Repetitive high-sustained gravitoinertial stress does not modulate pressure responsiveness to peripheral sympathetic stimulation.

PURPOSE: We evaluated the hypothesis that repetitive gravitoinertial stress would augment the arterial-pressure response to peripheral sympathetic stimulation. METHODS: Before and after a 5-weeks G-training regimen conducted in a human-use centrifuge, twenty healthy men performed a hand cold-pressor test, and nine of them also a foot cold-pressor test (4 min; 4 °C water). Arterial pressures and total peripheral resistance were monitored. RESULTS: The cold-induced elevation (P ≤ 0.002) in arterial pressures and total peripheral resistance did not vary between testing periods, either in the hand [mean arterial pressure: Before = + 16% vs. After = + 17% and total peripheral resistance: Before = + 13% vs. After = + 15%], or in the foot [mean arterial pressure: Before = + 19% vs. After = + 21% and total peripheral resistance: Before = + 16% vs. After = + 16%] cold-pressor tests (P > 0.05). CONCLUSION: Present results demonstrate that 5 weeks of prolonged iterative exposure to hypergravity does not alter the responsiveness of sympathetically mediated circulatory reflexes.

In vivo pressure-flow relation of human cutaneous vessels following prolonged iterative exposures to hypergravity.

The study examined intra- and interlimb variations in cutaneous vessel responsiveness to acute and repeated transmural pressure elevations. In 11 healthy men, red blood cell flux was assessed via laser-Doppler flowmetry on both glabrous and nonglabrous skin regions of an arm (finger and forearm) and leg (toe and lower leg), across a wide range of stepwise increasing distending pressures imposed in the vessels of each limb separately. The pressure-flux cutaneous responses were evaluated before and after 5 wk of intermittent (40 min, 3 sessions per week) exposures to hypergravity (∼2.6-3.3 G; G training). Before and after G training, forearm and lower leg blood flux were relatively stable up to ∼210 and ∼240 mmHg distending pressures, respectively; and then they increased two- to threefold (P < 0.001). Finger blood flux dropped promptly (P < 0.001), regardless of the G training (P = 0.64). At ≤120-mmHg distending pressures, toe blood flux enhanced by ∼40% (P ≤ 0.05); the increase was augmented after the G training (P = 0.01). At high distending pressures, toe blood flux dropped by ∼70% in both trials (P < 0.001). The present results demonstrate that circulatory autoregulation is more pronounced in glabrous skin than in nonglabrous skin, and in nonglabrous sites of the leg than in those of the arm. Repetitive high-sustained gravitoinertial stress does not modify the pressure-flow relationship in the dependent skin vessels of the arm nor in the nonglabrous sites of the lower leg. Yet it may partly inhibit the myogenic responsiveness of the toe's glabrous skin.

Acral skin vasoreactivity and thermosensitivity to hand cooling following 5 days of intermittent whole body cold exposure.

We sought to examine whether short-term, whole body cold acclimation would modulate finger vasoreactivity and thermosensitivity to localized cooling. Fourteen men were equally assigned to either the experimental (CA) or the control (CON) group. The CA group was immersed to the chest in 14°C water for ≤120 min daily over a 5-day period while the skin temperature of the right-hand fingers was clamped at ∼35.5°C. The CON group was instructed to avoid any cold exposure during this period. Before and after the intervention, both groups performed, on two different consecutive days, a local cold provocation trial consisting of a 30-min hand immersion in 8°C water while immersed to the chest once in 21°C (mild-hypothermic trial; 0.5°C fall in rectal temperature from individual preimmersion values) and on the other occasion in 35.5°C (normothermic trial). In the CA group, the cold-induced reduction in finger temperature was less (mild-hypothermic trial: P = 0.05; normothermic trial: P = 0.02), and the incidence of the cold-induced vasodilation episodes was greater (in normothermic trials: P = 0.04) in the post- than in the preacclimation trials. The right-hand thermal discomfort was also attenuated (mild-hypothermic trial: P = 0.04; normothermic trial: P = 0.01). The finger temperature responses of the CON group did not vary between testing periods. Our findings suggest that repetitive whole body exposure to severe cold within a week may attenuate finger vasoreactivity and thermosensitivity to localized cooling. These regional thermo-adaptions were ascribed to central neural habituation produced by the iterative, generalized cold stimulation.

Human cardiovascular adaptation to hypergravity.

Despite decades of experience from high-gravitoinertial (G) exposures in aircraft and centrifuges, information is scarce regarding primary cardiovascular adaptations to +Gz loads in relaxed humans. Thus, effects of G-training are typically evaluated after regimens that are confounded by concomitant use of anti-G straining maneuvers, anti-G suits, and pressure breathing. Accordingly, the aim was to evaluate cardiovascular adaptations to repeated +Gz exposures in the relaxed state. Eleven men underwent 5 wk of centrifuge G training, consisting of 15 × 40 min +Gz exposures at G levels close to their individual relaxed G-level tolerance. Before and after the training regimen, relaxed G-level tolerance was investigated during rapid onset-rate (ROR) and gradual onset-rate (GOR) G exposures, and cardiovascular responses were investigated during orthostatic provocation and vascular pressure-distension tests. The G training resulted in: 1) a 13% increase in relaxed ROR G tolerance (P < 0.001), but no change in GOR G tolerance, 2) increased pressure resistance in the arteries and arterioles of the legs (P < 0.001), but not the arms, and 3) a reduced initial drop in arterial pressure upon ROR high G, but no change in arterial pressure under basal resting conditions or during GOR G loading, or orthostatic provocation. The results suggest +Gz adaptation via enhanced pressure resistance in dependent arteries/arterioles. Presumably, this reflects local adaptations to high transmural pressures, resulting from the +Gz-induced exaggeration of the intravascular hydrostatic pressure gradients.

Cognitive performance, fatigue, emotional, and physiological strains in simulated long-duration flight missions.

Pilots in long-duration flight missions in single-seat aircraft may be affected by fatigue. This study determined associations between cognitive performance, emotions and physiological activation and deactivation - measured by heart rate variability (HRV) - in a simulated 11-h flight mission in the 39 Gripen aircraft. Twelve participants volunteered for the study. Perceived fatigue was measured by the Samn-Perelli Fatigue Index (SPFI). Cognitive performance was measured by non-executive and executive tasks. Emotions were assessed by the Circumplex Affect Space instrument. HRV was considered in relation to the cognitive tasks in four time points - Hours 3, 5, 7, 9 - and their associations with emotional ratings. Results indicated a decrease in performance in the non-executive task after approximately 7 h. This result was correlated with self-reported measures of fatigue. HRV, assessed by indices of parasympathetic modulation, remained unchanged for both non-executive and executive tasks over time (p > .05 for all). Significant correlations were observed between emotions and HRV; with increased boredom, increased passiveness, decreased stimulation, and decreased activeness, HRV indicators increased (p < .05). This suggests that a low self-regulatory effort for maintaining performance in these conditions was prevalent and that pilots could adapt to some degree to the demands and fatigue of long-duration missions.

Differential responsiveness of glabrous and nonglabrous skin to local transmural pressure elevations: impact of 5 weeks of iterative local pressure loading.

We examined the in vivo pressure-flow relationship in human cutaneous vessels during acute and repeated elevations of local transmural pressure. In 10 healthy men, red blood cell flux was monitored simultaneously on the nonglabrous skin of the forearm and the glabrous skin of a finger during a vascular pressure provocation, wherein the blood vessels of an arm were exposed to a wide range of stepwise increasing distending pressures. Forearm skin blood flux was relatively stable at slight and moderate elevations of distending pressure, whereas it increased approximately three- to fourfold at the highest levels (P = 0.004). Finger blood flux, on the contrary, dropped promptly and consistently throughout the provocation (P < 0.001). Eight of the subjects repeated the provocation trial after a 5-wk pressure-training regimen, during which the vasculature in one arm was exposed intermittently (40 min, 3 times/wk) to increased transmural pressure (from +65 mmHg week 1 to +105 mmHg week 5). The training regimen diminished the pressure-induced increase in forearm blood flux by ∼34% (P = 0.02), whereas it inhibited the reduction in finger blood flux (P < 0.001) in response to slight and moderate distending pressure elevations. The present findings demonstrate that during local pressure perturbations, the cutaneous autoregulatory function is accentuated in glabrous compared with in the nonglabrous skin regions. Prolonged intermittent regional exposures to augmented intravascular pressure blunt the responsiveness of the glabrous skin but enhance arteriolar pressure resistance in the nonglabrous skin.

Finger constrictor and thermoperceptual responsiveness to localised cooling following 5 weeks of intermittent regional exposures to moderately augmented transmural vascular pressure.

PURPOSE: To examine the effects of prolonged intermittent exposures to moderately increased transmural pressure on finger vasoreactivity and thermoperception to localised cooling. METHODS: Eleven men completed a 5-week regimen (3 sessions·week-1; 55 min·session-1), during which the vasculature in one arm (EXP) was exposed intermittently (10-min exposure: 5-min pause) to increased transmural pressure (from +65 mmHg week-1 to +105 mmHg week-5). Before and after the regimen, finger cutaneous vascular conductance (CVC), temperature (Tavg), and thermoperception (thermal sensation, discomfort and pain) were monitored during a 30-min hand cold (8 °C water) provocation trial. The responses of the non-trained hand were examined during an additional cold trial. RESULTS: After the regimen, baseline finger CVC and Tavg were higher in both hands (p ≤ 0.01). During cooling, neither finger CVC nor Tavg were modified (p > 0.05). Yet the magnitude of the cold-induced drop of CVC was augmented in both hands, and to a similar extent (p ≤ 0.02). The regimen alleviated thermal pain in both hands (p ≤ 0.02); the sensation of coldness and thermal discomfort were attenuated mainly in the EXP hand (p = 0.02). CONCLUSIONS: Present findings indicate that iterative local exposures to augmented intravascular pressure do not alter finger vasoreactivity to localised cooling. The pressure training, however, might impair finger basal vasomotor tone, and aggravate the magnitude of constrictor responsiveness to cooling. The pressure training also elicits thermoperceptual desensitisation to noxious thermal stimulus. To large extent, these vascular and perceptual adjustments seem to be transferred to the cutaneous vasculature of the non-trained limb.

Hypoxia gradually augments metabolic and thermoperceptual responsiveness to repeated whole-body cold stress in humans.

NEW FINDINGS: What is the central question of this study? In male lowlanders, does hypoxia modulate thermoregulatory effector responses during repeated whole-body cold stress encountered in a single day? What is the main finding and its importance? A ∼10 h sustained exposure to hypoxia appears to mediate a gradual upregulation of endogenous heat production, preventing the progressive hypothermic response prompted by serial cold stimuli. Also, hypoxia progressively degrades mood, and compounds the perceived thermal discomfort, and sensations of fatigue and coldness. ABSTRACT: We examined whether hypoxia would modulate thermoeffector responses during repeated cold stress encountered in a single day. Eleven men completed two ∼10 h sessions, while breathing, in normobaria, either normoxia or hypoxia ( PO2 : 12 kPa). During each session, subjects underwent sequentially three 120 min immersions to the chest in 20°C water (CWI), interspersed by 120 min rewarming. In normoxia, the final drop in rectal temperature (Trec ) was greater in the third (∼1.2°C) than in the first and second (∼0.9°C) CWIs (P < 0.05). The first hypoxic CWI augmented the Trec fall (∼1.2°C; P = 0.002), but the drop in Trec did not vary between the three hypoxic CWIs (P = 0.99). In normoxia, the metabolic heat production ( Ṁ ) was greater during the first half of the third CWI than during the corresponding part of the first CWI (P = 0.02); yet the difference was blunted during the second half of the CWIs (P = 0.89). In hypoxia, by contrast, the increase in Ṁ was augmented by ∼25% throughout the third CWI (P < 0.01). Regardless of the breathing condition, the cold-induced elevation in mean arterial pressure was blunted in the second and third CWI (P < 0.05). Hypoxia aggravated the sensation of coldness (P = 0.05) and thermal discomfort (P = 0.04) during the second half of the third CWI. The present findings therefore demonstrate that prolonged hypoxia mediates, in a gradual manner, metabolic and thermoperceptual sensitization to repeated cold stress.

Interactions of mild hypothermia and hypoxia on finger vasoreactivity to local cold stress.

We examined the interactive effects of mild hypothermia and hypoxia on finger vasoreactivity to local cold stress. Eight male lowlanders performed, in a counterbalanced order, a normoxic and a hypoxic (partial pressure of oxygen: ~12 kPa) hand cold provocation (consisting of a 30-min immersion in 8°C water), while immersed to the chest either in 21°C [cold trials; 0.5°C fall in rectal temperature (Trec) from individual preimmersion values], or in 35.5°C water, or while exposed to 27°C air. The duration of the trials was kept constant in each breathing condition. Physiological (Trec, skin temperature, cutaneous vascular conductance, oxygen uptake) and perceptual (thermal sensation and comfort, local pain, affective valence) reactions were monitored continually. Hypoxia accelerated the drop in Trec by ~14 min (P = 0.06, d = 0.67). In the air-exposure trials, hypoxia did not alter finger perfusion during the local cooling, whereas it impaired the finger rewarming response following the cooling (P < 0.01). During the 35.5°C immersion, the finger vasomotor tone was enhanced, especially in hypoxia (P = 0.01). Mild hypothermia aggravated finger vasoconstriction instigated by local cooling (P < 0.01), but the response did not differ between the two breathing conditions (P > 0.05). Hypoxia tended to attenuate the sensation of coldness (P = 0.10, r = 0.40) and thermal discomfort (P = 0.09, r = 0.46) in the immersed hand. Both in normoxia and hypoxia, the whole body thermal state dictates the cutaneous vasomotor reactivity to localized cold stimulus.

PlanHab* : hypoxia does not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone.

KEY POINTS: Superposition of hypoxia on 21 day bed rest did not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone. A significant impairment of maximal oxidative performance was identified downstream of cardiovascular O2 delivery, involving both the intramuscular matching between O2 supply and utilization and mitochondrial respiration. These chronic adaptations appear to be relevant in terms of exposure to spaceflights and reduced gravity habitats (Moon or Mars), as characterized by low gravity and hypoxia, in patients with chronic diseases characterized by hypomobility/immobility and hypoxia, as well as in ageing. ABSTRACT: Skeletal muscle oxidative function was evaluated in 11 healthy males (mean ± SD age 27 ± 5 years) prior to (baseline data collection, BDC) and following a 21 day horizontal bed rest (BR), carried out in normoxia ( PIO2  = 133 mmHg; N-BR) and hypoxia ( PIO2  = 90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement ( PIO2  = 90 mmHg; H-AMB) were also assessed. Pulmonary O2 uptake ( V̇O2 ), vastus lateralis fractional O2 extraction (changes in deoxygenated haemoglobin + myoglobin concentration, Δ[deoxy(Hb + Mb)]; near-infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one-leg knee-extension exercise (reduced constraints to cardiovascular O2 delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibres. V̇O2peak decreased (P < 0.05) after N-BR (0.98 ± 0.13 L min-1 ) and H-BR (0.96 ± 0.17 L min-1 ) vs. BDC (1.05 ± 0.14 L min-1 ). In the presence of a decreased (by ∼6-8%) thigh muscle volume, V̇O2peak normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)]peak decreased (P < 0.05) after N-BR (65 ± 13% of limb ischaemia) and H-BR (62 ± 12%) vs. BDC (73 ± 13%). H-AMB did not alter V̇O2peak or Δ[deoxy(Hb + Mb)]peak . An overshoot of Δ[deoxy(Hb + Mb)] was evident during the first minute of unloaded exercise after N-BR and H-BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP-stimulated mitochondrial respiration decreased (P < 0.05) after all interventions vs. control. In 21 day N-BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O2 delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O2 supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.

Effects of training with flow restriction on the exercise pressor reflex.

PURPOSE: We hypothesized that 5 weeks of endurance training with blood flow restriction (R-training), providing relative ischemia and stimulation of the muscle chemoreflex, would decrease the exercise pressor reflex (EPR) when compared to training with the same workload in a free-flow condition (NR-training). METHODS: 10 subjects performed one-leg knee-extension training four times a week during a 5-week period. Both legs were trained with identical workload, with one leg being trained during flow-restriction induced by lower body positive pressure. The EPR was assessed by measuring the increase in heart rate (HR) and mean arterial pressure (MAP) during an isometric knee extension of 35% of max torque for 90 s, this was done before (C), and after training in each leg (R and NR, respectively). RESULTS: At the end of isometric contraction, the increase in mean AP (MAP) in the NR-trained leg and in the control condition were 41 ± 4 and 38 ± 4 mmHg, respectively, whereas the increase in the R-trained leg was 30 ± 4 mmHg (p < 0.05 R vs C and NR), corresponding to a decrease of about 25%. A similar patter was observed with respect to responses in HR, where the increase was 28 ± 3 and 28 ± 3 bpm in the NR and C, and 22 ± 4 in the R condition (p < 0.05 R vs C and NR). CONCLUSIONS: Peripheral metabolic changes induced by relative ischemia are important in modifying the EPR in response to exercise training.

In Shackleton's trails: Central and local thermoadaptive modifications to cold and hypoxia after a man-hauling expedition on the Antarctic Plateau.

Cold and hypoxia constitute the main environmental stressors encountered on the Antarctic Plateau. Hence, we examined whether central and/or peripheral acclimatisation to the combined stressors of cold and hypoxia would be developed in four men following an 11-day man-hauling expedition on this polar region. Before and after the journey, participants performed a static whole-body immersion in 21 °C water, during which they were breathing a hypoxic gas (partial pressure of inspired O2: ~97 mmHg). To evaluate their local responses to cold, participants also immersed the hand into 8 °C water for 30 min, while they were whole-body immersed and mildly hypothermic [i.e. 0.5 °C fall in rectal temperature (Trec) from individual pre-immersion values]. Trec and skin temperature (Tsk), skin blood flux, and oxygen uptake (reflecting shivering thermogenesis) were monitored throughout. The polar expedition accelerated by ~14 min the drop in Trec [final mean (95% confidence interval) changes in Trec: Before = -0.94 (0.15) °C, After: - 1.17 (0.23) °C]. The shivering onset threshold [Before: 19 (22) min, After: 25 (19) min] and gain [Before: - 4.19 (3.95) mL min-1 kg-1, After: - 1.70 (1.21) mL min-1 kg-1] were suppressed by the expedition. Tsk did not differ between trials. The development of a greater post-expedition hypothermic state did not compromise finger circulation during the hand-cooling phase. Present findings indicate therefore that a hypothermic pattern of cold acclimatisation, as investigated in hypoxia, was developed following a short-term expedition on the South Polar Plateau; an adaptive response that is characterised mainly by suppressed shivering thermogenesis, and partly by blunted cutaneous vasoconstriction.

No association between hand and foot temperature responses during local cold stress and rewarming.

PURPOSE: The purpose was to examine whether associations exist between temperature responses in the fingers vs. toes and hand vs. foot during local cold-water immersion and rewarming phases. METHODS: Seventy healthy subjects (58 males, 12 females) immersed their right hand or right foot, respectively, in 8 °C water for 30 min (CWI phase), followed by a 15-min spontaneous rewarming (RW) in 25 °C air temperature. RESULTS: Temperature was lower in the toes than the fingers during the baseline phase (27.8 ± 3.0 vs. 33.9 ± 2.5 °C, p < 0.001), parts of the CWI phase (min 20-30: 8.8 ± 0.7 vs. 9.7 ± 1.4 °C, p < 0.001), and during the RW phase (peak temperature: 22.5 ± 5.1 vs. 32.7 ± 3.6 °C, p < 0.001). Cold-induced vasodilatation (CIVD) was more common in the fingers than in the toes (p < 0.001). Within the first 10 min of CWI, 61% of the subjects exhibited a CIVD response in the fingers, while only 6% of the subjects had a CIVD response in the toes. There was a large variability of temperature responses both within and between extremities, and there was a weak correlation between finger- and toe temperature both during the CWI (r = 0.21, p = 0.08) and the RW phases (r = 0.26, p = 0.03). CONCLUSIONS: Results suggest that there is generally a lower temperature in the toes than the fingers after a short time of local cold exposure and that the thermal responses of the fingers/hands are not readily transferable to the toes/foot.

PlanHab: hypoxia exaggerates the bed-rest-induced reduction in peak oxygen uptake during upright cycle ergometry.

The study examined the effects of hypoxia and horizontal bed rest, separately and in combination, on peak oxygen uptake (V̇o2 peak) during upright cycle ergometry. Ten male lowlanders underwent three 21-day confinement periods in a counterbalanced order: 1) normoxic bed rest [NBR; partial pressure of inspired O2 (PiO2 ) = 133.1 ± 0.3 mmHg]; 2) hypoxic bed rest (HBR; PiO2 = 90.0 ± 0.4 mmHg), and 3) hypoxic ambulation (HAMB; PiO2 = 90.0 ± 0.4 mmHg). Before and after each confinement, subjects performed two incremental-load trials to exhaustion, while inspiring either room air (AIR), or a hypoxic gas (HYPO; PiO2 = 90.0 ± 0.4 mmHg). Changes in regional oxygenation of the vastus lateralis muscle and the frontal cerebral cortex were monitored with near-infrared spectroscopy. Cardiac output (CO) was recorded using a bioimpedance method. The AIR V̇o2 peak was decreased by both HBR (∼13.5%; P ≤ 0.001) and NBR (∼8.6%; P ≤ 0.001), with greater drop after HBR (P = 0.01). The HYPO V̇o2 peak was also reduced by HBR (-9.7%; P ≤ 0.001) and NBR (-6.1%; P ≤ 0.001). Peak CO was lower after both bed-rest interventions, and especially after HBR (HBR: ∼13%, NBR: ∼7%; P ≤ 0.05). Exercise-induced alterations in muscle and cerebral oxygenation were blunted in a similar manner after both bed-rest confinements. No changes were observed in HAMB. Hence, the bed-rest-induced decrease in V̇o2 peak was exaggerated by hypoxia, most likely due to a reduction in convective O2 transport, as indicated by the lower peak values of CO.

The arterial baroreflex and inherent G tolerance.

PURPOSE: High G tolerance is based on the capacity to maintain a sufficient level of arterial pressure (AP) during G load; therefore, we hypothesized that subjects with high G tolerance (H group) would have stronger arterial baroreflex responses compared to subjects with low G tolerance (L group). The carotid baroreflex was evaluated using the neck pressure method (NP), which assesses open-loop responses. METHODS: The carotid baroreflex was tested in 16 subjects, n = 8 in the H and L group, respectively, in the supine and upright posture. Heart rate and AP were measured. RESULTS: There were no differences between groups in the maximum slopes of the carotid baroreflex curves. However, the H group had a larger systolic and mean AP (SAP, MAP) increase to the initial hypotensive stimuli of the NP sequence in the upright position compared to the L group, 7.5 ± 6.6 vs 2.0 ± 2.4 and 4.1 ± 3.4 vs 1.1 ± 1.1 mmHg for SAP and MAP, respectively. Furthermore, the L group exhibited an increased latency between stimuli and response in AP in the upright compared to supine position, 4.1 ± 1.0 vs 3.1 ± 0.9 and 4.7 ± 1.1 vs 3.6 ± 0.9 s, for SAP and MAP. No differences in chronotropic responses were observed between the groups. CONCLUSIONS: It is concluded that the capacity for reflexive vasoconstriction and maintained speed of the vascular baroreflex during orthostatic stress are coupled to a higher relaxed GOR tolerance.

Body height and arterial pressure in seated and supine young males during +2 G centrifugation.

It is known that arterial pressure correlates positively with body height in males, and it has been suggested that this is due to the increasing vertical hydrostatic gradient from the heart to the carotid baroreceptors. Therefore, we tested the hypothesis that a higher gravito-inertial stress induced by the use of a human centrifuge would increase mean arterial pressure (MAP) more in tall than in short males in the seated position. In short (162-171 cm; n = 8) and tall (194-203 cm; n = 10) healthy males (18-41 yr), brachial arterial pressure, heart rate (HR), and cardiac output were measured during +2G centrifugation, while they were seated upright with the legs kept horizontal (+2Gz). In a separate experiment, the same measurements were done with the subjects supine (+2Gx). During +2Gz MAP increased in the short (22 ± 2 mmHg, P < 0.0001) and tall (23 ± 2 mmHg, P < 0.0001) males, with no significant difference between the groups. HR increased more (P < 0.05) in the tall than in the short group (14 ± 2 vs. 7 ± 2 bpm). Stroke volume (SV) decreased in the short group (26 ± 4 ml, P = 0.001) and more so in the tall group (39 ± 5 ml, P < 0.0001; short vs. tall, P = 0.047). During +2Gx, systolic arterial pressure increased (P < 0.001) and SV (P = 0.012) decreased in the tall group only. In conclusion, during +2Gz, MAP increased in both short and tall males, with no difference between the groups. However, in the tall group, HR increased more during +2Gz, which could be caused by a larger hydrostatic pressure gradient from heart to head, leading to greater inhibition of the carotid baroreceptors.

G tolerance and the vasoconstrictor reserve.

PURPOSE: Because leg arterial stiffness is higher in subjects with high G tolerance, we hypothesized that subjects with high G tolerance would have larger capacity for vasoconstriction. METHODS: Sixteen subjects, eight with high and eight with low G tolerance (H and L group, respectively), were exposed to a cold pressor test (CPT) in supine and upright posture. Heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were measured, and total peripheral resistance (TPR) and stroke volume (SV) were calculated. RESULTS: In the supine position, CPT increased TPR more in the H group; 31 ± 18% than in the L group; 11 ± 7% (p < 0.05). The L group had larger increases in CO than the H group; 17 ± 16 vs. 3.4 ± 7% (p = 0.06). In the upright position, the H group had a larger MAP response to CPT than the L group; 26 ± 14 vs. 14 ± 7% (p = 0.06). The H group, but not the L group, had significant increases in TPR whereas the L group had significant increases in CO and SV. CONCLUSIONS: In response to CPT, the high G tolerance group elevated MAP by increasing TPR, whereas the low G tolerance group showed a dependency on increased CO. The H group seemed to have a larger vasoconstrictor reserve. The results further suggest that vasoconstrictor reserve capacity could constitute the link between the recent finding that indicates a relationship between G tolerance and arterial distensibility in the legs.

Blood pressure regulation V: in vivo mechanical properties of precapillary vessels as affected by long-term pressure loading and unloading.

Recent studies are reviewed, concerning the in vivo wall stiffness of arteries and arterioles in healthy humans, and how these properties adapt to iterative increments or sustained reductions in local intravascular pressure. A novel technique was used, by which arterial and arteriolar stiffness was determined as changes in arterial diameter and flow, respectively, during graded increments in distending pressure in the blood vessels of an arm or a leg. Pressure-induced increases in diameter and flow were smaller in the lower leg than in the arm, indicating greater stiffness in the arteries/arterioles of the leg. A 5-week period of intermittent intravascular pressure elevations in one arm reduced pressure distension and pressure-induced flow in the brachial artery by about 50%. Conversely, prolonged reduction of arterial/arteriolar pressure in the lower body by 5 weeks of sustained horizontal bedrest, induced threefold increases of the pressure-distension and pressure-flow responses in a tibial artery. Thus, the wall stiffness of arteries and arterioles are plastic properties that readily adapt to changes in the prevailing local intravascular pressure. The discussion concerns mechanisms underlying changes in local arterial/arteriolar stiffness as well as whether stiffness is altered by changes in myogenic tone and/or wall structure. As regards implications, regulation of local arterial/arteriolar stiffness may facilitate control of arterial pressure in erect posture and conditions of exaggerated intravascular pressure gradients. That increased intravascular pressure leads to increased arteriolar wall stiffness also supports the notion that local pressure loading may constitute a prime mover in the development of vascular changes in hypertension.

Effects of physical fitness on relaxed G-tolerance and the exercise pressor response.

Fighter pilots are commonly recommended strength training as a means of improving the tolerance to withstand high gravitoinertial (G) loads. Previous studies on the effect of short-term strength-training regimens on G-endurance show equivocal results, with a majority of the studies suggesting improved G-endurance. The mechanisms underlying such improvement are unknown. Presumably, any change in G-tolerance induced by physical training habits should be manifest following long-term training. We also reasoned that during repeated straining maneuvers--as during certain G-endurance protocols--the relaxed G-tolerance and the exercise pressure response may play a significant role in maintaining adequate arterial pressure, and hence that different training modalities might alter G-endurance, by altering the exercise pressor response. Three groups of males were studied, long-term (>6 months) endurance-trained (E; n = 17), strength-trained (S; n = 16) and untrained (U; n = 17) individuals. The pressor response was studied during sustained (40 s) isometric knee extensions at 50 % of the maximal contraction level. Relaxed gradual onset-rate G-tolerance was determined. G-tolerance was similar in the E (4.6 ± 0.5 G), S (4.9 ± 0.8 G) and U (4.6 ± 0.8 G) groups. The mean arterial pressure increase during isometric exercise was higher in the S (36 ± 7 mmHg = mean ± SD) and U (35 ± 16 mmHg) groups than in the E group (28 ± 8 mmHg). The results suggest that relaxed G-tolerance is unaffected by physical training habits, and that the training modality affects the magnitude of the exercise pressor response. However, it seems that the response is blunted by endurance training rather than enhanced by strength training.

G tolerance vis-à-vis pressure-distension and pressure-flow relationships of leg arteries.

During increased gravitoinertial (G) load in the head-to-foot direction, pressures in dependent vascular beds are commonly raised to levels capable of distending precapillary vessels, which, in turn, may reduce arterial pressure, and hence compromise the capacity to withstand G load (G tolerance). We hypothesized that distensibility in precapillary leg vessels would be lower in a group of subjects possessing high G tolerance (H; n = 7; relaxed G tolerance = 6.6 ± 0.8 G) than in a group with low G tolerance (L; n = 8; G tolerance = 3.9 ± 0.3 G). The groups were matched with regard to gender, age, weight, height, and resting arterial pressure. Arterial pressure-distension and pressure-flow experiments were performed with the subject supine in a pressure chamber with a lower leg protruding to the outside. Increased intravascular pressure in the blood vessels of the outside leg was accomplished by stepwise increasing chamber pressure to 240 mmHg. Diameter and flow in the posterior tibial artery were measured by ultrasonographic/Doppler techniques. Pressure-induced increments in arterial diameter and flow were more pronounced (p < 0.03) in the L (14.1 ± 4.2% and 32 ± 21 ml/min respectively) than in the H (1.7 ± 5.0% and 1.6 ± 25 ml/min) group, and the pressure thresholds at which these increments commenced were lower (by 52 and 48 mmHg, respectively) in the L than in the H group (p < 0.04). Negative correlations were observed between G tolerance and the increments in diameter and flow (p < 0.02). Thus, the wall stiffness of precapillary leg vessels is greater in individuals with high relaxed G tolerance; whether a causal relationship exists remains to be established.