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

Energy Intake of Men With Excess Weight During Normobaric Hypoxic Confinement

Due to the observations of weight loss at high altitude, normobaric hypoxia has been considered as a method of weight loss in obese individuals. With this regard, the aim of the present study was to determine the effect of hypoxia per se on metabolism in men with excess weight. Eight men living with excess weight (125.0 ± 17.7 kg; 30.5 ± 11.1 years, BMI: 37.6 ± 6.2 kg⋅m–2) participated in a randomized cross-over study comprising two 10-day confinements: normobaric (altitude of facility ≃ 940 m) normoxia (NORMOXIA; PIO2 = 133 mmHg), and normobaric hypoxia (HYPOXIA). The PIO2 in the latter was reduced from 105 (simulated altitude of 2,800 m) to 98 mmHg (simulated altitude of 3,400 m over 10 days. Before, and at the end of each confinement, participants completed a meal tolerance test (MTT). Resting energy expenditure (REE), circulating glucose, GLP-1, insulin, catecholamines, ghrelin, peptide-YY (PYY), leptin, gastro-intestinal blood flow, and appetite sensations were measured in fasted and postprandial states. Fasting REE increased after HYPOXIA (+358.0 ± 49.3 kcal⋅day–1, p = 0.03), but not after NORMOXIA (−33.1 ± 17.6 kcal⋅day–1). Postprandial REE was also significantly increased after HYPOXIA (p ≤ 0.05), as was the level of PYY. Furthermore, a tendency for decreased energy intake was concomitant with a significant body weight reduction after HYPOXIA (−0.7 ± 0.2 kg) compared to NORMOXIA (+1.0 ± 0.2 kg). The HYPOXIA trial increased the metabolic requirements, with a tendency toward decreased energy intake concomitant with increased PYY levels supporting the notion of a hypoxia-induced appetite inhibition, that could potentially lead to body weight reduction. The greater postprandial blood-glucose response following hypoxic confinement, suggests the potential development of insulin resistance

Distensibility in Arteries, Arterioles and Veins in Humans : Adaptation to Intermittent or Prolonged Change in Regional Intravascular Pressure

The present series of in vivo experiments in healthy subjects, were performed to investigate wall stiffness in peripheral vessels and how this modality adapts to iterative increments or sustained reductions in local intravascular pressures. Vascular stiffness was measured as changes in arterial and venous diameters, and in arterial flow, during graded increments in distending pressures in the vasculature of an arm or a lower leg. In addition, effects of intravascular pressure elevation on flow characteristics in veins, and on limb pain were elucidated. Arteries and veins were stiffer (i.e. pressure distension was less) in the lower leg than in the arm. The pressure-induced increase in arterial flow was substantially greater in the arm than in the lower leg, indicating a greater stiffness in the arterioles of the lower leg. Prolonged reduction of intravascular pressures in the lower body, induced by 5 wks of sustained horizontal bedrest (BR), decreased stiffness in the leg vasculature. BR increased pressure distension in the tibial artery threefold and in the tibial vein by 86 %. The pressure-induced increase in tibial artery flow was greater post bedrest, indicating reduced stiffness in the arterioles of the lower leg. Intermittent increases of intravascular pressures in one arm (pressure training; PT) during a 5-wk period decreased vascular stiffness. Pressure distension and pressure-induced flow in the brachial artery were reduced by about 50 % by PT. PT reduced pressure distension in arm veins by 30 to 50 %. High intravascular pressures changed venous flow to arterial-like pulsatile patterns, reflecting propagation of pulse waves from the arteries to the veins either via the capillary network or through arteriovenous anastomoses. High vascular pressures induced pain, which was aggravated by BR and attenuated by PT; the results suggest that the pain was predominantly caused by vascular overdistension. In conclusion, vascular wall stiffness constitutes a plastic modality that adapts to meet demands imposed by a change in the prevailing local intravascular pressure. That increased intravascular pressure leads to increased arteriolar wall stiffness supports the notion that local pressure load may serve as a “prime mover” in the development of vascular changes in hypertension.medicine doktorsexamen QC 2010110

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

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 &lt; 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 &lt; 0.01). Regardless of the breathing condition, the cold-induced elevation in mean arterial pressure was blunted in the second and third CWI (P &lt; 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.QC 20201130</p

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 increasingdistending pressures imposed in the vessels of each limb separately. The pressure-flux cutaneous responses were evaluatedbefore and after 5 wk of intermittent (40 min, 3 sessions per week) exposures to hypergravity (2.6–3.3 G; G training). Beforeand 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 &lt; 0.001). Finger blood flux dropped promptly (P &lt; 0.001), regardlessof the G training (P = 0.64). At 120-mmHg distending pressures, toe blood flux enhanced by 40% (P  0.05); the increasewas augmented after the G training (P = 0.01). At high distending pressures, toe blood flux dropped by 70% in both trials (P &lt;0.001). The present results demonstrate that circulatory autoregulation is more pronounced in glabrous skin than in nonglabrousskin, and in nonglabrous sites of the leg than in those of the arm. Repetitive high-sustained gravitoinertial stress does not modifythe pressure-flow relationship in the dependent skin vessels of the arm nor in the nonglabrous sites of the lower leg. Yet it maypartly inhibit the myogenic responsiveness of the toe’s glabrous skin.QC 20230630</p

Human cardiovascular adaptation to hypergravity.

Despite decades of experience from high-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 weeks 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 (ROR) and gradual (GOR) onset-rate G exposures, and cardiovascular responses were investigated during orthostatic provocation and vascular pressure-distension tests. The G training resulted in: (i) a 13% increase in relaxed ROR G tolerance (P &lt; 0.001), but no change in GOR G tolerance, (ii) increased pressure resistance in the arteries and arterioles of the legs (P &lt; 0.001), but not the arms, (iii) 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.QC 20220530</p

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.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

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⋅week1; 55 min⋅session1), during which the vasculature in one arm (EXP) was exposed intermittently (10-min exposure: 5-min pause) to increased trans-mural pressure (from +65 mmHg week-1 to +105 mmHg week-5). Before and after the regimen, finger cuta-neous 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 &gt;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. QC 20210720</p