INTRODUCTION Hypertension remains among the most prevalent cardiovascular disease risk factors world‐wide. Aerobic exercise training is the current gold‐standard non‐pharmacological intervention for lowering blood pressure, yet passive heat therapy is an effective alternative means of reducing blood pressure and improving cardiovascular health for individuals that are unable or unwilling to engage in traditional exercise training. However, the effectiveness of heat therapy versus exercise training has not been compared in adults with untreated hypertension. Therefore, the purpose of this ongoing clinical trial is to compare the effectiveness of hot water immersion (HWI) versus aerobic exercise training (EX) in lowering blood pressure and improving cardiovascular function. Data presented are preliminary (mid‐point) comparisons following 15 sessions of either HWI or EX. HYPOTHESIS It was hypothesized that hot water immersion would be more effective than traditional aerobic exercise training in reducing blood pressure and improving cardiovascular function in adults with untreated hypertension. METHODS Prior to randomization, all subjects (n=6, 1F) completed resting vascular function testing, including measurements of blood pressure (automated sphygmomanometer), cardiac output (acetylene wash‐in method), and carotid‐femoral pulse wave velocity (PWV). Systemic vascular conductance (SVC) was calculated as cardiac output/mean arterial pressure (MAP). Following pre‐testing (PRE), subjects were randomized into either HWI (n=4, 1F) or EX (n=2). During HWI, subjects were immersed to the level of the sternum in 40.5°C water for 45 minutes. EX consisted of upright cycling at 60% of heart rate reserve (HRR) for 40 min, with 5 min each for warm‐up and cool‐down at 30% of HRR. Participants completed 15 sessions of either HWI or EX prior to mid‐point (MID) testing. Combined data are presented as the change from PRE as mean ± SD and were analyzed using a paired‐samples t test. Group mean data for HWI versus EX are presented as the change from PRE as means ± SD and were analyzed using an unpaired two sample t‐test. RESULTS Following 15 sessions of either HWI or EX, systolic blood pressure tended to be reduced (‐5±4 mmHg; p=0.10). The change in systolic blood pressure (SBP) was directionally similar between HWI and EX (∆ from PRE, HWI vs. EX; ‐3±5 vs. ‐7±7 mmHg; p=0.59), whereas the change in diastolic blood pressure (DBP) was divergent between HWI and EX (‐3±8 vs. +5±10 mmHg; p=0.43). Accordingly, changes in MAP were disparate between HWI and EX (‐3±7 vs. +2±9 mmHg; p=0.61). Cardiac output was similar between HWI and EX (‐0.09±0.71 vs. ‐0.76±1.07 L/min; p=0.53), as were changes in SVC (‐0.3±6.6 vs. ‐7.6±15.9 mL•min‐1•mmHg‐1; p=0.63). Overall, PWV was reduced by both interventions (‐0.6±0.3 m/s; p=0.01) and changes in PWV were similar between HWI and EX (‐0.6±0.4 vs. ‐0.5±0.4 m/s; p=0.72). CONCLUSIONS Preliminary data from this ongoing clinical trial suggest both hot water immersion and exercise are similarly effective in lowering s...
Introduction Kidney injury is a top cause of hospitalization during extreme heat events. Currently, wet bulb temperatures (Twet) during extreme heat events rarely exceed 31°C. However, it is predicted that Twet during future extreme heat events will exceed 34˚C, the limit of compensability in humans. We previously reported that, compared to a Twet of 31˚C, an 8 h resting exposure to a Twet of 34˚C elevated the risk of kidney injury risk, as quantified via the FDA‐approved kidney injury risk biomarker – the product of urine insulin‐like growth factor binding‐protein 7 and urine tissue inhibitor of metalloproteinases 2 ([IGFBP7·TIMP‐2]). This kidney injury risk is likely of tubular origin, and while the mechanisms underlying this extreme heat mediated tubular injury are unknown, an inflammatory etiology occurring secondary to oxidative stress has been speculated. Purpose Test the hypothesis that kidney injury risk during prolonged passive extreme heat exposure is contributed to by oxidative stress and inflammation. Methods Fifteen healthy men underwent 8 h resting exposures in Twet of 31°C and 34°C. Blood and urine samples were collected at 0 and 8 h. Following observations of elevations in [IGFBP7·TIMP‐2] in 34°C vs. 31°C (p<0.01), assays were conducted for urine liver‐type fatty acid binding‐protein (uL‐FABP ‐ a marker of tubular injury caused by oxidative stress), urine thiobarbituric acid reactive substances (uTBARS ‐ a marker of renal oxidative stress), urine interleukin‐18 (uIL‐18 ‐ a marker of tubular injury and inflammation), and plasma interleukin‐17a (pIL‐17a ‐ a circulating marker of inflammation, n=10). Serum TBARS (sTBARS) was measured to assess systemic oxidative stress. Data are reported as a change from 0 h (mean ± SD). Urine markers were normalized to urine flow rate. Results uL‐FABP increased in 34°C (+42 ± 64 ng/min, p<0.01) but not 31°C (+11 ± 20 ng/min, p=0.75) and was different between trials at 8 h (p<0.01). uTBARS increased in 34°C (+43 ± 37 nmol/min, p<0.01) but not 31°C (+14 ± 13 nmol/min, p=0.27) and was different between trials at 8 h (p<0.01). sTBARS did not change in 34°C (+1.2 ± 4.0 nmol/mL, p=0.08) nor 31°C (+0.3 ± 2.9 nmol/mL, p=0.92) and did not differ between trials at 8 h (p=0.16). uIL‐18 increased in 34°C (+27 ± 19 pg/min, p<0.01) and 31°C (+20 ± 25 pg/min, p<0.01) and was higher in 34°C at 8 h (p=0.05). pIL‐17a increased in 34°C (+199 ± 90 fg/dL, p<0.01) but not 31°C (+9 ± 96 fg/dL, p=0.94) and was different between trials at 8 h (p<0.01). Conclusion Increases in uL‐FABP and uTBARS, in the absence of differences in sTBARS, support that renal tubular injury in 34°C is likely due to oxidative stress. pIL‐17a is selectively elevated in ischemic kidney injury. Thus, elevations in pIL‐17a in 34°C indicates inflammation of renal origins and this was translated to greater increases in uIL‐18 in 34°C. These findings support that kidney injury risk during prolonged passive extreme heat exposure is contributed to by oxidative stress and inflammation.
PURPOSE:Although maximal cushioning shoes are popular among recreational runners, few studies have assessed the effects of shoe type on running economy, and fewer have observed the influence of footwear condition on females. Therefore, this pilot study aims to investigate the effects of shoe type on running economy in female runners. METHODS: Participants (age: 21) reported to Whittier College's Human Movement Laboratory twice. During the first testing session, participants completed a VO 2MAX test using a CosMed T-150 treadmill and Cardiopulmonary Exercise Test (CPET) to determine baseline values. On the second visit, participants ran two 15-minute bouts at 70% of their VO 2max . Participants wore their own shoes (OS) for one bout, and a maximalist (MAX) lab shoe for the other. The order of footwear conditions was counterbalanced. Paired samples t-tests will assess differences in oxygen consumption, respiratory quotient, and rate of perceived exertion between shoe type (α=0.05). RESULTS: Analysis of preliminary data suggest oxygen consumption does not differ between footwear conditions (MAX: 31.99 ± 3.78 ml/kg/min, OS: 31.48 ± 3.78 ml/kg/min). Additionally, RQ and RPE did not differ between the MAX shoe (RQ: 0.90 ± 0.04; RPE: 12.93 ± 2.76) and OS (RQ: 0.91 ± 0.03; RPE: 12.57 ± 1.91). CONCLUSIONS: Based on preliminary data, shoe type may not affect running economy in female runners. A more complete analysis of the influence of footwear on running economy will occur as the data collection increases to the target sample size. If changes in running economy occur, the results of this study may determine if those changes are due to habituation or perturbation. In addition, this study's data regarding running economy may be beneficial for footwear development and consumer decision-making specifically for female runners.
METHODS: Data was collected on 41 active adults who completed a 11km road race. Age (mean±standard deviation [SD]): 44.7±15.7 years; VO 2 max: 42.7±9.2 ml/kg/min; percent body fat: 22.4±9.6%. CRI was assessed at baseline for 10 minutes in a supine position in a thermoneutral environment. At the road race, CRI was assessed for 2 minutes pre-race and post-race in the supine position. Heart rate and oxygen saturation were assessed alongside CRI. Environmental conditions were captured surrounding the race. Core temperature was assessed post-race. Descriptive statistics (mean±SD) were calculated and paired-samples t-tests were utilized to compare baseline to pre-race, baseline to post-race, and pre-race to post-race. RESULTS: Post-race CRI (mean ± SD: 0.70±0.32) significantly diminished compared to baseline values (0.91±0.07; p<0.001). Post-race CRI was significantly diminished (p<0.001) compared to pre-race CRI measures (mean±SD: 0.88±0.09). Resting heart rate increased from baseline (mean±SD: 59.6±10.4 bpm) to pre-race (65.4±11.2 bpm) and to post-race (85.1±16.9 bpm). Runners were characterized as hyperthermic following the race (core temperature: 38.90±1.20 ºC). Environmental conditions upon finishing the race were 22.78 ºC, 53% RH, and 21.67 ºC WBGT. CONCLUSIONS: Following physically demanding exercise in the heat, CRI monitoring may be able to detect changes resulting from increased physiological stress and may be utilized to prevent collapse. Future studies should assess the extent to which thermal stress is correlated to changes in CRI.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.