Reduced central blood volume and cardiac output and increased vascular resistance during static handgrip exercise in postural tachycardia syndrome

Abstract

Postural tachycardia syndrome (POTS) is characterized by exercise intolerance and sympathoactivation. To examine whether abnormal cardiac output and central blood volume changes occur during exercise in POTS, we studied 29 patients with POTS (17-29 yr) and 12 healthy subjects (18-27 yr) using impedance and venous occlusion plethysmography to assess regional blood volumes and flows during supine static handgrip to evoke the exercise pressor reflex. POTS was subgrouped into normal and low-flow groups based on calf blood flow. We examined autonomic effects with variability techniques. During handgrip, systolic blood pressure increased from 112 ± 4 to 139 ± 9 mmHg in control, from 119 ± 6 to 143 ± 9 in normal-flow POTS, but only from 117 ± 4 to 128 ± 6 in low-flow POTS. Heart rate increased from 63 ± 6 to 82 ± 4 beats/min in control, 76 ± 3 to 92 ± 6 beats/min in normal-flow POTS, and 88 ± 4 to 100 ± 6 beats/min in low-flow POTS. Heart rate variability and coherence markedly decreased in low-flow POTS, indicating uncoupling of baroreflex heart rate regulation. The increase in central blood volume with handgrip was absent in low-flow POTS and blunted in normal-flow POTS associated with abnormal splanchnic emptying. Cardiac output increased in control, was unchanged in lowflow POTS, and was attenuated in normal-flow POTS. Total peripheral resistance was increased compared with control in all POTS. The exercise pressor reflex was attenuated in low-flow POTS. While increased cardiac output and central blood volume characterizes controls, increased peripheral resistance with blunted or eliminated in central blood volume increments characterizes POTS and may contribute to exercise intolerance. Keywords orthostatic intolerance; mechanoreflex; metaboreflex; regional blood volume; exercise intolerance Chronic orthostatic intolerance is identified with the postural tachycardia syndrome (POTS) (10). Reduced exercise tolerance is frequently found in POTS (22). On the one hand, it could be argued that exercise intolerance in POTS is directly related to limitations of venous HHS Public Access Author manuscriptAm J Physiol Heart Circ Physiol. Author manuscript; available in PMC 2015 July 22. Author Manuscript Author ManuscriptAuthor Manuscript Author Manuscript return that occur in most POTS patients (44,61); this is consistent with data showing reduced cardiac output in many POTS patients (16). On the other hand, mechanisms originating in exercising muscle could contribute to effort impairment similar to what is seen in heart failure (52).Voluntary muscle contraction evokes central command (8) and the exercise pressor reflex (24,40,53), which depends on the stimulation of sensory afferents from exercising muscle (32). The exercise pressor reflex comprises the muscle mechanoreflex and muscle metaboreflex (25,54). These produce vagal withdrawal (13) and sympathetic activation (28) and together increase heart rate (HR) and blood pressure (BP) during exercise. The absence of peripheral vasoconstriction in canine models refl...

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

“…As a result, we found no association between the CO response during exercise and PEMI-induced changes in cardiac parasympathetic tone or BRS. In contrast to our earlier studies (22,65) and the present results, which showed an increase in BRS during PEMI, BRS has also reportedly attenuated during isometric handgrip exercise (32,58,59). This discrepancy might be attributable to differences in cardiac parasympathetic tone, since the reduction in BRS during exercise is linked to vagal withdrawal (45).…”

“…For correlations between ⌬LVR and ⌬MAP, ⌬CO, or ⌬TPR from the rest period to the exercise period, n ϭ 31 subjects; for all other correlations, n ϭ 35 subjects. *P Ͻ 0.05; †P Ͻ 0.01. ric exercise, as was suggested by measurements of renal and splanchnic vascular resistance and blood flow in both animals (8,12,63) and humans (39,42,(57)(58)(59)64). This might explain our observation that individual differences in LVR and CO responses were dissociated during exercise, despite a strong relationship between TPR and CO responses.…”

“…While the increase in arterial pressure during isometric exercise is a well-established response, the responses of the components mediating the pressor response, cardiac output (CO) and total peripheral vascular resistance (TPR), remain controversial. In fact, previous studies have shown that, during isometric handgrip exercise in healthy humans, the pressor response occurs via an increase in CO (16,32,[34][35][36]57), an increase in TPR (6, 17), or both of those (3,31,58,59,61,62). The variability of those findings leads one to speculate that there are considerable individual differences in the components of the pressor response to exercise, which is in stark contrast to the nearly invariant arterial pressure response.…”

“…grip exercise in healthy humans, the pressor response occurs via an increase in CO (16, 32, 34 -36, 57), an increase in TPR (6,17), or both of those (3,31,58,59,61,62). The variability of those findings leads one to speculate that there are considerable individual differences in the components of the pressor response to exercise, which is in stark contrast to the nearly invariant arterial pressure response.…”

Higher postural heart rate increments on head-up tilt correlate with younger age but not orthostatic symptoms

“…The pathophysiological mechanisms of orthostatic dysfunction in POTS have been well studied in younger populations, revealing specific roles for hypovolemia and peripheral and splanchnic blood flow and their relationship to the reninaldosterone system. The renin-aldosterone system in addition to angiotensin II levels has been strongly implicated in the pathophysiology of POTS (13,19,20). In younger patients with POTS, angiotensin II is increased, with an associated low distal lower extremity peripheral blood flow and hypovolemia (16).…”