Sex-specific effect of blood O2 carrying capacity on orthostatic tolerance in older individuals

Blood oxygen (O2) carrying capacity is reduced with ageing and has been previously linked with the capacity to withstand the upright posture, i.e., orthostatic tolerance (OT). This study experimentally tested the hypothesis that a definite reduction in blood O2 carrying capacity via hemoglobin (Hb) manipulation differently affects the OT of older women and men as assessed by lower body negative pressure (LBNP). Secondary hemodynamic parameters were determined with transthoracic echocardiography throughout incremental LBNP levels for 1 hour or until presyncope in healthy older women and men (total n=26) matched by age (64±7 vs. 65±8 yr, P<0.618) and physical activity levels. Measurements were repeated within a week period after a 10 % reduction of blood O2 carrying capacity via carbon monoxide rebreathing and analyzed via two-way ANCOVA. In the assessment session, OT time was similar between women and men (53.5±6.1 vs. 56.4±6.0 min, P=0.238). Following a 10 % reduction of blood O2 carrying capacity, OT time was reduced in women compared with men (51.3±7.0 vs. 58.2±2.8 min, P=0.003). The effect of reduced O2 carrying capacity on OT time differed between sexes (mean difference (MD)=-5.30 min, P=0.010). Prior to presyncope. reduced O2 carrying capacity resulted in lower left ventricular end-diastolic volume (MD=-8.11 ml∙m -2, P=0.043) and stroke volume (MD=-8.04 ml∙m -2, 95 % CI=-14.36, -1.71, P=0.018) in women relative to men, even after adjusting for baseline variables. In conclusion, present results suggest that reduced blood O2 carrying capacity specifically impairs OT and its circulatory determinants in older women.

Remotely Supervised Home-Based Resistance Training and Orthostatic Tolerance in Young Physically Inactive Women During COVID-19

Introduction: Orthostatic intolerance (OI) is the inability of the cardiovascular system to adequately adjust to gravity upon standing, resulting in lightheadedness or syncope. OI can be characteristic of pathology (e.g. postural orthostatic tachycardia syndrome), which disproportionately affect women, and is compounded by inactivity. Thus, we tested the effects of remotely supervised home-based, 4-week resistance training (RT) program vs. control on the orthostatic stress response of previously inactive young females using the NASA Lean Test (NLT). Methods: Systolic (SBP) and diastolic (DBP) blood pressures, and heart rate (HR) were assessed during the NLT, pre- and post-training, along with fitness and body composition in females randomized to RT or control (n=7). Results: RT improved fitness (group*intervention, p=0.047) and fat-mass (-3.4±2.9 vs. +0.3±0.7Δlbs, p=0.037) over control. The NLT significantly altered SBP, DBP, and HR (all, p<0.01). For SBP, the interaction of group*intervention approached significance (p=0.071), lowering SBP in the RT group with the intervention. In DBP, the group*intervention was not significant (p=0.558). For HR, the group*intervention interaction approached significance (p=0.066). Conclusions: In the current study, short-term remotely-supervised RT using bands tended to decrease SBP and HR during orthostatic stress in young, otherwise healthy, previously inactive females, suggesting improved health but perhaps not orthostatic tolerance.

Abstract P204: Sinusoidal Galvanic Stimulation Improves Orthostatic Symptoms In Patients With Postural Tachycardia.

Postural Tachycardia Syndrome (POTS) is characterized by frequent orthostatic symptoms and excessive heart rate increase (>= 30 bpm) on standing in the absence of orthostatic hypotension for more than 6 months. We and others have described a vestibulo-sympathetic reflex that can be engaged by galvanic vestibular stimulation to modulate sympathetic activity (Biaggioni et al., 2000; Kaufmann et al., 2002; Monahan & Ray, 2002; Ray & Carter, 2003, Bent, Macefield et al. 2006). We hypothesize that habituation to sinusoidal galvanic vestibular stimulation will improve orthostatic tolerance. We studied 6 patients with POTS (30.5+/6.0 years, BMI 22.8+/-2.9 kg/m 2 ) in two sessions using sinusoidal galvanic vestibular stimulation (sGVS 0.025 Hz, 2mA) or sham (0.01 mA). Stimulation was applied near mastoid process for 30 min in semi-recumbent position before orthostatic challenge. Patient were upright for a maximum of 15 minutes after each stimulation. Orthostatic change in Vanderbilt Orthostatic Symptom Score (dVOSS), orthostatic heart rate increase (dHR) and blood pressure response were recorded. Non-parametric Wilcoxon test for paired measures with significance level p<0.05 was used. sGVS stimulation reduced overall orthostatic symptom score (dVOSS sham: 32.5+/-9.3 bpm vs dVOSS sGVS: 10.5+/-5.5, p=0.03) and tended to reduce orthostatic HR increase (dHR sham: 65.83+/-11.5 vs dHR sGVS: 46.5+/-10.7 bpm, p=0.06). Blood pressure and tilt time did not change. This pilot study suggests that habituation to sinusoidal vestibular could be used to improve orthostatic symptoms and orthostatic tolerance.

Abstract P192: Orthostatic Tolerance Before And After 60 Days Of Strict Head Down Tilt Bedrest With And Without Daily Artificial Gravity Training

Background: Orthostatic intolerance occurs after space flight, immobilization and in patients with autonomic diseases, so there is a need for more effective countermeasures. We hypothesized that daily artificial gravity elicited through short-arm centrifugation attenuates plasma volume loss and orthostatic intolerance following 60 days of HDTBR, which models cardiovascular responses to weightlessness. Methods: We studied 24 healthy persons (8 women, 33.4±9.3 yr, 24.3±2.1 kg/m2) exposed to 60d HDTBR. Subjects were assigned to 30 min/d continuous short arm centrifugation (cAG), 6x5 min short arm centrifugation (iAG), or a control group (ctr, no countermeasures). Head-up tilt testing (15 min of 80°) followed by incremental lower body negative pressure (-10 mmHg every 3 min) until presyncope was performed before and at the end of HDTBR. Plasma volume was measured (CO rebreathing) 12-2 days before and after 56d of HDTBR. Stroke volume was measured by cMRI. Norepinephrine, epinephrine, aldosterone, and renine plasma levels were measured before and after HDTBR. Results: Time to presyncope decreased in all groups following bedrest (ctr: 22:56 min pre and 9:35 min post, cAG 15:34 min pre and 10:11 min post; iAG 14:56 min pre and 10:00 min post, p<0.001). The significant interaction (p=0.025) between bedrest and intervention was explained by greater baseline orthostatic tolerance time in the ctr. AG Data was pooled analysis. The reduction in stroke volume (ctr, pre: 93±19 ml, HDTBR: 69±13 ml, AG, pre: 88±20 ml, HDTBR: 67±17 ml) and plasma volume was similar (ctr, pre: 4155±1085 ml, HDTBR: 3855±1087 ml, AG, pre: 4114±1250 ml, HDTBR: 3674± 1313 ml). Catechols and aldosterone did not change significantly during bedrest. The increase in renine was similar between groups (ctr pre: 18±12 mE/L, HDTBR: 21±8 mE/L, AG pre: 21±10 mE/L, HDTBR: 31±12 mE/L). Conclusions: 30 min daily AG didn’t prevent a reduction in orthostatic tolerance following 60d HDTBR. Whether numerically smaller reductions in orthostatic tolerance in the AG groups indicate efficacy or result from baseline differences can’t be ascertained. A stronger AG stimulus or combination with other countermeasures might be required to maintain orthostatic tolerance and to attenuate the volume reduction.

Post-exercise Body Cooling: Skin Blood Flow, Venous Pooling, and Orthostatic Intolerance

Athletes and certain occupations (e.g., military, firefighters) must navigate unique heat challenges as they perform physical tasks during prolonged heat stress, at times while wearing protective clothing that hinders heat dissipation. Such environments and activities elicit physiological adjustments that prioritize thermoregulatory skin perfusion at the expense of arterial blood pressure and may result in decreases in cerebral blood flow. High levels of skin blood flow combined with an upright body position augment venous pooling and transcapillary fluid shifts in the lower extremities. Combined with sweat-driven reductions in plasma volume, these cardiovascular alterations result in levels of cardiac output that do not meet requirements for brain blood flow, which can lead to orthostatic intolerance and occasionally syncope. Skin surface cooling countermeasures appear to be a promising means of improving orthostatic tolerance via autonomic mechanisms. Increases in transduction of sympathetic activity into vascular resistance, and an increased baroreflex set-point have been shown to be induced by surface cooling implemented after passive heating and other arterial pressure challenges. Considering the further contribution of exercise thermogenesis to orthostatic intolerance risk, our goal in this review is to provide an overview of post-exercise cooling strategies as they are capable of improving autonomic control of the circulation to optimize orthostatic tolerance. We aim to synthesize both basic and applied physiology knowledge available regarding real-world application of cooling strategies to reduce the likelihood of experiencing symptomatic orthostatic intolerance after exercise in the heat.

EFFECT OF 14-DAY HEAD UP BEDREST ON ORTHOSTATIC TOLERANCE IN HUMANS

Effect of 14-day head up bedrest (HUBR) on the human orthostatic tolerance studied with participation of 23 essentially healthy male subjects at the age of 18 to 35 years. HUBR with the head-end tilted up at +9.6º was to imitate physiological effects of the lunar gravity. Orthostatic tolerance was tested on the day prior to and immediately after HUBR completion with subjects tilted up to +70° for 20 min maximum. The parameters registered before, during and after the tilt test included blood pressure, ECG and heart rate. In comparison with the baseline testing, HUBR reduced the number of completed tests and increased the number (10 vs. 4) of tests terminated for the reason of precollapse (p < 0.05). The group mean time of OS test tolerance decreased by 3.8 minutes (p < 0.01) and time interval between the test onset and precollapse decreased by 4.7 minutes (p = 0.055). For the most part, orthostatic disorders following HUBR were described as a vasodepressor type hypotension collapse with high activity of the chronotropic function of the heart. Several cases of vagus-mediated HR slowing pointed to a sharp decline of the sympathetic nervous activity which is an important mechanism of hemodynamics regulation in changed postural conditions.