Relation between resting spleen volume and apnea-induced increases in hemoglobin mass.

Introduction: Indigenous populations renowned for apneic diving have comparatively large spleen volumes. It has been proposed that a larger spleen translates to heightened apnea-induced splenic contraction and elevations in circulating hemoglobin mass (Hbmass), which, in theory, improves O2 carrying and/or CO2/pH buffering capacities. However, the relation between resting spleen volume and apnea- induced increases in Hbmass is unknown. Therefore, we tested the hypothesis that resting spleen volume is positively related to apnea-induced increases in total Hbmass. Methods: Fourteen healthy adults (six women; 29 ± 5 years) completed a two-minute carbon monoxide rebreathe procedure to measure pre-apneas Hbmass and blood volume. Spleen length, width, and thickness were measured pre-and post-five maximal apneas via ultrasound. Spleen volume was calculated via the Pilström equation (test-retest CV:2 ± 2%). Hemoglobin concentration ([Hb]; g/dl) and hematocrit (%) were measured pre- and post-apneas via capillary blood samples. Post-apneas Hbmass was estimated as post-apnea [Hb] x pre-apnea blood volume. Data are presented as mean ± SD. Results: Spleen volume decreased from pre- (247 ± 95 mL) to post- (200 ± 82 mL, p<0.01) apneas. [Hb] (14.6 ± 1.2 vs. 14.9 ± 1.2 g/dL, p<0.01), hematocrit (44 ± 3 vs. 45 ± 3%, p=0.04), and Hbmass (1025 ± 322 vs. 1046 ± 339 g, p=0.03) increased from pre- to post-apneas. Pre-apneas spleen volume was unrelated to post-apneas increases in Hbmass (r=-0.02, p=0.47). O2 (+28 ± 31 mL, p<0.01) and CO2 (+31 ± 35 mL, p<0.01) carrying capacities increased post-apneas. Conclusion: Larger spleen volume is not associated with a greater rise in apneas-induced increases in Hbmass in non-apnea-trained healthy adults.

Arterial oxygen desaturation during moderate hypoxia hinders sensorimotor performance.

INTRODUCTION: Moderate hypoxia may impact cognitive and sensorimotor performance prior to self-recognized impairments. Therefore, rapid and objective assessment tools to identify people at risk of impaired function during moderate hypoxia is needed. PURPOSE: Test the hypothesis that reductions in arterial oxygen saturation during moderate normobaric hypoxia (FiO2 = 14%) decreases gamified sensorimotor performance as measured by alterations of motor acuity. METHODS: Following three consecutive days of practice, thirty healthy adults (25 ± 5 y, 10 females) completed three bouts of the tablet-based gamified assessment (Statespace Labs, Inc.) of motor acuity at Baseline and 60 and 90 min after exposure to 13.8 ± 0.2% (hypoxia) and 20.1 ± 0.4% (normoxia) oxygen. The gamified assessment involved moving the tablet to aim and shoot at targets. Both conditions were completed on the same day and were administered in a single-blind, block randomized manner. Performance metrics included shot time and shot variability. Arterial oxyhemoglobin saturation estimated via forehead pulse oximetry (SpO2). Data were analyzed using linear mixed effects models. RESULTS: Compared to normoxia (99±1%), SpO2 was lower (p<0.001) at 60 (89±3%) and 90 (90±2%) min of hypoxia. Shot time was unaffected by decreases in SpO2 (0.012, p = 0.19). Nor was shot time affected by the interaction between SpO2 decrease and baseline performance (0.006, p = 0.46). Shot variability was greater (i.e., less precision, worse performance) with decreases in SpO2 (0.023, p = 0.02) and depended on the interaction between SpO2 decrease and baseline performance (0.029, p< 0.01). CONCLUSION: Decreases in SpO2 during moderate hypoxic exposure hinders sensorimotor performance via decreased motor acuity, i.e., greater variability (less precision) with no change in speed with differing decreases in SpO2. Thus, personnel who are exposed to moderate hypoxia and have greater decreases in SpO2 exhibit lower motor acuity, i.e., less precise movements even though decision time and movement speed are unaffected.

Facial fanning reduces heart rate but not tolerance to a simulated hemorrhagic challenge following exercise heat stress in young healthy humans.

We investigated whether reducing face skin temperature alters arterial blood pressure control and lower body negative pressure (LBNP) tolerance after exercise heat stress. Eight subjects (1 female; age, 27 ± 9 yr) exercised at ∼63% V̇o2max until core temperature had increased ∼1.5°C before undergoing LBNP to presyncope either with fanning to return face skin temperature to baseline (Δ-5°C, Fan trial) or without (No Fan trial). LBNP tolerance was quantified as cumulative stress index (CSI; mmHg·min). Before LBNP, whole body and face skin temperatures were elevated from baseline in both trials (38.0 ± 0.5°C and 36.3 ± 0.5°C, respectively, both P < 0.001). During LBNP, face skin temperature decreased in the Fan trial (30.9 ± 1.0°C) but was unchanged in the No Fan trial (36.1 ± 0.6°C, between trials P < 0.001). Mean arterial pressure was not different between trials (P = 0.237) and was similarly reduced at presyncope in both trials (from 82 ± 7 to 67 ± 8 mmHg, P < 0.001). During LBNP, heart rate was attenuated in the Fan trial at Mid LBNP (146 ± 16 vs. 158 ± 12 beats/min, P = 0.036) and at peak heart rate (158 ± 15 vs. 170 ± 15 beats/min; P < 0.001). LBNP tolerance was not different between trials (321 ± 248 vs. 328 ± 115 mmHg·min, P = 0.851). In exercise heat-stressed individuals, lowering face skin temperature to normothermic values suppressed heart rate thereby altering cardiovascular control during a simulated hemorrhagic challenge without reducing tolerance.

Gamified assessment of cognitive performance during moderate hypoxia.

INTRODUCTION: There is a need for rapid and objective assessment tools to identify people at risk of impaired cognitive function during hypoxia. PURPOSE: To test the hypotheses that performance on gamified cognitive tests examining the cognitive domains of executive function (Gridshot), working memory (Capacity) and spatial tracking (Multitracker) will be reduced during normobaric exposure to moderate normobaric hypoxia. METHODS: Following three consecutive days of practice, twenty-one healthy adults (27 ± 5 y, 9 females) completed five 1-min rounds of the tablet-based games Gridshot, Capacity, and Multitracker (Statespace Labs, Inc.) at Baseline and 60 and 90 min after exposure to 14.0 ± 0.2% (hypoxia) and 20.6 ± 0.3% (normoxia) oxygen. Both conditions were completed on the same day and were administered in a single-blind, block randomized manner. Arterial oxyhemoglobin saturation was estimated via forehead pulse oximetry (SpO2). Data were analyzed using ANCOVA with a covariate of Baseline. RESULTS: Compared to normoxia (98 ± 1%), SpO2 was lower (p < 0.001) at 60 (91 ± 3%) and 90 (91 ± 2%) min of hypoxia. No condition x time interaction effects were identified for any gamified cognitive tests (p ≥ 0.32). A main effect of condition was identified for Capacity (p = 0.05) and Multitracker (p = 0.04), but not Gridshot (p = 0.33). Post hoc analyses of the composite scores for both Capacity (p = 0.11) and Multitracker (p = 0.73) demonstrated no difference between conditions. CONCLUSION: Performance on gamified cognitive tests was not consistently affected by acute normobaric moderate hypoxic exposure.

Increased spleen volume provoked by temperate head-out-of-water immersion.

This study tested the hypotheses that 1) spleen volume increases during head-out-of-water immersion (HOWI) and returns to pre-HOWI values postdiuresis, and 2) the magnitude of apnea-induced spleen contraction increases when preapnea spleen volume is elevated. Spleen volume was measured before and after a set of five apneas in 12 healthy adults (28 ± 5 yr, 3 females) before, during (at 30 and 150 min), and 20 min after temperate temperature (36 ± 1°C) HOWI. At each time point, spleen length, width, and thickness were measured via ultrasound, and spleen volume was calculated using the Pilström equation. Compared with pre-HOWI (276 ± 88 mL), spleen volume was elevated at 30 (353 ± 94 mL, P < 0.01) and 150 (322 ± 87 mL, P < 0.01) min of HOWI but returned to pre-HOWI volume at post-HOWI (281 ± 90 mL, P = 0.58). Spleen volume decreased from pre- to postapnea bouts at each time point (P < 0.01). The magnitude of reduction in spleen volume from pre- to postapneas was elevated at 30 min of HOWI (-69 ± 24 mL) compared with pre-HOWI (-52 ± 20 mL, P = 0.04) but did not differ from pre-HOWI at 150 min of HOWI (-54 ± 16 mL, P = 0.99) and post-HOWI (-50 ± 18 mL, P = 0.87). Thus, spleen volume is increased throughout 180 min of HOWI, and whereas apnea-induced spleen contraction is augmented after 30 min of HOWI, the magnitude of spleen contraction is unaffected by HOWI thereafter.

High-intensity interval exercise reduces tolerance to a simulated haemorrhagic challenge in heat-stressed individuals.

NEW FINDINGS: What is the central question of this study? In heat-stressed individuals, does high-intensity interval exercise reduce tolerance to a simulated haemorrhagic challenge (lower body negative pressure, LBNP) relative to steady state exercise? What is the main finding and its importance? LBNP tolerance was lower in heat-stressed individuals following high-intensity interval exercise relative to steady state exercise. This was likely owing to the greater cardiovascular strain required to maintain arterial blood pressure prior to and early during LBNP following high-intensity interval exercise. These findings are of importance for individuals working in occupations in which combined heat stress and intense intermittent exercise are common and where the risk of haemorrhagic injury is increased. ABSTRACT: This study investigated whether tolerance to a simulated haemorrhagic challenge (lower body negative pressure, LBNP) was lower in heat-stressed individuals following high-intensity interval exercise relative to steady state exercise. Nine healthy participants completed two trials (Steady State and Interval). Participants cycled continuously at ∼38% (Steady State) or alternating between 10 and ∼88% (Interval) of the maximal power output whilst wearing a hot water perfused suit until core temperatures increased ∼1.4°C. Participants then underwent LBNP to pre-syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg min). Mean skin and core temperatures were elevated in both trials following exercise prior to LBNP (to 38.1 ± 0.6°C and 38.3 ± 0.2°C, respectively, both P < 0.001 relative to baseline) but not different between trials (both P > 0.05). In the Interval trial, heart rate was greater (122 ± 12 beats min-1 ) prior to LBNP, relative to the Steady State trial (107 ± 8 beats min-1 , P < 0.001) while mean arterial pressure was similarly reduced in both trials prior to LBNP (from baseline 89 ± 5 to 77 ± 7 mmHg; P = 0.001) and at pre-syncope (to 62 ± 9 mmHg, P < 0.001). CSI was lower in the Interval trial (280 ± 194 vs. 550 ± 234 mmHg min; P = 0.0085). In heat-stressed individuals, tolerance to a simulated haemorrhagic challenge is reduced following high-intensity interval exercise relative to steady state exercise.

Tolerance to Central Hypovolemia Is Greater Following Caffeinated Coffee Consumption in Habituated Users.

We investigated the influence of caffeinated coffee consumption on cardiovascular responses and tolerance to central hypovolemia in individuals habituated to caffeine. Thirteen participants completed three trials, consuming caffeinated coffee, decaffeinated coffee or water before exposure to central hypovolemia via lower body negative pressure (LBNP) to pre syncope. Tolerance to central hypovolemia was quantified as cumulative stress index (CSI: LBNP level multiplied by time; mmHg × min). Prior to the consumption of caffeinated coffee, decaffeinated coffee, and water, heart rate (HR: 62 ± 10, 63 ± 9 and 61 ± 8 BPM, respectively), stroke volume (SV: 103 ± 23, 103 ± 17 and 102 ± 18 mL/beat, respectively), and total peripheral resistance (TPR: 14.2 ± 3.0, 14.0 ± 3.0, and 14.3 ± 2.7 mmHg/L/min, respectively), were not different between trials (all P > 0.05). Mean arterial pressure (MAP) increased following consumption of all drinks (Post Drink) (Caffeinated coffee: from 86 ± 8 to 97 ± 7; Decaffeinated coffee: from 88 ± 10 to 94 ± 7; and Water: from 87 ± 10 to 96 ± 6 mmHg; all P = 0.0001) but was not different between trials (P = 0.247). During LBNP, HR increased (P = 0.000) while SV decreased (P = 0.000) relative to post drink values and TPR as unchanged (P = 0.109). HR, SV, and TPR were not different between trials (all P > 0.05). MAP decreased at pre syncope in all trials (60 ± 5, 60 ± 7, and 61 ± 6 mmHg; P < 0.001). LBNP tolerance was greater following caffeinated coffee (914 ± 309 mmHg × min) relative to decaffeinated coffee and water (723 ± 336 and 769 ± 337 mmHg × min, respectively, both P < 0.05). Tolerance to central hypovolemia was greater following consumption of caffeinated coffee in habituated users.