Santiago Lorenzo

Heat acclimation improves exercise performance

This study examined the impact of heat acclimation on improving exercise performance in cool and hot environments. Twelve trained cyclists performed tests of maximal aerobic power (VO2max), time-trial performance, and lactate threshold, in both cool [13°C, 30% relative humidity (RH)] and hot (38°C, 30% RH) environments before and after a 10-day heat acclimation (∼50% VO2max in 40°C) program. The hot and cool condition VO2max and lactate threshold tests were both preceded by either warm (41°C) water or thermoneutral (34°C) water immersion to induce hyperthermia (0.8-1.0°C) or sustain normothermia, respectively. Eight matched control subjects completed the same exercise tests in the same environments before and after 10 days of identical exercise in a cool (13°C) environment. Heat acclimation increased VO2max by 5% in cool (66.8 ± 2.1 vs. 70.2 ± 2.3 ml·kg(-1)·min(-1), P = 0.004) and by 8% in hot (55.1 ± 2.5 vs. 59.6 ± 2.0 ml·kg(-1)·min(-1), P = 0.007) conditions. Heat acclimation improved time-trial performance by 6% in cool (879.8 ± 48.5 vs. 934.7 ± 50.9 kJ, P = 0.005) and by 8% in hot (718.7 ± 42.3 vs. 776.2 ± 50.9 kJ, P = 0.014) conditions. Heat acclimation increased power output at lactate threshold by 5% in cool (3.88 ± 0.82 vs. 4.09 ± 0.76 W/kg, P = 0.002) and by 5% in hot (3.45 ± 0.80 vs. 3.60 ± 0.79 W/kg, P < 0.001) conditions. Heat acclimation increased plasma volume (6.5 ± 1.5%) and maximal cardiac output in cool and hot conditions (9.1 ± 3.4% and 4.5 ± 4.6%, respectively). The control group had no changes in VO2max, time-trial performance, lactate threshold, or any physiological parameters. These data demonstrate that heat acclimation improves aerobic exercise performance in temperate-cool conditions and provide the scientific basis for employing heat acclimation to augment physical training programs.

Human cutaneous reactive hyperaemia: role of BKCa channels and sensory nerves

Reactive hyperaemia is the increase in blood flow following arterial occlusion. The exact mechanisms mediating this response in skin are not fully understood. The purpose of this study was to investigate the individual and combined contributions of (1) sensory nerves and large‐conductance calcium activated potassium (BKCa) channels, and (2) nitric oxide (NO) and prostanoids to cutaneous reactive hyperaemia. Laser‐Doppler flowmetry was used to measure skin blood flow in a total of 18 subjects. Peak blood flow (BF) was defined as the highest blood flow value after release of the pressure cuff. Total hyperaemic response was calculated by taking the area under the curve (AUC) of the hyperaemic response minus baseline. Infusates were perfused through forearm skin using microdialysis in four sites. In the sensory nerve/BKCa protocol: (1) EMLA® cream (EMLA, applied topically to skin surface), (2) tetraethylammonium (TEA), (3) EMLA®+ TEA (Combo), and (4) Ringer solution (Control). In the prostanoid/NO protocol: (1) ketorolac (Keto), (2) NG‐nitro‐l‐arginine methyl ester (l‐NAME), (3) Keto +l‐NAME (Combo), and (4) Ringer solution (Control). CVC was calculated as flux/mean arterial pressure and normalized to maximal flow. Hyperaemic responses in Control (1389 ± 794%CVCmax s) were significantly greater compared to TEA, EMLA and Combo sites (TEA, 630 ± 512, P= 0.003; EMLA, 421 ± 216, P < 0.001; Combo, 201 ± 200, P < 0.001%CVCmax s). Furthermore, AUC in Combo (Keto +l‐NAME) site was significantly greater than Control (4109 ± 2777 versus 1295 ± 368%CVCmax s). These data suggest (1) sensory nerves and BKCa channels play major roles in the EDHF component of reactive hyperaemia and appear to work partly independent of each other, and (2) the COX pathway does not appear to have a vasodilatory role in cutaneous reactive hyperaemia.

Heat acclimation improves cutaneous vascular function and sweating in trained cyclists

The aim of this study was to explore heat acclimation effects on cutaneous vascular responses and sweating to local ACh infusions and local heating. We also sought to examine whether heat acclimation altered maximal skin blood flow. ACh (1, 10, and 100 mM) was infused in 20 highly trained cyclists via microdialysis before and after a 10-day heat acclimation program [two 45-min exercise bouts at 50% maximal O(2) uptake (Vo(2max)) in 40°C (n = 12)] or control conditions [two 45-min exercise bouts at 50% Vo(2max) in 13°C (n = 8)]. Skin blood flow was monitored via laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC) was calculated as LDF ÷ mean arterial pressure. Sweat rate was measured by resistance hygrometry. Maximal brachial artery blood flow (forearm blood flow) was obtained by heating the contralateral forearm in a water spray device and measured by Doppler ultrasound. Heat acclimation increased %CVC(max) responses to 1, 10, and 100 mM ACh (43.5 ± 3.4 vs. 52.6 ± 2.6% CVC(max), 67.7 ± 3.4 vs. 78.0 ± 3.0% CVC(max), and 81.0 ± 3.8 vs. 88.5 ± 1.1% CVC(max), respectively, all P < 0.05). Maximal forearm blood flow remained unchanged after heat acclimation (290.9 ± 12.7 vs. 269.9 ± 23.6 ml/min). The experimental group showed significant increases in sweating responses to 10 and 100 mM ACh (0.21 ± 0.03 vs. 0.31 ± 0.03 mg·cm(-2)·min(-1) and 0.45 ± 0.05 vs. 0.67 ± 0.06 mg·cm(-2)·min(-1), respectively, all P < 0.05), but not to 1 mM ACh (0.13 ± 0.02 vs. 0.18 ± 0.02 mg·cm(-2)·min(-1), P = 0.147). No differences in any of the variables were found in the control group. Heat acclimation in highly trained subjects induced local adaptations within the skin microcirculation and sweat gland apparatus. Furthermore, maximal skin blood flow was not altered by heat acclimation, demonstrating that the observed changes were attributable to improvement in cutaneous vascular function and not to structural changes that limit maximal vasodilator capacity.

Quantitative myocardial-perfusion SPECT: Comparison of three state-of-the-art software packages

BackgroundWe almed to compare the automation and diagnostic performance in the detection of coronary artery disease (CAD) of the 4DMSPECT (4DM), Emory Cardiac Toolbox (EMO), and QPS systems for automated quantification of myocardial perfusion.Methods and ResultsWe studied 328 patients referred for rest/stress Tc-99m sestamibi imaging, 140 low-likelihood patients and 188 with angiography. Contours were corrected when necessary. All other processing was fully automated. A 17-segment analysis was performed, and a summed stress score (SSS) ≥4 was considered abnormal. The average SSSs (±SD) for 4DM, EMO, and QPS were 10.5±9.4, 11.1±8.3, and 10.1±8.9 respectively (P=.02 for QPS versus EMO). The receiver operator characteristics areas-under-the-curve for the detection of CAD (±SEM) were 0.84±0.03, 0.76±0.04, and 0.88±0.03 for 4DM, EMO, and QPS, respectively (P=.001 for QPS versus EMO, and P=.03 for 4DM versus EMO), Normalcy rate was higher for QPS and 4DM versus EMO, at 91% and 94% versus 77%, respectively (P=.02). Sensitivity was higher for QPS (87%) versus 4DM (80%) (P=.045). Specificity was higher for QPS (71%) versus EMO (49%) (P=.01). The accuracy rate was higher for QPS versus 4DM and EMO, at 83% versus 77% and 76%, respectively, (P=.05).ConclusionsThere are differences in myocardial-perfusion quantification, diagnostic performance, and degree of automation of software packages.

Quantitative Diagnostic Performance of Myocardial Perfusion SPECT with Attenuation Correction in Women

Attenuation correction (AC) for myocardial perfusion SPECT (MPS) had not been evaluated separately in women despite specific considerations in this group because of breast photon attenuation. We aimed to evaluate the performance of AC in women by using automated quantitative analysis of MPS to avoid any bias. Methods: Consecutive female patients—134 with a low likelihood (LLk) of coronary artery disease (CAD) and 114 with coronary angiography performed within less than 3 mo of MPS—who were referred for rest–stress electrocardiography-gated 99mTc-sestamibi MPS with AC were considered. Imaging data were evaluated for contour quality control. An additional 50 LLk studies in women were used to create equivalent normal limits for studies with AC and with no correction (NC). An experienced technologist unaware of the angiography and other results performed the contour quality control. All other processing was performed in a fully automated manner. Quantitative analysis was performed with the Cedars-Sinai myocardial perfusion analysis package. All automated segmental analyses were performed with the 17-segment, 5-point American Heart Association model. Summed stress scores (SSS) of ≥3 were considered abnormal. Results: CAD (≥70% stenosis) was present in 69 of 114 patients (60%). The normalcy rates were 93% for both NC and AC studies. The SSS for patients with CAD and without CAD for NC versus AC were 10.0 ± 9.0 (mean ± SD) versus 10.2 ± 8.5 and 1.6 ± 2.3 versus 1.8 ± 2.5, respectively; P was not significant (NS) for all comparisons of NC versus AC. The SSS for LLk patients for NC versus AC were 0.51 ± 1.0 versus 0.6 ± 1.1, respectively; P was NS. The specificity for both NC and AC was 73%. The sensitivities for NC and AC were 80% and 81%, respectively, and the accuracies for NC and AC were 77% and 78%, respectively; P was NS for both comparisons. Conclusion: There are no significant diagnostic differences between automated quantitative MPS analyses performed in studies processed with and without AC in women.

Quantification of Cardiorespiratory Fitness in Healthy Nonobese and Obese Men and Women

BACKGROUND The quantification and interpretation of cardiorespiratory fitness (CRF) in obesity is important for adequately assessing cardiovascular conditioning, underlying comorbidities, and properly evaluating disease risk. We retrospectively compared peak oxygen uptake (VO(2)peak) (ie, CRF) in absolute terms, and relative terms (% predicted) using three currently suggested prediction equations (Equations R, W, and G). METHODS There were 19 nonobese and 66 obese participants. Subjects underwent hydrostatic weighing and incremental cycling to exhaustion. Subject characteristics were analyzed by independent t test, and % predicted VO(2)peak by a two-way analysis of variance (group and equation) with repeated measures on one factor (equation). RESULTS VO(2)peak (L/min) was not different between nonobese and obese adults (2.35 ± 0.80 [SD] vs 2.39 ± 0.68 L/min). VO(2)peak was higher (P < .02) relative to body mass and lean body mass in the nonobese (34 ± 8 mL/min/kg vs 22 ± 5 mL/min/kg, 42 ± 9 mL/min/lean body mass vs 37 ± 6 mL/min/lean body mass). Cardiorespiratory fitness assessed as % predicted was not different in the nonobese and obese (91% ± 17% predicted vs 95% ± 15% predicted) using Equation R, while using Equation W and G, CRF was lower (P < .05) but within normal limits in the obese (94 ± 15 vs 87 ± 11; 101% ± 17% predicted vs 90% ± 12% predicted, respectively), depending somewhat on sex. CONCLUSIONS Traditional methods of reporting VO(2)peak do not allow adequate assessment and quantification of CRF in obese adults. Predicted VO(2)peak does allow a normalized evaluation of CRF in the obese, although care must be taken in selecting the most appropriate prediction equation, especially in women. In general, otherwise healthy obese are not grossly deconditioned as is commonly believed, although CRF may be slightly higher in nonobese subjects depending on the uniqueness of the prediction equation.

Lactate threshold predicting time-trial performance: impact of heat and acclimation

The relationship between exercise performance and lactate and ventilatory thresholds under two distinct environmental conditions is unknown. We examined the relationships between six lactate threshold methods (blood- and ventilation-based) and exercise performance in cyclists in hot and cool environments. Twelve cyclists performed a lactate threshold test, a maximal O(2) uptake (Vo(2max)) test, and a 1-h time trial in hot (38°C) and cool (13°C) conditions, before and after heat acclimation. Eight control subjects completed the same tests before and after 10 days of identical exercise in a cool environment. The highest correlations were observed with the blood-based lactate indexes; however, even the indirect ventilation-based indexes were well correlated with mean power during the time trial. Averaged bias was 15.4 ± 3.6 W higher for the ventilation- than the blood-based measures (P < 0.05). The bias of blood-based measures in the hot condition was increased: the time trial was overestimated by 37.7 ± 3.6 W compared with only 24.1 ± 3.2 W in the cool condition (P < 0.05). Acclimation had no effect on the bias of the blood-based indexes (P = 0.51) but exacerbated the overestimation by some ventilation-based indexes by an additional 34.5 ± 14.1 W (P < 0.05). Blood-based methods to determine lactate threshold show less bias and smaller variance than ventilation-based methods when predicting time-trial performance in cool environments. Of the blood-based methods, the inflection point between steady-state lactate and rising lactate (INFL) was the best method to predict time-trial performance. Lastly, in the hot condition, ventilation-based predictions are less accurate after heat acclimation, while blood-based predictions remain valid in both environments after heat acclimation.

Ventilatory Responses at Peak Exercise in Endurance-Trained Obese Adults

BACKGROUND Alterations in respiratory mechanics predispose healthy obese individuals to low lung volume breathing, which places them at risk of developing expiratory flow limitation (EFL). The high ventilatory demand in endurance-trained obese adults further increases their risk of developing EFL and increases their work of breathing. The objective of this study was to investigate the prevalence and magnitude of EFL in fit obese (FO) adults via measurements of breathing mechanics and ventilatory dynamics during exercise. METHODS Ten (seven women and three men) FO (mean ± SD, 38 ± 5 years, 38% ± 5% body fat) and 10 (seven women and three men) control obese (CO) (38 ± 5 years, 39% ± 5% body fat) subjects underwent hydrostatic weighing, pulmonary function testing, cycle exercise testing, and the determination of the oxygen cost of breathing during eucapnic voluntary hyperpnea. RESULTS There were no differences in functional residual capacity (43% ± 6% vs 40% ± 9% total lung capacity [TLC]), residual volume (21% ± 4% vs 21% ± 4% TLC), or FVC (111% ± 13% vs 104% ± 15% predicted) between FO and CO subjects, respectively. FO subjects had higher FEV1 (111% ± 13% vs 99% ± 11% predicted), TLC (106% ± 14% vs 94% ± 7% predicted), peak expiratory flow (123% ± 14% vs 106% ± 13% predicted), and maximal voluntary ventilation (128% ± 15% vs 106% ± 13% predicted) than did CO subjects. Peak oxygen uptake (129% ± 16% vs 86% ± 15% predicted), minute ventilation (128 ± 35 L/min vs 92 ± 25 L/min), and work rate (229 ± 54 W vs 166 ± 55 W) were higher in FO subjects. Mean inspiratory (4.65 ± 1.09 L/s vs 3.06 ± 1.21 L/s) and expiratory (4.15 ± 0.95 L/s vs 2.98 ± 0.76 L/s) flows were greater in FO subjects, which yielded a greater breathing frequency (51 ± 8 breaths/min vs 41 ± 10 breaths/min) at peak exercise in FO subjects. Mechanical ventilatory constraints in FO subjects were similar to those in CO subjects despite the greater ventilatory demand in FO subjects. CONCLUSION FO individuals achieve high ventilations by increasing breathing frequency, matching the elevated metabolic demand associated with high fitness. They do this without developing meaningful ventilatory constraints. Therefore, endurance-trained obese individuals with higher lung function are not limited by breathing mechanics during peak exercise, which may allow healthy obese adults to participate in vigorous exercise training.

Oxygen cost of breathing and breathlessness during exercise in nonobese women and men

INTRODUCTION Although it has been reported that the work of breathing may be higher in women, inconsistencies among studies leaves this important question unresolved. Also, the association between the oxygen cost of breathing and rating of perceived breathlessness (RPB) during exercise has not been examined between women and men. PURPOSE This study aimed to measure oxygen cost of breathing during eucapnic voluntary hyperpnea and RPB (Borg 0-10 scale) during 6 min of constant work rate cycling at 60 and 90 W, respectively, in healthy, nonobese women and men. METHODS A total of 9 women (27 yr, body mass index = 21 kg·m(-2)) and 10 men (29 yr, body mass index = 25 kg·m(-2)) participated. All subjects underwent pulmonary function testing, exercise cycling, and determination of oxygen cost of breathing during eucapnic voluntary hyperpnea. Oxygen cost of breathing was obtained from the slope of the oxygen uptake (mL·min(-1)) and ventilation (L·min(-1)) relationship. RPB and cardiorespiratory measures were collected during minute 6 of the exercise. Data were analyzed by independent t-test and regression analysis. RESULTS Age and pulmonary function were similar between the nonobese women and men. Oxygen cost of breathing was similar between the nonobese women (1.17 ± 0.26 mL·L(-1)) and men (1.21 ± 0.42 mL·(-1)L). RPB during exercise was similar between the women (2.1 ± 1.3) and men (2.6 ± 1.2) and was correlated (P < 0.05) with relative oxygen uptake (r = 0.55) but not the oxygen cost of breathing. CONCLUSIONS In nonobese women and men, oxygen cost of breathing is not different over the ventilatory ranges studied and RPB is similar at the same relative exercise intensity. In addition, the oxygen cost of breathing was not associated with RPB during constant work rate exercise.

Corrected End-Tidal P CO 2 Accurately Estimates Pa CO 2 at Rest and During Exercise in Morbidly Obese Adults

BACKGROUND Obesity affects lung function and gas exchange and imposes mechanical ventilatory limitations during exercise that could disrupt the predictability of Pa(CO(2)) from end-tidal P(CO(2)) (P(ETCO(2))), an important clinical tool for assessing gas exchange efficiency during exercise testing. Pa(CO(2)) has been estimated during exercise with good accuracy in normal-weight individuals by using a correction equation developed by Jones and colleagues (P(JCO(2)) = 5.5 + 0.9 x P(ETCO(2)) – 2.1 x tidal volume). The purpose of this project was to determine the accuracy of Pa(CO(2)) estimations from P(ETCO(2)) and P(JCO(2)) values at rest and at submaximal and peak exercise in morbidly obese adults. METHODS Pa(CO(2)) and P(ETCO(2)) values from 37 obese adults (22 women, 15 men; age, 39 ± 9 y; BMI, 49 ± 7; [mean ± SD]) were evaluated. Subjects underwent ramped cardiopulmonary exercise testing to volitional exhaustion. P(ETCO(2)) was determined from expired gases simultaneously with temperature-corrected arterial blood gases (radial arterial catheter) at rest, every minute during exercise, and at peak exercise. Data were analyzed using paired t tests. RESULTS P(ETCO(2)) was not significantly different from Pa(CO(2)) at rest (P(ETCO(2)) = 37 ± 3 mm Hg vs Pa(CO(2)) = 38 ± 3 mm Hg, P = .14). However, during exercise, P(ETCO(2)) was significantly higher than Pa(CO(2)) (submaximal: 42 ± 4 vs 40 ± 3, P < .001; peak: 40 ± 4 vs 37 ± 4, P < .001, respectively). Jones’ equation successfully corrected P(ETCO(2)), such that P(JCO(2)) was not significantly different from Pa(CO(2)) (submax: P(JCO(2)) = 40 ± 3, P = .650; peak: 37 ± 4, P = .065). CONCLUSION P(JCO(2)) provides a better estimate of Pa(CO(2)) than P(ETCO(2)) during submaximal exercise and at peak exercise, whereas at rest both yield reasonable estimates in morbidly obese individuals. Clinicians and physiologists can obtain accurate estimations of Pa(CO(2)) in morbidly obese individuals by using P(JCO(2)).