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Ground-level ozone (O 3 ) is a potent air pollutant well recognized to acutely induce adverse respiratory symptoms and impairments in pulmonary function. However, it is unclear how the hyperpnea of exercise may modulate these effects, and the subsequent consequences on exercise performance. We tested the hypothesis that pulmonary function and exercise capability would be diminished, and symptom development would be increased during peak real-world levels of O 3 exposure compared with room air. Twenty aerobically trained participants [13 M, 7 F; maximal O 2 uptake (V̇o 2max ), 64.1 ± 7.0 mL·kg -1 ·min -1 ] completed a three-visit double-blinded, randomized crossover trial. Following a screening visit, participants were exposed to 170 ppb O 3 or room air (<10 ppb O 3 ) on separate visits during exercise trials, consisting of a 25-min moderate-intensity warmup, 30-min heavy-intensity bout, and a subsequent time-to-exhaustion (TTE) performance test. No differences in O 2 uptake or ventilation were observed during submaximal exercise between conditions. During the TTE test, we observed significantly lower end-exercise O 2 uptake (-3.2 ± 4.3%, P = 0.004), minute ventilation (-3.2 ± 6.5%, P = 0.043), tidal volume (-3.6 ± 5.1%, P = 0.008), and a trend toward lower exercise duration in O 3 compared with room air (-10.8 ± 26.5%, P = 0.092). As decreases in O 2 uptake and alterations in respiratory pattern were also present at matched time segments between conditions, a limitation of oxygen transport seems likely during maximal exercise. A more comprehensive understanding of the direct mechanisms that limit oxygen transport during exercise in high-pollutant concentrations is key for mitigating performance changes. NEW & NOTEWORTHY We demonstrate that in highly trained endurance athletes, exposure to peak real-world levels of O 3 air pollution (170 ppb) significantly diminishes O 2 uptake along with corresponding changes in ventilation during maximal exercise. As no differences were observed during extended submaximal exercise, a combined effect of effective dose of pollution and exercise intensity on severity of responses seems likely.

Background: The physical environment can facilitate or hinder physical activity. A challenge in promoting physical activity is ensuring that the physical environment is supportive and that these supports are appropriately tailored to the individual or group in question. Ideally, aspects of the environment that impact physical activity would be enhanced, but environmental changes take time, and identifying ways to provide more precision to physical activity recommendations might be helpful for specific individuals or groups. Therefore, moving beyond a "one size fits all" to a precision-based approach is critical., Main Body: To this end, we considered 4 critical aspects of the physical environment that influence physical activity (walkability, green space, traffic-related air pollution, and heat) and how these aspects could enhance our ability to precisely guide physical activity. Strategies to increase physical activity could include optimizing design of the built environment or mitigating of some of the environmental impediments to activity through personalized or population-wide interventions., Conclusions: Although at present non-personalized approaches may be more widespread than those tailored to one person's physical environment, targeting intrinsic personal elements (e.g., medical conditions, sex, age, socioeconomic status) has interesting potential to enhance the likelihood and ability of individuals to participate in physical activity.

Background: Type 1 diabetes mellitus (T1DM) is associated with an increased risk for cardiovascular disease (CVD) related morbidity and premature mortality. Regular physical activity plays an important role in the primary and secondary prevention of CVD, improving overall health and wellbeing. Previous observational studies have examined the associations between self-reported physical activity and CVD risk factors in largely adult Caucasian populations. However, limited work has evaluated the relationship between objectively measured physical activity and CVD risk factors in other ethnicities, particularly Chinese youth living with T1DM., Methods: This cross-sectional study assessed CVD risk factors, physical activity, and aerobic fitness (and their associations) in Chinese youth living with T1DM (n = 48) and peers (n = 19) without T1DM. Primary outcomes included blood pressure, lipid profiles, and physical activity (accelerometry). Statistical differences between groups were determined with chi-square, independent-samples t-tests, or analysis of covariance. The associations between aerobic fitness, daily physical activity variables, and CVD risk factors were assessed with univariate and multivariate linear regression analyses., Results: Results were summarized using means and standard deviation (SD) for normally distributed variables and medians and 25-75th quartile for non-normally distributed variables. In comparison to peers without diabetes, youth living with T1DM showed higher levels of total cholesterol (3.14 ± 0.67 vs. 4.03 ± 0.81 mmol·L -1 , p = 0.001), low-density lipoprotein cholesterol (1.74 ± 0.38 vs. 2.31 ± 0.72 mmol·L -1 , p = 0.005), and triglycerides (0.60 ± 0.40 vs. 0.89 ± 0.31 mmol·L -1 p = 0.012), and lower maximal oxygen power (44.43 ± 8.29 vs. 35.48 ± 8.72 mL·kg -1 ·min -1 , p = 0.003), total physical activity counts (451.01 ± 133.52 vs. 346.87 ± 101.97 counts·min -1 , p = 0.004), metabolic equivalents (METs) (2.41 ± 0.60 vs. 2.09 ± 0.41 METs, p = 0.033), moderate-to-vigorous intensity physical activity [MVPA: 89.57 (61.00-124.14) vs (53.19 (35.68-63.16) min, p = 0.001], and the percentage of time spent in MVPA [11.91 (7.74-16.22) vs 8.56 (6.18-10.12) %, p = 0.038]. The level of high-density lipoprotein cholesterol was positively associated with METs (β = 0.29, p = 0.030, model R 2  = 0.168), and the level of triglycerides was negatively associated with physical activity counts (β = - 0.001, p = 0.018, model R 2 = 0.205) and METs (β = - 0.359, p = 0.015, model R 2 = 0.208), and positively associated with time spent in sedentary behaviour (β = 0.002, p = 0.041, model R 2  = 0.156) in persons living with T1DM., Conclusions: Chinese youth with T1DM, despite their young age and short duration of diabetes, present early signs of CVD risk, as well as low physical activity levels and cardiorespiratory fitness compared to apparently healthy peers without diabetes. Regular physical activity is associated with a beneficial cardiovascular profile in T1DM, including improvements in lipid profile. Thus, physical activity participation should be widely promoted in youth living with T1DM.

New Findings: What is the central question of this study? How does sternocleidomastoid blood flow change in response to increasing ventilation and whole-body exercise intensity? What is the main finding and its importance? Sternocleidomastoid blood flow increased with increasing ventilation. For a given ventilation, sternocleidomastoid blood flow was lower during whole-body exercise compared to resting hyperpnoea. These findings suggest that locomotor muscle work exerts an effect on respiratory muscle blood flow that can be observed in the sternocleidomastoid., Abstract: Respiratory muscle work influences the distribution of blood flow during exercise. Most studies have focused on blood flow to the locomotor musculature rather than the respiratory muscles, owing to the complex anatomical arrangement of respiratory muscles. The purpose of this study was to examine how accessory respiratory (i.e. sternocleidomastoid, and muscles in the intercostal space) muscle blood flow changes in response to locomotor muscle work. Seven men performed 5 min bouts of constant load cycling exercise trials at 30%, 60% and 90% of peak work rate in a randomized order, followed by 5 min bouts of voluntary hyperpnoea (VH) matching the ventilation achieved during each exercise (EX) trial. Blood-flow index (BFI) of the vastus lateralis, sternocleidomastoid (SCM) and seventh intercostal space (IC) were estimated using near-infrared spectroscopy and indocyanine green and expressed relative to resting levels. BFI SCM was greater during VH compared to EX (P = 0.002) and increased with increasing exercise intensity (P = 0.036). BFI SCM reached 493 ± 219% and 301 ± 215% rest during VH and EX at 90% peak work rate, respectively. BFI IC increased to 242 ± 178% and 210 ± 117% rest at 30% peak work rate during VH and EX, respectively. No statistically significant differences in BFI IC were observed with increased work rate during VH or EX (both P > 0.05). Moreover, there was no observed difference in BFI IC between conditions (P > 0.05). BFI SCM was lower for a given minute ventilation during EX compared to VH, suggesting that accessory respiratory muscle blood flow is influenced by whole-body exercise., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Purpose: To examine the association between day-to-day resting cardiac parasympathetic variability over consecutive non-training days (i.e. weekend) and accumulated exercise stress when quantified using indices of cardiovascular strain. Methods: Twelve international calibre female field hockey players training as part of a national team were participants over a four-week mesocycle prior to a 2016 Olympic qualifying tournament. On-field exercise stress was examined using heart rate (HR) dynamics and quantified as; (1) training load and (2) time (min) spent above anaerobic threshold. The square root of the mean squared differences of successive cardiac cycles (R-R intervals) recorded on Saturday and Sunday were individually calculated and log-transformed prior to being averaged (Ln rMSSDweekend). Day-to-day variation in Ln rMSSD over the weekend was expressed using the coefficient of variation (Ln rMSSD CV ). Non-linear regression analysis examined the association between accumulated exercise stress and Ln rMSSD CV . Results: A quadratic association between each index of exercise stress and Ln rMSSD CV was identified. After converting the coefficient of determination into a correlation coefficient (90% CL), the respective association between Ln rMSSD CV and training load (AU); r  = 0.40 (0.16:0.59) and time above threshold; r  = 0.35 (0.06:0.59) were observed. Conclusion: Ln rMSSD CV derived over consecutive non-training days displayed a moderate, yet significant association between accumulated exercise stress when expressed as global or high-intensity indices of cardiovascular strain. Weekend assessments may offer a practical and appropriate juncture between microcycles to assess the magnitude of perturbation in cardiac autonomic homeostasis prior to entering subsequent training periods.

Background: The combined effects of physical activity and air pollution exposure on vascular function are insufficiently understood, particularly after the inhalation of a β 2 -agonist, a vasodilating agent., Objective: To assess the micro- and macrovascular response to physical activity after β 2 -agonist use while breathing diesel exhaust (DE) in individuals with exercise-induced bronchoconstriction., Methods: On four exposure visits, eighteen adults inhaled either 400 μg of the β 2 -agonist salbutamol or placebo before resting for 60 min, followed by a 30-min cycling bout. During rest and cycling, participants inhaled filtered air (FA) or DE (300 μg/m 3 of PM 2.5 ). Microvascular (central retinal arteriolar and venular equivalents, CRAE and CRVE, respectively) and macrovascular parameters (blood pressure (BP)) and heart rate (HR)) were assessed at baseline (T 1 ), 10 min (T 2 ) and 70 min (T 3 ) after cycling., Results: The cycling bout increased CRAE (T 2 -T 1 difference (95th % confidence interval): 4.88 μm (4.73, 5.00 μm), p < 0.001; T 3 -T 1 difference: 2.10 μm (1.62, 2.58 μm), p = 0.031) and CRVE (T 2 -T 1 difference: 3.78 μm (3.63, 3.92 μm), p < 0.001; T 3 -T 1 difference: 3.73 μm (3.63, 3.92 μm), p < 0.001). The exposure to DE had no effect on CRAE (FA-DE difference at T 2 : 0.46 μm (-0.02, 0.92 μm); p = 0.790; FA-DE difference at T 3 : 1.76 μm (1.36, 2.16 μm), p = 0.213) and CRVE (FA-DE difference at T 2 : 0.26 μm (-0.35, 0.88 μm), p = 0.906; FA-DE difference at T 3 : 0.55 μm (0.05, 1.06 μm), p = 0.750). Compared to T 1 , systolic BP was decreased at T 2 by 2.5 mmHg (2.8, 2.3 mmHg, p = 0.047), independent of inhaled exposure. Heart rate at T 2 was significantly increased by 3 bpm (2, 3 bpm, p = 0.025) after the DE-exposure when compared to FA., Discussion: Acute physical activity induces a vasodilatory response in the micro- and macrovasculature in healthy adults by increasing CRAE and CRVE, and by reducing systolic BP post exercise, despite breathing DE. The DE-associated increase in HR might be indicative of an increased sympathetic response to physical activity while breathing DE., Competing Interests: Declaration of competing interest MSK acted as a consultant for GlaxoSmithKline, a manufacturer of salbutamol on November 4th, 2016. The other authors declare they have no actual or potential competing financial interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Perrotta, AS, Taunton, JE, Koehle, MS, White, MD, and Warburton, DER. Monitoring the prescribed and experienced heart rate-derived training loads in elite field hockey players. J Strength Cond Res 33(5): 1394-1399, 2019-This study examined the congruence between the prescribed and experienced heart rate-derived training loads over a 5-week periodized mesocycle. Twenty-four elite female field hockey players training as part of a national team were monitored before an (FIH) Hockey World League tournament. Three on-field training sessions per week were prospectively designed focusing on technical, tactical, and physiologically oriented hockey drills. A training load value, modeling the periodized weekly loading scheme, was prescribed for each training session and was calculated using normative training load responses from performing on-field hockey drills. Magnitude-based inferences focusing on the effect size (ES) and a Pearson correlation coefficient (r) were used to examine the degree of difference and the strength of correlation between the prescribed and experienced training loads. A significant correlation was observed between the experienced and prescribed training loads over the 5-week mesocycle (r = 0.92, 90% confidence limit [CL] [0.84-0.96]). The percentage difference and the ES between the achieved and prescribed training loads were as follows: week 1 demonstrated a 2.0% difference (ES = 0.10, 90% CL [-0.22-0.41]), week 2 a -5.4% difference (ES = -0.41, 90% CL [-0.75 to -0.07]), week 3 a -1.5% difference (ES = -0.09, 90% CL [-0.37 to 0.20]), week 4 a 7.1% difference (ES = 0.46, 90% CL [0.14-0.78]), and week 5 a 3.5% difference (ES = 0.18, 90% CL [-0.17 to 0.53]). This investigation demonstrates the efficacy for coaches to prospectively design on-field training sessions using normative training load data to enhance the congruence between the prescribed and experienced training loads over a periodized mesocycle.

Background: Exposure to air pollution impairs aspects of pulmonary and autonomic function and causes pulmonary inflammation. However, how exercising in air pollution affects these indices is poorly understood. Therefore, the purpose of this study was to determine the effects of low-intensity and high-intensity cycling with diesel exhaust (DE) exposure on pulmonary function, heart rate variability (HRV), fraction of exhaled nitric oxide (FeNO), norepinephrine and symptoms., Methods: Eighteen males performed 30-min trials of low-intensity or high-intensity cycling (30 and 60% of power at VO 2peak ) or a resting control condition. For each subject, each trial was performed once breathing filtered air (FA) and once breathing DE (300μg/m 3 of PM 2.5 , six trials in total). Pulmonary function, FeNO, HRV, norepinephrine and symptoms were measured prior to, immediately post, 1 h and 2 h post-exposure. Data were analyzed using repeated-measures ANOVA., Results: Throat and chest symptoms were significantly greater immediately following DE exposure than following FA (p < 0.05). FeNO significantly increased 1 h following high-intensity exercise in DE (21.9 (2.4) vs. 19.3 (2.2) ppb) and FA (22.7 (1.7) vs. 19.9 (1.4)); however, there were no differences between the exposure conditions. All HRV indices significantly decreased following high-intensity exercise (p < 0.05) in DE and FA. The exception to this pattern was LF (nu) and LF/HF ratio, which significantly increased following high-intensity exercise (p < 0.05). Plasma norepinephrine (NE) significantly increased following high-intensity exercise in DE and FA, and this increase was greater than following rest and low-intensity exercise (p < 0.05). DE exposure did not modify any effects of exercise intensity on HRV or norepinephrine., Conclusions: Healthy individuals may not experience greater acute pulmonary and autonomic effects from exercising in DE compared to FA; therefore, it is unclear if such individuals will benefit from reducing vigorous activity on days with high concentrations on particulate matter.

New Findings: What is the central question of this study? Does manipulation of the work of breathing during high-intensity exercise alter respiratory and locomotor muscle blood flow? What is the main finding and its importance? We found that when the work of breathing was reduced during exercise, respiratory muscle blood flow decreased, while locomotor muscle blood flow increased. Conversely, when the work of breathing was increased, respiratory muscle blood flow increased, while locomotor muscle blood flow decreased. Our findings support the theory of a competitive relationship between locomotor and respiratory muscles during intense exercise. Manipulation of the work of breathing (WOB) during near-maximal exercise influences leg blood flow, but the effects on respiratory muscle blood flow are equivocal. We sought to assess leg and respiratory muscle blood flow simultaneously during intense exercise while manipulating WOB. Our hypotheses were as follows: (i) increasing the WOB would increase respiratory muscle blood flow and decrease leg blood flow; and (ii) decreasing the WOB would decrease respiratory muscle blood flow and increase leg blood flow. Eight healthy subjects (n = 5 men, n = 3 women) performed a maximal cycle test (day 1) and a series of constant-load exercise trials at 90% of peak work rate (day 2). On day 2, WOB was assessed with oesophageal balloon catheters and was increased (via resistors), decreased (via proportional assist ventilation) or unchanged (control) during the trials. Blood flow was assessed using near-infrared spectroscopy optodes placed over quadriceps and the sternocleidomastoid muscles, coupled with a venous Indocyanine Green dye injection. Changes in WOB were significantly and positively related to changes in respiratory muscle blood flow (r = 0.73), whereby increasing the WOB increased blood flow. Conversely, changes in WOB were significantly and inversely related to changes in locomotor blood flow (r = 0.57), whereby decreasing the WOB increased locomotor blood flow. Oxygen uptake was not different during the control and resistor trials (3.8 ± 0.9 versus 3.7 ± 0.8 l min -1 , P > 0.05), but was lower on the proportional assist ventilator trial (3.4 ± 0.7 l min -1 , P < 0.05) compared with control. Our findings support the concept that respiratory muscle work significantly influences the distribution of blood flow to both respiratory and locomotor muscles., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

Key Points: High work of breathing and exercise-induced arterial hypoxaemia (EIAH) can decrease O 2 delivery and exacerbate exercise-induced quadriceps fatigue in healthy men. Women have a higher work of breathing during exercise, dedicate a greater fraction of whole-body V̇O2 towards their respiratory muscles and develop EIAH. Despite a greater reduction in men's work of breathing, the attenuation of quadriceps fatigue was similar between the sexes. The degree of EIAH was similar between sexes, and regardless of sex, those who developed the greatest hypoxaemia during exercise demonstrated the most attenuation of quadriceps fatigue. Based on our previous finding that women have a greater relative oxygen cost of breathing, women appear to be especially susceptible to work of breathing-related changes in quadriceps muscle fatigue., Abstract: Reducing the work of breathing or eliminating exercise-induced arterial hypoxaemia (EIAH) during exercise decreases the severity of quadriceps fatigue in men. Women have a greater work of breathing during exercise, dedicate a greater fraction of whole-body V̇O2 towards their respiratory muscles, and demonstrate EIAH, suggesting women may be especially susceptible to quadriceps fatigue. Healthy subjects (8 male, 8 female) completed three constant load exercise tests over 4 days. During the first (control) test, subjects exercised at ∼85% of maximum while arterial blood gases and work of breathing were assessed. Subsequent constant load exercise tests were iso-time and iso-work rate, but with EIAH prevented by inspiring hyperoxic gas or work of breathing reduced via a proportional assist ventilator (PAV). Quadriceps fatigue was assessed by measuring force in response to femoral nerve stimulation. For both sexes, quadriceps force was equally reduced after the control trial (-27 ± 2% baseline) and was attenuated with hyperoxia and PAV (-18 ± 1 and -17 ± 2% baseline, P < 0.01, respectively), with no sex difference. EIAH was similar between the sexes, and regardless of sex, subjects with the lowest oxyhaemoglobin saturation during the control test had the greatest quadriceps fatigue attenuation with hyperoxia (r 2  = 0.79, P < 0.0001). For the PAV trial, despite reducing the work of breathing to a greater degree in men (men: 60 ± 5, women: 75 ± 6% control, P < 0.05), the attenuation of quadriceps fatigue was similar between the sexes (36 ± 4 vs. 37 ± 7%). Owing to a greater relative V̇O2 of the respiratory muscles in women, less of a change in work of breathing is needed to reduce quadriceps fatigue., (© 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society.)

In this study we tested the hypothesis that inspiring a low-density gas mixture (helium-oxygen; HeO2) would minimize mechanical ventilatory constraints and preferentially increase exercise performance in females relative to males. Trained male (n = 11, 31 yr) and female (n = 10, 26 yr) cyclists performed an incremental cycle test to exhaustion to determine maximal aerobic capacity (V̇o2max; male = 61, female = 56 ml·kg(-1)·min(-1)). A randomized, single-blinded crossover design was used for two experimental days where subjects completed a 5-km cycling time trial breathing humidified compressed room air or HeO2 (21% O2:balance He). Subjects were instrumented with an esophageal balloon for the assessment of respiratory mechanics. During the time trial, we assessed the ability of HeO2 to alleviate mechanical ventilatory constraints in three ways: 1) expiratory flow limitation, 2) utilization of ventilatory capacity, and 3) the work of breathing. We found that HeO2 significantly reduced the work of breathing, increased the size of the maximal flow-volume envelope, and reduced the fractional utilization of the maximal ventilatory capacity equally between men and women. The primary finding of this study was that inspiring HeO2 was associated with a statistically significant performance improvement of 0.7% (3.2 s) for males and 1.5% (8.1 s) for females (P < 0.05); however, there were no sex differences with respect to improvement in time trial performance (P > 0.05). Our results suggest that the extent of sex-based differences in airway anatomy, work of breathing, and expiratory flow limitation is not great enough to differentially affect whole body exercise performance., (Copyright © 2015 the American Physiological Society.)

Purpose: An acute reduction in blood pressure observed after a single bout of exercise is termed post-exercise hypotension (PEH). In contrast to moderate intensity aerobic exercise, little is known about the PEH response following high-intensity interval exercise. The present purpose is to assess how sex and training status impact PEH following high-intensity interval exercise., Methods: Cardiac volumes and function via echocardiography were measured in 40 normotensive, endurance-trained (ET) and normally active (NA) men and women (Age ± SD = 30.5 ± 5.7) following high-intensity interval cycle exercise. Continuous measurements of ECG and beat-by-beat blood pressure were collected before and 30 min post-exercise for determination of cardiovagal baroreflex function (BRS and αLF), spectral analysis of heart rate and systolic blood pressure (SBP LF)., Results: Post-exercise systolic BP was significantly reduced from baseline, occurring to a greater degree in ET compared with NA (-12.9 vs. -5.3 mmHg, P = 0.008), while mean arterial pressure was similarly reduced in all groups (-4.6 mmHg, P = 0.003). Despite reduced SVI and TPRI, CI was increased post-exercise (P < 0.01). ET experienced a greater decrease in αLF (P = 0.037) and increase in SBP LF (P = 0.017) than NA. Lean body mass was a significant predictor of change in SBP LF (Std. β = 0.735, P = 0.008)., Conclusions: These results characterize greater depressions in cardiovagal baroreflex function, and increased sympathetic activity, following vigorous exercise in endurance-trained individuals compared with normally active participants. This heightened sympathovagal balance after high-intensity exercise may be a compensatory mechanism in response to greater peripheral blood flow demands following vigorous exercise.

Exercise-induced arterial hypoxemia (EIAH) occurs in some healthy humans at sea-level, whereby the most aerobically trained individuals develop the most severe hypoxemia. A female competitive runner completed 2 maximal exercise tests. Maximal oxygen consumption increased by 15% between testing days, but the degree of hypoxemia remained similar (PaO2, SaO2; 82 and 80 mm Hg; 93.8% and 92.8%; first and second test, respectively). Our case indicates that EIAH does not necessarily worsen with aerobic training.

The health benefits of exercise are well known. Many of the most accessible forms of exercise, such as walking, cycling, and running often occur outdoors. This means that exercising outdoors may increase exposure to urban air pollution. Regular exercise plays a key role in improving some of the physiologic mechanisms and health outcomes that air pollution exposure may exacerbate. This problem presents an interesting challenge of balancing the beneficial effects of exercise along with the detrimental effects of air pollution upon health. This article summarizes the pulmonary, cardiovascular, cognitive, and systemic health effects of exposure to particulate matter, ozone, and carbon monoxide during exercise. It also summarizes how air pollution exposure affects maximal oxygen consumption and exercise performance. This article highlights ways in which exercisers could mitigate the adverse health effects of air pollution exposure during exercise and draws attention to the potential importance of land use planning in selecting exercise facilities.

High-intensity exercise induces marked physiological stress affecting the secretion of catecholamines. Sustained elevations in catecholamines are thought to desensitize cardiac beta receptors and may be a possible mechanism in impaired cardiac function following strenuous exercise. In addition, attenuated arterial-ventricular coupling may identify vascular mechanisms in connection with postexercise attenuations in ventricular function. Thirty-nine normally active (NA) and endurance-trained (ET) men and women completed an echocardiographic evaluation of left ventricular function before and after an acute bout of high-intensity interval exercise (15 bouts of 1:2 min work:recovery cycling: 100% peak power output and 50 W, respectively). Following exercise, time to peak twist and peak untwisting velocity were delayed (P < 0.01) but did not differ by sex or training status. Interactions for sex and condition (rest vs. exercise) were found for longitudinal diastolic strain rate (men, 1.46 ± 0.19 to 1.28 ± 0.23 s(-1) vs. women, 1.62 ± 0.25 to 1.63 ± 0.26 s(-1); P = 0.01) and arterial elastance (men 2.20 ± 0.65 to 3.24 ± 1.02 mmHg · ml(-1) · m(-2) vs. women 2.51 ± 0.61 to 2.93 ± 0.68 mmHg · ml(-1) · m(-2); P = 0.04). No cardiac variables were found associated with catecholamine levels. The change in twist mechanics was associated with baseline aortic pulse-wave velocity (r(2) = 0.27, P = 0.001). We conclude that males display greater reductions in contractility in response to high-intensity interval exercise, independent of catecholamine concentrations. Furthermore, a novel association of arterial stiffness and twist mechanics following high-intensity acute exercise illustrates the influence of vascular integrity on cardiac mechanics.

The purpose of this study was to characterize exercise-induced arterial hypoxaemia (EIAH), pulmonary gas exchange and respiratory mechanics during exercise, in young healthy women. We defined EIAH as a >10 mmHg decrease in arterial oxygen tension ( ) during exercise compared to rest. We used a heliox inspirate to test the hypothesis that mechanical constraints contribute to EIAH. Subjects with a spectrum of aerobic capacities (n = 30; maximal oxygen consumption ( ) = 49 ± 1, range 28-62 ml kg(-1) min(-1)) completed a stepwise treadmill test and a subset (n = 18 with EIAH) completed a constant load test (~85% ) with heliox gas. Throughout exercise arterial blood gases, oxyhaemoglobin saturation ( ), the work of breathing (WOB) and expiratory flow limitation (EFL) were assessed. Twenty of the 30 women developed EIAH with a nadir and ranging from 58 to 88 mmHg and 87 to 96%, respectively. At maximal exercise, was inversely related to (r = -0.57, P < 0.05) with notable exceptions where some subjects with low aerobic fitness levels demonstrated EIAH. Subjects with EIAH had a greater (51 ± 1 vs. 43 ± 2 ml kg(-1) min(-1)), lower end-exercise (93.2 ± 0.5 vs. 96.1 ± 0.3%) and a greater maximal energetic WOB (324 ± 19 vs. 247 ± 23 J min(-1)), but had similar resting pulmonary function compared to those without EIAH. Most subjects developed EIAH at submaximal exercise intensities, with distinct patterns of hypoxaemia. In some subjects with varying aerobic fitness levels, mechanical ventilatory constraints (i.e. EFL) were the primary mechanism associated with the hypoxaemia during the maximal test. Mechanical ventilatory constraints also prevented adequate compensatory alveolar hyperventilation in most EIAH subjects. Minimizing mechanical ventilatory constraints with heliox inspiration partially reversed EIAH in subjects who developed EFL. In conclusion, healthy women of all aerobic fitness levels can develop EIAH and begin to do so at submaximal intensities. Mechanical ventilatory constraints are a primary mechanism for EIAH in some healthy women and prevent reversal of hypoxaemia in women for whom it is not the primary mechanism.

Purpose: To determine the effect of pre-exercise exposure to diesel exhaust (DE) on 20-km cycling performance, pulmonary function, and cardio-respiratory variables during exercise., Methods: Eight endurance-trained males participated in the study. Test days consisted of a 60-min exposure to either filtered air (FA) or DE, followed by a 20 km cycling time trial. Exposures to DE were at a concentration of 300 µg/m³ of PM(2.5). Forced expiratory volume in 1 s (FEV₁) and forced vital capacity (FVC) were measured before and after exposure, and after exercise. Oxygen consumption (VO₂) and carbon dioxide production (VCO₂), minute ventilation (V(E)), tidal volume (V(T)), breathing frequency (F(B)), heart rate and oxyhemoglobin saturation (SpO₂), were collected during the time trials. The effect of condition on time trial duration, an order effect, and mean cardio-respiratory variables were each analysed using paired T-tests. Repeated-measures ANOVA were used to assess the effect of DE exposure on pulmonary function., Results: There was a main effect of condition (FA vs. DE) on the change in FEV₁ from baseline, and in exercise heart rate. Post hoc tests revealed that exercise-induced bronchodilation was significantly attenuated following DE compared to FA. There were no main effects of condition on 20 km cycling performance, or VO₂, VCO₂, V(E), V(T), F(B) and SpO₂ during a 20 km time trial., Conclusion: A 60-min exposure to DE prior to exercise significantly attenuated exercise-induced bronchodilation and significantly increased heart rate during exercise. Pre-exercise exposure to diesel exhaust did not significantly impair 20 km cycling time trial performance.

A healthy 36-year-old untrained (maximal oxygen consumption (V(O2max)): 39 mL/kg/min) woman completed multiple graded exercise tests on a treadmill. Temperature-corrected arterial blood samples were obtained in addition to esophageal pressure. Significant hypoxemia (-13 mm Hg arterial oxygen tension decrease) and arterial oxyhemoglobin desaturation (-6% decrease) was observed relative to rest and occurred during submaximal exercise and worsened at maximal intensities. Expiratory flow limitation (28-40% intersection of tidal volume) was present at near-maximal intensities. Relieving mechanical ventilatory constraints with a helium inspirate (79% He:21% O(2)) partially reversed the hypoxemia. Conversely, increasing chemical ventilatory stimuli, with hypercapnia (3.5% CO(2)), failed to increase ventilation. Maintaining oxyhemoglobin saturation, via a mildly hyperoxic (26% O(2)) inspirate, increased exercise duration (+45 s) and V(O2max) (+5 mL/kg/min). We attribute the hypoxemia to an excessive A-a(O2) resulting from ventilation-perfusion mismatch and secondarily to mechanical ventilatory constraints. We conclude that a healthy untrained woman can develop EIAH and this remains stable over a period of 6 months., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The purpose of this study was to determine if healthy young women of various aerobic fitness levels are vulnerable to intrapulmonary arteriovenous shunts (IPAVS) at sub maximal work rates. Female volunteers (n=24) performed semi-recumbent cycling exercise to exhaustion and agitated saline contrast echocardiography was used to determine the presence of IPAVS at rest, during exercise, and post exercise. Subjects were classified as untrained (UT, n=8), moderately trained (MT, n=6) and highly trained (HT, n=10) based on their respective (V(O(2,peak)) (UT=35±5; MT=43±1 and HT = 50 ± 3 ml kg(-1) min(-1)). We found that the % (V(O(2,peak)) at IPAVS onset was not significantly different between women of varying fitness (P>0.05). The majority of individuals exhibited IPAVS during modest levels of exercise intensity. In conclusion, there is no association between aerobic capacity or exercise intensity at IPAVS onset in women performing semi-recumbent cycle exercise., (Copyright © 2012 Elsevier B.V. All rights reserved.)

We tested the hypothesis that following an acute bout of exercise cardiovascular and cerebrovascular responses to lower-body negative pressure (LBNP) would be altered due to post-exercise hypotension (PEH). Ten healthy, male, endurance-trained athletes (mean age +/- SD = 29.6 +/- 5) were assessed for cardiovascular and cerebrovascular responses to LBNP following acute bouts of interval and continuous exercise. Mean arterial pressure (MAP), cardiac output, total peripheral resistance, heart rate variability, and total cerebral oxygen index were determined during a baseline LBNP session. These indices were also determined during two other LBNP sessions: following an acute bout of interval exercise, and following an acute bout of continuous exercise. Compared with baseline, MAP was reduced after both exercise conditions, similar to values previously reported (10 mmHg; p < 0.05 vs. pre-exercise). Total peripheral resistance was significantly reduced following both exercise bouts, and heart rate was significantly increased post-exercise (rest: 59.6 +/- 11.2; interval: 77.8 +/- 12.8; continuous: 80.3 +/- 15.2 beats.min(-1)). Both cardiac output and stroke volume responses to LBNP following exercise were not altered when compared with baseline measurements. Tissue oxygenation during -40 mmHg (interval: 74.31% +/- 7.82% vs. continuous: 69.13% +/- 5.23%) was significantly lower than during normobaric pressure (interval: 77.14% +/- 1.30% vs. continuous: 74.41% +/- 0.94%). It appears from these observations that although young, endurance-trained males experience PEH following acute bouts of interval or continuous exercise, this hypotension does not alter the cardiovascular and cerebrovascular responses to a moderate orthostatic stress.

Sex differences in neuroendocrine and metabolic responses to prolonged strenuous exercise (PSE) have been well documented. The aim of this investigation was to examine sex differences in left ventricular function and cardiac beta-receptor responsiveness following a single bout of PSE. Nine male and eight female triathletes were examined during three separate sessions: before, immediately after, and 24 h following a half-ironman triathlon using dobutamine stress echocardiography. Steady-state graded infusions of dobutamine were used to assess beta-receptor responsiveness. Slopes calculated from linear regressions between dobutamine doses and changes in heart rate and contractility for each participant were used as an index of beta-receptor responsiveness. Despite no change in preload, fractional area change decreased from baseline after the race in both men and women, with a greater decrease in men [men: 54.1% (SD 2.1) to 50.7% (SD 3.4) vs. women: 55.4% (SD 2.7) to 53.3% (SD 2.5); P < 0.05]. The amount of dobutamine necessary to increase heart rate by 25 beats/min [men: 29.6 microg x kg(-1) x min(-1) (SD 6.6) to 42.7 microg x kg(-1) x min(-1) (SD 12.9) vs. women: 23.5 microg x kg(-1) x min(-1) (SD 4.0) to 30.0 microg x kg(-1) x min(-1) (SD 7.8); P < 0.05] and contractility by 10 mmHg/cm2 [men: 20.9 microg x kg(-1) x min(-1) (SD 5.1) to 37.0 microg x kg(-1) x min(-1) (SD 11.5) vs. women: 22.6 microg x kg(-1) x min(-1) (SD 6.4) to 30.7 microg x kg(-1) x min(-1) (SD 7.2); P < 0.05] was greater in both men and women postrace. However, the amount of dobutamine required to induce these changes was greater in men, reflecting larger beta-receptor alterations in male triathletes following PSE relative to women. These data suggest that following an acute bout of PSE, male triathletes demonstrate an attenuated chronotropic and inotropic response to beta-adrenergic stimulation compared with female triathletes.

Ventilatory responsiveness to hypoxia (HVR) has been reported to be different between highly trained endurance athletes and healthy sedentary controls. However, a linkage between aerobic capacity and HVR has not been a universal finding. The purpose of this study was to examine the relationship between HVR and maximal oxygen consumption (VO2 max) in healthy men with a wide range of aerobic capacities. Subjects performed a HVR test followed by an incremental cycle test to exhaustion. Participants were classified according to their maximal aerobic capacity. Those with a VO2 max of >or=60 ml x kg(-1) x min(-1) were considered highly trained (n = 13); those with a VO2 max of 50-60 ml x kg(-1) x min(-1) were considered moderately-trained (n = 18); and those with a VO2 max of <50 ml x kg(-1) x min(-1) were considered untrained (n = 24). No statistical differences were detected between the three groups for HVR (P > 0.05), and the HVR values were variable within each group (range: untrained = 0.28-1.61, moderately trained = 0.23-2.39, and highly trained = 0.08-1.73 l x min.%arterial O2 saturation(-1)). The relationship between HVR and VO2 max was not statistically significant (r = -0.1723; P > 0.05). HVR was also unrelated to maximal minute ventilation and ventilatory equivalents for O2 and CO2. We found that a spectrum of hypoxic ventilatory control is present in well-trained endurance athletes and moderately and untrained men. We interpret these observations to mean that other factors are more important in determining hypoxic ventilatory control than physical conditioning per se.

Recent studies claim a higher prevalence of exercise-induced arterial hypoxemia (EIAH) in women relative to men and that diminished peripheral chemosensitivity is related to the degree of arterial desaturation during exercise in male endurance athletes. The purpose of this study was to determine the relationship between the acute ventilatory response to hypoxia (AHVR) and EIAH and the potential influence of gender in trained endurance cyclists and untrained individuals. Healthy untrained males (n = 9) and females (n = 9) and trained male (n = 11) and female (n = 10) cyclists performed an isocapnic AHVR test followed by an incremental cycle test to exhaustion. Oxyhemoglobin saturation (Sa(O(2)) was lower in trained men (91.4 +/- 0.9%) and women (91.3 +/- 0.9%) compared to their untrained counterparts (94.4 +/- 0.8% versus 94.3 +/- 0.7%) (P < 0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P < 0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P > 0.05). We conclude that resting AHVR does not have a significant role in maintaining Sa(O(2)) during sea-level maximal cycle exercise in men or women.