An interventional study of Passive heating in Aging, sponsored by University of Portsmouth. Completed at 1 site in United Kingdom. Open to participants aged 55 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2025-08-06.
Sponsored by University of Portsmouth · Not applicable, Interventional, and Treatment
Aging is associated with a decline in cardiovascular health, cognitive function and losses in muscle strength, with half or more of those over age 65 suffering from two or more comorbidities (e.g., heart disease, type 2 diabetes). The worldwide population of older adults is growing rapidly, with one in six people expected to be over age 65 by 2050. This will place further financial burden from chronic diseases on already stressed healthcare systems. While studies show that frequent exercise is an effective way for older adults to maintain or improve cardiovascular and metabolic health, older individuals are less physically active and do not adhere well to exercise programs, often due to physical or medical limitations. Therefore, alternative methods for older adults to get the same health benefits as exercise require further exploration. Recent work has shown a single session of passive heat therapy could be an alternative way to improve cardiovascular health and cognitive function in various populations, however, the length of time that these benefits last is yet to be explored.
Aging is associated with declines in cardiovascular health and cognitive function as well as chronic inflammation and the development of neurodegenerative conditions such as Alzheimer's and Parkinson's disease. Additionally, ageing results in a loss of muscle size and strength, commonly referred to as sarcopenia, leading to increased risk of falls or adverse exercise-related events. It is well understood that frequent exercise improves cardiovascular and metabolic health whilst lowering the risk of disease and all-cause mortality, acting as a treatment for many different health conditions. Despite the evidence of its efficacy, many individuals struggle with adherence to exercise programmes, particularly older adults and clinical populations, with many individuals within these populations unable to perform exercise due to physical limitations or medical contraindications. With one in six people expected to be over the age of 65 years by 2050 and corresponding increases in non-communicable diseases (e.g., cancer, diabetes, cardiovascular disease) anticipated from this aging population, the development of adjunct treatments or alternatives to exercise to improve general health in older populations is needed.
Recent work has shown one such potential solution could be the use of passive heat therapy (PHT) (e.g., hot water immersion, sauna), which can achieve health benefits comparable to exercise. Acute PHT induces vascular improvements including increased blood flow, reduced blood pressure. and macro- and microvascular dilator function in various populations. Acute PHT has also been shown to increase reaction time, while mixed results have been seen in its effect on executive function in both young and older populations. The mechanisms for these improvements, however, are currently unclear, and may be related to increases in nitric oxide activity or reductions in biomarkers of inflammation.
One potential mechanism for the physiological benefits obtained from PHT is the increase of cytoprotective heat shock proteins (HSP) (specifically HSP27, HSP60, HSP70 and HSP90) intracellularly (i) and extracellularly (e) in response to increases in deep body temperature. Increases in the expression of these HSPs have been shown to play a role in reducing inflammation and protecting the vasculature via increases in endothelial nitric oxide synthase activity. Increased HSP concentrations may also prevent the accumulation of harmful biomarkers in the brain that play a role in cognitive decline and development of neurodegenerative diseases. There is also evidence that increased preoperative levels of both iHSP70 and eHSP70 are correlated with improved postoperative outcomes following cardiac surgery. Aging, however, is associated with a reduction in HSP transcription activity in various tissues, resulting in an impaired heat shock response and development of a pro-inflammatory state.
Previous work using acute hot water immersion has shown mixed results, with various studies showing increases in eHSP70, iHSP70 and iHSP90, while others have reported no change in expression. Heating stimuli applied in these studies has varied in magnitude, duration and whole body or not, and measurements of HSPs have taken place at various time points before, during and after PHT. Therefore, it is possible that upregulation of HSPs may have been missed, as no time course relationship exists between a single bout of PHT and upregulation of HSPs. Additionally, the duration for acute vascular and cognitive benefits from PHT and when function is returned to baseline is yet to be determined. A time course relationship study to determine the peak HSP response to acute passive heat therapy in older adults would provide insight into the relationship between acute changes in vascular or cognitive function and concurrent upregulation of both intracellular and extracellular HSPs, as well as its potential implications for improved surgical outcomes.
University of Portsmouth is the lead sponsor of 32 studies on the registry; 6 are open to participants now.
Counted across the registry records on this site, refreshed daily.
Exclusion Criteria:
1 h hot water immersion (to the clavicle, @40°C, rectal temperature \~38.5°C and \<39°C)
Other: Passive heating
1 h hot water immersion (to the clavicle, @40°C, rectal temperature \~38.5°C and \<39°C)
Brachial artery flow-mediated dilation
Percentage change in brachial artery diameter and return to baseline as assessed by ultrasound.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Brachial and carotid artery blood flow velocity
Change from baseline in blood flow velocity of the brachial artery and right common carotid artery as assessed via ultrasound. cm/s is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Carotid vessel diameter
Change in vessel diameter of the right common carotid artery and return to baseline as assessed via ultrasound. mm is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Carotid intima-media thickness
Change in intima-media thickness of the right common carotid artery and return to baseline as assessed via ultrasound. mm is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Carotid compliance
Change in compliance of the right common carotid artery and return to baseline as assessed via ultrasound. µm\^2 per kilopascal is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Carotid distensibility
Change in distensibility of the right common carotid artery and return to baseline as assessed via ultrasound. 10\^-3/kPa is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Carotid stiffness
Change in stiffness of the right common carotid artery and return to baseline as assessed via ultrasound. Meters per second is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Microvascular function
Change in microvascular function and return to baseline as assessed via iontophoresis on the forearm with acetylcholine (Ach) and Insulin, Area under the curve is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Stroke volume
Change in stroke volume and return to baseline measured noninvasively via thoracic impedance. mL/m\^2 is the unit
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Total peripheral resistance
Change in total peripheral resistance and return to baseline measured noninvasively via thoracic impedance
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Cardiac output
Change in cardiac output and return to baseline measured noninvasively via thoracic impedance. L/min is the unit.
Time frame: Pre hot water immersion, then 1 hour, 3 hours, 24 hours and 48 hours post
Intracellular HSP27 concentration
Change in iHSP27 concentration and return to baseline. Measured via immunoblotting in peripheral blood mononuclear cells (PBMCs).
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Intracellular HSP60 concentration
Change in iHSP60 concentration and return to baseline. Measured via immunoblotting in peripheral blood mononuclear cells (PBMCs).
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Intracellular HSP70 concentration
Change in iHSP70 concentration and return to baseline. Measured via immunoblotting in peripheral blood mononuclear cells (PBMCs).
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Intracellular HSP90 concentration
Change in iHSP90 concentration and return to baseline. Measured via immunoblotting in peripheral blood mononuclear cells (PBMCs).
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Plasma eHSP27 concentration
Change in plasma eHSP27 concentration and return to baseline. Measured via ELISA.
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Plasma eHSP60 concentration
Change in plasma eHSP60 concentration and return to baseline. Measured via ELISA.
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Plasma eHSP70 concentration
Change in plasma eHSP70 concentration and return to baseline. Measured via ELISA.
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Plasma eHSP90 concentration
Change in plasma eHSP90 concentration and return to baseline. Measured via ELISA.
Time frame: Pre hot water immersion, then immediately post, 1 hour, 2 hours, 3 hours, 6 hours, 12 hours, 24 hours and 48 hours post
Reaction time
Change in reaction time and return to baseline as assessed using ANAM: Automated Neurophysiological Assessment Metrics.
Time frame: Pre hot water immersion, then immediately post, 3 hours, 24 hours and 48 hours post
Logical reasoning
Change in logical reasoning and return to baseline as assessed using ANAM: Automated Neurophysiological Assessment Metrics.
Time frame: Pre hot water immersion, then immediately post, 3 hours, 24 hours and 48 hours post
Memory
Change in memory function and return to baseline as assessed using ANAM: Automated Neurophysiological Assessment Metrics.
Time frame: Pre hot water immersion, then immediately post, 3 hours, 24 hours and 48 hours post
Cerebral oxygenation
Change in cerebral oxygenation and return to baseline. Assessed using Near-infrared spectroscopy (NIRS) attached to the forehead
Time frame: Pre hot water immersion, then immediately post, 3 hours, 24 hours and 48 hours post
Plan to share: Yes — All data will be anonymized and raw data uploaded to the University of Portsmouth repository.
Supporting information: Study protocol
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This study is completed, as verified in Mar 2025. You cannot join it, but the record below documents what was studied.
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