firewatcher

The endurance-trained group had a significantly larger LV end-diastolic volume normalized by body surface area (vs. sedentary and resistance-trained groups), whereas the resistance-trained group had a significantly higher LV wall thickness and aortic pulse wave velocity (PWV) compared with the endurance-trained group. My take understanding of this statement is that the endurance trained group moved more blood (LV end-diastolic volume), but the resistance trained group had thicker heart muscle walls, pushing the blood harder through the system. (Please correct me if I am wrong.) In response to 60-degree head-up tilt (HUT), mean arterial pressure (MAP) rose in the resistance-trained group (+6.5±1.6 mmHg, P<0.05) but did not change significantly in sedentary and endurance-trained groups. Systolic blood pressure (SBP) decreased in endurance-trained group (-8.3±2.4 mmHg, P<0.05) but did not significantly change in sedentary and resistance-trained groups. When tilted, the endurance trained group had a drop in SBP, and the resistance trained group had no change in SBP, but had a rise in arterial pressure. Furthermore, the change in stroke volume significantly correlated with LV wall thickness A thicker heart wall meant more muscle to push the blood through the system. I'd have to read the whole article, but it would appear that exercises like running expand the blood volume and move it through the heart muscle...but leave you prone to fainting when not in motion...and lifters have "stronger" hearts that push the blood harder through the system... I've always felt better when lifting or doing strength exercises.

"As mental challenge activates the sympathetic system..." Since being upright is already a huge challenge, thinking hard for something like a test or taxes, etc. just ramps our sympathetic nervous system even more! I think that this is why it is so exhausting to think and concentrate for long periods of time...and also why stress is such a big crash inducer for us.

Physiol Behav. 2012 Feb 25. [Epub ahead of print] Delaying orthostatic syncope with mental challenge: A pilot study. Goswami N, Roessler A, Hinghofer-Szalkay H, Montani JP, Steptoe A. Source Institute of Physiology, Medical University of Graz, Austria. Abstract At orthostatic vasovagal syncope there appears to be a sudden decline of sympathetic activity. As mental challenge activates the sympathetic system, we hypothesized that doing mental arithmetic in volunteers driven to the end point of their cardiovascular stability may delay the onset of orthostatic syncope. We investigated this in healthy male subjects. Each subject underwent a head up tilt (HUT)+ graded lower body negative pressure (LBNP) up to presyncope session (control) to determine the orthostatic tolerance time, OTT (Time from HUT commencement to development of presyncopal symptoms/signs). Once the tolerance time was known, a randomized crossover protocol was used: either 1) Repeat HUT+LBNP to ensure reproducibility of repeated run or 2) HUT+LBNP run but with added mental challenge (2min before the expected presyncope time). Test protocols were separated by 2weeks. Our studies on five male test subjects indicate that mental challenge improves orthostatic tolerance significantly. Additional mental loading could be a useful countermeasure to alleviate the orthostatic responses of persons, particularly in those with histories of dizziness on standing up, or to alleviate hypotension that frequently occurs during hemodialysis or on return to earth from the spaceflight environment of microgravity. Copyright © 2012 Elsevier Inc. All rights reserved. PMID: 22387271 [PubMed - as supplied by publisher] Dang, I can't do math even lying down!!!!!

J Appl Physiol. 2012 Mar 15. [Epub ahead of print] Impact of Chronic Exercise Training on the Blood Pressure Response to Orthostatic Stimulation. Sugawara J, Komine H, Miyazawa T, Imai T, Fisher JP, Ogoh S. Source 1National Institute of Advanced Industrial Science and Technology. Abstract Exercise training elicits morphological adaptations in the left ventricle (LV) and large conduit arteries that are specific to the type of training performed (i.e., endurance vs. resistance exercise). We investigated whether the mode of chronic exercise training, and the associated cardiovascular adaptations, influence the blood pressure responses to orthostatic stimulation in 30 young healthy men (10 sedentary, 10 endurance-trained, and 10 resistance-trained). The endurance-trained group had a significantly larger LV end-diastolic volume normalized by body surface area (vs. sedentary and resistance-trained groups), whereas the resistance-trained group had a significantly higher LV wall thickness and aortic pulse wave velocity (PWV) compared with the endurance-trained group. In response to 60-degree head-up tilt (HUT), mean arterial pressure (MAP) rose in the resistance-trained group (+6.5±1.6 mmHg, P<0.05) but did not change significantly in sedentary and endurance-trained groups. Systolic blood pressure (SBP) decreased in endurance-trained group (-8.3±2.4 mmHg, P<0.05) but did not significantly change in sedentary and resistance-trained groups. A forward stepwise multiple regression analysis revealed that LV wall thickness and aortic PWV were significantly and independently associated with the MAP response to HUT, explaining ~41% of its variability (R(2)=0.414, P<0.001). Likewise, aortic PWV and the corresponding HUT mediated change in stroke volume were significantly and independently associated with the SBP response to HUT, explaining ~52% of its variability (R(2)=0.519, P<0.0001). Furthermore, the change in stroke volume significantly correlated with LV wall thickness (r=0.39, P<0.01). These results indicate that chronic resistance and endurance exercise training differentially affect the BP response to HUT, and that this appears to be associated with training-induced morphological adaptations of the LV and large conduit arteries. PMID: 22422799 [PubMed - as supplied by publisher]

J Pediatr. 2012 Mar 14. [Epub ahead of print] Twenty-Four-Hour Urinary Sodium Excretion and Postural Orthostatic Tachycardia Syndrome. Zhang Q, Liao Y, Tang C, Du J, Jin H. Source Department of Pediatrics, Peking University First Hospital, Beijing, China. Abstract OBJECTIVE: To investigate whether 24-hour urinary sodium excretion could be an indicator of the effectiveness of salt supplementation in children with postural orthostatic tachycardia syndrome (POTS). STUDY DESIGN: The patient group comprised 30 children with POTS, and the control group comprised 10 healthy children. Serum sodium and 24-hour urinary sodium excretion were measured in all children, and the relationship between 24-hour urinary sodium and symptom severity was analyzed in the 30 patients. At 1 month after initiation of salt supplementation, the receiver operating characteristic curve was used to explore the probability of correctly discriminating responders to salt supplementation from nonresponders using 24-hour urinary sodium excretion as an indicator. RESULTS: Patients with POTS had lower 24-hour urinary sodium excretion than controls (P = .022). Symptom severity was negatively correlated with 24-hour urinary sodium excretion (OR, -0.754; P = .000). The receiver operating characteristic curve demonstrated a sensitivity of 76.9% and specificity of 93% for correct prediction of responders and nonresponders to salt supplementation when a 24-hour urinary sodium excretion of 124 mmol/24 hours was used as the cutoff value. CONCLUSION: Our results indicate that 24-hour sodium excretion of <124 mmol/24 hours is an indicator of the effectiveness of salt supplementation in children and adolescents with POTS. Copyright © 2012 Mosby, Inc. All rights reserved.

I was told that I had GERD based on endoscopy and manometry (slow esophageal transit/peristalsis) BUT....it turned out to actually be my gallbladder. My GERD symptoms disappeared once I'd had mine taken out!

Hang in there! I have done this at least twice for testing. It is not beyond you!!! You made it without this med, and you will make it again! The last bit is the hardest to come off: Klonopin has a 36 hour half-life...so it is still in your system up to 36 hours after taking it. Be kind to yourself and don't push yourself too hard. Of all the pain/panic meds, Klonopin is one of the hardest to come off of, and you have already done it. Ride it out, but don't hesitate to call your doc if things turn "wonky." Just take one breath at a time if you have to!(((( ))))))

I take in about half what I put out, unless medicated. I can lose 8lbs in a day and it is always clear and of low osmolality. I have been diagnosed with partial diabetes insipidus. If your first morning urine is clear, that is a big tell...but with DI there is no such thing as a "first" unless you count the midnight, 2 am, 4 am, and 6 am trips to the toilet!

This was one of the first drugs I was started on. Initially, it was an 80mg dose, but that was WAY to much. It was quickly lowered to two 20mg doses until it was shown that unmedicated, I had bradycardia at night. That cut out the evening dose. Now I take 20mg once a day in the morning. In me, it wears off about 12 hours later, which is my OK time anyway. Once I take melatonin, that controls the upright tachycardia until bedtime. This is one of the three drugs (including dDAVP and Klonopin) that has helped me the most...its an "oldie" but a goodie for me. I do notice that it both Klonopin and Propranolol work better together for me, just one won't do much without the other.

Yes, my doc did suggest that either my hypothalamus or pituitary is "shot." I don't have anyone looking into anything at all at the moment. Right now, they expect it and are just waiting...I hope a LONG time! As for hypo-pit, there can also be vasopressin that needs to be replaced. Head trauma can cause diabetes insipidus as well as incomplete pituitary failure.

http://www.americanautonomicsociety.org/ This site is a pretty good resource for finding docs and clinical trials too. One of the other interesting notes is the Streeten Fund, which is as big a contributor to this symposium. My doc at Vandy is on the donor list, as is Dr. Stewart and other names we know. If you want a charity to give to for POTS/ANS dysfunction research, this site could pool enough to get its name on the donor list! As for the three Big Pharma companies that donate...Bless them! They are at least interested!

I've had three of my docs make the connection. The problem is: there is no way to fix it and almost no way to treat it! We/they don't even understand all the connections between the hypothalamus and the rest of the body! Even now, no one understands what all the hormones do in the body! I can cite countless examples from melatonin levels triggering puberty to vasopressin effecting agression/bonding. The only thing that I've had in acknowledgement of this was a comment by my OB/GYN: "Either your pituitary or your hypothalamus is shot, there is nothing we can do till it fails completely...and then we just replace the hormones with pills." HOWEVER! Head trauma is a well known cause of pituitary dysfunction and your pituitary hormone levels should probably be checked just to make sure something can't be done to help. I had to go to a specific Pituitary Endocrinologist for this.

Always had it, but relapsing/remitting with progression. Birthdays are like that too.

Hyper/Hypo POTS are not universally accepted "groups." Usually, if you have upright hypertension and increased "sympathetic activity," like tremors, flushing or sweating, we tend to classify ourselves as Hyper. Some of us have measurably high levels of norepinephrine or catecholamines while upright. My doc at Vanderbilt labeled me based on my ANS test responses.

I have seen one yearly for many years. I have dysplastic moles (precancerous,) so I have to have a yearly checkup. She doesn't do much for my POTS, but she takes my questions seriously and doesn't blow me off like other docs have. She also knows that I do not react well to adhesives and has investigated several unusual skin reactions that I have had!

I have a cardiologist. He does nothing other than collect my copay once a year, BUT, he has actually heard of POTS (which is a huge plus.) My previous cardiologists had not heard of POTS, and did not care to educate themselves either. I am torn between just dropping a cardiologist altogether or finding a new one. While I am stable, I have no motivation to put myself through the pain of "the hunt." But, if I have an issue, I know I'll wish that I had. How helpful can cardiologists be? Should I even bother to have one? I really don't want to go to one and have them insist on a rigorous exercise program or monkey with my meds......

When I get a virus, this happens to me too. I can have the flu and never run a fever. I feel like I'd gladly die from fatigue and I hurt all over and the tachy is thru the roof. I happened to have a pulse ox test one night into getting the flu and it showed supine HR fluctuations between 42 BPM- 170 BPM. Just stay in bed and KEEP DRINKING! Even though you are hot, pile on the covers; if you can break a sweat (I rarely can) it may help. I HATE getting sick! Be well!

I was asked several times if I was on cocaine because of the size of my pupils. I'm guessing that it gives you really big pupils because I've never taken it! I even had one guy ask if I had "any more for him?" He did not believe that I was not "on" anything. I've also had many questions about why I "shake so much." They get really apologetic when I tell them I have a tremor!

http://www.sciencedaily.com/releases/1999/02/990209072908.htm Early link between Autoimmunity and Heart Failure. http://www.sclerodermatt.org/articles/news/407-clinical-manifestations-of-heart-disease-in-autoimmune-disorders Clinical Manifestations of Heart Disease in autoimmune Disorders This one has some risk reduction suggestions

I take a tiny dose, 20mg a day, once a day. It is enough to take the orthostatic edge off, but not "clinically" significant for most "normal" people. Vandy had an article about this drug with the tag "less is more." It is out of my system within 12 hours, so it is fairly short acting (at least for me.) I use it for orthostatic hypertension, tachycardia and tremor.

What interested me in the article was that these patients show NO "symptoms" or lab indications other than positive antibodies. But, the antibodies are enough to predispose the body to dysautonomia!

Tohoku J Exp Med. 2012;226(3):191-5. Cardiac autonomic regulation is disturbed in children with euthyroid hashimoto thyroiditis. Kilic A, Gulgun M, Tascilar ME, Sari E, Yokusoglu M. Source Department of Pediatric Cardiology, Gulhane Medical Academy. Abstract Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common form of thyroiditis in childhood. Previous studies have found autonomic dysfunction of varying magnitude in patients with autoimmune diseases, which is considered a cardiovascular risk factor. We aimed to evaluate the heart rate variability (HRV), a measure of cardiac autonomic modulation, in children with euthyroid Hashimoto thyroiditis (eHT). The study included 32 patients with eHT (27 girls and 5 boys; mean age 11 ± 4.1 years, range 8-16; body mass index 0.47 ± 0.69 kg/m(2)), as judged by normal or minimally elevated serum TSH levels (normal range: 0.34-5.6 mIU/l) and normal levels of free thyroid hormones (FT4 and FT3) and 38 euthyroid age-matched controls. Patients with eHT and control subjects underwent physical examination and 24-hour ambulatory ECG monitoring. Time-domain parameters of HRV were evaluated for cardiac autonomic functions. Children with eHT displayed significantly lower values of time-domain parameters of SDANN (standard deviation of the averages of NN intervals), RMSSD (square root of the mean of the sum of the squares of differences between adjacent NN intervals), NN50 counts (number of pairs of adjacent NN intervals differing by more than 50 ms) and PNN50 (NN50 count divided by the total number of all NN intervals) for each 5-min interval, compared to healthy controls (p < 0.05 for each), indicating the decreased beat-to-beat variation of heart rate. In conclusion, eHT is associated with disturbed autonomic regulation of heart rate. Hence, the children with eHT are at higher risk for developing cardiovascular diseases. PMID: 22343434

I have awful post exercise muscle soreness/weakness. It is so bad that it takes me 4-5 days to recover from one hour of exercise. I also wake up most mornings with moderate pain in my legs, almost like I've been climbing stairs all night. It eases up through the day, but I don't remember a day in the last 10 years without pain.

http://www.theshorthorn.com/index.php/news/university/29435-expert-women-at-cardiac-disadvantage Women at Cardiac Disadvantage: Dr. Fu (and Levine) lecture at University of Texas Arlington about POTS. Most interesting was the response from a lecture attendee, who refutes some of what the article says. I wonder how much of this is simply bad reporting? On the other hand, why, in this age of increased "sensitivity" would a doctor continue to use a term to describe his patients that the patients themselves find so offensive?

I had one exactly like this and it did ride up on me. It also stretched out pretty quickly. It was a great help until I found the athletic compression garments (compression shorts.) Now I can get by with something more like a girdle.