University of Tasmania
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Haemodynamic responses to climate variations in healthy individuals and those with Type 2 diabetes mellitus

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posted on 2023-05-26, 01:49 authored by King, SGK
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 21vÄv¿C with 40% RH (control), 21vÄv¿C with 80% RH (humid), 12vÄv¿C with 40% RH (mild-cold), 36vÄv¿C with 40% RH (hot-dry), and 36vÄv¿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¬¨‚àûC 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.


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Copyright 2013 the author

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