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Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes

This article below bears directly on previous discussions on coronary atherosclerosis including my recent post Can an Extreme Endurance Athlete Have an Early Heart Attack?.

METs are a measure of oxygen consumption, with one MET corresponding to about 70 KCal. My caloric burn per hour when training intensively is about 740 calories per here, let»s round that down to 10 METs when rounded. During a double century, that typically drops to 650 to 680 KCal/hour depending on the course and how good I am feeling.

The last 4 days alone I have expended 8200 KCal* ~= 117 MET-hours. If I have that correct, than that is 117 * 60 = ~7000 MET-min, which far exceeds the study’s cutoff of 2000 MET-min/week—and the week has 3 days left. Having done this for years, it would surely explain my CT coronary calcium score.

* According to my highly accurate SRM power meter. Right now I am having problems with my SRM PC8 connecting to the computer and it may need to be fixed, but I plan to show an entire week’s overload-cycle spring training.

Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes

Participants in the >2000 MET-min/wk group had a higher prevalence of CAC and atherosclerotic plaques. The most active group, however, had a more benign composition of plaques, with fewer mixed plaques and more often only calcified plaques. These observations may explain the increased longevity typical of endurance athletes despite the presence of more coronary atherosclerotic plaque in the most active participants.

The key take-aways from the article are:

  • Physically highly active individuals may have substantial, asymptomatic coronary atherosclerosis.
  • The plaque types of the most active group are more benign calcified plaques and need more study to understand the implications.
  • The relationship between high exercise volume and coronary artery calcification and plaque is as yet poorly understood.
  • The more calcified plaques in high volume athletes may offset calcification scores and contribute to superior life expectancy of athletes.
  • ...possible that it is not the duration of exercise that is most important in the development of coronary atherosclerosis but the intensity of exercise.
  • Underlying mechanisms for higher prevalence of CAC/plaque and increased calcification in athletes with the highest exercise volume and intensity are unknown.

This adds yet more context to the relatively context-free paint-by-numbers evaluation of heart disease favored in doctor’”s offices. Also, the data does not seem to have distinguished runners from cyclists, and runners take much more of a beating/pounding, which could affect the health of arteries.

See also

Various Interesting Health Findings in Science Daily: Exercise and Hidden Fat, Extreme Exercise and Heart Disease, Fasting, Brain and Fasting, Peripheral Neuropathy

MESA 10-Year CHD Risk With Coronary Artery Calcification

ACCEL: Detecting CAD in Older Athletes and What to Recommend When You Find

Expert Opinion: "Crazy for Ketones" – The Ketogenic Diet in Athletes: Variable Effects on Athletic Performance with Potential for Cardiovascular Harm

Expert Opinion: Fat for Thought – Any Role for the Ketogenic Diet in Athletic Training?

Coronary Atherosclerosis in Masters Athletes: Mechanisms and Implications for Cardiovascular Disease Risk

Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification


Up to 1527MB/s sustained performance

Can an Extreme Endurance Athlete Have an Early Heart Attack? CT Coronary Calcium Scan, HDL Cholesterol, LDL Cholesterol, Statins, etc (UPDATE with a cardiologist viewpoint)

A new challenge: reversing early arteriosclerosis. I think I may have to get down to 5% body fat to see if it can be done. There is no consensus on whether getting body fat that low can reverse arterial plaque. My working theory is that the body will scavenge soft plaque), but I do know that when I was at 8% body fat with only 1 pound of visceral fat (!), my cholesterol was the lowest it had ever been over a period of 22 years—see the graph.

The core problem I face in researching this issue is that as a layman, sorting through conflicting expert opinions is difficult. What is clear is that the evidence for heart disease root causes is exceedingly weak, and based on epidemiological studies of large numbers of mostly obese people who never exercised and ate garbage all their lives (e.g. Americans—just go visit Walmart one day!).

Worse, the link to diet is weak to say the least, let alone the role of the microbiome, exercise, genetics, epigenetics, etc. Given the fiascoes in nutrition revealed in recent years by new research, it is very hard to accept any recommendations as having merit. Heck, medical science can’t even figure out trivially simple (by comparison) glycemic index, which varies hugely for the same food for different people.

23 year cholesterol history: total cholesterol, HDL, LDL, triglycerides

Background

Just under two years ago in late March of 2018 I had a CT Coronary Calcium Scan which showed arteriosclerosis placing me in the 81st percentile for my age (mid 50's), the 99th percentile being the worst, 0th the best. Meaning that out of 100 men, 88 or so would have less arterial plaque for my age.

Visual assessment of the coronary arteries shows moderate coronary artery calcification centered within the LAD. Quantitative calcium score provided by the 3D Lab is 91.2, which places the patient in the 81st percentile for age and gender.

Heart: normal in size, no significant valvular calcification.
Pericardium: no pericardial effusion.
Pulmonary arteries: not enlarged.
Thoracic aorta: no significant abnormality.

That was a shocker, given my exercise and diet, but I seem to have inherited a genotype or have had epigenetic triggers or a gut microbiome that is unfavorable for cholesterol. See my 22 year cholesterol chart further below, which suggests that it’s pretty much the way my body works.

The CT calcium scan is not very helpful, so I am looking into a heartflow scan. Do I have 10% blockage, 30%, what? No meaningful risk assessment can be made with such vague information IMO, particularly in weighing against all the potential downsides of statins, which appear to be much higher than the medical industry wants to acknowledge, and such risks are always framed in epidemiological terms which means mainly high risk people who never exercised much or at all, and ate badly as a life habit. And... maybe it is all about inflammation and sugar and has nothing to do with dietary cholesterol.

I’m willing to do what it takes to halt and hopefully reverse arteriosclerosis, but the more questions I ask, the more I find that doctors have no idea how to do that! Meaning it’s all vague recommendations that on average might help. But the more I learn about the gut microbiome, the more I think that much of that is averaged-out epidemiological bullshit for any particular individual. Basically, the science is crap when it comes to an individual cases and there isn’t even agreement on the side effect profile. So how do I assess if I’m going to collapse and die of a heart attack in five or ten years and weigh that against the risks that no one can properly assess?

Seems like one huge guinea pig experiment: New Study Adds to Debate Over Statin Use to Prevent CVD

The authors consistently found that the harms outweighed the benefits until 10-year CVD risk thresholds substantially exceeded those recommended in current guidelines... anywhere from 50 to 200 people who don’t have CVD must take a statin to prevent just 1 heart attack over 5 years. Meanwhile, many of these patients will develop muscle pains and they are also at higher risk of developing type 2 diabetes.

Moreover, studies I’ve found suggest that the majority of pro athletes cannot tolerate statins. What does that say for me, doing double centuries and the training for it? Moreover, statins can attenuate fitness gains and fitness gains can offset the risks from high LDL.

Worse, how does one make intelligent choices without monthly lipid profiles to see what works and what doesn’t? Good science means changing one variable and seeing if it helps (e.g., using psyllium husk or oatmeal or whatever for a month, or dropping 10 pounds of body fat, etc). I have had exceptional dietary discipline before (recording food to the gram, etc), but more than a month is discouraging without feedback.... are the changes working for me or not? That is the massive flaw in the whole system.

Data for 2020-02-14 shows HDL (good) cholesterol level of 111 mg/dL, which is sort of off the charts. While HDL is called “good cholesterol” for its scrubbing of LDL cholesterol, the latest science now ponders if too much HDL may be associated with increased risk of heart attack and death:

...more research is needed to elucidate the mechanisms of this paradoxical association. "While the answer remains unknown, one possible explanation is that extremely elevated HDL cholesterol may represent 'dysfunctional HDL' which may promote rather than protect against cardiovascular disease," he said.

I know that my HDL rises the more I lose body fat, while LDL decreases. This seems paradoxical, just as the above states. But could my latest HDL of 111 (extremely high) be associated with LDL, sort of rising in tandem? That would violate past patterns in which HDL rise is associated with LDL decrease. Go figure.

23 year cholesterol history: total cholesterol, HDL, LDL, triglycerides

Statin?

Last week my internist said I would likely have a heart attack within 7 years if I did not get my LDL cholesterol down (further buildup). ALL other tests are poster-perfect including blood pressure of 116/68.

All of my doctors say I should be on a statin. A statin is a medication that reduces cholesterol with alleged reductions of 24% to 36% reduced risk of heart attack, which is not much IMO and why the hell the wide range? Seems sketchy at best.

I am loathe to take a statin because the “rare” side effects are likely not so. I know from personal experience with Metronidazole that doctors DO NOT report adverse effects properly, or at all. So statistics on side effects are almost certainly total bullshit. And for those in poor health (most), side effects are both less important and less noticed and maybe a reasonable tradeoff.

My specific concerns with taking a statin are :

  • Risk of nerve inflammation. After severe nerve damage from Metronidazole that took two years to recover from, the least thing I want in my body is anything that carries any risk of nerve damage.
  • Cognitive impairment—years from now maybe we’ll find that dementia and similar are made worse by statins. Statins can affect cognitive function (“reversible cognitive impairing effect in some patients”, “clinical trials were not originally designed to detect cognitive impairment”) but science is in doubt as to benefit or impairment. And with my brain finally mostly back in order after a concussion, the last thing I want is to fuck it up with a statin or find out that “reversible” is really a lie from big pharma—big money means bigger lies.
    A double blind placebo-controlled trial of lovastatin’s effect on cognitive functioning and mood showed detrimental effects on cognitive performance on four neuropsychological tests assessing attention, working memory, and overall mental efficiency... Post-marketing surveillance has continued to uncover case reports of cognitive effects associated with statin use since the FDA report
  • 100% to 200% increased risk of diabetes with some statins.
  • Risk of life threatening muscle damage with some statins; rare but one drug was withdrawn from the market for that reason. Or just muscle aches and pains, a total non-starter for me as an athlete.
  • Liver inflammation—what does a statin do to the liver during extreme stress such as in a double century? I doubt there is any science at all on such things.

Scientific studies

Scientific studies are so dubious these days: there is disconcerting evidence of sloppy work or money involved 75% of the time. So call me a skeptic on statins and the $billions involved in selling statins to millions of obese sedentary people, versus someone like myself doing double centuries and exercising 10 times as much every day as most of those statistical people do in a week.

While every doctor I’ve seen (two internists and a cardiologist) have recommended a statin to me, no doctor has ever offered a credible risk assessment of the side effects of statins, or even brought the issue up. That’s a huge red flag, a “halfpinion”—it’s bad science, bad medicine, bad risk management to offer a “solution” without also considering the negatives.

No one is an epidemiological statistic. A recommendation that works on average—that’s like saying every woman is 13.7% pregnant, which is obviously idiotic. Some people are damaged by some medications, sometimes fatally. What I want is a tailored personal recommendation based on my lifestyle, my genetics along with my current gut microbiome, my diet. But that doesn’t exist AFAIK with regards to arteriosclerosis.

Every person responds differently to medications, as I learned the hard way. PLUS, I am an extreme outlier with respect to epidemiological statistics for arteriosclerosis, as follows:

  • I am an ultra endurance athlete.
  • I have been active nearly all my life.
  • I regularly take my body fat to 10% or so, sometimes lower.
  • I have an off-the-chart HDL cholesterol of 111 out of a 250 total cholesterol. Medical science cannot agree on how protective this “good” HDL cholesterol is, but I am certainly several standard deviations away from any normal.
  • Both my parents are at or near 80, and have never had a heart attack or stroke. My mother has high cholesterol, my father’s is very good.
  • I eat a far healthier diet than most Americans. my diet being 100% free of cheeseburgers and sodas and processed foods and the garbage that most people eat. I eat the good stuff. My main dietary failing is having eaten 2-3 quarts of full-fat Greek yogurt the past 5 months, a great travel food when burning an extra 2000 calories a day in the cold.

How I plan to handle it

I am strongly averse to a statin, which aside from the risk discussed above, seems like a bad idea without first making all reasonable efforts on diet and body fat, which do not carry risks.

  • Reduce body fat by 10 pounds to get to 8% body fat. I have done this before, so it can be done.
  • (stretch goal) Get to 5% body fat in hopes that this will REVERSE arteriosclerosis.
  • Increase consumption of psyllium husk, oatmeal. Add 4000 mg omega 3. Continue olive oil and similar friendly oils, avocado, etc. These items together in theory could cut blood cholesterol by 20% or more.
  • Reduce consumption of whole fat yogurt to no more than one quart per week.
  • Continue with favorable diet for gut microbiome including

Based on past assessments, achieving 8% body fat should drop total cholesterol to 190 or so (2011-05-20 in graph). Since I cannot maintain that low level of body fat, I will have to rely on diet for most of the year.

See also

MESA 10-Year CHD Risk With Coronary Artery Calcification

ACCEL: Detecting CAD in Older Athletes and What to Recommend When You Find

Expert Opinion: "Crazy for Ketones" – The Ketogenic Diet in Athletes: Variable Effects on Athletic Performance with Potential for Cardiovascular Harm

Expert Opinion: Fat for Thought – Any Role for the Ketogenic Diet in Athletic Training?

Coronary Atherosclerosis in Masters Athletes: Mechanisms and Implications for Cardiovascular Disease Risk

Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification

Cardiologist viewpoint

Emphasis added.

From Jon L (a recently retired academic cardiologist).

“Can endurance athletes die of premature heart attack?”
The answer is yes.  Perhaps the most notable case is that of the runner Jim Fixx.  From Wikipedia: 
          “Fixx died on July 20, 1984 at age 52 of a fulminant heart attack, during his daily run on Vermont Route 15 in Hardwick.[1] The autopsy, conducted by Vermont's chief medical examiner, Dr. Eleanor McQuillen, revealed that atherosclerosis had blocked one coronary artery 95%, a second 85%, and a third 70%.[4] (His father Calvin Fixx had died of a second heart attack at age 43.[5])
        “In 1986 exercise physiologist Kenneth Cooper published an inventory of the risk factors that might have contributed to Fixx's death.[6] Granted access to his medical records and autopsy, and after interviewing his friends and family, Cooper concluded that Fixx was genetically predisposed - his father died of a heart attack at 43 after a previous one at 35, and Fixx himself had a congenitally enlarged heart - and had an unhealthy life: Fixx was a heavy smoker before beginning running at age 36, had a stressful occupation, had undergone a second divorce, and his weight before he took up running had ballooned to 214 pounds (97 kg).[7] Medical opinion continues to uphold the link between moderate exercise and longevity.[8]

At issue is what risk any individual has for developing atherosclerotic vascular disease (ASVD).  Risk is assessed using data from population studies (“derived from pooled cohort estimates”).  As you suggest, endurance athletes are poorly represented in these pooled cohorts.  Given the fact that exercise is generally accepted as reducing risk of ASVD, risk assessed using these tools may overestimate risk for endurance athletes.  Although it is generally accepted that moderate exercises reduces cardiovascular risk, there is evidence that this benefit diminished with the highest levels of exercise (most notably in marathon runners). 

In contrast to Fixx, the estimate of your risk, based on the data you have provided (age, gender, cholesterol levels, negative family history of premature disease, etc,) would be on the order of 2% which is considered low.  Even adding your coronary calcium score, (which would not be recommended in your case given the low basal risk), your risk would still be considered low (3.8% with ≤ 5% considered low risk). 

The presence of coronary calcification indicates the presence of atherosclerosis.  Recent studies suggest that the prevalence of coronary calcification is higher in endurance athletes, and that coronary calcification scores may be elevated in response to vigorous exercise.  These studies are not large enough to clearly establish whether the increased coronary calcium was associated with an increase in ASVD events.  See DeFina et al, JAMA Cardiol, 2019;4(2):174-181.  Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification.  Additional studies with CT angiography suggest that these lesions are more densely calcified, thought to be more stable, and less likely to rupture and cause an event. 

You correctly point out that our understanding of the pathogenesis of ASVD remains incomplete.  There is good evidence to support the presence of diabetes, hypertension, chronic kidney disease, unfavorable cholesterol levels, smoking and family history as major risk factors for premature ASVD.  Current research is focused on the role of the gut microbiome, inflammation and other factors.  The role of gut microbiome is being addressed by informatics and analysis of large datasets (stool DNA analysis) where the role of artificial intelligence may come to into play.

As regards your high levels of total cholesterol, the significance is offset by the high HDL cholesterol, normal LDL cholesterol and triglycerides.  

You raise the question of what further tests might be considered to refine further your individual risk of premature ASVD.  Assessment of coronary blood flow by myocardial perfusion imaging would be of limited value given your low pre-test likelihood and excellent exercise tolerance.  Elevation of high-sensitivity C-reactive protein (hs-CRP) has been used as a marker of subclinical inflammation and has been considered to provide additional information as to risk.  Asymptomatic individuals with elevated hs-CRP have been shown to benefit from statin therapy with a reduction in ASVD events (Jupiter trials).  This finding has not been assessed in endurance athletes

The next question is how would the results of additional testing change the approach to further risk reduction.  Some authorities would recommend statins.  However, given your overall low risk, the benefit of statins might be expected to be low.  Moreover, as you correctly point out, statins are not well tolerated in athletes.  Similarly, aspirin which has proven benefit in patients with manifest ASVD events, would not be indicated for you given that the risk of increased bleeding would outweigh any potential benefit (particularly if you had another bike crash while cycling!).

All of the aforementioned discussions are predicated on the information you have provided.  As indicated in the 2019 AHA/ACC Guidelines for Primary Prevention of ASVD, shared decision making between you and your doctors should determine the best strategies top reduce your risk.  Your case is further complicated by the lack of clear data for high endurance athletes.  Moreover, our current health care systems do not provide physicians the time to have detailed discussion of the relative risks and benefits of interventions with their patients (and may in fact penalize the physician if they “…spend too much time…” with a patient.  Many patients are looking for a pill to fix their problem and they are rewarded with a statin.  The patient is happy because he got a pill and the physician is happy because he has done something to meet the patient’s expectations.  Additionally, should the patient have an atherosclerotic event, the physician would not be faced with the question “Why didn’t you start the patient on a statin?”.

For now, the most important thing would be to watch for unexplained changes in your exercise tolerance, shortness of breath or the development of new chest tightness.  The onset of new symptoms or decrease in exercise tolerance should prompt further cardiac evaluation.  Continued extreme exercise does carry some risk of a cardiac event, but there is little compelling evidence to suggest how that risk might be reduced further.  Again, these recommendations should be considered relatively unique to your situation and not necessarily appropriate for other endurance athletes.

WIND: I felt vigorous at 14252' elevation (4344m) just last August, along with weeks spent at 10K to 12K feet last fall and hiking faster with a load than most people half my age... that the low partial pressure of oxygen would have a high likelihood of flushing out a heart blockage issue, particularly at max heart rate at 14K feet while sprinting to the summit. No issues whatsoever.

Making the available data even more tenuous, I am a cyclist and I wonder if runners could have different risks due to much higher impact and stress versus cycling. In cycling, the body when properly fitted and positioned acts as a shock absorbing spring, sparing the chest from stress. In a runner the stresses may be quite high if descending, but even on flat ground there is joint-killing pounding going on continually.

Another cardiologist weighs in:

Based on your numbers, I wouldn't put you on a statin. You're healthy, your HDL is excellent, and you have no family history of CAD. Trust me, I've saved way more lives putting people on statins than putting in stents. They are good and safe drugs. That being said, I wouldn't put on a statin. Sure, you've got some coronary calcium - it's not too uncommon - but I'd probably hold off for now. If you wanted the lowest cardiovascular risk, then you could take a statin, but with your family history and high HDL, I don't think you're entirely likely to benefit from it.

As an aside, getting down to that low of a body fat percentage is sketchy. the TdF riders that can do that only get that low briefly. The risk for illness and increased inflammation may be higher. I don't know, but be careful.

WIND: I have felt very healthy at 8% body fat, but I looked like a skinny teenager, and lower than that is probably risky.

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2017 Mercedes Sprinter: Is it Going to KILL ME by Failing to Move at a Crucial Time?

Prior post:

Mercedes Sprinter Issues and Breakdowns: Sprinter Will Not Go, RPMs Drop Very Low (Normal idle, put into D or R, RPMs drop, Engine Lugs

I had quite a scare about a week ago.

Returning from a daylong hike with temperatures in the 40's, I started up the Sprinter, let it warm up for a minute or so.

Checking in both directions for traffic (none seen), I put it into D (drive) and being pointed downhill, it rolled away easily. Cranking the wheel to turn uphill, I was now straddling both lanes on a blind corner at night. The accelerator pedal had NO EFFECT, just as described.

I immediately floored the accelerator pedal and held it there. The Sprinter would not move. The engine did not die, but it would not go anywhere either. I do not recall if the RPMs dropped in this case, being more shocked and afraid of being hit by an oncoming vehicle, but at the least there was no increase in RPMs.

Slowly, reluctantly, about 30 seconds later, the Sprinter started going and I drove away. Once warmed up, it behaved normally as is always the case.

Lately, even on relatively warm nights (not much below freezing), I cannot get the Sprinter to move (R or D) until warmed up several minutes. With colder temperatures, it 8 to 10 minutes to go anywhere, dropping to 500 rpm and lugging badly and going nowhere. Put into N or P, the engine RPMS are as high as 1400 when cold, and the engine revs freely when pressing the accelerator pedal.

Diagnostic code

The following diagnostic code is found:

ECM-EngineControl ($7E0) P0506 PowerTrain Confirmed Idle Air Control System RPM Lower Than Expected


MacPerformanceGuide.com

Biodiesel is the Kiss of Death for Mercedes Sprinter

I keep meeting Mercedes Sprinter owners who fail to break-in their Sprinter properly (the fault of Mercedes using inappropriate oil* for break-in), who change the oil far to infrequently (naively following the service interval).

And... some who have fueled up with biodiesel B20 or worse, covered in detail in:

Mercedes Sprinter Maintenance: Biodiesel is the Kiss of Death for Your Sprinter

Biodiesel should not be confused with renewable diesel, which is a far higher quality product, arguably better than petroleum diesel, albeit with dubious lubrication properties due to its ultra ultra low sulfur content (~5 ppm vs 15 ppm for ULSD), which in theory could result in fuel pump failur due to inadequate lubrication from the low sulfur content.

* Using 5W 30 oil will not break in a diesel engine properly because the piston rings will not seat properly into the cylinders, the oil being too “thin” (low viscosity). So you get 1% or 2% better fuel mileage for a few thousand miles when new, but the engine now has leaky piston rings forever. Thus it leaks fuel into crankcase oil (“fuel accretion”), particularly during a DPF burnoff cycle, which dilutes the crankcase oil and damages its lubrication properties. Over time, the engine suffers increasingly premature wear, which results in shortened lifespan along with reduced fuel economy over its usable lifetime. Mercedes won’t tell you any of this, which is awful, but regulatory bodies hold all the cards and call the shots, so Mercedes isn’t going to fess up on any of it.

2017 Mercedes Sprinter: Is it Going to Strand Me in a Remote Place?

Update: this blog post will not be updated further. The topic needs its own page, including an issue history and log. See:

Mercedes Sprinter Issues and Breakdowns: Sprinter Will Not Go, RPMs Drop Very Low (Normal idle, put into D or R, RPMs drop, Engine Lugs

... original post, not updated follows below...

Today’s problem‚ something new or just a symptom?

Today, my 2017 Mercedes Sprinter would start, but then lugs badly at 2 seconds at 500 rpm, then quit. Plenty of cranking amps no question. Repeated failures.

Temperature overnight hit maybe as low as 15°F at 1000' elevation, but Sprinter console showed 19°F at 8AM when failures occurred. Tried 3 or 4 times, then gave up and went for a hike. At 3PM it started up fine at 37°F. Ran fine once started in the afternoon, but I did let it idle 30 minutes to be safe before trying to move, because of ongoing issues detailed below.

OK, just for giggles, one might blame it on fuel but that seems unlikely—not really cold enough and no other issues noted on same tank of fuel for a week. Even though not winter blend fuel (AFAIK), it just did not get cold enough.

Today’s failure is actually not my main concern, as it may only be a symptom of the more insidious and ongoing issue, which is getting worse and worse, plaguing me before and after Service B (so not the fuel filter) for around a YEAR. So it's not a particular tank of fuel or a fuel filter or a particular temperature.

SYNOPSIS: normal idle, put into D or R, Sprinter goes nowhere, rpms drop and engine lugs

Having mentioned this problem to more than one service department on service visits, and getting little more than shrugs, my hopes are not high for seeing this resolved. I want a dealer to call Tech Service and track this down! I have one dealer in mind who might get the job done. My confidence in another is near zero.

Maybe all it is is software, but the truth is that mechanics hate doing them—my information is that Mercedes pays them very poorly for piecework that can take hours yet pays only for 30 minutes or so (not paid by hour). So one never knows if all software is up to date or not and it can be like pulling teeth to get the latest software.

Contact Lloyd with ideas or similar issues.

  1. Start engine, give it half a minute or so to warm up. Observe rpms at 900 to 1300, depending on altitude and temperature.
  2. Put into D or R (doesn’t matter).
  3. PROBLEM: observe rpms drop to 500-600, engine lugs badly (audibly bad).
  4. Floor accelerator pedal: absolutely nothing happens, even for minutes.
  5. Put back into P: rpms return to normal. Rev engine—revs up to any rpm freely
  6. Repeat ad nauseum. After some indeterminate period (2 to 10 minutes), the problem may resolve with the Sprinter reluctantly moving away. However, if there is any up-slope, it may have trouble for another minute or so.

Part 1, after idling 2 minutes to warm up:
https://www.youtube.com/watch?v=QHUHEwtjgOA

Part 2, after idling 9 minutes to warm-up:
https://www.youtube.com/watch?v=Gb9JglzSItg

Notes

  • Might be altitude related, but this is not certain; I don’t start my Sprinter at home much, but it has not failed at home (500 feet altitude). Failures seen at 6000/9000/10000/112660 feet elevation.
  • Goes into gear; does not appear to be transmission related—just makes no power
  • Seen at least a dozen times over a year from 6000 to 11600 feet
  • Happens over a wide temperature range, at least 14°F to 54°F, so if temperature related, does not have to be more than just cool temperatures.
  • Intermittent problems so hard to diagnose.
  • Full service B done in April 2019, problem occurs before and after a year, maybe more.

Possibilities

  • Lack of turbo boost due to faulty altitude or other sensor(s)?
  • Faulty ECU software? No problems seen prior to Feb 2018 ECU software update

Updates / log

2019-10-01: 9000’ elevation, 25°F @ 10PM dipping to 9°F overnight, started up fine @ 8:30AM @ 27°F idling @ 1300 rpm slightly rough idle, just let it warm up, and once warmed, it would roll in reverse without issue.

2019-09-30: 8100’ elevation, 27°F @ 10PM dipping to 20°F overnight, started up fine @ 8AM @ 28°F idling @ 1300 rpm slightly rough idle, died when tried to move with parking brake slightly applied on level ground after one minute of warmup. After two minutes warmup, was able to reverse on level ground (no brake), rolled away in D on level to downhill, engine steadily warmed up and behaved normally.

2019-09-29: stranded most of day as per full description.

2019-09-28: Sprinter would not go as per detailed description

2019/2018 year prior: perhaps a dozen such “no go” problems, ranging from a minute to 10 minutes in delay. All at altitude of 6000 feet or higher as far as I can remember.

Reader comments

Joe writes:

I have exactly the same experience.

First, I know my science is sub par to your excellent work but my ramblings may shed some light on it.

1) Because you like science I suggest the most knowledgeable MB dealer on “ cold” is Lone Star MB in Calgary,AB. Before calling them check their website blog - not sure if it has this item but it may be & they do have some useful info I have read.

2) My prior Diesel + Cold experience was with a Ford Excursion 6.0 Diesel. That puppy was dead at 20F & no amount of glow plug action could start it. Only spraying Ether in the Breather would work but I hate that stuff because strips the oil off the piston rings. The SOP was to wait until temps got above 25F & it would start reluctantly (assuming one had not totally depleted the 2 batteries during the failed Glow plug attempts)

3) In my experience the Sprinter will fairly well start above 20F but run rough. As the the temperature drops below 20F it requires successive Glow Plug cycles (without actually engaging the starter!) At 18F I found that it would require at lest 6-8 cycles. And it would start & stumble & cough etc etc, always die on the first full start attempt and then require 2 or 3 of the prior procedures to finally get it to run (very very rough & not quit).

Now for the next hurdle: assuming you got the engine running for awhile, at least to the point it “sounds “ normal (maybe 15 minutes) the Sprinter acts like its stuck to the ground. Without any authority I am fairly certain it’s due to the fact the transmission is still 15F & the fluid like glue. Since there are no shared fluids with the engine you are relying on plain old heat transfer from the adjacent engine block which might take 20 minutes of engine running to get the transmission to respond (& even at that, sluggishly).

4). The solution: install an Espar Hydronic Diesel water heater to solely to pre-heat the engine to 180F 🤪. Engine starts like its in Miami & the Tranny goes along for the ride. Then it never matters how cold it is ! (Bonus it saves all that ritual unassisted cold weather starting procedure which has to be hard on the engine.

DIGLLOYD: I never had these problems the first six months of operation. But after the Feb 2018 ECU update required by the California Air Resources Board (with sticker required to smog check), things seemed to not run so well. So I am dubious that it is a 'hardware' issue. And if it runs rough at start, it has always settled down pretty quickly in the past.

Moreover the Sprinter hardly ever pauses for glow plug operation... I didn’t even know it really had them! It had no pause whatsoever trying to start it today. Which raises the question as to whether they are working at all?

I’ve had the Sprinter start many times in sub-freezing conditions and run normally. But the sub-25°F experience is more limited. Last December I had it exhibit the symptoms going to bed at 25°F (engine still warm) but a warm front had moved in and it was 43°F when I started it, and had been for some hours from what I could tell. And I’ve had the no-go issue into the high 40°F range (and did not keep track all this time) I think also the low 50°F range. So I don’t think the no-go issue is heating issue. The does-not-start-and-stay-on issue today is all new, and definitely not the coldest temps I’ve been in it with—and I had gone to bed with a nice warm engine.

Still, the Espar Hydronic Diesel water heater might be worthwhile, but I admit to it being intimidating on who to have install it and inspire confidence that it won’t spring a leak or cause issues of its own.

Mark G writes:

Dang. Sorry to hear that. I have almost given up on the Mercedes Sprinter. Backed out of custom order at the last minute. Now waiting to test drive a 2020 Transit AWD with ecoboost (most powerful) gas engine. Planning on some custom suspension mods to improve ground clearance if I decide AWD is good enough for my needs.

I want a Sprinter for many specific strengths but diesel engine and all its related concerns are just too much to ignore. There's a good sprintersource post about block heaters and this issue you describe somewhere on the forum. They found a specific issue that was something related to the turbo, or some other part that a certain dealership had identified. They had an overnight test they could do in the dead of winter to diagnose. MB was made aware. That's all I remember. Let me know if you find a solution.

Hang in there sir!

DIGLLOYD: I guess one half-assed solution is to drive around and make the engine hot before going to bed, then wake up at 2 AM and (bad for a Sprinter) idle it for 20 minutes, then pray for morning.

The question of the turbo is a good one—my guess is a software bug and/or altitude sensor bug that causes the turbo to provide no boost. After all, how many people regularly camp out at 10K feet or (often) 11600 feet? Tonight I am at 8100' and I will see how it behaves in the morning. I parked where I have a cell signal and sunlight will hit early and it's flat, just in case!

My Strongest Ride Yet in 2019

Nice day/date for it!

Two antibiotics really got to me, requiring two months to feel normal again, which was very discouraging. I kept at it (riding) but performance was record slow (for me) in this year’s Eastern Sierra Double.

About 10 days ago I felt my strength increasing. Three days ago I had a strong ride with confirming signs of a body “happy” again.

Today I had the strongest ride of 2019. It’s so satisfying when my body works at its best—high power output with a sense of ease and fluidity, and only minor issues (a bit of patella pain starting at mile 52 or so, resolved by stretching bit between intervals).

The important thing is to keep at it, knowing that slumps and problems occur and will resolve!

Click for larger chart.

2019-07-04: Year’s Strongest Workout
4:38, 88.3 miles, 3712 kJ / 3549 calories
222W / NP=230W, HR=138 bpm, TSS=392, 4217 ft ascent

Up to 1527MB/s sustained performance

Gut Bacteria May Play a Role in Autism

The gut is a “second brain”. The brain controls the body, but the gut and its microbes also control the brain, as does blood and probably other things too.

In late 2014 Scientific American reported in Gut Bacteria May Play a Role in Autism that:

Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder's behavioral symptoms.

...

The Economist May 30 2019 in More evidence that autism is linked to gut bacteria reports that:

What causes ASD has baffled psychiatrists and neurologists since the syndrome was first described, in the mid-20th century, by Hans Asperger and Leo Kanner. But the evidence is pointing towards the bacteria of the gut. That suggestion has been reinforced by two recently published studies—one on human beings and one on laboratory rodents.

...

Two years ago they tested a process called microbiota transfer therapy (mtt) on 18 autistic children aged between seven and 16. Of their participants 15 were regarded, according to the Childhood Autism Rating Scale, as having “severe” autism.

...

Crucially, these changes in gut bacteria have translated into behavioural changes. Even 18 weeks after treatment started the children had begun showing reduced symptoms of autism. After two years, only three of them still rated as severe, while eight fell below the diagnostic cut-off point for asd altogether. These eight thus now count as neurotypical.

...

Meanwhile, the success of the study in Arizona has prompted America’s Food and Drug Administration (FDA) to look into the matter. A firm called Finch Therapeutics Group, based in Massachusetts, hopes to commercialise the use of mtt as a treatment for autism and the fda has now granted this effort “fast track” status, which should speed up the review process

WIND: how awesome that there is now hope of reducing or even curing autism—with gut bacteria of all things!

Siloed specialized knowledge has let autism wreak its havoc, and I daresay many maladies suffer the same fate until multiple specialists put their heads together. Perhaps AI will overcome that in the future and suggest posssibilities for curing many more human health issues.

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Which Lenses to Choose?🌈


Avoid costly mistakes and get the ideal system for your needs: diglloyd photographic consulting.

Three Top Notch Professionals to Help Your Body Health and Cycling Performance

Here are three individuals that I am very impressed with, and highly recommend.

Imagine your body working at its best!

3D Bike Fit

Kevin Bailey, 3DBikeFit.com (San Francisco)

Kevin at 3DBikeFit.com (see https://3dbikefit.com/bike-fits) gets bike fitting right, with the most meticulous attention to detail I’ve seen—the very best. Kevin is the reason I can ride double centuries without pain. I also ride a saddle of his design, the best I have ever found (and I have half a dozen other ones in a box!).

Kevin also makes custom orthotics which are awesome—I rode a double century two days after he made my pair, with zero issues—that’s amazing, and a proper footbed means better power transfer and no pain.

 

 

 

 

 

Rikki Johansen

Dr. Rikki Johanseen CCSP, DACBSP, DACBR (Palo Alto, CA)

Also, certified triathlon coach and a USA Cycling, Level II certified cycling coach.

Rikke Chiropractic and about Rikke Johansen.

When I have any injury or problem with my body (muscular, tendon, left/right imbalance, and related pains or similar injuries), I go see Rikke first because she knows how to fix it, and fix it quickly—including casese that bothered me for weeks that improve immediately.

Rikki knows hers stuff and is not any ordinary “crack your back” chiropracter; she’s a cut way above that. She likes to fix things in one visit if possible (for me, that has been true with most injuries!).

I don’t bother going to doctors for sports injuries and similar anymore because they really don’t know how to fix things (expensive brief visits just result in a PT referral)! Unless it’s a broken bone or torn ligament or other true medical surgery-type issue, go so Rikke first.

 

 

 


Dee Sickles, MMT, LMT

Dee Sickles, MMT, LMT (Flagstaff, AZ)

See Intractable or Problematic Physical Issue? Medical Massage with Dee Sickles.

There is massage, there is medical massage, and then there are gifted hands with medical massage. If you have a seemingly intractable physical issue that doctors say is “impossible” to fix without surgery, think again, because what do you have to lose? All feedback from people I’ve recommended Dee to has been enthusiastic.

In 2018, after my 25 mph crash into an embankment with moderate-to-severe concussion, a twisted spine and torso and mashed-in ribs were not going to go away on their own, but Dee cleared it all up. I’ve had both injuries and massage before but never fixes like that. Problems solved.

Dee’s uncanny ability to zero in on the issue was startling to me. Pains I had for weeks after my crash were solved for good.

Reader comments below

anon writes:

I can attest to the importance of having a good massage therapist.

This past month, I was driven to near madness by mysterious tension headaches, neck discomfort and weird sensations. I attributed it all to job stress and started worrying if I'd be able to continue to work or even worse, that I had a serious health condition. Turns out it was just bad posture.

After a visit to a skilled massage therapist with myoskeletal experience, I learned I had Upper Cross Syndrome- pairs of weak and tense muscle groups caused by years of texting on a cellphone and hunched office work. After 3 hours of intense back and neck work my symptoms were 70%+ alleviated, permanently. Massage therapy saved my job, and sanity.

DIGLLOYD: nice outcome.

Mark N writes:

Thank you very much for your post about the products at 3DBikeFit. I am interested in their bike seat and would like to know which seat you use. Either the Throne GT or RS. It appears we have a similar body habitus.

DIGLLOYD: great to hear it’s useful—such stuff is why I bother—hoping someone can profit from sharing my experience. I ride the 3DBikeFit “Throne GT” saddle. As per Kevin Bailey of 3DBikeFit.com:

Lloyd has the Throne GT, and now we have another revised new version of it with a larger cut out. It’s same foam but front has longer channel. Looks better is more refined and has longer rails and new atoms base where cover raps under top base at front and back.

Protect Your Phone
NuGard KX Case for iPhones and iPads.
Outstanding protection against drops and impact!
Plus, excellent grip for wet hands, cycling, etc.

Science News: Gut microbes might help elite athletes boost their physical performance

I have a pretty solid personal feeling that gut microbes have a TON of influence on not just athletic peformance—from personal observation over 20 years of athletic and other performance.

Great preliminary work that deserves further study. The whole microbiome area is incredible and in my view will result in life-changing benefits once understood with “miracle” cures coming.

Science news: Gut microbes might help elite athletes boost their physical performance

Microbes that flourished in the guts of some runners after a marathon boosted the time that lab mice ran on a treadmill, researchers report June 24 in Nature Medicine. These particular microbes seem to take lactate, pumped out by muscles during exercise, and turn it into a compound that may help with endurance.

...

In the study, researchers collected stool samples from 15 elite runners for five days before and after they ran in the 2015 Boston Marathon, and compared the samples’ microbial makeup with that of poop collected from 10 nonrunners. The runners’ samples showed a bump in the abundance of bacteria from the genus Veillonella after the race. The team also saw an increase in Veillonella in a group of 87 ultramarathoners and Olympic trial rowers after a workout.

This finding raised the question of whether these microbes were mere bystanders or were actually helping their hosts. So the researchers cultured one strain, Veillonella atypica, from a runner and fed it to mice. Not all of the 32 mice responded to the treatment, but on average, mice that received the microbes ran for 13 percent longer in experiments than mice in a control group.

The work shows that “a single bout of exercise can have effects on your microbiome,” says Jeffrey Woods, an exercise physiologist at the University of Illinois at Urbana-Champaign. But he is skeptical of whether the improvement in the mice’s stamina is important, noting that the mice were tested in a series of short runs that “isn’t anything like the marathon run.” The researchers might have found other microbes at play if more stool samples had been studied, he says.

The authors, however, say that the microbes could boost athletic performance. In a race, “sometimes people worry about a fraction of a second … this could be much more than that,” says biotechnologist George Church at Harvard University.

...


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Every Year is a Challenge, the Key is Having Faith in Recovery: Antibiotics Are Dangerous

I’m not a spring chicken any more, so I am coming to expect aging issues. Ah, to be young again, because no matter the attitude, the body just doesn’t perform as well.

This post is mostly about antibiotics: back in 2014 I sustained nerve damage from the antibiotic Metronidazole, taking nearly two years to fully recover (the worst symptoms were gone within 4 months), making me very leery of all antibiotics. But every few years, something pops up.

Beating a urinary tract infection

This is a postscript to what follows below: after the Eastern Sierra double century, I had burning while urinating two days later. I did NOT want to take antibiotics yet again.

While I obtained more Cipro as a precaution (being in a remote area), I did not take it, deciding instead to force a lot of extra fluid (with electrolytes) through my system, the idea being that steady flow of urine might help flush out kidneys an urinary tract.

I did so for a week, taking in about an up to an extra gallon of fluid each day (with electrolytes). The discomfort was mostly gone after 12 hours and gone with only mild sense of it for a few days, then it disappeared and did not return, and has not 3 weeks later. Hooray!

Antibiotics for UTI and Prostatitis

In March after the Solvang Double Century where my body worked supremely well, I came down with a urinary tract infection (UTI) a week later. I had not had such an infection since 2012. It only got worse, so I took the antibiotic nitrofurantoin (Macrobid). It was nasty stuff doing a job on my insides and even worse when done. It the UTI, but unfortunately it seems that prostatitis was probably the root cause/source of the infection, and nitrofurantoin does not get into the tissues and thus won’t cure prostatitis.

About two weeks after finishing the Nitrofurantoin, I was getting my strength back and resuming training, when prostatitis struck, which was uncomfortable and also made cycling impossible. It held steady at a tolerable level of discomfort but it was not improving, so I had to take a 10 day course of ciprofloxacin (Cipro), which surprisingly was much less troublesome than Nitrofuran tin.

By the time I was done with the Cipro, I was severely weakened, not just from losing fitness, but by damaging effects to body and brain. Even baseline rides were tiring. Worse, one or both of those antibiotics brought back certain post-concussion symptoms, which in terms of a self employment situation is a very serious side problem. I would say that more than half the days of the week, my productivity was cut in half or worse—unable to focus or concentrate, very easily distracted, etc.

I was weakened enough that I skipped three key double centuries, and had my doubts about doing one, but I did complete the Eastern Sierra Double by keeping cadence higher and power lower (I was also concerned about tendon rupture, a black box warning for Cipro, so I had kept training very aerobic). For the first 80 miles, my legs muscles and tendons were right as drums, a daily condition since the antibiotics (another cyclist told me of also experiencing the same tightness following antibiotic use).

Starting out dead last, I finished 5th and 90 minutes slower than 2018, though conditions this year were ideal compared to last year’s heat , so I deem that 2 hours slower. But I got it done, which restored some confidence. Setbacks happen, and if I cannot bounce back, I can at least roll over and stand up!

Summarizing antibiotics

  • Maintain a strong aversion antibiotics; the cure can be worse than the disease.
  • Antibiotics often have all sorts of side affects, including on body and brain.
  • The gut is a second brain; since antibiotics kill the gut microbiome (and probably skin and other microbiomes in some cases), antibiotics in effect cause a sort of mild brain damage from which you can recover “fully” but the microbiome in the gut and body will NEVER be the same again.

IMO, antibiotics are far more dangerous than a similar course of narcotics or benzodiazepines! Because antibiotics for just 10-14 days can inflict changes from which there is no true recovery to prior condition.


Up to 1527MB/s sustained performance

Can Modern Technology Ever Make a Better Shoelace?

Shoelaces have long been a problem with just about every shoe I buy—premature failure.

See also Gear for the Mountains.

This is ridiculous—I’ve hardly worn these FiveTen Guide Tennie approach shoes. The laces ruptured into nearly useless junk. Now that Adidas bought FiveTen, the quality may go downhill further as costs are surely cut, and FiveTen was quite good at least in terms of the shoe itself.

One reader suggested parachute cord, which I tried, but it turned out to be useless—even worse—suffering the same sheath/core disintegration as the original laces, and there is no easy way to make stiff ends to feed through the holes.

A much better solution is to buy shoelaces for hiking shoes (63 inch length for these shoes)—which I did and will report on the quality when I try them.

Update: the DELELE 2 Pair Round Wave Shape Non Slip Heavy Duty and Durable Outdoor Climbing Shoelaces fit great and are a close match for the original laces, but look to be better made.

Shoelace failure with FiveTen (now Adidas) Guide Tennie approach shoes
f1.8 @ 1/30 sec, ISO 64; 2019-06-19 12:18:01
iPhone 7 Plus + iPhone 7 Plus 4.0 mm f/1.8 @ 28mm equiv (4mm) ENV: altitude 196 ft / 60 m

[low-res image for bot]

 

OWC Thunderbolt 3 Dock
Ideal for any Mac with Thunderbolt 3


Dual Thunderbolt 3 ports
USB 3 • USB-C
Gigabit Ethernet
5K and 4K display support plus Mini Display Port
Analog sound in/out and Optical sound out

Works on any Mac with Thunderbolt 3

The Fungus that Can Kill You—Candida Auris Spreading and Very Hard to Decontaminate

Candida Auris is about as scary a threat as one might imagine: a fungus that is multidrug resistant, hard to identify, and very had to clean/kill from hospital settings.

Be afraid, be very afraid because assuming hospitals are going to make patients aware of an outbreak is something only those born yesterday will find credible. State governments are suppressing information about it, a Low State that will surely lead to unnecessary deaths going forward.

From NYT: How a Chicago Woman Fell Victim to Candida Auris, a Drug-Resistant Fungus:

Nearly 600 cases of C. auris have been reported in the United States, the majority of them in New York, New Jersey and Illinois. According to the Centers for Disease Control and Prevention, nearly half of people who contract the illness die within 90 days. But the true death rate is difficult to quantify because most patients have other medical conditions and their deaths may be attributed to other causes.

...on Tuesday, the C.D.C. confirmed that it has learned in the last month of the first known cases in the United States of so-called “pan-resistant” C. auris — a strain resistant to all major antifungals.

It often has been hard to gather details about the path of C. auris because hospitals and nursing homes have been unwilling to publicly disclose outbreaks or discuss cases, creating a culture of secrecy around the infection. States have kept confidential the locations of hospitals where outbreaks have occurred, citing patient confidentiality and a risk of unnecessarily scaring the public.

It’s not just fungus, there was a new deadly bacteria outbreak in Mexico that the CDC noted in January 2019 in Drug-Resistant Infections in Patients Who Had Weight-Loss Surgery in Mexico.


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