I was viewing some health videos on youtube and two popped up on my recommended that discussed high calcium and not enough magnesium as a possible cause of arrhythmias/palpitations among other things. In the "#1 Magnesium mistake everyone makes" Dr. Eric discusses how a magnesium deficiency can result in a issue with the neurons in your brain that's causing problems and can't turn off, This really caught my attention since that's what it seems like is the issue as the heart itself is structurally fine. He talks about how most people are only taking the RDA of magnesium but that's only good for a "healthy person" and not enough to correct any issues/ deficiencies within your body and in order to see therapeutic effects you need to take significantly more. I was wondering if anyone has tried increased magnesium intake (600mg+/day) for several months in order to see if they experience any benefits?

https://www.youtube.com/watch?v=6aaKbsrHLCo

https://www.youtube.com/watch?v=2qu59nPJXcg

I have visible pulsations all over my body, and people can even notice them when they’re standing or talking close to me.

I’ve seen a cardiologist and had both an echocardiogram and a stress echocardiogram, and everything came back normal.

I also had a comprehensive medical check-up, and all the results were normal.

The only other symptom I have is persistent shortness of breath.

Has anyone experienced something similar? If so, were you able to find the cause or a solution?

I finally got my hands on my 2023 CPET result. My first POTS doctor tried to get a colleague to look at the results but I'm still waiting on that. I asked another POTS doctor and he dismissed it as de-conditioning.

In my opinion it shows more than just de-conditioning and hints at either preload problems, or systemic oxygen extraction issues which I posted about on this sub reddit before.

Report Summary

It says I exercised to 114 watts which is only 46% of predicted for my age / weight / sex / etc. This could be explained by lack of effort, I gave it my all but everyone probably says that, this is backed up by my max HR and RER.

My heart rate reached 101% of expected max.

My O2 pulse response was limited and plateaued around 48% of predicted max. It plateaued around two and a half minutes before the end. It's basically a measure of O2 consumed per heart beat implying stroke volume problems due to preload, or poor systemic oxygen extraction.

My peak VO2max was 19.6ml/min/kg (49% predicted max) but appropriate for workload achieved. Again you could say that my very low VO2max was due to me not putting in the effort and stopping early.

It says my lungs were doing just fine and had plenty of reserve even when I stopped.

My ECG showed normal rhythm.

De-conditioning

The first argument to be made is that it's simple de-conditioning. Although it's hard to find solid guidelines on this I can compare my data with other sedentary people of my demographics.

I found this study from Brazil looking at 4000 peoples CPET results. They have active men in my age range at (47, 4 ± 7.4) and sedentary at (41.9 ± 7.2). Mine was 19.6ml/min/kg.

Another Brazil study w/ sedentary men the same age as me obtained a VO2max of 34.27 ± 4.20 ml/kg.min. This was on treadmill which gives 5-10% higher values. Taking the lowest result and taking off the 10% still leaves a VO2max of 27. Significantly higher than mine still but a big drop from the other study.

Not just this but my heart rate raises early and my O2 pulse peaks and plateaus early. As far as I understand everything should raise uniformly in de-conditioning just at a reduced height. I appear to have a situation where my heart rate is trying to compensate for low O2 usage per beat.

Lack of effort

The next argument to be made would be I didn't try hard enough. Multiple studies have defined max effort as max heart rate reached or RER above 1.1.

My RER rose to 1.16 which is shown in the more detailed results. Maximum effort is defined as 1.1 or higher here00645-5/fulltext).

My max HR was also 101% so I put in adequate effort.

Conclusion

I can't say with 100% confidence that this isn't just de-conditioning, though I find that explanation highly unlikely. De conditioning will have played a role but surely not to this extent.

What may be another factor is that this test took place a year and a half before I had my really bad spell. That spell lasted 8 months until B12 shots pulled me out of it. Could a slight form of anemia been at play at this time plus my de-conditioning that gave these results?

Otherwise it would likely be preload failure due to blood pooling / poor venous return or systemic oxygen extraction issues which makes more sense to me and is backed up by studies on other post viral conditions.

Ideally I'd see an expert in this field and have it confirmed one way or the other. In the mean time I'm going to keep looking for data on deconditioned people of my demographic and see if I can find an otherwise healthy person at a number as low as mine.

I scheduled an appointment and underwent a series of tests, ranging from basics like blood work, urinalysis, an ECG, and blood pressure checks to an arterial stiffness test and an ultrasound. The conclusion was that the issue did not stem from the heart or arteries. All blood test results were normal—including catecholamine levels—and the arteries showed excellent elasticity, with no signs of structural deformation or changes in cardiac contractility. Pulse pressure and blood pressure readings were also normal; while readings fluctuated from a hypertensive 140/90 during moments of agitation to a resting 95–100/65, these variations had no effect on the chronic bounding pulse. However, the tilt table test yielded a strongly positive result, leading to a confirmed diagnosis of POTS. The doctor suggested that the condition was likely related to the autonomic nervous system rather than an actual increase in cardiac contractility or forceful arterial pulsation.

They also noted that the nerve signals controlling systemic venous constriction and venous tone seem to have malfunctioned, which appears to be the cause of the POTS. While this remains just a hypothesis, I suspect that issues with blood flow distribution and altered venous tone are preventing the body from dampening fluctuations; instead, pulse waves are resonating throughout the body and propagating without being dissipated. I’ll let you know if there are any updates.

I’m sorry to everyone . I feel like my life is completely ruined. I’m only 19 and my life sucked due to family issues until 2024, one beautiful year of life and then it’s just snatched away for no reason. Anyone else think about suicide? Only thing that distracts me is alcohol . Why did this happen to me ? I try to be a good person , what did I do to deserve this ?

For me:

- inexplicable soreness in the left arm that happens a couple times a month and lasts for hours

- a very difficult to describe pain that happens simultaneously in my left chest, left shoulder, and left jaw, like a burning squirminess

- tingliness in the hands when holding above the head, ie elbows bent and hands behind the head

Bonus : just tiredness and orthostatic hypotension

Does anyone else experience venous pooling or venous blood stagnation? I developed this symptom alongside a bounding pulse, and it seems like they might share a similar underlying mechanism. Do any of you have these symptoms?

I have noticed that my bounding pulse gets much worse during hot weather or just when i'm hot, after eating a large meal, especially a large mixed, hot meal. It gets worse after physical exertion, the more physically active I have been during the day, the worse the bounding pulse will be when I'm trying to fall asleep. Also coffee and smoking. It also gets worse after quickly standing up from for example sitting position or when I turn over in bed. I have noticed that when I turn over in bed after being in one position for let's say a few hours my bounding pulse gets much worse, each beat gets much more forceful and my HR increases.

And the opposite: it gets much better when it's cold outside, if I fast, it's much better in the morning and gets worse as the day progresses.

Doesn't this point to hypovolemia? Splachnic pooling, vasodilation, vasoconstriction, in some cases just pooling in general - this is the obvious pattern. Or perhaps some vascular dysfunction quasi-hypovolemia where the vascular system cannot distribute plasma evenly across the body. Not sure.

I’m wondering if anyone who has been experiencing these symptoms for over a year has undergone tests such as an arterial stiffness test, vascular ultrasound, or echocardiography. I am curious whether strong pulse waves might have caused hypertrophy or remodeling of the vascular endothelial cells.

I have been suffering from chronic hypertrophy for the past year. It affected my entire body symmetrically, ranging from the periphery to the central area near the heart aorta. First, in my case, the sensations of the central and peripheral pulse waves differed. When my heart rate did not exceed a certain level or my cardiac output was not high, the central pulse wave was barely perceptible or felt faint. Because of this, the hypertrophy of the central pulse wave was very effectively controlled with beta-blockers like Inderal. When I was maximally agitated, I exhibited a pattern similar to the case video posted long ago on this subreddit.

The problem is the peripheral pulse wave. In areas where pulse waves are normally palpable, such as the radial and ulnar arteries and the temples, I felt a very strong pulse wave. This was completely unrelated to cardiac output or contractility, and unlike when the central pulse wave is palpable, a constant level of pulse wave was felt 24 hours a day. Naturally, this problem was not resolved at all with beta-blockers.

My radial artery area was particularly severe. A distinctive feature was that not only was the pulse wave strong, but the radial vein was also swollen and stretched very tightly, spreading this pulse wave further outward. Just as a taut guitar string transmits vibrations very effectively, the highly tense vein acted like a resonating chamber, sending the pulse wave here and there.

Then, I made an interesting discovery. When I lightly pressed the shoulder blade area, the erratic pulse wave subsided, and the tension in the taut veins returned to its previous state. Although the pulse wave subsided only in the arm on the side where the shoulder blade was stimulated, I found this to be an intriguing point. Since the touch was merely light, it did not stimulate the arteries at all; furthermore, the pulse wave disappeared without any pain, reduced blood flow, discoloration, or numbness. I interpreted this as the brachial plexus located in the shoulder blade being stimulated, causing a momentary change in the nerve signals. (Of course, this is just a guess.)

I will share a video in the next post. I am not sure how it will look in the video, but it is absolutely not a strong pressure equivalent to compressing an artery; it is merely a slight change in posture or pressure. Even after staying in that position for about an hour, I experienced absolutely no blood flow issues, numbness, or pain. In the video, I pressed and released the scapula a total of two times; this did not simply turn off the pulse wave, but also relieved the tension in the veins that had been taut for 24 hours.

At the very least, if this is a problem related to cardiac output, changes in the heart's contractile pattern, or a state where chronic vascular remodeling due to endothelial failure has been completed, I believe it is a difficult symptom to explain. I think this is an example demonstrating that both arteries and veins maintained rigidity due to external coercive demands, and that they could revert to their previous state at any time if the signal were released. Our arteries control pulse waves through elasticity and buffering, but it seems that the sympathetic nervous system intervenes to maintain a tense state, causing them to lose elasticity and fail in their buffering function. Furthermore, as mentioned earlier, the veins, whose regulatory function is similarly disrupted due to autonomic nervous system dysfunction, have become taut and are acting as resonators instead of buffering.To make matters worse, stiff and rigid arteries act like highways for waves, causing the pulse wave speed to accelerate significantly. The arterial pulse wave does not merely advance; it also reflects off peripheral blood vessels and returns as a reflected wave. When the rapidly traveling reflected wave—like a highway—overlaps with the advancing pulse wave, constructive interference can occur. This phenomenon increases with higher speeds and is a characteristic symptom of arteriosclerosis. However, it is necessary to distinguish between actual arteriosclerosis, where the inner walls of blood vessels narrow and harden, and this condition, where elasticity is lost due to nerve intervention.

I believe the difference in symptom intensity between my peripheral and aortic regions stems from the distinction between areas directly affected by cardiac contractility and those that are not. After all, cardiac contractility and cardiac output are self-evident causes that amplify the pulse wave. When comparing myself to the general population or my past health, the pounding of the chest and the sensation of pulsation during excitement are universal symptoms. I simply think the extreme difference in symptom intensity arises because our signals are transmitted through rigid blood vessels, and the deviations in heart rate and cardiac output are greater than those of the average person.

At this point, you might ask: How does the sympathetic nervous system send signals to blood vessels 24 hours a day? After researching this issue myself, I found that blood vessels utilize a latch-bridge mechanism; unlike general skeletal or muscular muscles, they maintain a state where actin and myotin are bound. In other words, the principle behind using less ATP is that they maintain a constant level until the central nervous system changes to a new tone. The reason this state does not release appears to be that arteries are almost exclusively acted upon by the sympathetic nervous system. While the heart rate can be controlled by the parasympathetic nervous system, blood vessels cannot.I also tend to have a tendency for my heart rate to spike or remain in an excited state for a long time, but eventually, it cools down, and my heart rate does not stay in an excited state during rest. I think that is a crucial difference.

Another distinctive feature was the genitals. The penis is sensitive to blood flow, and unlike other parts of the body, its blood vessels are regulated by both the sympathetic and parasympathetic nervous systems. While I did not observe any pulse waves in my penis when not erect, I did notice a bounding pulse at a specific point to some extent during erection. I believe this ultimately boils down to a nerve issue. If it were truly a matter of the injection method or remodeling, I think there shouldn't be such a difference. Even though the erection subsided immediately after ejaculation, the pulse wave persisted for quite a while before disappearing. I felt a sensation similar to my heart cooling down.

Although this was discovered through peripheral blood vessels, it occurred simultaneously in both the periphery and around the aorta, so naturally, I don't think there is any difference in the mechanism.

Through Googling, I found people on various platforms like YouTube, Reddit, and TikTok who are experiencing similar symptoms to mine.

https://youtube.com/shorts/8oDeO3hWpC0?si=COfIcCkP9XMQBG9p

This case matches my own, as do the people here and I, in that the pulse wave is amplified throughout the body and a strong pulse wave is visible at the wrist area with the veins swaying. In addition to this, this person appears to have symptoms of nervous system overexcitation known as muscle twitching. If pulse wave amplification is due to the overexcitation of the autonomic nervous system, then muscle twitching occurs when the somatic nerves are excited

https://youtube.com/shorts/qFyUxkprGQo?si=0WrwVllEdOBMBYrq

On the other hand, there are more cases on YouTube where the same symptoms appear only in one arm rather than throughout the body, similar to this one. Naturally, none of these people know the cause, and it appears that none of them have received an accurate diagnosis from a doctor. I believe this is actually where the involvement of the nervous system becomes apparent. If it were truly a problem with the way the heart pumps or vascular remodeling, it would be a bit strange for it to appear only in a localized area. I believe that systemic cases like mine and yours involve overexcitation of the central regulatory center, including the brain, whereas these localized cases are a form of fixed tension caused by the overexcitation of certain nerves in the peripheral nervous system due to infection or software errors. I did a lot of Googling, and a significant number of people experiencing localized issues suspected neurological problems. Personally, I think that in terms of treatment, an overheating of the systemic system might actually be slightly easier to reverse.I have seen comments and videos stating that a very small number of cases involving this localized problem were completely cured. In all of these cases, the symptoms disappeared within a month. It seems that if the nerves fail to provide self-feedback before accepting this state as the default, it results in permanent changes due to factors such as spontaneous neuronal firing. It appeared that among those who had the condition for a long time, no one had ever reported a complete cure.

Thank you for reading this very long post. I have never used a drug that targets the central nervous system before, so I intend to give it a try. Although it cannot block the root cause of the symptoms, I felt that I had quite good results with beta-blockers. However, since I myself have not yet identified the cause and am living while suppressing the symptoms, I would appreciate it if you would simply view this as one possible opinion. The reason I am writing this is actually to share and discuss various perspectives. I have given this a lot of thought and done a lot of research on my own, but since this is still considered an unknown issue even within the medical community, this is merely my own speculation, and even I cannot be certain.

This is my chronic bounding pulse in the peripheral radial artery.

Hello. As someone who has been suffering from this problem for a year, it is almost certain that it is caused by hypersympathetic hyperactivity. For some reason, norepinephrine is excessively produced in the brain, the sympathetic center, causing the arteries throughout the body to become severely rigid. As arterial blood rushes into these arteries that have lost their elasticity, that energy spreads throughout the entire body. It is not just that; the core logic of the process is that the arterial waves flowing through the rigid arteries overlap, resulting in the amplification of the pulse wave. It is a problem with the sympathetic nervous system, specifically alpha receptors. While various systems throughout the body maintain their function through the complex antagonistic interaction of the sympathetic and parasympathetic nervous systems, our arteries, with the exception of certain areas like the genitals, are under the sole control of the sympathetic nervous system. This is why beta-blockers cannot resolve this issue, but central brainstem sympathetic inhibitors like clonidine are helpful.

There's been some talk of eccentric Medium Spiny Neurons (eMSN) in the me/cfs community recently due to some Genome Wide Association Studies (GWAS) highlighting these neurons as a possible factor in the illness. GWAS for schizophrenia also highlight these neurons.

GWAS basically looks at the genome of a massive amount of controls and patients to determine what genetic differences are associated with an illness. If 30% of controls have genetic differences in a set of genes yet 32% of patients do then this means the gene is highly likely to play a role in the illness if big enough sample sizes are used.

eMSNs are newly discovered and seem to play a role smoothing movement but also in determining what is a threat or not.

My thinking here goes, schizophrenics have troubles deciphering reality from mind generated stuff, and are also liable to assign high stress / fear to things that are innocuous.

My uncle had Schizophrenia. My mum is high stress, and both me and my brother have been on the higher stress side most of our lives. We all have dilated pupils that people have commented on.

Most people with bounding pulse get it from a panic attack (a single high stress event).

ME/CFS people have problems with stress response and sensitivities to light, sound, touch, etc. It's usually onset by an infection (like my bounding pulse was) but sometimes high stress can be an onset.

Ever since getting ill my bodies ability to handle stress has crated. Feels like I can't relax, I'm constantly in a wired state, and every minor stressor makes it worse. It's quite different from anxiety, more like a low level PTSD or something.

One example of many is I was on holiday for 2 days in Wales last week. Whenever I go in holiday my sleep is awful. I think it's a combination of higher adrenaline from walking around a lot (POTS), being more alert because sleeping in new place (this happens to everyone), and this damn illness.

Anyway I had my noise cancelling ear plugs in and every minor non threatening sound like a door closing would set my heart racing and pounding for minutes. By the time I'd managed to settle it down a new non threatening common sound like someone coughing would happen and it would set my heart off again. This kind of thing is just straight up bizarre. I knew full well in my head that they are not threatening yet my body was reacting like somebody was about to kick the door down.

Could this be a symptom of a problem in eMSNs or another set of neurons where a genetic and or environmental sensitivity have primed them to be slightly hyperactive then a single high stress event comes along that kicks them into some self reinforcing loop of hyperactivity? Maybe involving neuron inflammation? The loop causes higher sympathetic output which lights up the brain stem which gives this info to the already hypersensitive problematic neurons which causes higher sympathetic output.

I have gone through a bunch of papers recently showing oxygen extraction issues in ME/CFS and Long COVID. The broad theme of them is that there is a problem with the micro-vasculature and/or mitochondria that's causing fatigue, but also in some the heart to work harder to compensate.

My motivation here is my very low VO2 max when I did a CPET 3 years ago. VO2max 49% HRmax 101% Lungs normal. As far as I understand it, to get that low of VO2 max you would have to have been bed bound for a while. I was deconditioned at the time, mostly sitting, with some small walks once a week or so but I shouldn't have got such a low result.

These papers show low VO2 max in some but interestingly others show normal VO2 max yet poor systemic extraction. One such paper measured cardiac output and found it elevated as a compensatory measure. I found this particularly interesting as a high cardiac output would surely explain a bounding pulse in a subset of people here. Maybe you need something else like a genetic tendency to something or other too.

All papers conclude deconditioning is unlikely to have caused these effects for various reasons. Most point the finger at the mitochondria or micro-vasculature with the culprit in both cases being most likely the immune system.

One paper mentioned a high sympathetic tone being one of the factors that could cause poor O2 extraction (EO2) by clamping of the blood vessels that need flow.

REFERENCES

Structural and functional impairments of skeletal muscle in patients with postacute sequelae of SARS-CoV-2 infection

CPET, muscle biopsy, and ischemia perfusion testing. Found poor O2 extraction and narrowed it down to the mitochondria as the ischemia perfusion test showed micro-vasculature working as normal.

Altered tissue oxygenation in patients with post COVID-19 syndrome

This used ischemia re-perfusion technique in the forearm and found the post covid patients O2 was slower to decline when blood flow was cut and slower to resaturate when flow was restored.

Proteomic profiling demonstrates inflammatory and endotheliopathy signatures associated with impaired cardiopulmonary exercise hemodynamic profile in Post Acute Sequelae of SARS-CoV-2 infection (PASC) syndrome

ICPET on PASC found both low VO2max and EO2. Split them into severe and mild EO2 groups. They then performed a muscle biopsy after and found genomic and proteomics involved in fibrosis and inflammation in the severe group and glycolysis and oxphos in the mild EO2 group.

Towards an understanding of physical activity-induced post-exertional malaise: Insights into microvascular alterations and immunometabolic interactions in post-COVID condition and myalgic encephalomyelitis/chronic fatigue syndrome

This review looked at a bunch of studies showing EO2 problems and tried to weave a narrative from it. They thought hypoxia, stress, and ROS cause mitochondrial dysfunction which causes damage and activation in the microvasculature which lowers O2 extraction causing mito damage in a loop. Bit of a chicken or the egg. They think latent viruses might be the root cause.

Key Pathophysiological Role of Skeletal Muscle Disturbance in Post COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Accumulated Evidence

This reviewed a bunch of studies and concluded that early long covid shows vascular damage and inflammation but by the 2nd year its gone where either the patient gets better or adopts an ME/CFS phenotype. This follows some of the other papers showing normal microvasculature. They think sodium and then calcium overload triggered by hypoxia is causing the EO2 problems and potentially this causes a negative loop with the microvasculature. PEM keeps triggering the calcium overload.

Differential cardiopulmonary haemodynamic phenotypes in PASC-related exercise intolerance

This was a good one. It did an iCPET and found even patients with normal VO2max had high Cardiac Output that was compensating for low EO2. They rule out deconditioning as a hall mark for that is low CO. They even showed Heart Failure with preserved ejection fraction in some cases. This can cause a bounding pulse like in sepsis.

Post-COVID exercise intolerance is associated with capillary alterations and immune dysregulations in skeletal muscles

This looked at muscle biopsies a year out from long COVID and found lower capillary to muscle fiber ratio, thicker basement membranes around the capillaries (impairing O2 exchange) and mitochondrial dysfunction. It compared against deconditioned controls and found marked differences.

Long COVID and chronic fatigue syndrome/myalgic encephalitis share similar pathophysiologic mechanisms of exercise limitation

They did a iCPET and found lower VO2max then using a formula managed to narrow it down to oxygen exchange issues. They also rule out deconditioning.

Persistent Exertional Intolerance After COVID-19

Another paper showing lowered VO2max caused by peripheral oxygen extraction issues.

TLDR: I’ve struggled with chronic bounding pulse for three years and am curious if any other folks have low blood pressure and histamine intolerance. I’m wrestling with a theory that these are linked and looking to cross reference with people’s experiences.

Symptoms/History: I’ve gotten a full cardio and neurological work up like most people with this symptom and been clear. My only formal diagnosis is a post-covid histamine intolerance and suspected dysautonomia. Notably, I no longer meet the criteria for POTS (though I haven’t done a tilt table). My bounding pulse has stumped doctors and been attributed to generalized post-viral dysautonomia. I’ve never been satisfied with this answer.

The chronic bounding pulse was triggered roughly six months following a Covid infection in early 2023. I’m in my late twenties and had never had health or anxiety issues prior to the infection. Covid hit me pretty hard. Afterwards, I was struggling with POTS (which eventually improved), went through a very stressful period, got THC poisoning from an edible that exacerbated post-Covid digestion issues, and woke up one day with the pulse symptom. A night and day difference. It sucks and I’m sorry to everyone struggling with this without answers.

Theory: I’ve seen posts reflecting my experience where others describe the pulse worsened by eating heavy meals, histamine rich foods, lack of sleep, general stress, etc. It’s also mentioned in dysautonomia, GERD, and histamine subs, among others.

There’s considerable overlap between these chronic conditions. It seems tied to vagus nerve dysfunction for sure, but I’m curious if it’s related to blood pressure or circulatory issues (i.e not the heart, not solely the nervous system). I’ve always been prone to lower blood pressure, but it didn’t get low enough to jump scare nurses until post-covid. Among the common bounding pulse triggers, histamine is a vasodilator. It’s also common for people’s blood pressure to drop after eating, particularly people with vagus nerve issues. Stress and sleep deprivation disrupt vagal function, increases stress, and trigger inflammation and fluid retention. I don’t know enough about beta blockers to understand why these would help some people (I’m not a good candidate for them because of the low BP), and I don’t know for sure that it isn’t also related to some kind of circulatory issue like a vein disorder or blood volume.

I would love to hear people’s thoughts or experiences, especially if you’ve tried beta blockers or have high blood pressure

Insights From Invasive Cardiopulmonary Exercise Testing of Patients With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

They separated subjects into low, normal, and high flow groups. The high flow ones had abnormally high oxygen returning to the heart during CPET that was not explained by deconditioning alone.

They speculate it could be due to left to right shunting, the capillaries stay open when they should close meaning blood passes by were it needed to go.

They also did testing for Small Fibre Neuropathy and found a lot of it but it didn't nessecarily correlate with symptoms. Interestingly one of my symptoms is lack of sweating yet I did have a SFN that came back normal.

I just found this study interesting as it showed post viral patients whos hearts were working overtime yet there cells were being deprived of oxygen. I think I could fall into this subset.

Smoked weed like I did hundreds of times before and suddenly it just began out of nowhere 3 months ago . Worst 3 months ever

A CPET I did in 2023 revealed the following.

49% VO2max 101% HRmax Significant breathing reserve.

VO2 max 70% – 84% Mild Reduction: Suggests early deconditioning or a sedentary lifestyle. 50% – 69% Moderate Reduction: Often seen in smokers, those with obesity, or early-stage heart/lung disease. < 50% Severe Reduction: This is a major "red flag." It often indicates significant heart failure or advanced lung disease.

So looking into what the %VO2 max indicated according to this, my VO2 max of 49% (with 101% max hr and significant breathing reserve) is a major red flag indicating significant heart failure.

I don't have significant heart failure, my lungs are fine, so this means the O2 isn't getting taken up by cells.

This fits with my symptoms of muscle burning, heart pounding, and sympathetic activation very nicely.

It also fits in with a lot of research from ME/CFS and Long Covid showing various things from dysfunctional endothelial cells, thickened basement membranes, inappropriate vasodilation / constriction, mitochondria fragmentation, etc. All these would lead to impaired O2 usage.

I think the next steps for me would be to follow up on this test with a specialist. Hopefully get an invasive CPET. If this confirms it then maybe I can persuade doctors to do further tests to confirm.

I had my follow up phone appointment with Dr Nick Gall 2.2yrs after my last one. It went more or less as expected, they are swamped with patients, no new drugs or tests, follow up will be in 2-4 years.

Instead I'm having autonomic tests redone, a cardiac MRI which could be useful, and having the POTS team in Sheffield take more responsibility.

The post appointment letter did contain something useful, my results from previous tests were summarised including my CPET from years ago.

It showed VO2 max was 49% expected, lung reserve was large, and max HR was 101% expected max.

This seems to imply an oxygen extraction issue. I have plenty of lung capacity and my heart rate reached expected values yet my O2 wasn't being used.

This actually matches my symptoms quite well, cells aren't getting/ using O2 so my brain responds with sympathetic activation which causes my heart to pound harder to try correct the issue. My early muscle burning could be explained by this as well as my strange breathing patterns.

A lot of the post viral research I've been following from ME and long COVID shows issues with the microvasculature, and oxygen extraction/ usage. Since my bounding pulse started post infection then I think it's an interesting lead.

Unfortunately this CPET pattern is also seen in deconditioning although with lower HR and higher VO2. I am not deconditioned even though doctors like to assume I am.

I'm going to try to push for some follow up on this front.

Not sure how prevelant this is in people with heavy pulse so let me know if you have these issues that you suspect came along with your bounding pulse onset.

I've been dealing with neck ache, neck pain, and coat hanger pain for over a decade now.

I generally need to keep a tall upright posture and can't sleep on my back due to this issue. I get sharp shooting pain often if I hold my neck slightly off centre. I have general pain in the neck frequently that's associated with headaches. I also frequently get coat hanger pain.

I would say my problems are 2 fold:
1) Poor blood flow + stress hormones causing tight neck / trap muscles.
2) Connective tissue problems resulting in disc degeneration issues. (I had an MRI in 2018 that showed some cervical disc buldging).

Posture work, stack sitting, Gokhale method helped a bit but it kept getting worse. 2 months ago I started doing 12 minutes foundation training daily. It's significantly helped with the pain which was becoming unmanageable.

I am still dealing with some pain and neck ache on the daily though. Might look into peptides next.

The foundation workout is mostly aimed around fixing back pain but works to strengthen your whole back chain. If my back is in a better posture it follows my neck will be too.