated muscle fibers. Overall, these results revealed that advanced aging separately reduces the number and fCSA of each muscle fiber type, but long-term CR can ameliorate this age-related sarcopenic muscle atrophy.
Caloric restriction in humans: Potential pitfalls and health concerns
'Caloric restriction is the only non-genetic intervention that
consistently slows the intrinsic rate of aging in mammals. The
classic regimen of CR most often used in experimental animal
models is a ~40% reduction in caloric intake, as compared to
the ad libitum diet, while maintaining all essential nutrients.
The health and longevity benefits of such a diet regimen are
numerous, however, is not without potential negative side
effects applicable to the human life. These include hypotension,
loss of libido, menstrual irregularities, infertility, bone thinning
and osteoporosis, cold sensitivity, loss of strength and stamina,
slower wound healing, and psychological conditions such as
depression, emotional deadening, and irritability. '
... and they do not even mention the aesthetic aspect.
When are cyborgs are Artificial Intelligence going to become a reality? We still cannot even find a cure for balding yet.. We should be further along now..
If CR worked for humans you would expect to see lower mortality at lower BMI but that is not the case. A BMI of 19 has about the same mortality risk as a BMI of 30.
22.5 - 25 is the sweet spot.
Too low muscle mass. Maybe there just isn't enough reserve if your BMI is under 22 no matter how lean you are.
Malnutrition. Would there be less mortality with precision nutrition?
To Lee: Don´t we have to distinguish between malignant and benignant causes of very low BMI,
just a simple BMI number may not be useful ?
And: precision nutrition indeed might work, but are we not rather far away from valid results ?