According to James LaValle, slower recovery stems from less blood flow (adrenaline stiffens blood vessels, too little NO, high blood pressure) and weaker immune system (that does the repair). He spoke about chronic inflammation coming from chronic unmanaged stress (cortisol and adrenaline) and leaky gut (which can come from chronic stress and other insults). Jim says, get the stress under control (many options) to get better sleep and a normal cortisol curve (vs on all the time). Slowly build the gut back to a diverse microbiome and a non leaky gut to feel great and recover like a younger you.
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Good point. I agree injuries are another matter, and can create permanent damage. The tiny bits of damage from hard use might add up to scarring. I don’t think my muscles are getting scarred from my weight lifting that is creating some sort of stress or damage (I do get sore), but if I twisted or over stretched or tore something that took more than 24 hours…that would logically be more like an injury vs. a training stress. I’m not a scientists, but I think that chronic inflammation and declining immune function are then main drivers of the decline in my body’s function. Inflammation is a cause and effect of many things. The one thing i am trying to resolve for myself right now is nitric oxide which declines as we age, and low NO causes many issues including less protection for the heart in hypoxia, poor blood circulation, weakened endothelium health as well as lower athletic performance. It’s a tough nut to crack so far.
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Thanks, Joe! Good stuff.
It goes without saying that microtrauma is what we’re seeking whenever we train or exercise, regardless of the modality, right? So, it’s a good thing, until we reach a threshold of sorts and the trauma ends up lingering or multiplying - perhaps simply because our ability to deal with the damage and repair it is reduced. I’d also offer that, overstating the obvious, the stress and trauma that’s created as a by-product of strength training is a different type of stress than is upper/steady z2, to cardiac muscle.
I agree that chronic inflammation is a huge factor…how could it not be? Cause and effect, as you say. Yes. And again, to some degree, the build-up of all of these factors would clearly lead to an increased risk of minor circulating levels of inflammation becoming more problematic with age. And after all, I gave it an entire chapter in my book…and Vince, your recent podcast guest, certainly feels the same way. As an aside, are the high levels of carbohydrates that EA typically consume also a factor? I am thinking it might be…
As for NO, I’ve written and read about this a fair amount…the one thing I recommend over and over to people is nose breathing vs mouth breathing. I talk about this in the book numerous times, including discussing using mouth tape for sleeping. I realize this may read to someone as smart as you as being ridiculously elementary, but that being said, if we add up the hours we use our mouth to breathe when we shouldn’t, it has an impact on NO production…
I hammer breathing ONLY through the nose in z1/low z2 training to every athlete I’ve ever coached…it’s the best non-gadgety determinant of true intensity that I can think of…
As an aside, you’re certainly right about endothelial cell health being a HUGE factor in our overall risk of not only performance losses, but more importantly, heart disease/atherosclerosis…
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Totally agree re immune function and endothelial NO as very important underlying factors for many age related diseases, especially the most important ones like CVD and cancer.
One of my favorite supplements for NO is pine bark extract combined with low dose cialis.
For a whole multitude of sins, I really like PEA and have been on it for years.
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It does seem to mirror aging. When I first started rapa my recovery time was greatly improved. The effect waned over time ( maybe I should have taken breaks to reduce tolerance).
Of everything, sleep seems to impact my recovery more than anything. If I have a hard exercise day and then sleep poorly, I’m royally screwed the next day. I’ve added in the sleep agent Dayvigo for this purpose. It allows your brain to really calm down and results in a more restorative sleep.
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Thanks, Joe. The supplements can start to get crazy…there’s a lot to consider.
I’m thinking Vince’s inflammation cocktail might be seriously worth considering. I think I’m going to order some. Maybe you could put in a good word and see if he’ll do an affiliate relationship? As I build this B.E.A.T. Aging coaching program, I’m sure they’ll be more people interested… 
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Will do. Good idea. I’ll let you know.
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Paul, thank you for your input. I had replied to Joe but also meant to mention I appreciated your input…
Furthermore, a high VO2 max is one of the most potent predictors of all-cause mortality. Individuals with greater levels of aerobic fitness have lower all-cause mortality compared to less-fit individuals. The lowest risk is observed in people with so-called “elite” levels of aerobic fitness. In other words, there’s a high ceiling for the benefits of cardiorespiratory fitness when it comes to reducing your risk of death.
Despite these well-known benefits of exercise, in the recent decade, a series of interesting data have emerged that raise cautions about the potentially harmful effects of “too much” exercise.
There’s a hypothesis that athletes — namely competitive endurance athletes — by pushing their cardiovascular system to its limit for years upon years, may actually be doing more harm than good to their heart. High-intensity exercise, we must remember, is stressful. Blood pressure and heart rate spike, blood flow becomes turbulent, and the heart and arteries are subjected to high levels of mechanical stress and inflammation. Over time, these mechanisms may promote vascular remodeling, fibrosis, scarring, and atherosclerosis.
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What is the socioeconomic status of an elite athlete compared to the average person? How does the diet compare? Lots of confounding issues.
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Thank you, @rivasp12 : PCA is now another supplement that I had no idea existed. I don’t believe I’ve seen it listed in anyone’s “stack” posts. From reading your attached paper It seems to positively impact so much. Any thought as to why it isn’t better known (or at least “better known to me”)?
I read your attracted article and noticed “ Other neuroprotective actions include inhibiting apoptosis and autophagy” (in the brain health section). Isn’t this the opposite of what we are attempting to accomplish with Rapamycin ? (And I guess, cycling different impacts at different times?)
Stupid question: it seems from what I read it comes from fat (?) but is an endocannabinoid. Will it trigger drug tests (ie if I travel from the U.S. will I be put to death in another country for using it)?
I really enjoy medical history so I accidentally ran across palmitoylethanolamide while reading about how egg yolks used to protect children from getting rheumatic fever. Turns out it was the PEA.
Then in WW1 soldiers were dying from influenza so they did an experiment with giving some of them PEA and it protected them.
So we have 2 examples of a substance having dramatic benefits in humans. Other trials have substantiated these findings so I almost view it as more of a drug than a supplement. I take it at about 1000 mg every other day.
You haven’t heard of it because medical science lost interest with the advent of antibiotics. We tend to throw the baby out with the bath water. I could give you other examples.
I’ve never seen it show up on a drug test.
Autophagy is very complicated and needs to be just right, but we can’t measure autophagic flux in humans with any degree of accuracy, so I think it’s good to cycle the autophagy influencers.
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Although I intend trying out PEA It is worth noting about the review paper that
Conflicts of Interest
M.H., N.B. and S.S. are employed by Gencor Pacific, who own the patented PEA formulations, Levagen® and Levagen®+. R.V. has personal relations to one of the members of Gencor Pacific. There is no other conflict of interest involved.[quote]
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Sounds intriguing. Do you have sources for these?
Thank you for sharing this. I have no doubt that there is some validity and that in particular, sustained upper z2/z4 training that is typical for competitive cyclists/runners that may result in an increase in scarring and fibrosis.
As I sit here and look back on 40+ years with some periods of sustained intense training and racing…would I trade what I’ve accomplished and the fitness I now have at 63 (and along with it the associated risks of that training) with someone who was a recreational exerciser during that same period of time?
The answer is a resounding NO. For so many reasons.
At the same time, I’ve been very transparent about my decision to not continue to train at those levels or continue competing at the same kinds of events as I have in the past. My running now is comprised of primarily two types of approaches. 1. Very easy, short duration z1/z2, breathing only through the nose. 2. Intense, short duration “sprint” type efforts that are highly variable, e.g. short bursts followed by longer very easy walk/jog recovery. IOW, the exact opposite of upper steady/threshold type efforts typical of marathon racing.
It’s been my observation that we collectively stand and applaud when we see 60-70-80-year-olds finishing marathons and Ironman tris. This is a double-edged sword. Often, those older athletes are people who started their endurance journey at a much later time in their life, often in their 40s and 50s. As a result, they don’t have the history of repeated chronic stress (as discussed in the bradyholmer article) that might have some negative consequences. But for others who have been at it consistently since the teens/20s, it’s a different story.
In the end, there are so many variables that determine our individual risk. It’s important for every person to know more about their own body (via all of the important testing that’s available-CAC, blood, etc), health/family history, and decide what is most important to them so as to make the smartest choices while trusting their intuition.
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Here’s an interesting look at some of the history of PEA :
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It’s interesting that PEA isn’t marketed more widely as an anti inflammatory. Drug store shelves are lined with generic medications.
More on hypoxia here. In mice.
Very interesting connection between hypoxia and mitochondrial dysfunction
- Low mitochondria function leads to excess oxygen in brain (oxygen not fully used by mitochondria)
- hypoxia (anemia, high altitude) can lower impact of mitochondrial dysfunction
