Non-invasive Measures of Core Temperature versus Ingestible Thermistor during Exercise in the Heat

International Journal of Exercise Science 10(2): 225-233, 2017 The accuracy of core temperature (Tc) thermometry from temporal, tympanic, and oral thermometry devices has been variable during exercise in a hot, humid environment. The purpose of the present study was to cross-validate temporal, two tympanic devices, and oral devices compared to an ingestible thermistor during exercise in a hot, humid environment. Fourteen young, active adults (6 women) completed a graded exercise test until voluntary exhaustion in an environmental chamber (35.5 ± 0.6 °C, 53.9 ± 5.8 % RH). There was no statistical difference in mean temperature between tympanic device 1 and pill-based core temperature (PBTc) measurements across all time points and were positively correlated (0.357; P\u3c0.001). Temperatures of tympanic device 2 were statistically higher than PBTc (37.8 ± 0.7 ºC vs. 37.6 ± 1.0 ºC; respectfully) (P=0.008). At all time points, temperatures for the second tympanic device and PBTc were positively correlated (0.192; P=0.043). Temporal and PBTc values did not differ across time points and were positively correlated (0.262; P=0.005) across all time points. Mean oral temperature was significantly less than mean PBTc across all time points. (37.0 ± 0.4 ºC vs. 37.6 ± 1.0 ºC, respectively) (P\u3c0.001). Across all time points, oral and PBTc were positively correlated (0.262; P=0.010). Tympanic and temporal devices can reflect Tc while exercising in a hot, humid environment. However, care should be taken when selecting the tympanic or temporal measurement device and validation is advised prior to heat illness mitigation in the field

Effects of Acute Cold Exposure on Plasma Biomarkers Associated with Cardiovascular Disease

Inflammatory cytokines and lipid mediators are used as biomarkers for CVD risk. Cold exposure has been suggested to improve some of these biomarkers. We measured cardiovascular inflammatory and lipid biomarkers to expand our knowledge of cold exposure and CVD risk. Interleukin-1 Beta (IL-1 B) and Chemokine Ligand 2 (CCL2) are inflammatory cytokines associated with various disease states. Free fatty acids (FFA) are released from fat cells in response to stress. We evaluated the effects of acute 30 min cold exposure on these blood biomarkers. We hypothesized that the inflammatory markers and plasma FFA levels would increase at 2-h post-cold exposure. Twenty subjects (9 females, 23.9±2.7sd y, 1.71±10.2sd m, 74.2±13.5sd kg, 19.4±7.4sd %BF, 64.5±15.3sd kg FFM) were subjected to a 30-min seated cold exposure while metabolic data was collected via indirect calorimetry. Shivering started immediately upon cold exposure and ceased within 10 seconds following cold exposure. Estimated resting energy expenditure (kcal/min) during the exposure period (1.73±0.7sd, 1.47±0.6sd, 1.36±1.0sd for min 5, 15, and 30, respectively) was two-fold higher than pre-cold. Venous plasma was collected at pre-cold period, immediately after cold exposure, and 2 h post-cold, centrifuged, and stored at -80 ºC for subsequent biomarker analysis. ELISAs were used to measure plasma inflammatory cytokines; interlukin-1 beta (IL-1 B) and chemokine ligand 2 (CCL2) biomarkers and plasma free fatty acid (FFA) during and following cold exposure. Pre-cold IL-1B (pg/ml), CCL2 (pg/ml), and FFA (mM) values were 19±3.6se, 2.4±0.7se, and 507±87se, respectively. Immediate post-cold values were 18±3.8se, 3.4±1.2se, and 412±42se, respectively. Finally, 2 h post-cold values were 20±3.6se, 2.6±0.7se, and 458±48se, respectively. There was a 3.4±0.7se (p\u3c0.05) increase in IL-1 B plasma levels immediately after cold exposure that lasted up to two hours. CCL2 plasma levels and FFA were not different from baseline during the post-cold period. We conclude that acute cold exposure may worsen CVD risk through a select inflammatory response. Additional analyses of our samples will expand the possible list of affected CVD risk biomarkers. Whether or not extended exposure to cold would exacerbate these marker levels or affect the other markers measured is not known

Cardiorespiratory Responses during 2-Person CPR using Two Assisted CPR Devices Versus Manual CPR

Active Compression-decompression-CPR (ACD-CPR) requires rescuers to perform work during both phases of CPR. ACD-CPR provides active pre-loading of a patient’s heart with venous return as well as enhanced stroke volume during resuscitation. Prolonged, one-person CPR is exhausting and associated with decayed CPR quality over time. Active compression-decompression-CPR (ACD-CPR) requires the rescuer to actively work during both phases of CPR. We evaluated the metabolic cost of manual CPR (M-CPR), ACD-CPR1, and ACD-CPR2 (with adhesive pad) during a 10-min resuscitation period. We hypothesized that the metabolic cost for the devices would be similar to M-CPR. Twenty (10 female) participants (23.5±3.5y, 165.8±25.6cm, 72.5±12.2kg) completed 3 randomized trials with performance feedback by investigators. Expired air was analyzed for estimations of metabolic cost via indirect calorimetry. Participants rested for 10 minutes before the baseline data collection followed by 10 min of CPR to simulate one-person CPR. Treatment effects were observed for VO2, METS, VCO2, RR, RQ, blood lactate, SBP, and RPE. No such effects were observed with HR and DBP as the observed condition differences for HR and DBP were not significantly different from each other. Blood lactate and SBP were significantly higher using ACD-CPR1 compared to MCPR and ACD-CPR2. Although a trend for elevated DBP was observed with ACD-CPR1, this was not significantly different. RQ values for the ACD-CPR1 device (1.0 ± 0.0) were significantly higher than the RQ values for M-CPR (0.9 ± 0.0) and ACD-CPR2 (0.9 ± 0.0). Assisted CPR using the ACD-CPR1 device is more stressful to the cardiorespiratory system as reflected by the higher SBP compared to the ACD-CPR1 or standard MCPR. Metabolically, the ACD-CPR1 required more VO2 and elicited higher RQ, RPE, and lactate values during 10-min simulated one-person resuscitation compared to M-CPR and ACD-CPR1. However, the ACD-CPR2 cardiorespiratory results were similar to that of M-CPR, despite the latter method’s higher rate of compressions (110/min) and passive decompressions

Effects of Acute Vaporized Nicotine in Non-tobacco Users at Rest and During Exercise

Smokers, and even non-smokers, may utilize vaporized nicotine delivered by electronic cigarette (EC) due to the perception that EC are “healthier” than traditional tobacco cigarettes. The effects of vaporized nicotine delivered by EC on resting blood pressure (BP) and metabolic rate (RMR), or BP and aerobic power during exercise have not been studied. This investigation tested the effects of acute vaporized nicotine inhalation by EC on resting BP and RMR and cycle exercise BP, metabolic responses, and aerobic power in young, normotensive non-smokers. Using a double-blind design, 20 subjects (10 female; 23.1±2.5 years, 1.69±0.1 m, 70.6±14.9 kg; 22.1±11.0% body fat) self-reporting as healthy and non-smoking participated. All subjects participated in two randomized trials: placebo (0 mg nicotine) or nicotine (18 mg nicotine). Participants inhaled from EC once every 30 s for 10 min (20 inhalations total) during each trial. RMR was assessed 40 min later by indirect calorimetry followed by an incremental cycle test. Participants’ pre-inhalation SBP, DBP, and HR were also not significantly different between conditions or from those averaged over the last 5 min of the indirect calorimetry protocol. Cotinine, a stable nicotine metabolite, was assessed on post-inhalation (i.e., 10 min) urine samples. The cotinine concentration ranges, as scored using the semi-quantitative urine analysis kit strips, were significantly higher (p-1) compared to placebo (0-10 ng•ml-1). RMR was assessed ~40 min after the last EC inhalation. RMR (p=0.39), VO2 (p=0.5), RQ (p=0.15), and HR (p=0.47) were not significantly different between the placebo and nicotine trials. Compared to the placebo trial, nicotine use resulted in a 3.7 mmHg lower resting SBP (p=0.04) but a 3.0 mmHg higher DBP (p=0.04). VO2peak was not different between the nicotine trial (2.3±0.8 L•min-1) and placebo trial (2.3±0.7 L•min-1) trials (p=0.77). No statistically distinguishable difference was observed for Wpeak between nicotine (201.0±53.8 W) and placebo (204.8±57.8 W) (p=0.29). There was a main effect of time over the cycle test for VO2 , energy expenditure, RQ, and HR but no between treatment effects. A main treatment effect was identified for DBP, which was higher following nicotine compared to placebo at all time points during the test (p=0.05). No time by treatment interaction was identified for any variable during exercise. Exercise DBPpeak after nicotine (79.4±7.6) was significantly higher (p=0.02) than placebo (74.9±8.3 mmHg). Peak SBP was not different between trials (p=0.14). Our results show that acute vaporized nicotine inhalation via EC increases resting and exercise DBP but does not affect RMR or cycle aerobic power in young, normotensive non-smokers

Energy Expenditure following Acute Cold Exposure

TACSM Abstract - Energy Expenditure following Acute Cold Exposure Stelly S, Bravo D, Hines N, Koehler L, Levi M and Fogt D Exercise Biochemistry & Metabolism Laboratory; Department of Kinesiology, Health & Nutrition; The University of Texas at San Antonio; San Antonio, TX Category: Masters Advisor / Mentor: Fogt, Donovan ([email protected]) ABSTRACT Whole body energy expenditure (i.e., RMR) increases during acute cold exposure. Whether this increase in energy expenditure persists in the post-cold term in humans due to non-shivering thermogenesis has not yet been evaluated. Therefore we tested the hypothesis that RMR would be different directly following acute cold exposure. RMR (kcal•min-1) was assessed via indirect calorimetry on eight (8) males and seven (7) females at six time points: prior to cold exposure (T1), at the end of 30 minutes of cold exposure (T2), immediately post-cold-post-shivering (T3), at 35 minutes post-cold (T4), at 75 minutes post-cold (T5), and at 115 minutes post-cold (T6). This RMR data for the aforementioned time points was analyzed using paired, dependent t-tests and one way ANOVA; the significance level was placed at p \u3c 0.05. The RMR data for each time point was as follows: T1 (1.19±0.21), T2 (2.30±0.94), T3 (1.37±0.25), T4 (1.12±0.19), T5 (1.14±0.22), and T6 (1.14±0.22). The analysis of the RMR data showed a significant difference between the cold (T2) data and all other time points (T1, T3, T4, T5, and T6). Additionally there was a significant difference between the pre-cold (T1) and the immediately post-cold (T3) data. However there was no significant difference between the pre-cold (T1) data when compared with the remaining post-cold data (T4 – T6). These results suggest that the human body is capable of returning RMR to baseline levels relatively immediately following the cessation of acute cold exposure

Determination of Anaerobic Threshold by Heart Rate or Heart Rate Variability using Discontinuous Cycle Ergometry

International Journal of Exercise Science 7(1) : 45-53, 2014. The purpose was to determine if heart rate (HR) and heart rate variability (HRV) responses would reflect anaerobic threshold (AT) using a discontinuous, incremental, cycle test. AT was determined by ventilatory threshold (VT). Cyclists (30.6±5.9y; 7 males, 8 females) completed a discontinuous cycle test consisting of 7 stages (6 min each with 3 min of rest between). Three stages were performed at power outputs (W) below those corresponding to a previously established AT, one at W corresponding to AT, and 3 at W above those corresponding to AT. The W at the intersection of the trend lines was considered each metric’s “threshold”. The averaged stage data for Ve, HR, and time- and frequency-domain HRV metrics were plotted versus W. The W at the “threshold” for the metrics of interest were compared using correlation analysis and paired-sample t-test. In all, several heart rate-related parameters accurately reflected AT with significant correlations (p≤0.05) were observed between AT W and HR, mean RR interval (MRR), low and high frequency spectral energy (LF and HR, respectively), high frequency peak (fHF), and HFxfHF metrics’ threshold W (i.e., MRRTW, etc.). Differences in HR or HRV metric threshold W and AT for all subjects were less than 14 W. The steady state data from discontinuous protocols may allow for a true indication of steady-state physiologic stress responses and corresponding W at AT, compared to continuous protocols using 1-2 min exercise stages

Changes in whole body bone mineral composition in a community-based pilot study designed for Mexican-American women at risk for type II diabetes

Changes in whole body bone mineral composition in a community-based pilot study designed for Mexican-American women at risk for type II diabetes David C. Castillo, B.S., Maria G. Placeres, B.S., Arely Perez, M.S., Danielle M. Bravo, B.S., Donovan L. Fogt, Ph.D., Zenong Yin, Ph.D. Mobile Health Laboratory, Department of Health and Kinesiology The University of Texas at San Antonio Classification of First Author (Master’s) Background: Osteoporosis is a serious public health concern in the United States that is expected to increase over the next several years, especially in women. The US Surgeon General’s Report on Bone Health states that individuals can decrease the risk of developing osteoporosis with proper combinations of nutrition and physical activity. Diet and exercise are two important factors that have been shown to prevent or delay the onset of type II diabetes, another national top health concern. Intensive lifestyle interventions, such as The Diabetes Prevention Program have shown that type II diabetes can be delayed or prevented by losing moderate amounts of weight through dietary changes and increased physical activity. It is not clear if a lifestyle intervention can impact bone health. Purpose: This pilot study examined the effects of lifestyle intervention (dietary and physical activity behavior modification) on bone mineral density (BMD) and bone mineral content (BMC). The intervention was a 14-week community-based pilot study, based on The Diabetes Prevention Program, designed to reduce risk for type II diabetes in high-risk Mexican American women. The research questions were: Did the lifestyle intervention affect the outcome measures (BMC and BMD)? Were there differences in BMC and BMD between age groups (low-age ≤45 yrs. vs. high-age \u3e45 yrs.)? Were there differences in BMC and BMD between body weight groups (≤78 kg vs. \u3e78.1 kg)? Methods: The study used a one-group pre- and post-test design. Twenty-five non-diabetic Mexican-American females (average age = 45, SD = 10.9; BMI 25-40) participated in a 14-week lifestyle intervention pilot study. Changes in BMD (g/cm2) and BMC (g) were measured at baseline and 14 weeks after baseline using whole body dual-energy x-ray absorptiometry (DXA). Results: results of paired t-test showed a significant increase in whole body BMC (p\u3c .0001) and a marginally significant increase in whole body BMD (p\u3c .06). Results of Analysis of Covariance revealed no significant difference in BMC between age groups and a marginally significant increase of BMD (p\u3c .07) in younger participants compared to older participants, after controlling pretest measure. There was a significant increase in BMC (p\u3c .01) and a marginally significant increase in BMD (p\u3c .08) in the high-body weight group compared to the low weight group after controlling for pretest measure. Conclusions: A lifestyle intervention that utilized a combination of physical activity and dietary modification showed great promise toward preventing the onset of osteoporosis, especially in heavier Mexican-American women

The Valsalva Maneuver for Assessment of Cardiovagal Baroreflex Sensitivity

The cardiovagal baroreflex is fundamental to understanding normal autonomic neural function, but can be difficult to assess. PURPOSE: In this study, we highlight the utility of the Valsalva maneuver for the assessment of cardiovagal baroreflex sensitivity during both vagal inhibition and activation. METHODS: Thirteen supine male subjects (21 ± .7 yrs; 173 ± 2 cm; 78 ± 4 kg) were instrumented with an electrocardiogram and a finger photoplethysmograph (Finometer, to assess beat-by-beat arterial pressure). Subjects then exhaled against resistance to an expiratory pressure of 40 mmHg for 15 s followed by a 2-min recovery. Subjects performed three trials, and we averaged systolic arterial pressure (SAP) reductions during phase II straining, and SAP increases during phase IV release from strain. Cardiovagal baroreflex sensitivity during vagal inhibition (phase II) and activation (phase IV) was assessed by calculating linear regressions between SAP and R-R interval. RESULTS: During phase II straining, SAP decreased by 26 ± 4 mmHg (mean ± SE), and during phase IV increased by 39 ± 6 mmHg. Correlation coefficients (r) during phase II were .92 ± .02, and .75 ± .04 during phase IV. Cardiovagal baroreflex sensitivity (β1x) was 11 ± 2 ms/mmHg during phase II, and 10 ± 2 ms/mmHg during phase IV. CONCLUSION: Our results demonstrate that the Valsalva maneuver is a simple, yet informative non-invasive technique yielding insight into dynamic changes of the cardiovagal baroreflex during both vagal inhibition and activation. This descriptive study identifies responses of apparently healthy, college-age men, and provides baseline data from which comparisons might be made with other matched subjects with conditions characterized by autonomic dysfunction

Arterial Pulse Wave Velocities are Unchanged Following 12 Weeks of Circuit Weight Training

Arterial stiffness is decreased after vigorous endurance training and increased after high-intensity resistance training. The effects of a combined program of moderate endurance and resistance exercise on arterial stiffness have not been determined. PURPOSE: To determine whether12 weeks of circuit weight training will decrease both central and peripheral arterial stiffness as estimated from pulse wave velocity (PWV). METHODS: Thirteen males and eight females (age 22 ± 2, height 162 ± 8 cm, weight 78 ± 20 kg) were assigned to control (n = 10) or exercise (n = 11) groups. Aerobic capacity and muscular strength were assessed before and at the end of the 12 week period. Arterial pressures and PWV (Doppler) were recorded every four weeks. Velocities from the carotid to femoral artery and from the femoral to dorsalis pedis artery were used as estimates of central and peripheral stiffness. RESULTS: Muscular strength increased by 26% (P = .001) and VO2 max increased by 17% (P = .06) following circuit training in the exercise group, but was unchanged for controls. Circuit weight training did not affect arterial pressures, (systolic = 117 ± 3, diastolic = 74 ± 3 mmHg; pooled across groups), or central and peripheral PWV (central PWV = 6.2 ± 0.6, peripheral PWV = 9.5 ± 0.7 m ∙ s-1; pooled across groups). CONCLUSIONS: In contrast to other reports of increases in arterial stiffness following high-intensity resistance training, increases in muscular strength following moderate-intensity exercise in the current study were not associated with increased arterial stiffness. Circuit training may be an appropriate exercise prescription to increase muscular strength for patients at risk for peripheral artery disease

Metabolic Responses of Two Assisted CPR Devices Versus Manual CPR during 1-Person CPR

Prolonged, one-person CPR is exhausting and associated with decayed CPR quality over time. Active compression-decompression-CPR (ACD-CPR) requires the rescuer to actively work during both phases of CPR. We evaluated the metabolic cost of manual CPR (M-CPR), ACD-CPR1, and ACD-CPR2 (with adhesive pad) during a 10-min resuscitation period. We hypothesized that the metabolic cost for the devices would be similar to M-CPR. Twenty (10 female) participants (23.5±3.5y, 165.8±25.6cm, 72.5±12.2kg) completed 3 randomized trials with performance feedback by investigators. Expired air was analyzed for estimations of metabolic cost via indirect calorimetry. Participants rested for 10 minutes before the baseline data collection followed by 10 min of CPR to simulate one-person CPR. Treatment effects were observed for VO2, METS, VCO2, HR, RR, blood lactate, and RPE. No such effect was observed for RQ, SBP, or DBP. VO2 (ml/kgBW/min) was significantly higher with ACD-CPR1 (17.8±1.4) vs. MCPR and ACD-CPR2 (15.9±0.9 and 14.2±1.1, respectively). Metabolic equivalent (MET) was significantly lower with ACD-CPR2 (4.1±0.3) vs. MCPR and ACD-CPR1 (4.7±0.3 and 5.1±0.4, respectively). All three groups’ blood lactate data differed significantly with ACD-CPR1 \u3e M-CPR \u3e ACD-CPR2. The RR required by the ACD-CPR1 during a 10 min CPR simulation is significantly higher than the ACD-CPR2 and M-CPR. No group differences were observed for RQ, SBP, or DBP. CPR performance metrics were averaged over the 10-min resuscitation period. RPE was significantly higher following ACD-CPR1 compared to both M-CPR and ACD-CPR2. The metabolic work required by the ACD-CPR2 during 10-min simulated one-person resuscitation (80/min) is far less than the ACD-CPR1. However, the ACD-CPR2 metabolic cost is similar to that of M-CPR, despite the latter method’s higher rate of compressions (110/min) and passive decompressions