The best source I’ve seen on the topic is this Physiological Reviews article (I’ve read other sources as well, but didn’t keep around links for most of them).
Reversibility is specifically addressed—age-related muscle loss (aka sarcopenia) is not really reversible. There are things people can do at any age to add muscle (e.g. exercise), but muscle is lost if exercise/diet/etc is held constant. Masters athletes are a visible example of this.
Also, it’s not just skeletal muscle. For example, the pupil muscle squeezes the lens of the eye to adjust focus. In old age, that muscle loses mass, resulting in slower focusing speed. (Source: Physiological Basis of Aging and Geriatrics; the chapter on the eye is one of the best in the book). And of course there’s loss of muscle mass in various sphincters, resulting in e.g. incontinence and other digestive problems. None of those muscles are suffering from lack of use.
Looking into the term sarcopenia (I avoided it earlier as it seemed inconsistently used and I was getting confused mass +/- function loss) here’s some snippets and thoughts.
ArticleIn his closing comments to a scientific congress in 1989, Dr. Irwin Rosenberg suggested that one way to bring greater attention to the issue of the decline in muscle mass with ageing was to give it a Greek name. Although two terms were suggested (“sarcomalacia” being the other one), “sarcopenia” was the term adopted by the field …
unfortunately in recent years the term has increasingly come to be synonymous with its operational definitions … the term sarcopenia is appearing in other clinical literature in which muscle atrophy is present but ageing per se is not the cause.
Among the most widely observed histological features of ageing muscle is its remarkable fiber size heterogeneity.
… the available evidence strongly implicates sporadic and repeating cycles of denervation-re-innervation in the histopathology of ageing muscle
Primary loss of muscle mass versus secondary loss of muscle mass after loss of innervation—paresis/paralysis—loss of function—atrophy. From what I’ve read sarcopenia is a secondary loss of muscle, and I’d classify sphincter incompetence as an innervation issue rather than a primary loss of muscle mass issue. No idea if/what the significance of distinguishing between primary and secondary is but something to be aware of.
Fascinating subject, my initial comment was poorly worded/wrong depending on what age “ageing” begins—I was thinking 30+ where loss of muscle may be noted but reversed (quickly found article) but by 60+ sarcopenia with strict definition occurs. Another article I found: sarcopenia v. non-sarcopenia.
(Just enjoying being able to interact on LW as so much stuff goes straight over my head!)
One of the main questions I haven’t found a satisfying answer to yet is whether denervation/renervation is causal for sarcopenia. Apparently a huge amount of resources went into imaging neuromuscular junctions for a while—the physiological reviews article I linked spends half the article on the topic—but that seems to be driven by historical accident more than anything. After wading through a ton of it I still haven’t seen any decisive evidence on whether denervation is the main cause of muscle atrophy, or muscle atrophy causes nerve atrophy. It sounds like either is sufficient to cause the other experimentally, but it’s not clear which actually comes first in aging. (And of course research is made difficult by authors sometimes making statements about causality which their data/experimental procedure doesn’t actually establish.)
The best source I’ve seen on the topic is this Physiological Reviews article (I’ve read other sources as well, but didn’t keep around links for most of them).
Reversibility is specifically addressed—age-related muscle loss (aka sarcopenia) is not really reversible. There are things people can do at any age to add muscle (e.g. exercise), but muscle is lost if exercise/diet/etc is held constant. Masters athletes are a visible example of this.
Also, it’s not just skeletal muscle. For example, the pupil muscle squeezes the lens of the eye to adjust focus. In old age, that muscle loses mass, resulting in slower focusing speed. (Source: Physiological Basis of Aging and Geriatrics; the chapter on the eye is one of the best in the book). And of course there’s loss of muscle mass in various sphincters, resulting in e.g. incontinence and other digestive problems. None of those muscles are suffering from lack of use.
Exercise increases the size of individual muscle cells but not their number. When muscle cells die it doesn’t replenish them.
Looking into the term sarcopenia (I avoided it earlier as it seemed inconsistently used and I was getting confused mass +/- function loss) here’s some snippets and thoughts.
Primary loss of muscle mass versus secondary loss of muscle mass after loss of innervation—paresis/paralysis—loss of function—atrophy. From what I’ve read sarcopenia is a secondary loss of muscle, and I’d classify sphincter incompetence as an innervation issue rather than a primary loss of muscle mass issue. No idea if/what the significance of distinguishing between primary and secondary is but something to be aware of.
Fascinating subject, my initial comment was poorly worded/wrong depending on what age “ageing” begins—I was thinking 30+ where loss of muscle may be noted but reversed (quickly found article) but by 60+ sarcopenia with strict definition occurs. Another article I found: sarcopenia v. non-sarcopenia.
(Just enjoying being able to interact on LW as so much stuff goes straight over my head!)
One of the main questions I haven’t found a satisfying answer to yet is whether denervation/renervation is causal for sarcopenia. Apparently a huge amount of resources went into imaging neuromuscular junctions for a while—the physiological reviews article I linked spends half the article on the topic—but that seems to be driven by historical accident more than anything. After wading through a ton of it I still haven’t seen any decisive evidence on whether denervation is the main cause of muscle atrophy, or muscle atrophy causes nerve atrophy. It sounds like either is sufficient to cause the other experimentally, but it’s not clear which actually comes first in aging. (And of course research is made difficult by authors sometimes making statements about causality which their data/experimental procedure doesn’t actually establish.)