A number of studies have investigated whether loading with intravenous hydration solutions (saline, etc) or with a volume expander such as dextran can ameliorate symptoms associated with deconditioning. These studies have found that volume expansion (also called fluid or volume loading) can improve a number of symptoms in deconditioned patients, but does not improve exercise capacity. Multiple studies have found the best effects from intravenous saline in conjunction with exercise.
Shibata investigated whether orthostatic intolerance could be mitigated following bed rest with exercise and/or fluid loading (Shibata 2010). This study found that OI could be dextran solution (IV fluids) given after twenty days of bed rest was insufficient to control OI symptoms, but that it was successful when used in conjunction with a daily exercise program. This finding was important, as it indicated that low blood volume was not the exclusive factor in orthostatic intolerance.
Figueroa et al looked at the relationship between blood volume and exercise capacity in POTS patients (Figueroa 2014). They found that acute volume loading with IV saline reduces heart rate and improves orthostatic tolerance and other symptoms in POTS patients. Importantly, IV saline significantly increased the stroke volume, cardiac output and reduced systemic vascular resistance. However, IV saline did not affect peak exercise capacity or improve cardiovascular markers during exercise. So while IV saline does help symptoms in these deconditioned patients, it does not improve exercise capacity. The author notes that for this purpose, acute infusion may not be sufficient and may need to undergone chronically to see benefits on exercise physiology.
Whole body heating is known to increase cardiac output, constrict the blood vessels in the abdominal cavities, increase sympathetic nerve activity in the muscles and decrease vascular resistance in the skin. Taken together, these factors stress the regulatory mechanism of the cardiovascular system. One study (Keller 2009) found that acute expansion of blood volume (with dextran) completely mitigated the impact of heat stress on orthostatic tolerance. In short, receiving an infusion that increased the blood volume allowed the cardiovascular system to function properly in the face of a known stressor.
One study looked at the effect of fluid loading on orthostatic intolerance and blood flow in the brain (Jeong 2012). They found that following bed rest, volume loading alone prevented larger reductions in cerebral blood flow, but did not prevent orthostatic intolerance. Exercise and volume loading prevented orthostatic intolerance but did not affect cerebral blood flow. Importantly, aerobic or resistance exercise before bed rest did not prevent development of decompensation.
A 2000 paper notes that POTS symptom scores improved significantly following administration of IV saline (Gordon 2000). Additionally, a 2013 study evaluated the frequency and characterization of “brain fog”, a common term for the cognitive deficits associated with this (and other) conditions (Joyner 2013). 86% (56/66) of patients reported that IV saline was the most effective treatment for brain fog.
In summary, bolus IV fluids or volume expanders have been found to improve a number of symptoms in deconditioned patients, although they have not been found to improve exercise capacity.
For this metric, a graded exercise program is recommended.
(Author’s note: I have recently been made aware that the data supporting use of graded exercise for chronic fatigue patients was hugely flawed. I retract this statement at this time. For details on this topic, please refer to this Lancet article: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60686-7/fulltext)
A 2008 paper compared POTS and deconditioning (Joyner 2008). The author pointed out that a number of parallels existed between the physiological changes seen in POTS patients and those seen in deconditioned patients. Additionally, he made note of the parallels between POTS, chronic fatigue syndrome and fibromyalgia and the fact that exercise training had seen benefits in all of them. Given the significant relationship between mast cell disease and POTS, and the large overlap in CFS, fibromyalgia and mast cell populations, it is a comfortable assumption that an effective treatment modality for CFS, POTS and fibromyalgia may also be effective for mast cell disease. It is my belief that this is the basis for the frequently discussed finding of mast cell patients that intravenous fluids ameliorate a number of symptoms.
Furthermore, there are special considerations for mast cell disease that make intravenous fluids likely to cause a positive change in symptom profile. The first is that mast cell degranulation can induce systemic effects on arterial tone, hypotension and vasodilation (Willingham 2009). The next is that hypotension is characteristic of systemic mastocytosis, and that hypotension and syncope may occur due to cerebral hypoperfusion (Ozdemir 2010). Lastly, it is well known that mast cell mediators, including histamine, serotonin and tryptase, can induce capillary leakage leading leading to edema, and that they can increase vascular permeability (He 1997). Taken together, these points indicate that a mast cell patient may lose volume from the bloodstream into the surrounding tissues, which can exacerbate an already existing tendency toward hypotension, in turn made worse by orthostatic intolerance.
Fluid loading in the form of intravenous fluids may decrease symptoms in mast cell patients due to deconditioning, orthostatic intolerance and the capillary leakage often seen as a result of mast cell disease, which is especially present following mast cell attacks and anaphylaxis.
Gordon VM., et al. Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome. Clin Auton Res. 2000 Feb; 10(1): 29-33.
Ross, Amanda J., et al. What is brain fog? An evaluation of the symptom in postural tachycardia syndrome. Clin Auton Res 2013 Dec; 23(6): 305-311.
Raj, Satish R., et al. Postural orthostatic tachycardia syndrome (POTS). Circulation 2013; 127: 2336-2342.
Rocío A. Figueroa, et al. Acute volume loading and exercise capacity in postural tachycardia syndrome. J Appl Physiol 117:663-668, 2014.
He, Shaoheng, Walls, Andrew F. Mast cell activation may be all that is sufficient and necessary for the rapid development of microvascular leakage and tissue edema. European Journal of Pharmacology 1997; 328(1): 89-97.
Ozdemir, D., et al. Hypotension, syncope and fever in systemic mastocytosis without skin infiltration and rapid response to corticosteroid and cyclosporine: a case report. Case Reports in Medicine, Volume 2010 (2010), Article ID 782595.
Willingham DL, et al. Unexplained and prolonged perioperative hypotension after orthotopic liver transplantation: undiagnosed systemic mastocytosis. Liver Transpl 2009 Jul; 15(7): 701-8.
Keller, David M., et al. Acute volume expansion preserves orthostatic tolerance during whole body heat stress in humans. J Physiol 2009 Mar; 587(5): 1131-1139.
Sung-Moon Jeong , Shigeki Shibata , Benjamin D. Levine , Rong Zhang. Exercise plus volume loading prevents orthostatic intolerance but not reduction in cerebral blood flow velocity after bed rest. American Journal of Physiology – Heart and Circulatory Physiology 2012 Vol. 302 no. 2.
Shizue Masuki , John H. Eisenach , William G. Schrage , Christopher P. Johnson , Niki M. Dietz , Brad W. Wilkins , Paola Sandroni , Phillip A. Low , Michael J. Joyner. Reduced stroke volume during exercise in postural tachycardia syndrome. Journal of Applied Physiology 2007 Vol. 103 no. 4, 1128-1135.