Device-estimated sleep metrics do not mediate the relation between race and blood pressure dipping in young black and white women.

Short, disturbed, and irregular sleep may contribute to blunted nocturnal blood pressure (BP) dipping, a predictor of cardiovascular disease. Black women (BLW) demonstrate less BP dipping and poorer sleep health than White women (WHW). However, it remains unclear whether device-estimated sleep health metrics mediate the relation between race and BP dipping in young women. We hypothesized that the relation between race and BP dipping would be partly mediated by sleep health metrics of sleep duration, sleep efficiency, and sleep regularity. Participants (20 BLW, 17 WHW) were 18-29 years old, normotensive, nonobese, and without evidence of sleep disorders. Systolic and diastolic BP dipping were derived from 24-h ambulatory BP monitoring. Habitual sleep duration and sleep efficiency were estimated via 14 days of wrist actigraphy. Sleep duration regularity was calculated as the standard deviation (SD) of nightly sleep duration (SDSD). Sleep timing regularity metrics were calculated as the SD of sleep onset and sleep midpoint (SMSD). Mediation analysis tested the mediating effect of each sleep metric on the relation between race and BP dipping. BLW experienced less systolic (P = .02) and diastolic (P = .01) BP dipping. Sleep duration (P = .14) was not different between groups. BLW had lower sleep efficiency (P < .01) and higher SDSD (P = .02), sleep onset SD (P < .01) and SMSD (P = .01). No sleep metrics mediated the relation between race and BP dipping (all indirect effects P > .38). In conclusion, mediation pathways of sleep health metrics do not explain racial differences in nocturnal BP dipping between young BLW and WHW.

Limb, sex, but not acute dietary capsaicin, modulate the near-infrared spectroscopy-vascular occlusion test estimate of muscle metabolism.

The downward slope during the near-infrared spectroscopy (NIRS)-vascular occlusion test (NIRS-VOT) is purported as a simplified estimate of metabolism. Whether or not the NIRS-VOT exhibits sex- or limb-specificity or may be acutely altered remains to be elucidated. Thus, we investigated if there is limb- or sex specificity in tissue desaturation rates (DeO2) during a NIRS-VOT, and if acute dietary capsaicin may alter this estimate of muscle metabolism. Young healthy men (n = 25, 21 ± 4 years) and women (n = 20, 20 ± 1 years) ingested either placebo or capsaicin, in a counterbalanced, single-blind, crossover design after which a simplified NIRS-VOT was conducted to determine the DeO2 (%/s), as an estimate of oxidative muscle metabolism, in both the forearm (flexors) and thigh (vastus lateralis). There was a significant limb effect with the quadriceps having a greater DeO2 than the forearm (-2.31 ± 1.34 vs. -1.78 ± 1.22%/s, p = 0.007, ηp 2 = 0.19). There was a significant effect of sex on DeO2 (p = 0.005, ηp 2 = 0.203) with men exhibiting a lesser DeO2 than women (-1.73 ± 1.03 vs. -2.36 ± 1.32%/s, respectively). This manifested in significant interactions of limb*capsaicin (p = 0.001, ηp 2 = 0.26) as well as limb*capsaicin*sex on DeO2 (p = 0.013, ηp 2 = 0.16) being observed. Capsaicin does not clearly alter O2-dependent muscle metabolism, but there was apparent limb and sex specificity, interacting with capsaicin in this NIRS-derived assessment.

Tissue-specific mitochondrial toxicity of cigarette smoke concentrate: consequence to oxidative phosphorylation.

Cigarette smoke exposure is a well-known risk factor for developing numerous chronic health conditions, including pulmonary disease and cardiometabolic disorders. However, the cellular mechanisms mediating the toxicity of cigarette smoke in extrapulmonary tissues are still poorly understood. Therefore, the purpose of this study was to characterize the acute dose-dependent toxicity of cigarette smoke on mitochondrial metabolism by determining the susceptibility and sensitivity of mitochondrial respiration from murine skeletal (gastrocnemius and soleus) and cardiac muscles, as well as the aorta to cigarette smoke concentrate (CSC). In all tissues, exposure to CSC inhibited tissue-specific respiration capacity, measured by high-resolution respirometry, according to a biphasic pattern. With a break point of 451 ± 235 µg/mL, the aorta was the least susceptible to CSC-induced mitochondrial respiration inhibition compared with the gastrocnemius (151 ± 109 µg/mL; P = 0.008, d = 2.3), soleus (211 ± 107 µg/mL; P = 0.112; d = 1.7), and heart (94 ± 51 µg/mL; P < 0.001; d = 2.6) suggesting an intrinsic resistance of the vascular smooth muscle mitochondria to cigarette smoke toxicity. In contrast, the cardiac muscle was the most susceptible and sensitive to the effects of CSC, demonstrating the greatest decline in tissue-specific respiration with increasing CSC concentration (P < 0.001, except the soleus). However, when normalized to citrate synthase activity to account for differences in mitochondrial content, cardiac fibers' sensitivity to cigarette smoke inhibition was no longer significantly different from both fast-twitch gastrocnemius and slow-twitch soleus muscle fibers, thus suggesting similar mitochondrial phenotypes. Collectively, these findings established the acute dose-dependent toxicity of cigarette smoke on oxidative phosphorylation in permeabilized tissues involved in the development of smoke-related cardiometabolic diseases.NEW & NOTEWORTHY Despite numerous investigations into the mechanisms underlying cigarette smoke-induced mitochondrial dysfunction, no studies have investigated the tissue-specific mitochondrial toxicity to cigarette smoke. We demonstrate that, while aorta is least sensitive and susceptible to cigarette smoke-induced toxicity, the degree of cigarette smoke-induced toxicity in striated muscle depends on the tissue-specific mitochondrial content. We conclude that while the mitochondrial content influences cigarette smoke-induced toxicity in striated muscles, aorta is intrinsically protected against cigarette smoke-induced mitochondrial toxicity.

Impact of high intensity interval exercise with and without heat stress on cardiovascular and aerobic performance: a pilot study.

BACKGROUND: Heat stress during aerobic exercise training may offer an additional stimulus to improve cardiovascular function and performance in a cool-temperate environment. However, there is a paucity of information on the additive effects of high-intensity interval exercise (HIIE) and acute heat stress. We aimed to determine the effects of HIIE in combination with acute heat stress on cardiovascular function and exercise performance. METHODS: Twelve active (peak O2 consumption [VO2peak]: 47 ± 8 ml·O2/min/kg) young adults were counterbalanced to six sessions of HIIE in hot (HIIE-H, 30 ± 1 °C, 50 ± 5% relative humidity [RH]) or temperate conditions (HIIE-T, 20 ± 2 °C, 15 ± 10% RH). Resting heart rate (HR), HR variability (HRV), central (cBP) and peripheral blood pressure (pBP), peripheral mean arterial pressure (pMAP), pulse wave velocity (PWV), VO2peak, and 5-km treadmill time-trial were measured pre- and post-training. RESULTS: Resting HR and HRV were not significantly different between groups. However, expressed as percent change from baseline, cSBP (HIIE-T: + 0.9 ± 3.6 and HIIE-H: -6.6 ± 3.0%, p = 0.03) and pSBP (HIIE-T: -2.0 ± 4.6 and HIIE-H: -8.4 ± 4.7%, p = 0.04) were lower in the heat group. Post-training PWV was also significantly lower in the heat group (HIIE-T: + 0.4% and HIIE-H: -6.3%, p = 0.03). Time-trial performance improved with training when data from both groups were pooled, and estimated VO2peak was not significantly different between groups (HIIE-T: 0.7% and HIIE-H: 6.0%, p = 0.10, Cohen's d = 1.4). CONCLUSIONS: The addition of acute heat stress to HIIE elicited additive adaptations in only cardiovascular function compared to HIIE alone in active young adults in temperate conditions, thus providing evidence for its effectiveness as a strategy to amplify exercise-induced cardiovascular adaptations.

We like to move it, move it: A perspective on performing passive leg movement as a non-invasive assessment of vascular function in pediatric populations.

The passive leg movement (PLM) technique is a non-invasive assessment of lower-limb vascular function. PLM is methodologically simple to perform and utilizes Doppler ultrasound to determine leg blood flow (LBF) through the common femoral artery at rest and in response to passive movement of the lower leg. LBF responses to PLM have been reported to be mostly nitric oxide (NO)-mediated when performed in young adults. Moreover, PLM-induced LBF responses, as well as the NO contribution to PLM-induced LBF responses, are reduced with age and in various diseased populations, demonstrating the clinical utility of this non-invasive test. However, no PLM studies to date have included children or adolescents. Since its conception in 2015, our laboratory has performed PLM on hundreds of individuals including a large cohort of children and adolescents. Thus, the purpose of this perspective article is threefold: 1) to uniquely discuss the feasibility of performing PLM in children and adolescents, 2) to report PLM-induced LBF values from our laboratory in 7-17-year-olds, and 3) to discuss considerations for making comparisons among pediatric populations. Based on our experiences performing PLM in children and adolescents (among various other age groups), it is our perspective that PLM can feasibly be performed in this population. Further, data from our laboratory may be used to provide context for typical PLM-induced LBF values that could be observed in children and adolescents, as well as across the lifespan.

Effects of cigarette smoke on in situ mitochondrial substrate oxidation of slow- and fast-twitch skeletal muscles.

Epidemiological and clinical evidence suggests that cigarette smoke exposure alters glucose and fatty acid metabolism, leading to greater susceptibility to metabolic disorders. However, the effects of cigarette smoke exposure on mitochondrial substrate oxidation in the skeletal muscle are still poorly understood. Accordingly, this study aimed to examine the acute effects of cigarette smoke on mitochondrial respiratory capacity, sensitivity, and concurrent utilization of palmitoylcarnitine (PC), a long-chain fatty acid, and pyruvate, a product of glycolysis, in permeabilized gastrocnemius and soleus muscle fibers exposed to an acute (1 h) dose (4 %) of cigarette smoke concentrate. Cigarette smoke decreased both mitochondrial respiratory capacity (CONTROL: 50.4 ± 11.8 pmolO2/s/mgwt and SMOKE: 22.3 ± 4.4 pmolO2/s/mgwt, p < 0.01) and sensitivity for pyruvate (CONTROL: 0.10 ± 0.04 mM and SMOKE: 0.11 ± 0.04 mM, p < 0.01) in the gastrocnemius muscle. In the soleus, only the sensitivity for pyruvate-stimulated mitochondrial respiration trended toward a decrease (CONTROL: 0.11 ± 0.04 mM and SMOKE: 0.23 ± 0.15 mM, p = 0.08). In contrast, cigarette smoke did not significantly alter palmitoylcarnitine-stimulated mitochondrial respiration in either muscle. In the control condition, pyruvate-supported respiration was inhibited by the concurrent addition of palmitoylcarnitine in the fast-twitch gastrocnemius muscle (-27.1 ± 19.7 %, p < 0.05), but not in the slow-twitch soleus (-9.2 ± 17.0 %). With cigarette smoke, the addition of palmitoylcarnitine augmented the maximal respiration rate stimulated by the concurrent addition of pyruvate in the gastrocnemius (+18.5 ± 39.3 %, p < 0.05). However, cigarette smoke still significantly impaired mitochondrial respiratory capacity with combined substrates compared to control (p < 0.05). Our findings underscore that cigarette smoke directly impairs mitochondrial respiration of carbohydrate-derived substrates and is a primary mechanism underlying cigarette smoke-induced muscle dysfunction, which leads to a vicious cycle involving excess glucose conversion into fatty acids and lipotoxicity.

Does sex influence near-infrared spectroscopy-derived indicators of microvascular reactivity and the response to acute dietary capsaicin.

Endothelial dysfunction is associated with cardiovascular disease development, nitric oxide (NO) deficiencies, and may be limb or sex-specific. Prior in vitro work indicated that the transient receptor potential vanilloid channel-1 (TRPV1) is expressed in human arteries and the TRPV1 agonist capsaicin alters vasodilation in an endothelium-dependent manner; however, it is unknown if this translates in vivo or is limb or sex-dependent. Therefore, we sought to determine if there was limb or sex-specificity in the effect of capsaicin on microvascular function using near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (StO2) reperfusion slope. In a blinded placebo-controlled crossover design, 45 young males (M: n = 25) and females (F: n = 20), the reperfusion slopes of the forearm and quadriceps were assessed, and a urine sample obtained to assay for nitrate/nitrite (NOx) concentrations and antioxidant capacity after acutely ingesting placebo or capsaicin. Under placebo, females had greater reperfusion rates in both the forearm (M: 0.44 ± 0.24 vs. F: 0.98 ± 0.46 %/sec; p = 0.002, d = -1.50) and quadricep (M: 0.86 ± 0.31 vs. F: 1.17 ± 0.43 %/sec; p = 0.010, d = -0.85). Capsaicin decreased microvascular responsiveness in the forearm of females (placebo: 0.98 ± 0.45 vs. capsaicin: 0.84 ± 0.45 %/sec) as compared to males (placebo: 0.45 ± 0.24 vs. capsaicin: 0.38 ± 0.16 %/sec, interaction p < 0.001, η2 = 0.475). There was a sex*treatment interaction for NOx concentrations, where males increased (placebo: 21.13 ± 12.83 vs. capsaicin: 23.82 ± 13.34 µM), while females decreased (placebo: 22.78 ± 14.40 vs. capsaicin: 14.43 ± 10.01 µM; p = 0.037, η2 = 0.042). Using NIRS to assess microvascular function, there is apparent limb and sex-specificity, and, for the first-time, document that acute oral capsaicin alters reperfusion slope in a sexually divergent manner.

Capsaicin and Its Effect on Exercise Performance, Fatigue and Inflammation after Exercise.

Capsaicin (CAP) activates the transient receptor potential vanilloid 1 (TRPV1) channel on sensory neurons, improving ATP production, vascular function, fatigue resistance, and thus exercise performance. However, the underlying mechanisms of CAP-induced ergogenic effects and fatigue-resistance, remain elusive. To evaluate the potential anti-fatigue effects of CAP, 10 young healthy males performed constant-load cycling exercise time to exhaustion (TTE) trials (85% maximal work rate) after ingestion of placebo (PL; fiber) or CAP capsules in a blinded, counterbalanced, crossover design, while cardiorespiratory responses were monitored. Fatigue was assessed with the interpolated twitch technique, pre-post exercise, during isometric maximal voluntary contractions (MVC). No significant differences (p > 0.05) were detected in cardiorespiratory responses and self-reported fatigue (RPE scale) during the time trial or in TTE (375 ± 26 and 327 ± 36 s, respectively). CAP attenuated the reduction in potentiated twitch (PL: -52 ± 6 vs. CAP: -42 ± 11%, p = 0.037), and tended to attenuate the decline in maximal relaxation rate (PL: -47 ± 33 vs. CAP: -29 ± 68%, p = 0.057), but not maximal rate of force development, MVC, or voluntary muscle activation. Thus, CAP might attenuate neuromuscular fatigue through alterations in afferent signaling or neuromuscular relaxation kinetics, perhaps mediated via the sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) pumps, thereby increasing the rate of Ca2+ reuptake and relaxation.

Borderline-low testosterone levels are associated with lower left ventricular wall thickness in firefighters: An exploratory analysis.

BACKGROUND: Low endogenous testosterone has been associated with increased cardiovascular risk in men. OBJECTIVES: To determine the prevalence of low serum testosterone level (TT) in a cohort of male US career firefighters and to examine its relation with left ventricular wall thickness (LVWT). MATERIALS AND METHODS: We conducted a cross-sectional study among 341 career firefighters, (age: 37.5 ± 10.3 years; BMI: 28.9 ± 4.5 kg/m2 ), who underwent an occupational medical screening examination. TT quartiles were determined, and LVWT distribution among them was plotted. Then, TT values were categorized as low (<264 ng/dL), borderline (264-399 ng/dL), reference range (400-916 ng/dL), and high (>916 ng/dL). To further investigate the association of mildly decreased TT on LVWT, we divided the borderline group into borderline-low (264-319 ng/dL) and borderline-high (320-399 ng/dL) ranges. LVWT values were classified as low LVWT when <0.6 cm. A multivariate model was used to compare LVWT, age, BMI, systolic blood pressure (SBP), and HbA1c among groups by TT values. RESULTS: The prevalence of low TT was 10.6% and of borderline was 26.4%, while 58.7% had levels in the reference range. The low-TT group was older and had higher BMI and SBP as compared to the reference group (P < .01). LVWT values were different among groups (P = .04) and significantly lower in firefighters with borderline-low TT as compared to the reference group (P < .05). This finding also occurred within obese firefighters (P = .03). The borderline-low group had a higher adjusted risk for a low LVWT as compared to the reference group [OR: 4.11 (95% CI: 1.79-9.43)]. DISCUSSION: Our findings highlight the possible relationship between a mild reduction in testosterone levels (borderline) and lower LVWT. CONCLUSIONS: A high prevalence of subnormal TT levels (low and borderline: 37%) was observed in this relatively homogeneous cohort of career firefighters. Mildly decreased TT levels and lower LVWT might represent a preclinical condition and a window of opportunity for cardiovascular preventive interventions in firefighters.

Physiologic strain of SCBA confidence course training compared to circuit training and live-fire training.

Firefighting is a dangerous occupation and even training carries substantial risks. Self-contained breathing apparatus confidence courses (SCBACC) are a common type of training. PURPOSE: Compare the physiological strain of SCBACC to live-fire training (LFT) and circuit training (CT) among academy cadets. METHODS: Cadets wore physiologic status monitors to assess heart rate (HR) and estimated core temperature (ECT) during CT, LFT, and SCBACC of similar duration (33-38 min). RESULTS: Data from 52 cadet firefighters (28 ±â€¯4 yrs old) were analyzed. ECT (38.6 ±â€¯0.4 vs 39.3 ±â€¯0.7 vs. 39.3 ±â€¯0.6ᵒC), peak HR (182.6 ±â€¯9.1 vs. 192.7 ±â€¯9.5 vs 195.9 ±â€¯9.6 bpm), and age-predicted maximal HR (APMHR%; 94.6 ±â€¯4.6 vs 99.9 ±â€¯4.9 vs. 101.5 ±â€¯4.8%) were significantly (p < 0.05) lower for CT than SCBACC and LFT, respectively. CONCLUSIONS: SCBACC produced physiological strain greater than CT and similar to LFT. SCBACC resulted in sustained HR at 100% of age-predicted maximal values, a peak ECT of 39.3 °C, and should be considered as physiologically stressful as LFT.

Rehydrating efficacy of maple water after exercise-induced dehydration.

Dehydration impairs physiological function and physical performance, thus understanding effective rehydration strategies is paramount. Despite growing interest in natural rehydrating beverages, no study has examined maple water (MW). PURPOSE: To investigate the rehydrating efficacy of MW after exercise-induced dehydration. METHODS: Using a single-blind, counterbalanced, crossover design, we compared the rehydrating efficacy of MW vs. maple-flavored bottled water (control) in 26 young healthy (22 ± 4 yrs., 24 ± 4 kg/m2) males (n = 13) and females (n = 13) after exercise-induced dehydration (~ 2.0%ΔBody Weight [BW]) in the heat (30 °C, 50% relative humidity [RH]). Hydration indicators (BW, salivary and urine osmolality [SOsm/UOsm], urine specific gravity [USG], urine volume [UV], urine color [UC]), thirst, fatigue, and recovery (heart rate [HR)], and HR variability [HRV]) were taken at baseline, post-exercise, 0.5, 1, and 2 h post-consumption of 1 L of MW or control. RESULTS: Following similar dehydration (~ 2%ΔBW), MW had no differential (p > 0.05) impact on any measure of rehydration. Likely due to greater beverage osmolality (81 ± 1.4 vs. 11 ± 0.7 mOsmol/kg), thirst sensation remained 12% higher with MW (p <  0.05). When sex was considered, females had lower UV, elevated UOsm (p < 0.05), trends for higher ΔBW, USG, but similar SOsm. Analysis of beverages and urine for antioxidant potential (AP) revealed a four-fold greater AP in MW, which increased peak urine AP (9.4 ± 0.7 vs. 7.6 ± 1.0 mmol, MW vs. control, p <  0.05). CONCLUSION: Electrolyte-containing MW, was similar in effectiveness to water, but has antioxidant properties. Furthermore, trends for sex differences were discovered in urinary, but not salivary, hydration markers, with discrepancies in kinetics between fluid compartments both warranting further study.

Effects of Wrist Cooling on Recovery From Exercise-Induced Heat Stress With Firefighting Personal Protective Equipment.

OBJECTIVE: To determine the effects of wrist cooling on recovery from exercise-induced heat stress (EIHS) from wearing firefighting personal protective equipment (PPE) and self-contained breathing apparatus. METHODS: Using a single-blind, counterbalanced, crossover-design, in 11 healthy men, we measured heart rate (HR), HR variability (HRV), core temperature (TCore), thermal strain (TS), and fatigue at rest, during 30-minute of exercise in PPE+SCBA, and during recovery while wearing a wrist cooling band (control[off] vs cool[on]). RESULTS: No differences were observed between trials at baseline or during exercise, in HR, TCore, TS, or fatigue. Time to 50% and recovery were not different between trials. Upon recovery, TCore was lower, while HR, fatigue, HRV, and TS were relatively indifferent with cooling. CONCLUSION: Wrist cooling after EIHS only modestly enhanced recovery, questioning its implementation during on-scene rehabilitation of firefighters.

Effects of a combined protein and antioxidant supplement on recovery of muscle function and soreness following eccentric exercise.

BACKGROUND: An acute bout of eccentric contractions (ECC) cause muscle fiber damage, inflammation, impaired muscle function (MF) and muscle soreness (MS). Individually, protein (PRO) and antioxidant (AO) supplementation may improve some aspects of recovery from ECC, though have yet to be combined. We sought to determine if combined PRO and AO supplementation (PRO + AO) improves MS and MF following damaging ECC over PRO alone. METHODS: Sixty sedentary college-aged males participated in a randomized, single-blind, parallel design study of peak isometric torque (PIMT), peak isokinetic torque (PIKT), thigh circumference (TC), and muscle soreness (MS) of knee extensor muscles measured at baseline, immediately after and 1, 2, 6, and 24 h after completion of 100 maximal ECC. Immediately, 6 h, and 22 h post-ECC, participants consumed either: carbohydrate control (CHO; n = 14), PRO (n = 16), or PRO + AO (n = 17). RESULTS: At baseline MS, TC, MF, macro- and micro-nutrient intakes, and total work during the ECC were not different between groups (p > 0.05). PIMT and PIKT (both -25%∆), TC (~1%∆) and MS (~35%∆) all changed with time (p < 0.05). We observed a group by time effect for PIKT (PRO + AO and PRO > CHO, p < 0.05). At 24 h post ECC, there was a trend towards improved relative PIMT (~11%) and PIKT (~17%) for PRO + AO (~17%) and PRO (~11%) compared to CHO. An interaction indicated PRO + AO had lowest MS over time (PRO + AO > PRO & CHO, p < 0.05). CONCLUSIONS: Our results suggest PRO facilitates recovery of muscle function within 24 h following ECC, and addition of AO ameliorates MS more than PRO or CHO alone.