POTS versus deconditioning: the same or different?
- 360 Downloads
The 2007 Streeten Lecture focused on the idea that physical deconditioning plays a key role in the symptomology and pathophysiology of POTS. Parallels were drawn between the physiological responses to orthostatic stress seen in POTS patients and the physiological responses seen in “normal” humans after prolonged periods of bedrest, deconditioning, or space flight. Additionally, the idea that endurance exercise training might ameliorate some of these symptoms was also advanced. Finally, potential parallels between POTS, chronic fatigue syndrome, and fibromyalgia were also drawn and the potential role of exercise training as a “therapeutic intervention” in all three conditions was raised. The conceptual model for the lecture was that after some “initiating event” chronic deconditioning plays a significant role in the pathophysiology of these conditions, and these physiological changes in conjunction with “somatic hypervigilence” explain many of the complaints that this diverse group of patients have. Additionally, the idea that systematic endurance exercise training might be helpful was advanced, and data supportive of this idea was reviewed. The main conclusion is that the medical community must retain their empathy for patients with unusual conditions but at the same time send a firm but empowering message about physical activity. As always, we must also ask what do the ideas about physical activity and inactivity and the conditions mentioned above not explain?
Keywordsorthostatic stress exercise somatic hypervigilance
The author’s work on this topic was supported by NS 32352. The author would also like to thank his many collaborators over the years, and especially Dr. Phillip A. Low, who first suggested that he conduct physiological studies on patients with orthostatic intolerance.
- 6.Fu Q, Shook RP, Shibata S, Hastings JL, Okazaki K, Conner CL, Palmer MD, Levine BD (2007) Vasomotor sympathetic and hemodynamic responses during upright tilt in postural orthostatic tachycardia syndrome. FASEB J 21:A879.Google Scholar
- 7.Fu Q, Shook RP, Shibata S, Okazaki K, Hastings JL, Dorfman T, Conner CL, Palmer MD, Jacob G, Levine BD (2006) Cardiac size: a potential mechanism for gender differences in orthostatic intolerance and POTS? Clin Auton Res 16:321.Google Scholar
- 9.Levine BD (2006) The Grinch syndrome: a new name for orthostatic hypotension and syncope. In: 2006 ACSM annual meeting named lectures [DVD]. American College of Sports Medicine, Monterey, healthy learning.Google Scholar
- 10.Levine BD, Pawelczyk JA, Ertl AC, Cox JF, Zuckerman JH, Diedrich A, Biaggioni I, Ray CA, Smith ML, Iwase S, Saito M, Sugyama Y, Mano T, Zhang R, Iwasaki K, Lane LD, Buckey JC Jr, Cooke WH, Baisch FJ, Eckberg DL, Blomqvist CG (2002) Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight. J Physiol 538:331–340.PubMedCrossRefGoogle Scholar
- 21.Streeten DH, Scullard TF (1996) Excessive gravitational blood pooling caused by impaired venous tone is the predominant non-cardiac mechanism of orthostatic intolerance. Clin Sci (Lond) 90:277–285.Google Scholar
- 24.Winker R, Barth A, Bidmon D, Ponocny, Weber M, Mayr O, Robertson D, Diedrich A, Maier R, Pilger A, Haber P, Rudiger HW (2005) Endurance exercise training in orthostatic intolerance: a randomized, controlled trial. Hypertension 45:391–398.Google Scholar