The effects of water temperature on cerebral blood flow during aquatic exercise.

PURPOSE: Recent studies suggest that episodic increases in cerebral blood flow (CBF) may contribute to the improvement in brain health associated with exercise training. Optimising CBF during exercise may enhance this benefit. Water immersion in ~ 30-32 °C augments CBF at rest and during exercise; however, the impact of water temperature on the CBF response has not been investigated. We hypothesised that cycle ergometry in water would increase CBF compared to land-based exercise, and that warm water would attenuate the CBF benefits. METHODS: Eleven young heathy participants (nine males; 23.8 ± 3.1 yrs) completed 30 min of resistance-matched cycle exercise in three separate conditions; non-immersion (Land), 32 °C and 38 °C water immersion up to the level of the waist. Middle cerebral artery velocity (MCAv), blood pressure, and respiratory measures were assessed throughout the exercise bouts. RESULTS: Core temperature was significantly higher in the 38 °C immersion than 32 °C (+ 0.84 ± 0.24 vs + 0.04 ± 0.16, P < 0.001), whilst mean arterial pressure was lower during 38 °C exercise compared to Land (84 ± 8 vs 100 ± 14 mmHg, P < 0.001) and 32 °C (92 ± 9, P = 0.03). MCAv was higher in 32 °C immersion compared to the Land and 38 °C conditions throughout the exercise bout (68 ± 10 vs 64 ± 11 vs 62 ± 12 cm/s, P = 0.03 and P = 0.02, respectively). CONCLUSION: Our findings suggest that cycle exercise in warm water attenuates the beneficial impact of water immersion on CBF velocity due to redistribution of blood flow to subserve thermoregulatory demand. Our findings suggest that, whilst water-based exercise can have beneficial effects on cerebrovascular function, water temperature is a key determinant of this benefit.

Effects of exercise during water immersion on arterial function in humans.

Flow-mediated dilation (FMD) provides a valid bioassay of vascular function in humans. Although water immersion induces hemodynamic effects that modify brachial artery shear stress, it is unclear whether water-based exercise modifies FMD. We hypothesized that exercise in 32°C water would decrease brachial artery shear and FMD relative to land-based exercise, whereas exercise in 38°C would increase brachial shear and FMD. Ten healthy participants (8 males; 23.9 ± 3.3 yr) completed 30 min of resistance-matched cycle exercise in three separate conditions: on land and in 32°C and 38°C water. Brachial artery shear rate area under the curve (SRAUC) was measured throughout each condition, with FMD measured pre- and postexercise. Brachial SRAUC increased during exercise in all conditions and was highest across the 38°C condition compared with Land and 32°C conditions (38°C: 27,507 ± 8,350 vs. Land: 9,908 ± 4,738 vs. 32°C: 13,840 ± 5,861 1/s, P < 0.001). Retrograde diastolic shear was greater during 32°C than both Land and 38°C conditions (32°C:-3,869 ± 2,198 vs. Land:-1,602 ± 1,334 vs. 32°C:-1,036 ± 1,754, P < 0.01). FMD increased as a result of 38°C (6.2 ± 1.9 vs. 8.5 ± 2.7%, P = 0.03), with no change in the Land exercise (6.3 ± 2.4 vs. 7.7 ± 2.4%, P = 0.10) or 32°C condition (6.4 ± 3.2 vs. 6.7 ± 3.2%, P = 0.99). Our findings indicate that cycle exercise in hot water attenuates retrograde shear, increases antegrade shear, and FMD. Exercise in 32°C water induces central hemodynamic changes relative to land-based exercise, but these do not translate to increases in FMD in either condition, likely due to the impact of increased retrograde shear. Our findings indicate that modification of shear has direct acute impacts on endothelial function in humans.

Improvements in vascular function in response to acute lower limb heating in young healthy males and females.

Regular exposure to passive heat stress improves vascular function, but the optimal heating prescription remains undefined. Local limb heating is more feasible than whole body heating, but the evidence demonstrating its efficacy is lacking. The purpose of this study was to determine whether acute improvements in vascular function can be achieved with lower limb heating in 16 young healthy individuals (8 female, 8 male). In separate visits, participants underwent 45 min of ankle- and knee-level hot water immersion (45°C). A subset of seven participants also participated in a time-control visit. Endothelial function was assessed through simultaneous brachial and superficial femoral artery flow-mediated dilation (FMD) tests. Macrovascular function was quantified by %FMD, whereas microvascular function was quantified by vascular conductance during reactive hyperemia. Arterial stiffness was assessed through carotid-femoral and femoral-foot pulse wave velocity (PWV). Plasma concentrations of interleukin-6 and extracellular heat shock protein-72 (eHSP72) were used as indicators of inflammation. Our findings showed that 45 min of lower limb heating-regardless of condition-acutely improved upper limb macrovascular endothelial function (i.e., brachial %FMD; Pre: 4.6 ± 1.7 vs. Post: 5.4 ± 2.0%; P = 0.004) and lower limb arterial stiffness (i.e., femoral-foot PWV; Pre: 8.4 ± 1.2 vs. Post: 7.7 ± 1.1 m/s; P = 0.011). However, only knee-level heating increased upper limb microvascular function (i.e., brachial peak vascular conductance; Pre: 6.3 ± 2.7 vs. Post: 7.8 ± 3.5 mL/min â‹… mmHg; P ≤ 0.050) and plasma eHSP72 concentration (Pre: 12.4 ± 9.4 vs. Post: 14.8 ± 9.8 ng/mL; P ≤ 0.050). These findings show that local lower limb heating acutely improves vascular function in younger individuals, with knee-level heating improving more outcome measures.NEW & NOTEWORTHY This study demonstrates that lower limb hot water immersion is an effective strategy for acutely improving vascular function in young, healthy males and females, thereby encouraging the development of accessible modes of heat therapy for vascular health.

The impact of the 24-h movement spectrum on vascular remodeling in older men and women: a review.

Aging is associated with increased risk of cardiovascular and cerebrovascular events, which are preceded by early, negative remodeling of the vasculature. Low physical activity is a well-established risk factor associated with the incidence and development of disease. However, recent physical activity literature indicates the importance of considering the 24-h movement spectrum. Therefore, the purpose of this review was to examine the impact of the 24-h movement spectrum, specifically physical activity (aerobic and resistance training), sedentary behavior, and sleep, on cardiovascular and cerebrovascular outcomes in older adults, with a focus on recent evidence (<10 yr) and sex-based considerations. The review identifies that both aerobic training and being physically active (compared with sedentary) are associated with improvements in endothelial function, arterial stiffness, and cerebrovascular function. Additionally, there is evidence of sex-based differences in endothelial function: a blunted improvement in aerobic training in postmenopausal women compared with men. While minimal research has been conducted in older adults, resistance training does not appear to influence arterial stiffness. Poor sleep quantity or quality are associated with both impaired endothelial function and increased arterial stiffness. Finally, the review highlights mechanistic pathways involved in the regulation of vascular and cerebrovascular function, specifically the balance between pro- and antiatherogenic factors, which mediate the relationship between the 24-h movement spectrum and vascular outcomes. Finally, this review proposes future research directions: examining the role of duration and intensity of training, combining aerobic and resistance training, and exploration of sex-based differences in cardiovascular and cerebrovascular outcomes.

The effects of local versus systemic passive heating on the acute inflammatory, vascular and glycaemic response.

The aim of this study was to compare the acute cardiometabolic and perceptual responses between local and whole-body passive heating. Using a water-perfused suit, 10 recreationally active males underwent three 90 min conditions: heating of the legs with upper-body cooling (LBH), whole-body heating (WBH) and exposure to a thermoneutral temperature (CON). Blood samples were collected before and up to 3 h post-session to assess inflammatory markers, while a 2 h oral glucose tolerance test was initiated 1 h post-session. Femoral artery blood flow and perceptual responses were recorded at regular intervals. The interleukin (IL)-6 incremental area under the curve (iAUC) was higher for LBH (1096 ± 851 pg/mL × 270 min) and WBH (833 ± 476 pg/mL × 270 min) compared with CON (565 ± 325 pg/mL × 270 min; p < 0.047). Glucose concentrations were higher after WBH compared with LBH and CON (p < 0.046). Femoral artery blood flow was higher at the end of WBH (1713 ± 409 mL/min) compared with LBH (943 ± 349 mL/min; p < 0.001), and higher in LBH than CON (661 ± 222 mL/min; p = 0.002). Affect and thermal comfort were more negative during WBH compared with LBH and CON (p < 0.010). In conclusion, local passive heating elevated blood flow and the IL-6 iAUC. However, while resulting in more positive perceptual responses, the majority of the included cardiometabolic markers were attenuated compared with WBH. Novelty: The increase in the IL-6 iAUC in response to passive heating is not reduced by upper-body cooling. Upper-body cooling attenuates the plasma nitrite, IL-1ra and femoral artery blood flow response to passive heating. Upper-body cooling leads to more positive perceptual responses to passive heating.

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives.

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/.

Emerging evidence for accelerated ageing and cardiovascular disease in individuals with cerebral palsy.

OBJECTIVE: To examine longitudinal changes in traditional and non-traditional risk factors for cardiovascular disease in individuals with cerebral palsy and to investigate relationships between age, Gross Motor Function Classification System (GMFCS) and risk of cardiovascular disease. METHODS: Individuals with cerebral palsy (n = 28 of 53 eligible participants; GMFCS levels I-V; follow-up mean age 35.1 years (standard deviation (SD) 14.4) participated in a longitudinal cohort study with 4.0 years (SD 1.2) follow-up. Traditional risk factors included waist circumference and systolic blood pressure. Non-traditional risk factors included carotid artery intima media thickness and distensibility, carotid-femoral pulse wave velocity, and flow-mediated dilation. RESULTS: Absolute (0.31 mm (SD 0.13) vs 0.22 mm (SD 0.08) , p = 0.045, 95% confidence interval (95% CI) 0.040, 0.151) and relative flow-mediated dilation (9.9 % (SD 4.7) vs 7.5 % (SD 2.6), p = 0.049, 95% CI 0.464, 4.42) decreased, while carotid artery intima media thickness (0.52 mm (SD 0.17) vs 0.67 mm (SD 0.33), p = 0.041, 95% CI -0.242, -0.074) increased from baseline to follow-up. No other risk factor changed significantly. Age at baseline was a significant independent predictor of carotid artery intima media thickness change (R-squared = 0.261, p = 0.031). CONCLUSION: Individuals with cerebral palsy experience significant changes in non-traditional risk factors for cardiovascular disease over 4 years, in the face of no changes in traditional risk factors. Compared with findings in the literature from the general population, these risk factors progress at a faster rate and at a younger age in individuals with cerebral palsy.

Peripheral artery endothelial function responses to altered shear stress patterns in humans.

NEW FINDINGS: What is the central question of this study? What is the effect of altered shear stress pattern, with or without concurrent neurohumoral and metabolic activation, on the acute endothelial function response assessed via brachial artery flow-mediated dilatation? What is the main finding and its importance? Despite generating distinctive shear stress patterns (i.e. increases in anterograde only, anterograde only with neurohumoral and metabolic activation, and both anterograde and retrograde), similar acute improvements were observed in the brachial artery flow-mediated dilatation response in all conditions, indicating that anterograde and/or turbulent shear stress might be the essential element to induce acute increases in endothelial function. ABSTRACT: Endothelial function is influenced by both the direction and the magnitude of shear stress. Acute improvements in endothelial function have mostly been attributed to increased anterograde shear, whereas results from many interventional models in humans suggest that enhancing shear stress in an oscillatory manner (anterograde and retrograde) might be optimal. Here, we determined the acute brachial artery shear stress (SS) and flow-mediated dilatation (FMD) responses to three shear-altering interventions [passive heat stress (HEAT), mechanical forearm compression (CUFF) and handgrip exercise (HGEX)] and examined the relationship between changes in oscillatory shear index (OSI) and changes in FMD. During separate visits, 10 young healthy men (22 ± 3 years old) underwent 10 min of HEAT, CUFF or HGEX in their left forearm. Anterograde and retrograde SS, Reynolds number, OSI and FMD were assessed at rest and during/after each intervention. Anterograde SS increased during all interventions in a stepwise manner (P < 0.05 between interventions), with the change in HGEX (∆37.7 ± 12.2 dyn cm-2 , P < 0.05) > CUFF (∆25.1 ± 11.9 dyn cm-2 , P < 0.05) > HEAT (∆14.5 ± 7.9 dyn cm-2 , P < 0.05). Retrograde SS increased during CUFF (∆-19.6 ± 4.3 dyn cm-2 , P < 0.05). Anterograde blood flow was turbulent (i.e. Reynolds number ≥ |2000|) during all interventions (P < 0.05). The relative FMD improved after all interventions (P = 0.01), and there was no relationship between ∆OSI and ∆FMD. We elicited changes in SS profiles including increased anterograde SS (HEAT and HGEX) and both increased anterograde and retrograde SS (CUFF); regardless of the SS pattern, FMD improved to the same extent. These findings suggest that the presence of anterograde and/or turbulent SS might be the key to optimizing endothelial function in acute assessment protocols.

Effect of heat stress on vascular outcomes in humans.

In addition to its role as an environmental stressor, scientists have recently demonstrated the potential for heat to be a therapy for improving or mitigating declines in arterial health. Many studies at both ends of the scientific controls spectrum (tightly controlled, experimental vs. practical) have demonstrated the beneficial effects of heating on microvascular function (e.g., reactive hyperemia, cutaneous vascular conductance); endothelial function (e.g., flow-mediated dilation); and arterial stiffness (e.g., pulse-wave velocity, compliance, ß-stiffness index). It is important to note that findings of beneficial effects are not unanimous, likely owing to the varied methodology in both heating protocols and assessments of outcome measures. Mechanisms of action for the effects of both acute and chronic heating are also understudied. Heat science is a very promising area of human physiology research, as it has the potential to contribute to approaches addressing the global cardiovascular disease burden, particularly in aging and at risk populations, and those for whom exercise is not feasible or recommended.

Cardiac and haemodynamic influence on carotid artery longitudinal wall motion.

NEW FINDINGS: What is the central question of this study? Carotid artery longitudinal wall motion (CALM) is a bidirectional forward and backward motion of the arterial wall; however, there is no evidence in humans for what controls CALM despite proposals for pulse pressure, left ventricular motion and shear rate. What is the main finding and its importance? Carotid artery longitudinal wall motion responses were heterogeneous when manipulating sympathetic activation and endothelium-independent vasodilatation, leading to non-significant group responses. However, individual CALM responses were associated with left ventricular rotation and shear rate. These findings are important when interpreting changes in CALM in humans with acute or chronic experimental designs. Carotid artery longitudinal wall motion (CALM) has recently attracted interest as an indicator of arterial health; however, the regulation of CALM is poorly understood. We conducted a series of studies aimed at manipulating pulse pressure (PP), left ventricular (LV) motion and carotid shear rate, which have been previously suggested to regulate various components of CALM pattern and magnitude. To determine the regulatory influences on CALM, 15 healthy men (22 ± 2 years old) were exposed to three acute interventions: the serial subtraction test (SST); the cold pressor test (CPT); and exposure to sublingual nitroglycerine (NTG). The SST elicited increases in PP (P < 0.01), apical LV rotation (P < 0.01) and carotid shear rate (P < 0.01), with no changes in CALM (P > 0.05). Likewise, the CPT elicited increases in PP (P = 0.01), basal LV rotation (P = 0.04) and carotid shear rate (P = 0.01), with no changes in CALM (P > 0.05). Conversely, exposure to NTG elicited no change in PP (P = 0.22), basal (P = 0.65) or apical LV rotation (P = 0.45), but did decrease carotid shear rate (P < 0.01), without altering CALM (P > 0.05). Considerable individual variability in CALM responses prompted further analyses where all three interventions were pooled for change scores. Changes in LV basal rotation were related to changes in systolic retrograde CALM (B = -0.025, P = 0.03), whereas changes in carotid shear rate were related to changes in diastolic CALM displacement (B = 0.0009, P = 0.01). The interventions were underpinned by relationships between CALM and both LV basal rotation and local shear rate at the individual level, indicating that cardiac and haemodynamic factors may influence CALM in humans.

Cardiovascular profile in postural orthostatic tachycardia syndrome and Ehlers-Danlos syndrome type III.

The cardiovascular profile of postural orthostatic tachycardia syndrome + Ehlers-Danlos syndrome hypermobility type (POTS + EDSIII) has not been described, despite suggestions that it plays a role in orthostatic intolerance. We studied nine individuals diagnosed with POTS + EDSIII and found that the arterial stiffness and cardiac profiles of patients with POTS + EDSIII were comparable to those of age- and sex-matched controls, suggesting an alternate explanation for orthostatic intolerance.