Academic literature on the topic 'Central aortic blood pressure, Pulse wave reflection, Augmentation Index'

Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 ± 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0°C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased ( P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 ± 3 vs. 15 ± 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: −1.4 ± 3.8 vs. 21.2 ± 3.0 and 19.9 ± 3.6%; PWV: 5.6 ± 0.2 vs. 6.5 ± 0.3 and 6.2 ± 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.

Introduction: Increasing arterial stiffness is a feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Multiple studies demonstrate divergence of carotid-femoral pulse wave velocity and augmentation index in persons with diabetes mellitus, though mechanisms responsible for this are unclear. Materials and methods: We tested the effect of acutely and independently increasing plasma glucose, plasma insulin, or both on hemodynamic function and markers of arterial stiffness (including carotid-femoral pulse wave velocity, augmentation index, forward and backward wave reflection amplitude, and wave reflection magnitude) in a four-arm, randomized study of healthy young adults. Results: Carotid-femoral pulse wave velocity increased only during hyperglycemic-hyperinsulinemia (+0.36 m/s; p = 0.032), while other markers of arterial stiffness did not change (all p > 0.05). Heart rate (+3.62 bpm; p = 0.009), mean arterial pressure (+4.14 mmHg; p = 0.033), central diastolic blood pressure (+4.16 mmHg; p = 0.038), and peripheral diastolic blood pressure (+4.09 mmHg; p = 0.044) also significantly increased during hyperglycemic-hyperinsulinemia. Conclusions: Hyperglycemic-hyperinsulinemia acutely increased cfPWV, heart rate, mean arterial pressure, and diastolic blood pressure in healthy humans, perhaps reflecting enhanced sympathetic tone. Whether repeated bouts of hyperglycemia with hyperinsulinemia contribute to chronically-enhanced arterial stiffness remains unknown.

The aims were to determine if childhood obesity is associated with increased central aortic blood pressure (BP) and to characterize haemodynamic and vascular changes associated with BP changes in obese children and adolescents by means of analyzing changes in cardiac output (stroke volume, SV), arterial stiffness (aortic pulse wave velocity, PWV), peripheral vascular resistances (PVR), and net and relative contributions of reflected waves to the aortic pulse wave amplitude. We included 117 subjects (mean/range age: 10 (5–15) years, 49 females), who were obese (OB) or had normal weight (NW). Peripheral and central aortic BP, PWV, and pulse wave-derived parameters (augmentation index, amplitude of forward and backward components) were measured with tonometry (SphygmoCor) and oscillometry (Mobil-O-Graph). With independence of the presence of dyslipidemia, hypertension, or sedentarism, the aortic systolic and pulse BP were higher in OB than in NW subjects. The increase in central BP could not be explained by the elevation in the relative contribution of reflections to the aortic pressure wave and higher PVR or by an augmented peripheral reflection coefficient. Instead, the rise in central BP could be explained by an increase in the amplitude of both incident and reflect wave components associated to augmented SV and/or PWV.

Mortality increases when acute coronary syndromes are complicated by stress-induced hyperglycemia. Early pulse wave reflection can augment central aortic systolic blood pressure and increase left ventricular strain. Altered pulse wave reflection may contribute to the increase in cardiac risk during acute hyperglycemia. Chronic ascorbic acid (AA) supplementation has recently been shown to reduce pulse wave reflection in diabetes. We investigated the in vivo effects of acute hyperglycemia, with and without AA pretreatment, on pulse wave reflection and arterial hemodynamics. Healthy male volunteers were studied. Peripheral blood pressure (BP) was measured at the brachial artery, and the SphygmoCor pulse wave analysis system was used to derive central BP, the aortic augmentation index (AIx; measure of systemic arterial stiffness), and the time to pulse wave refection ( Tr; measure of aortic distensibility) from noninvasively obtained radial artery pulse pressure (PP) waveforms. Hemodynamics were recorded at baseline and then every 30 min during a 120-min systemic hyperglycemic clamp (14 mmol/l). The subjects, studied on two separate occasions, were randomized in a double-blind, crossover manner to placebo or 2 g intravenous AA before the initiation of hyperglycemia. During hyperglycemia, AIx increased and Tr decreased. Hyperglycemia did not change peripheral PP but did magnify central aortic PP and diminished the normal physiological amplification of PP from the aorta to the periphery. Pulse wave reflection, as assessed from peripheral pulse wave analysis, is enhanced during acute hyperglycemia. Pretreatment with AA prevented the hyperglycemia-induced hemodynamic changes. By protecting hemodynamics during acute hyperglycemia, AA may have therapeutic use.

The augmentation index and central blood pressure increase with normal aging. Recently, cyclooxygenase (COX) inhibitors, commonly used for the treatment of pain, have been associated with transient increases in the risk of cardiovascular events. We examined the effects of the COX inhibitor indomethacin (Indo) on central arterial hemodynamics and wave reflection characteristics in young and old healthy adults. High-fidelity radial arterial pressure waveforms were measured noninvasively by applanation tonometry before (control) and after Indo treatment in young (25 ± 5 yr, 7 men and 6 women) and old (64 ± 6 yr, 5 men and 6 women) subjects. Aortic systolic (control: 115 ± 3 mmHg vs. Indo: 125 ± 5 mmHg, P < 0.05) and diastolic (control: 74 ± 2 mmHg vs. Indo: 79 ± 3 mmHg, P < 0.05) pressures were elevated after Indo treatment in older subjects, whereas only diastolic pressure was elevated in young subjects (control: 71 ± 2 mmHg vs. Indo: 76 ± 1 mmHg, P < 0.05). Mean arterial pressure increased in both young and old adults after Indo treatment ( P < 0.05). The aortic augmentation index and augmented pressure were elevated after Indo treatment in older subjects (control: 30 ± 5% vs. Indo 36 ± 6% and control 12 ± 1 mmHg vs. Indo: 18 ± 2 mmHg, respectively, P < 0.05), whereas pulse pressure amplification decreased (change: 8 ± 3%, P < 0.05). In addition, older subjects had a 61 ± 11% increase in wasted left ventricular energy after Indo treatment ( P < 0.05). In contrast, young subjects showed no significant changes in any of the variables of interest. Taken together, these results demonstrate that COX inhibition with Indo unfavorably increases central wave reflection and augments aortic pressure in old but not young subjects. Our results suggest that aging individuals have a limited ability to compensate for the acute hemodynamic changes caused by systemic COX inhibition.

Young African-American men have altered macrovascular and microvascular function. In this cross-sectional study, we tested the hypothesis that vascular dysfunction in young African-American men would contribute to greater central blood pressure (BP) compared with young white men. Fifty-five young (23 yr), healthy men (25 African-American and 30 white) underwent measures of vascular structure and function, including carotid artery intima-media thickness (IMT) and carotid artery β-stiffness via ultrasonography, aortic pulse wave velocity, aortic augmentation index (AIx), and wave reflection travel time (Tr) via radial artery tonometery and a generalized transfer function, and microvascular vasodilatory capacity of forearm resistance arteries with strain-gauge plethysmography. African-American men had similar brachial systolic BP (SBP) but greater aortic SBP ( P < 0.05) and carotid SBP ( P < 0.05). African-American men also had greater carotid IMT, greater carotid β-stiffness, greater aortic stiffness and AIx, reduced aortic Tr and reduced peak hyperemic, and total hyperemic forearm blood flow compared with white men ( P < 0.05). In conclusion, young African-American men have greater central BP, despite comparable brachial BP, compared with young white men. Diffuse macrovascular and microvascular dysfunction manifesting as carotid hypertrophy, increased stiffness of central elastic arteries, heightened resistance artery constriction/blunted resistance artery dilation, and greater arterial wave reflection are present at a young age in apparently healthy African-American men, and conventional brachial BP measurement does not reflect this vascular burden.

Arterial stiffness potently predicts mortality in dialysis patients. Pulse-wave analysis permits the non-invasive assessment of indices of arterial stiffness and the central pressure waveform by applanation tonometry. The aim of this study was to assess the reproducibility of pulse-wave analysis in patients with chronic renal failure. A total of 188 subjects (23 healthy controls, along with 71 pre-dialysis, 67 dialysis and 27 transplant patients) took part. Duplicate measurements were recorded of brachial blood pressure using the semi-automated Omron 705 device and of the radial artery pressure waveform using applanation tonometry. The central pressure aortic waveform was then obtained by application of a transfer function incorporated into the SphygmoCor software. Central aortic mean blood pressure (MBP), indices of arterial stiffness [augmentation index (AIx) and time to reflection (TR)] and the subendocardial viability ratio (SEVR) were analysed for intra-observer, inter-observer and long-term reproducibility using Bland-Altman plots. The mean (±S.D.) intra-observer difference was 0±4% for AIx, 0±20 ms for TR, 0±3 mmHg for aortic MBP and 0±18% for the SEVR. Inter-observer mean differences were 0±3% for AIx, 1±7ms for TR, 1±4mmHg for aortic MBP and 1±9% for the SEVR. For the long-term study, the mean differences were -1±9% for AIx, -2±13mmHg for aortic MBP, -2±12ms for TR and 1±29% for the SEVR. Pulse-wave analysis showed excellent reproducibility in all the studies, and is therefore suitable for use in all patients with chronic renal failure. Further prospective and interventional studies are now required to assess whether AIx and TR are important prognostic indices of cardiovascular events, and therefore relevant surrogate indices of arterial stiffness in this susceptible population.

Brachial artery pulse pressure is a predictor of (cardiovascular) morbidity, but its determinants in individuals with Type II diabetes and untreated mild hypertension have not been elucidated. We therefore cross-sectionally investigated determinants of brachial artery mean 24h pulse pressure in 60 individuals (40 males; age, mean±S.D., 57.8±7.5 years) with Type II diabetes [median diabetes duration (interquartile range), 6.3 (3.6-10.1) years] and untreated mild hypertension [sitting blood pressure >140/90mmHg and <190/120mmHg (mean of two consecutive auscultatory office measurements after 5min of rest)]. We measured (1) three potential determinants reflecting different aspects of central artery stiffness [the overall systemic arterial compliance, the aortic augmentation index and 1/(regional carotido-femoral transit time)], (2) structural and functional changes of the circulatory system often observed in Type II diabetes, and (3) diabetes-associated metabolic variables. After adjustment for age, gender and mean arterial pressure, brachial artery pulse pressure was associated with autonomic function [standardized regression coefficient (β), -0.27 (P = 0.01)], blood pressure decline during sleep [standardized β, -0.32 (P = 0.002)], fasting glucose concentration [standardized β, 0.26 (P = 0.01)], HbA1c concentration [standardized β, 0.27 (P = 0.003)] and diabetes duration [standardized β, 0.28 (P = 0.002)] in linear regression analyses. In a combined multivariate model, brachial artery pulse pressure was independently determined by gender [1 = male, 2 = female; standardized β, 0.24 (P = 0.01)], diabetes duration [standardized β, 0.18 (P = 0.03)], mean arterial pressure [standardized β, 0.32 (P = 0.002)], systemic arterial compliance [standardized β, -0.23 (P = 0.02)] and fasting glucose concentration [standardized β, 0.20 (P = 0.02)]. Aortic augmentation index and 1/(carotido-femoral transit time) were not independently associated with pulse pressure. In conclusion, in individuals with Type II diabetes and untreated mild hypertension, brachial artery pulse pressure is determined mainly by proximal aortic stiffness in a way which is not strongly influenced by peripheral pulse wave reflection. Approx. 60% of the variance in brachial artery pulse pressure could be explained by potentially modifiable determinants.

Endurance exercise is efficacious in reducing arterial stiffness. However, the effect of resistance training (RT) on arterial stiffening is controversial. High-intensity, high-volume RT has been shown to increase arterial stiffness in young adults. We tested the hypothesis that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume would not elicit increases in either central or peripheral arterial stiffness or alter aortic pressure wave reflection in young men and women. The RT group ( n = 24; 21 ± 1 years) performed two sets of 8–12 repetitions to volitional fatigue on seven exercise machines on 3 days/week for 12 weeks, whereas the control group ( n = 18; 22 ± 1 years) did not perform RT. Central and peripheral arterial pulse wave velocity (PWV), aortic pressure wave reflection (augmentation index; AIx), brachial flow–mediated dilation (FMD), and plasma levels of nitrate/nitrite (NOx) and norepinephrine (NE) were measured before and after RT. RT increased the one-repetition maximum for the chest press and the leg extension ( P < 0.001). RT also increased lean body mass ( P < 0.01) and reduced body fat (%; P < 0.01). However, RT did not affect carotid-radial, carotid-femoral, and femoral-distal PWV (8.4 ± 0.2 vs. 8.0 ± 0.2 m/sec; 6.5 ± 0.1 vs. 6.3 ± 0.2 m/sec; 9.5 ± 0.3 vs. 9.5 ± 0.3 m/sec, respectively) or AIx (2.5% ± 2.3% vs. 4.8% ± 1.8 %, respectively). Additionally, no changes were observed in brachial FMD, NOx, NE, or blood pressures. These results suggest that an RT protocol consisting of progressively higher intensity without concurrent increases in training volume does not increase central or peripheral arterial stiffness or alter aortic pressure wave characteristics in young subjects.

The α1-adrenoceptor agonist phenylephrine (PE) and Angiotensin II (Ang II) are both potent vasoconstrictors at peripheral resistance arteries. PE has pure vasoconstrictive properties. Ang II, additionally, modulates central nervous blood pressure (BP) control via sympathetic baroreflex resetting. However, it is unknown whether Ang II vs. PE mediated vasoconstriction at equipressor dose uniformly or specifically modifies arterial stiffness. We conducted a three-arm randomized placebo-controlled cross-over trial in 30 healthy volunteers (15 female) investigating the effects of Ang II compared to PE at equal systolic pressor dose on pulse wave velocity (PWV), pulse wave reflection (augmentation index normalized to heart rate 75/min, AIx) and non-invasive hemodynamics by Mobil-O-Graph™ and circulating core markers of endothelial (dys-)function. PE but not Ang II-mediated hypertension induced a strong reflex-decrease in cardiac output. Increases in PWV, AIx, total peripheral resistance and pulse pressure, in contrast, were stronger during PE compared to Ang II at equal mean aortic BP. This was accompanied by minute changes in circulating markers of endothelial function. Moreover, we observed differential hemodynamic changes after stopping either vasoactive infusion. Ang II- and PE-mediated BP increase specifically modifies arterial stiffness and hemodynamics with aftereffects lasting beyond mere vasoconstriction. This appears attributable in part to different interactions with central nervous BP control including modified baroreflex function.

Background Central aortic blood pressure has received in recent years more interest as a more accurate predictor of outcome than brachial artery blood pressure. Number of techniques exists to assess the aortic pressure. Objetive To compare the values of central systolic pressure and peripheral augmentation index in hypertensive patients calculated by the Omron and the SphygmoCor systems. Methods Eighty-four (84) hypertensive subjects (40 males and 44 females), mean aged 58 ± 12 years were examined at the Hypertension Unit at San Luca Hospital (Istituto Auxologico Italiano) Milan Italia. All 84 subjects were treated with antihypertensive therapy. Results Statistics Data were analyzed using Statistica software version 9.0 (StatSoft Tulsa, Oklahoma. Inc). Pearson product–moment correlation coefficient (r) was used to determine associations between variables. Bland–Altman plots were used to assess agreement between methods. Dependent t tests were used to compare means. 1) Comparison between central pressure values provided by Sphygmocor and by Omron. There was a good correlation between cSBPsphy and cSBPomr (r=0.76; r²=58, P=< 0.001), but with a mean difference of -16 ± 13 mmHg, indicating a systematic underestimation by Omron device. 2) Comparison between cSBPsphy and pSBP2omr values showed also a good correlation, r= 0.74; r²=55, P <0.001, with a mean difference of only -0.8 ± 13 mmHg, indicating a good mean agreement. 3) Peripheral augmentation index measured by both devices showed close correlation (r=0.66; r²= 43 P < 0.001) but a mean difference Sphy-Omr of 62 ± 19, indicating important overestimation by the Sphygmocor. Discussion When comparing the original pSBP2omr values with the cSBP calculated by SphygmoCor, the mean difference was only -0.8 ± 13 mmHg. Direct invasive measurements of aortic pressure must be developed for a better algorithm to convert pSBP2omr to cSBPomr. Peripheral augmentation index is calculated by the same formula in both devices, there was a good correlation between the values of pAIx calculated by each device (r=0.66; r²= 0.43, P=< 0.001), but a very poor agreement. In summary estimated cSBP provided by the Omron system good correlation and limited agreement with values obtained from the SphygmoCor system. Conversely cSBP with Sphygmocor showed good agreement with pSBP2 measured by OMRON. Further investigations should compare estimates of pSBP2 by the Omron system to direct measurements of aortic pressure by cardiac catheterisation. The results suggest that the Omron system has an accurate of pSBP2 which show strong correlations with those of the SphygmoCor device.

Background and aims Environmental cold and heat exposure are linked to increased cardiovascular (CV) morbidity and mortality. People with impaired vascular function and thermoregulation, such as individuals with type 2 diabetes mellitus (T2DM) are at higher risk of heat or cold-related illness. To date, very few studies on whole-body cold or heat exposure have included individuals with T2DM. Even fewer have used central haemodynamic indicators of CV risk such as aortic pulse wave velocity (PWV), which is a marker of aortic stiffness, or augmentation index (AIx), which signifies left ventricular (LV) load. Moreover, there are no data available of the effects of high humidity, with or without heat, on resting central hemodynamic measures in any population. The studies that comprise this thesis aimed to determine the effects of whole-body exposure to differing air temperature (cold and heat) and relative humidity (RH) on measures of central haemodynamics and arterial stiffness in resting healthy individuals, and those with T2DM. Methods Five climate trials were undertaken in two participant groups; a Healthy and a T2DM group. The Healthy group comprised 16 adults (10 men), aged 43±19 years, and the T2DM group included 14 participants with T2DM (8 men), aged 63 ± 7 years. Supine, resting measures included aortic and brachial PWV, aortic AIx, brachial and aortic blood pressures (BPs), and measures of aortic reservoir function including reservoir pressure (`P_(res`), excess pressure (`P_(ex)`), and timing of `P_(ex)`. The five climate conditions were 21˚C with 40% RH (control), 21˚C with 80% RH (humid), 12˚C with 40% RH (mild-cold), 36˚C with 40% RH (hot-dry), and 36˚C with 80% RH (hot-humid). Every participant in both groups completed all five climate trials on separate days, with a washout of at least 7 days between each trial. Time points for data collection were ambient baseline, then at 5 (T2DM group only), 10, 30, 60, and 90 minutes while in each climate condition. 300mL (Healthy group) and 250mL (T2DM group) of water was consumed following the 60 minute measures in each climate condition in every participant. For analysis and presentation of results, data were split into mild-cold vs. control, and heat and humidity vs. control results. Data from baseline to 60 minutes were used for main analyses, and data from 60 to 90 minutes for heat and humidity results were analysed separately in order to account for any possible effect of dehydration and rehydration in the hot conditions. Results Results indicate that in the Healthy group, a change from a comfortable ambient climate to a mild-cold climate, as commonly happens in day-to-day life, significantly increased augmentation pressure (AP; P = 0.01) and AIx (P = 0.01), and reduced time to `P_(ex)` (P = 0.01) compared to control, without significantly altering aortic PWV (P = 0.87). Conversely, in the T2DM group, mild-cold exposure significantly increased aortic PWV (P = 0.03) but elicited a smaller pressor response compared to that observed in healthy individuals; brachial and aortic systolic BPs, and mean BP increased within condition in mild-cold (all P < 0.05) in T2DM participants, but these measures did not change compared to control (all P > 0.24). In the heat and humidity trials, it was observed that humidity at 80% significantly reduced aortic PWV during heating at 36°C in both healthy individuals and those with T2DM (both groups P < 0.05); a result that was not apparent when each group was exposed to hot-dry conditions (each group P > 0.06). In healthy individuals, hot-humid conditions did not significantly change measures of LV load (mean BP and AIx both P > 0.05). However, in T2DM, mean BP was reduced similarly in all hot comparisons (all P < 0.005) and AIx was reduced by hot-humid (P = 0.03) but not hot-dry (P = 0.31) conditions. In the Healthy group, `P_(res)` was reduced only in hot-dry (P = 0.03) but not hothumid conditions. However, in the T2DM group `P_(res)` was reduced in all hot conditions (all P < 0.006). The only instance where `P_(ex)` was significantly affected during any climate trial was during humid-heating in T2DM participants, where `P_(ex)` was reduced (P < 0.05). Finally, the studies into heat and humidity demonstrated that compared to control, exposure to high humidity at room temperature (i.e. independently of heat) significantly reduced aortic systolic BP (P = 0.02), rate pressure product (P = 0.02) and aortic `P_(res)` (P = 0.03) in healthy individuals, and reduced AIx in people with T2DM (P = 0.04). Discussion and Conclusions The results from the mild-cold studies suggest that even a brief exposure to a mild-cold temperature can increase aortic stiffness (aortic PWV) in people with T2DM and increase haemodynamic stress and LV load (AP and AIx) in apparently healthy individuals. In healthy individuals, increased AP and AIx during mild-cold exposure were potentially the result of peripheral vasoconstriction causing reduced peripheral blood run-off and increased impedance to aortic outflow. This may create a transient situation in which aortic in-flow exceeds aortic out-flow volume for the duration of the cold exposure, and this imbalance may have increased AIx and altered timing of `P_(ex)` in this study. However, in a T2DM population, a greater aortic stiffness and smaller pressor response than observed in healthy individuals during cold exposure is potentially a normal response. This is because of the higher likelihood of autonomic dysfunction in individuals with T2DM which impairs normal vascular reactivity and pressor responses to cold exposure. Such acute increases in these indicators of CV risk during cold exposure may add to explanations of cold-associated morbidity and mortality in people with T2DM. The findings of the heat and humidity studies show that in healthy individuals, aortic PWV was reduced by humid-heat without affecting brachial or aortic systolic or mean BPs. In T2DM individuals, aortic PWV was similarly reduced by humid-heat, but pressor responses were more variable in the heat and humidity trials than were observed for healthy people. Reductions in aortic PWV in healthy individuals and those with T2DM during humid-heating are potentially due to the increased heat load which accompanies increasing humidity, which in turn may produce a passive relaxation of the elastic aorta. This reduction in aortic stiffness may occur via flow-mediated increases in shear stress which triggers release of nitric oxide and other endogenous vasodilators that decrease large artery stiffness, and can work independently of changes in BP. The more variable pressor responses observed in the T2DM group may be due to impaired vascular reactivity which accompanies T2DM and is due to the toxic effects of chronic hyperglycaemia. The T2DM heat and humidity data in this thesis are the first available that show `P_(ex)`, a measure of wave-related pressure and longitudinal wave reflections, was reduced only in response to whole-body humid-heat exposure in adults with T2DM. Aortic PWV is thought to be dependent on changes in mean BP, heart rate and AIx, and wave reflections. Given that in the T2DM group, mean BP was reduced and heart rates were increased similarly across all hot comparisons but aortic PWV was only reduced in hot-humid conditions, it is possible that the decreased aortic PWV in hot-humid conditions may be related to reduced wave motion, (i.e. `P_(ex)`), `P_(res)` and AIx in patients with T2DM. Findings from the heat and humidity studies in healthy individuals and those with T2DM suggest that high humidity, with and without heat, can reduce measures of aortic stiffness and LV load, which may be beneficial to the CV system. The lowering effect of high humidity on arterial stiffness and haemodynamics may have particular clinical relevance for reduction of CV risk in T2DM individuals. In conclusion, the results from this thesis show divergent haemodynamic responses between cooling and heating in people with T2DM and healthy individuals. During cooling, some haemodynamic responses to mild-cold were exaggerated in T2DM (i.e. increased aortic stiffness), and some were attenuated (i.e. pressor responses) compared to responses of healthy individuals. Conversely, during humid-heating, people with T2DM had greater pressor reductions yet similar magnitude reductions in aortic stiffness compared to healthy individuals. Results of this thesis highlight the similarities and differences between responses of healthy individuals and people with T2DM during sudden climate changes. The findings demonstrate that cold exposure is potentially detrimental to haemodynamic function, while short-term humid-heating is potentially beneficial to haemodynamic function in healthy individuals, but more particularly in individuals with T2DM.