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Ultramarathon participation is growing in popularity and exposes runners to unique stressors including extreme temperatures, high altitude, and exceedingly long exercise duration. However, the acute effects of ultramarathon participation on the cardiovascular system are not well understood. To determine the acute effects of trail ultramarathon participation on central artery stiffness and hemodynamics, 41 participants (9 F, 32 M) participating in the 2023 Western States Endurance Run underwent measures of carotid-femoral pulse wave velocity (cf-PWV) and pulse wave analysis pre- and <1 h post-race. Subendocardial viability ratio (SEVR) was calculated from central blood pressure (BP) waveforms. Serum was analyzed for creatine kinase (CK) activity as a measure of muscle damage. Normally distributed data are presented as means ± standard deviation (SD), and nonnormally distributed data are presented as median (interquartile range). Runners were middle-aged and generally lean [age = 44 ± 9 yr, body mass index (BMI) = 22.7 ± 1.8 kg·m−2]. There was no difference in cf-PWV from pre- to post-race (pre = 6.4 ± 1.0, post = 6.2 ± 0.85 m/s, P = 0.104), a finding that persisted after adjusting for mean arterial pressure (P = 0.563). Systolic and diastolic BPs were lower post-race (pre = 129/77 ± 9/7, post = 122/74 ± 10/8 mmHg, P < 0.001). Augmentation index (AIx; pre = 17.3 ± 12.2, post = 6.0 ± 13.7%, P < 0.001), AIx normalized to a heart rate of 75 beats/min (P = 0.043), reflection magnitude (pre = 55.5(49.0–60.8), post = 45.5(41.8–48.8)%, P < 0.001), and SEVR (pre = 173.0(158.0–190.0), post = 127.5(116.5–145.8)%, P < 0.001) were reduced post-race. CK increased markedly from pre- to post-race (pre = 111(85–162), post = 11,973(5,049–17,954) U/L, P < 0.001). Completing a 161-km trail ultramarathon does not affect central arterial stiffness and acutely reduces BP despite eliciting profound muscle damage. However, the reduced post-race SEVR suggests a short-term mismatch between myocardial work and coronary artery perfusion. NEW AND NOTEWORTHY Ultramarathon participation is growing dramatically. However, the acute cardiovascular effects of completing a 161-km trail ultramarathon remain unknown. We examined the acute effects of completing the 2023 Western States Endurance Run on arterial stiffness and central hemodynamics in a relatively large sample of males and females. We observed dramatic postexercise hypotension, reductions in reflected wave amplitude and reduced subendocardial viability ratio post-race. These findings suggest that ultramarathon participation has few negative effects on cardiovascular health. [ABSTRACT FROM AUTHOR]

In rodents and older patients with elevated blood pressure (BP), high dietary sodium increases excretion of biomarkers of kidney injury, but it is unclear whether this effect occurs in healthy young adults. The purpose of this study was to determine whether short-term high dietary salt increases urinary excretion of the kidney injury biomarkers neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in healthy young adults. Twenty participants participated in a double-blind, placebocontrolled, randomized crossover study. For 10 days each, participants were asked to consume salt (3,900 mg sodium) or placebo capsules. We measured BP during each visit, obtained 24-h urine samples for measurements of electrolytes, NGAL, and KIM-1, and assessed creatinine clearance. Compared with placebo, salt loading increased daily urinary sodium excretion (placebo: 130.3 ± 62.4 mmol/24 h vs. salt: 287.2 ± 72.0 mmol/24 h, P < 0.01). There was no difference in mean arterial BP (placebo: 77 ± 7 mmHg vs. salt: 77 ± 6 mmHg, P = 0.83) between conditions. However, salt loading increased the urinary NGAL excretion rate (placebo: 59.8 ± 44.4 ng/min vs. salt: 80.8 ± 49.5 ng/min, P < 0.01) and increased creatinine clearance (placebo: 110.5 ± 32.9 mL/min vs. salt: 145.0 ± 24.9 mL/min, P < 0.01). Urinary KIM-1 excretion was not different between conditions. In conclusion, in healthy young adults 10 days of dietary salt loading increased creatinine clearance and increased urinary excretion of the kidney injury biomarker marker NGAL but not KIM-1. [ABSTRACT FROM AUTHOR]

Females typically exhibit lower blood pressure (BP) during exercise than males. However, recent findings indicate that adjusting for maximal strength attenuates sex differences in BP during isometric handgrip (HG) exercise and postexercise ischemia (PEI; metaboreflex isolation). In addition, body size is associated with HG strength but its contribution to sex differences in exercising BP is less appreciated. Therefore, the purpose of this study was to determine whether adjusting for strength and body size would attenuate sex differences in BP during HG and PEI. We obtained beat-to-beat BP in 110 participants (36 females, 74 males) who completed 2 min of isometric HG exercise at 40% of their maximal voluntary contraction followed by 3 min of PEI. In a subset (11 females, 17 males), we collected muscle sympathetic nerve activity (MSNA). Statistical analyses included independent t tests and mixed models (sex × time) with covariate adjustment for 40% HG force, height 2 , and body surface area. Females exhibited a lower absolute 40% HG force than male participants ( P s < 0.001). Females exhibited lower Δsystolic, Δdiastolic, and Δmean BPs during HG and PEI than males (e.g., PEI, Δsystolic BP, 15 ± 11 vs. 23 ± 14 mmHg; P = 0.004). After covariate adjustment, sex differences in BP responses were attenuated. There were no sex differences in MSNA. In a smaller strength-matched cohort, there was no sex × time interactions for BP responses (e.g., PEI systolic BP, P = 0.539; diastolic BP, P = 0.758). Our data indicate that sex differences in exercising BP responses are attenuated after adjusting for muscle strength and body size. NEW & NOTEWORTHY When compared with young males, females typically exhibit lower blood pressure (BP) during exercise. Adjusting for maximal strength attenuates sex differences in BP during isometric handgrip (HG) exercise and postexercise ischemia (PEI), but the contribution of body size is unknown. Novel findings include adjustments for muscle strength and body size attenuate sex differences in BP reactivity during exercise and PEI, and sex differences in body size contribute to HG strength differences.

High salt consumption increases blood pressure (BP) and cardiovascular disease risk by altering autonomic function and increasing inflammation. However, it is unclear whether salt manipulation alters resting and exercising heart rate variability (HRV), a noninvasive measure of autonomic function, in healthy young adults. The purpose of this investigation was to determine whether short-term high-salt intake 1 ) alters HRV at rest, during exercise, or exercise recovery and 2 ) increases the circulating concentration of the inflammatory biomarker monocyte chemoattractant protein 1 (MCP-1). With the use of a randomized, placebo-controlled, crossover study, 20 participants (8 females; 24 ± 4 yr old, 110 ± 10/64 ± 8 mmHg) consumed salt (3,900 mg sodium) or placebo capsules for 10 days each separated by ≥2 wk. We assessed HRV during 10 min of baseline rest, 50 min of cycling (60% V̇o 2peak ), and recovery. We quantified HRV using the standard deviation of normal-to-normal RR intervals, the root mean square of successive differences (RMSSD), and additional time and frequency domain metrics of HRV. Plasma samples were collected to assess MCP-1 concentration. No main effect of high salt or condition × time interaction was observed for HRV metrics. However, acute exercise reduced HRV (e.g., RMSSD time: P < 0.001, condition: P = 0.877, interaction: P = 0.422). High salt elevated plasma MCP-1 (72.4 ± 12.5 vs. 78.14 ± 14.7 pg/mL; P = 0.010). Irrespective of condition, MCP-1 was moderately associated ( P values < 0.05) with systolic ( r = 0.32) and mean BP ( r = 0.33). Short-term high-salt consumption does not affect HRV; however, it increases circulating MCP-1, which may influence BP in young adults.

High dietary salt increases arterial blood pressure variability (BPV) in salt-resistant, normotensive rodents and is thought to result from elevated plasma [Na + ] sensitizing central sympathetic networks. Our purpose was to test the hypothesis that water deprivation (WD)-induced elevations in serum [Na + ] augment BPV via changes in baroreflex function and sympathetic vascular transduction in humans. In a randomized crossover fashion, 35 adults [17 female/18 male, age: 25 ± 4 yr, systolic/diastolic blood pressure (BP): 107 ± 11/60 ± 7 mmHg, body mass index: 23 ± 3 kg/m 2 ] completed two hydration protocols: a euhydration control condition (CON) and a stepwise reduction in water intake over 3 days, concluding with 16 h of WD. We assessed blood and urine electrolyte concentrations and osmolality, resting muscle sympathetic nerve activity (MSNA; peroneal microneurography; 18 paired recordings), beat-to-beat BP (photoplethysmography), common femoral artery blood flow (Doppler ultrasound), and heart rate (single-lead ECG). A subset of participants ( n = 25) underwent ambulatory BP monitoring during day 3 of each protocol. We calculated average real variability as an index of BPV. WD increased serum [Na + ] (141.0 ± 2.3 vs. 142.1 ± 1.7 mmol/L, P < 0.01) and plasma osmolality (288 ± 4 vs. 292 ± 5 mosmol/kg H 2 O, P < 0.01). However, WD did not increase beat-to-beat (1.9 ± 0.4 vs. 1.8 ± 0.4 mmHg, P = 0.24) or ambulatory daytime (9.6 ± 2.1 vs. 9.4 ± 3.3 mmHg, P = 0.76) systolic BPV. Additionally, sympathetic baroreflex sensitivity ( P = 0.20) and sympathetic vascular transduction were not different after WD ( P = 0.17 for peak Δmean BP following spontaneous MSNA bursts). These findings suggest that, despite modestly increasing serum [Na + ], WD does not affect BPV, arterial baroreflex function, or sympathetic vascular transduction in healthy young adults.

Previous studies have demonstrated an inverse relation between resting muscle sympathetic nerve activity (MSNA) and vasoconstrictor responsiveness (i.e., sympathetic transduction), such that those with high resting MSNA have low vascular responsiveness, and vice versa. The purpose of this investigation was to determine whether biological sex influences the balance between resting MSNA and beat-to-beat sympathetic transduction. We measured blood pressure (BP) and MSNA during supine rest in 54 healthy young adults (27 females: 23 ± 4 yr, 107 ± 8/63 ± 8 mmHg; 27 males: 25 ± 3 yr, 115 ± 11/64 ± 7 mmHg; means ± SD). We quantified beat-to-beat fluctuations in mean arterial pressure (MAP, mmHg) and limb vascular conductance (LVC, %) for 10 cardiac cycles after each MSNA burst using signal averaging, an index of sympathetic vascular transduction. In females, there was no correlation between resting MSNA (burst incidence; burst/100 heartbeats) and peak ΔMAP ( r  = -0.10, P = 0.62) or peak ΔLVC ( r  = -0.12, P = 0.63). In males, MSNA was related to peak ΔMAP ( r  = -0.50, P = 0.01) and peak ΔLVC ( r  = 0.49, P = 0.03); those with higher resting MSNA had blunted increases in MAP and reductions in LVC in response to a burst of MSNA. In a sub-analysis, we performed a median split between high- versus low-MSNA status on ΔMAP and ΔLVC within each sex and found that only males demonstrated a significant difference in ΔMAP and ΔLVC between high- versus low-MSNA groups. These findings support an inverse relation between resting MSNA and sympathetic vascular transduction in males only and advance our understanding on the influence of biological sex on sympathetic nervous system-mediated alterations in beat-to-beat BP regulation.

High dietary sodium intake has been linked to alterations in neurally mediated cardiovascular function, but the effects of high sodium on cardiovagal baroreflex sensitivity (cBRS) in healthy adults are unknown. The purpose of this study was to determine whether high dietary sodium alters cBRS and heart rate variability (HRV) and whether acute intravenous sodium loading similarly alters cBRS and HRV. High dietary sodium (300 mmol/day, 7 days) was compared with low dietary sodium (20 mmol/day, 7 days; randomized) in 14 participants (38 ± 4 yr old, 23 ± 1 kg/m 2 body mass index, 7 women). Acute sodium loading was achieved via a 23-min intravenous hypertonic saline infusion (HSI) in 14 participants (22 ± 1 yr old, 23 ± 1 kg/m 2 body mass index, 7 women). During both protocols, participants were supine for 5 min during measurement of beat-to-beat blood pressure (photoplethysmography) and R-R interval (ECG). cBRS was evaluated using the sequence method. Root mean square of successive differences in R-R interval (RMSSD) was used as an index of HRV. Serum sodium (137.4 ± 0.7 vs. 139.9 ± 0.5 meq/l, P < 0.05), plasma osmolality (285 ± 1 vs. 289 ± 1 mosmol/kgH 2 O, P < 0.05), cBRS (18 ± 2 vs. 26 ± 3 ms/mmHg, P < 0.05), and RMSSD (62 ± 6 vs. 79 ± 10 ms, P < 0.05) were increased following high-sodium diet intake compared with low-sodium diet intake. HSI increased serum sodium (138.1 ± 0.4 vs. 141.1 ± 0.5 meq/l, P < 0.05) and plasma osmolality (286 ± 1 vs. 290 ± 1 mosmol/kgH 2 O, P < 0.05) but did not change cBRS (26 ± 5 vs. 25 ± 3 ms/mmHg, P = 0.73) and RMSSD (63 ± 9 vs. 63 ± 8 ms, P = 0.99). These data suggest that alterations in dietary sodium intake alter cBRS and HRV but that acute intravenous sodium loading does not alter these indexes of autonomic cardiovascular regulation.