Sometimes, it’s just nice to spend the day geeking out on some research. Although this is not directly related to diabetes, age-related muscle loss is something that everyone thinks about at some point in their lives. I wanted to know if diet, particularly the keto diet, had any effect on slowing or preventing muscle loss.
Here’s the background ….
As we age, we tend to lose strength, lose muscle mass. The condition is known as primary sarcopenia, which is a progressive and systemic skeletal muscle disease that results from aging and can result in an increased risk of falls, disability and mortality.
Although the exact causes of sarcopenia remain unclear, some studies have shown abnormalities in the morphology of the neuromuscular junction (the connection between the motor nerve and the muscle) and changes in mitochondrial function (the mitochondria is the part of the cell that makes energy) in individuals with sarcopenia. These impairments could be potential contributing factors to the development of sarcopenia.
Mitochondria are enriched on both sides of the neuromuscular junction and that likely plays an important role in the stability of the neuromuscular junction and its ability to transmit signals. Because of this, mitochondrial dysfunction (e.g what fuel is being processed and how) is increasingly being recognized as a critical contributor to neuromuscular junction instability, which leads to skeletal muscle atrophy. (although some studies indicate no direct relationship between mitochondrial dysfunction and NMJ instability).
Right now, regular exercise, a ketogenic diet and a calorie-restricted diet have shown promise in preventing or mitigating neuromuscular junction and mitochondrial damage in sarcopenia. We’re going to look at the keto diet first.
The article that did the best job on discussing the effects of a ketogenic diet on muscles metabolism was a 2022 article by Yakupova et al. The reference is attached.
Muscle is a high energy-demanding tissue of the organism. Sufficient ATP production is necessary for muscle contraction and normal muscle function. Muscle has metabolic flexibility to various stimuli, including food or fuel consumed. Since the bulk of our ATP is produced is in the mitochondria, metabolic pathways and intermediates can affect the muscle and it’s mitochondria.
First, the authors considered skeletal muscle and looked at 14 studies done on rats and mice. All of the animals were fed a ketogenic diet, exercised, then various skeletal muscles examined. Results were mixed. They included everything from abolishment of age-related muscle loss, protection against muscle atrophy and prevention of intramuscular fat accumulation in old mice on the positive end to lower mitochondrial quantity, impairment of muscle regeneration, increased triglycerides and impairment of exercise performance. On the surface, it is difficult to draw a conclusion on the pros and cons of the ketogenic diet in the prevention of sarcopenia in skeletal muscles.
Secondly, the authors looked at studies on cardiac muscle. The heart is a muscle and has many similarities, as well as differences, from skeletal muscle on the cellular and molecular levels. Most of these studies were model studies and showed several potential benefits. One study showed infusion of 3-hydroxybutyrate, a ketone body (a fuel molecule produced by the ketogenic diet) could produce a 40% increase in cardiac output and 8% increase in left ventricular ejection fraction in patients with heart failure. Several models showed improvements such as increased coronary blood flow, improved heart remodeling and increased number of mitochondria. These studies seem to make it safe to conclude that a ketogenic diet (or the resulting increased 3-hydroxybutyrate) can bring beneficial effects in heart failure and I/R injury. However, some studies showed prolonged exposure resulting in hypertension and cardiac fibrosis.
This paper and several others left a list of pros and cons on the ketogenic diet when it comes to preventing sarcopenia. Something that wasn’t mentioned in any of the papers was the timeframe of anything. Fasting for as little as 3 days can increase our 3-hydroxybutyrate concentration. Do we just need 3-hydroxybutyrate intermittently or constantly? Although the ketogenic diet has shown great results in many other conditions, everything from epilepsy to polycystic ovarian syndrome, so has intermittent fasting. Is it possible that we can generate some ketones, maybe a sufficient amount to get the potential benefits, but not remain in ketosis, and reap the benefits of the ketone bodies? Maybe that will be the question for the next day of geeking!
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