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We recently explored the cardiopulmonary interactions during partial unloading of the respiratory muscles during exercise. Expanding upon this work, we present a noteworthy case study whereby we eliminated the influence of respiration on cardiac function in a conscious but mechanically ventilated human during exercise. This human was a young healthy endurance-trained male who was mechanically ventilated during semi-recumbent cycle exercise at 75 Watts (W) (∼30% W max ). During mechanically ventilated exercise, esophageal pressure was reduced to levels indistinguishable from the cardiac artefact which led to a 94% reduction in the power of breathing. The reduction in respiratory pressures and respiratory muscle work led to a decrease in cardiac output (-6%), which was due to a reduction in stroke volume (-13%), left ventricular end-diastolic volume (-15%), and left-ventricular end-systolic volume (-17%) that was not compensated for by heart rate. Our case highlights the influence of extreme mechanical ventilation on cardiac function while noting the possible presence of a maximal physiological limit to which respiration (and its associated pressures) impacts cardiac function when the power of breathing is maximally reduced., Competing Interests: The authors declare no competing interests.

There is a significant effect of sex and muscle mass on the cardiorespiratory response to the skeletal muscle metaboreflex during isometric exercise. We therefore tested the hypothesis that sex differences would be present when isolated following dynamic exercise. We also tested the hypothesis that single and double leg post-exercise circulatory occlusion (PECO) following heavy exercise would elicit a cardiorespiratory response proportional to the absolute muscle mass. Healthy (24 ± 4 years) males ( n  = 10) and females ( n  = 10) completed pulmonary function and an incremental cycle test to exhaustion. Participants completed two randomized, 6 min bouts of intense cycle exercise (84 ± 7% V̇O 2peak ). One exercise bout was immediately followed by 3 min PECO (220 mmHg) of the legs while the other exercise bout was followed by passive recovery. Males completed an additional session of testing with single leg PECO. The mean arterial pressure during PECO and control was greater in males compared to females ( p  = 0.004). The was a significant time by condition by sex interaction in the heart rate response to PECO ( p  = 0.027). There was also a significant condition by sex interaction in the ventilatory response to PECO ( p  = 0.026). In males, we observed a dose-dependent cardiovascular, but not ventilatory, response to muscle mass occluded (all p  < 0.05). Our findings suggest the metaboreflex contribution to cardiorespiratory control during dynamic exercise is greater in males compared to females. The ventilatory response induced by double-leg occlusion but not single-leg occlusion, suggests that the ventilatory influence of the metaboreflex is less sensitive than the cardiovascular response and may be linked to the greater afferent activation induced by double-leg occlusion., Competing Interests: The authors declare there are no competing interests.

In healthy adults, airway-to-lung (i.e., dysanapsis) ratio is lower and dyspnoea during exercise at a given minute ventilation (V̇ E ) is higher in females than in males. We investigated the relationship between dysanapsis and sex on exertional dyspnoea in healthy adults. We hypothesized that females would have a smaller airway-to-lung ratio than males and that exertional dyspnoea would be associated with airway-to-lung ratio in males and females. We analyzed data from n  = 100 healthy never-smokers aged ≥40 years enrolled in the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who underwent pulmonary function testing, a chest computed tomography scan, and cardiopulmonary exercise testing. The luminal area of the trachea, right main bronchus, left main bronchus, right upper lobe, bronchus intermedius, left upper lobe, and left lower lobe were 22%-37% smaller (all p  < 0.001) and the airway-to-lung ratio (i.e., average large conducting airway diameter relative to total lung capacity) was lower in females than in males (0.609 ± 0.070 vs. 0.674 ± 0.082; p  < 0.001). During exercise, there was a significant effect of V̇ E , sex, and their interaction on dyspnoea (all p  < 0.05), indicating that dyspnoea increased as a function of V̇ E to a greater extent in females than in males. However, after adjusting for age and total lung capacity, there were no significant associations between airway-to-lung ratio and measures of exertional dyspnoea, regardless of sex (all r  < 0.34; all p  > 0.05). Our findings suggest that sex differences in airway size do not contribute to sex differences in exertional dyspnoea., Competing Interests: The authors declare there are no competing interests.

Rating of perceived exertion (RPE) is used to subjectively quantify the perception of physical activity, breathlessness or dyspnea, and leg discomfort (RPE legs ) during exercise. However, it is unknown how dyspnea or RPE legs can be influenced by expectations. Thirty healthy, active participants (19 males, 11 females) completed five, 5-minute submaximal cycling trials at 60% peak work rate. We deceived participants by telling them they were inspiring different hypoxic and hyperoxic gases, when in fact they breathed room air. Cardiorespiratory variables were similar between the trials, however, dyspnea and RPE legs evaluated with a Borg scale changed in a dose-response manner. When participants believed they were breathing 15% O 2 , they significantly increased dyspnea +0.70 ± 0.2 units ( p  = 0.03) compared to room air, whereas RPE legs was unchanged +0.35 ± 0.1 units ( p  = 0.70). When participants believed they were breathing 15% O 2 , they significantly increased dyspnea +1.05 ± 0.4 units ( p  = 0.003) compared to 23% hyperoxic condition, whereas RPE legs was unchanged +0.35 ± 0.1 units ( p  = 0.70). We found that dyspnea during exercise is susceptible to expectancy, without any accompanying physiological changes. Given coaches and clinicians use perceived exertion to prescribe exercise intensity and evaluate treatments, our findings show that the effect of expectations must be considered when interpreting sensations of breathlessness.

Voluntary activation can be used to assess central fatigue of the diaphragm after tasks such as exercise or inspiratory muscle loading. Cervical magnetic stimulation (CMS) of the phrenic nerves elicits an involuntary contraction, or twitch, of the diaphragm. This twitch is quantified based on a measure of transdiaphragmatic pressure and can be used to evaluate diaphragm contractile function and diaphragm voluntary activation (diaphragm-VA). The test-retest reliability of diaphragm-VA using CMS is currently unknown. Thirteen participants (4 male, 9 female; aged 25 ± 3 years) performed a series of interpolated twitch manoeuvres, which included a maximal inspiratory effort against a semi-occluded mouthpiece and 2 CMS-stimuli, 1 during the inspiratory manoeuvre and 1 after when the participant returned to functional residual capacity to quantify diaphragm-VA. Intraclass correlation coefficients (ICCs) and standard error of measurement (SEM) measured between-day and within-session reliability of diaphragm-VA, respectively. Maximal diaphragm-VA values were 91% (SD: 6; SEM: 3.9) and 92% (SD: 5; SEM: 2.2) during visits 1 and 2 ( p = 0.68), respectively, and displayed "good" between-day reliability (ICC: 0.88; 95% confidence interval: 0.67-0.95; SEM: 2.7). Our results suggest that assessing diaphragm-VA using CMS is reliable in young healthy adults. Measuring diaphragm-VA may provide additional insight into the consequences and mechanisms of diaphragm fatigue. Novelty: Magnetic stimulation of the phrenic nerves can reliably measure voluntary activation of the diaphragm. Diaphragm voluntary activation can be used to provide additional insight into fatigability of the diaphragm.

Exercise-induced arterial hypoxemia (EIAH) is characterized by the decrease in arterial oxygen tension and oxyhemoglobin saturation during dynamic aerobic exercise. Since the time of the initial observations, our knowledge and understanding of EIAH has grown, but many unknowns remain. The purpose of this review is to provide an update on recent findings, highlight areas of disagreement, and identify where information is lacking. Specifically, this review will place emphasis on ( i ) the occurrence of EIAH during submaximal exercise, ( ii ) whether there are sex differences in the development and severity of EIAH, and ( iii ) unresolved questions and future directions.

There are known sex differences in blood pressure regulation. The differences are related to ovarian hormones that influence β-adrenergic receptors and the transduction of muscle sympathetic nerve activity. Oral contraceptives (OC) modulate the ovarian hormonal profile in women and therefore may alter the cardiovascular response. We questioned if OC would alter the absolute pressor response to static exercise and influence the day-to-day variability of the response. Healthy men (n = 11) and women (n = 19) completed a familiarization day and 2 experimental testing days. Women were divided into those taking (W-OC, n = 10) and not taking (W-NC, n = 9) OC. Each experimental testing day involved isometric handgripping exercise, at 30% of maximal force, followed by circulatory occlusion to isolate the metaboreflex. Experimental days in men were 7-14 days apart. The first experimental testing in W-OC occurred 2-7 days after the start of the active phase of their OC. Women not taking OC were tested during the early and late follicular phase of the menstrual cycle as determined by commercial ovulation monitor. The increase in mean arterial pressure (MAP) during exercise was significantly lower in W-NC (95 ± 4 mm Hg) compared with men (114 ± 4 mm Hg) and W-OC (111 ± 3 mm Hg) (P < 0.05), with the differences preserved during circulatory occlusion. The rise in MAP was significantly correlated between the 2 testing days in men (r = 0.72, P < 0.01) and W-OC (r = 0.77, P < 0.05), but not in W-NC (r = 0.17, P = 0.67), indicating greater day-to-day variation in W-NC. In conclusion, OC modulate the exercise pressor response in women and minimize day-to-day variability in the exercise metaboreflex.

Repeatedly performing exercise in hypoxia could elicit an independent training response and become an unintended co-intervention. The primary purposes of this study were to determine if hypoxic exercise responses changed across repeated testing and to assess the day-to-day variability of commonly used measures of cardiorespiratory and metabolic responses to hypoxic exercise. Healthy young males (aged 23 ± 2 years) with a maximal O2 consumption of 50.7 ± 4.7 mL·kg(-1)·min(-1) performed 5 trials (H1 to H5) over a 2-week period in hypoxia (fraction of inspired oxygen = 0.13). Participants completed 3-min stages at 20%, 40%, 60%, and 10% of individual peak power. With increasing cycle exercise intensity there were increases in minute ventilation, O2 consumption, CO2 production, respiratory exchange ratio, heart rate (HR), blood lactate concentration, and ratings of perceived exertion for legs and respiratory system along with a reduction in oxyhaemoglobin saturation (%SpO2) (all p < 0.001). There were no systematic changes from H1 to H5 (p > 0.05). Most measures were highly repeatable across testing sessions with the coefficient of variation (CV) averaging ≤10% of the mean value in all variables except O2 consumption (17%), CO2 production (11%) and blood lactate concentration (17%). For HR and %SpO2 the CV was <5%. The exercise protocol did not elicit a training response when repeated 5 times during a 2-week period and the variability of exercise responses was low. We conclude that this protocol allows detection of small changes in cardiorespiratory responses to hypoxic exercise that might occur during exposure to hypoxia.

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.

Dyspnea, the subjective feeling of shortness of breath, is a hallmark feature of chronic obstructive pulmonary disease (COPD). Pulmonary rehabilitation (PR) programs aim to improve dyspnea, thereby increasing exercise tolerance and health-related quality of life in patients with COPD. Exercise training is proven to be an essential component of PR; however, there is no consensus regarding which training modality confers the greatest therapeutic benefit. Secondary to pulmonary impairment, many COPD patients develop limb muscle dysfunction (LMD), particularly in the leg muscles. Mounting evidence suggests that peripheral limitation to exercise as a result of LMD is frequent in patients with COPD. LMD of the legs, or lower limb muscle dysfunction, has been shown to markedly influence ventilatory and dyspnea responses to exercise. Accordingly, isolated training of leg muscles may contribute to reducing dyspnea and increase exercise tolerance in patients with COPD. Indeed, relative to the largely irreversible impairment of the pulmonary system, the leg muscles are an important site by which to improve patients' level of function and quality of life. Isolated leg exercises have been shown to improve LMD and may constitute an effective training modality to improve dyspnea and exercise tolerance in COPD within the context of PR.

The objective of this study was to measure the magnitude of the muscle metaboreflex in people with chronic obstructive pulmonary disease (COPD) compared with healthy controls and to assess the relationships between disease severity, exercise capacity, and the magnitude of the muscle metaboreflex. Nine people with mild-to-severe COPD and 11 age- and gender-matched healthy controls performed isometric handgrip exercise (IHG), followed by postexercise circulatory occlusion (PECO) while hemodynamic changes were measured. Continuous measures of heart rate, arterial pressure, leg blood flow, leg vascular resistance, and total peripheral resistance were obtained. Participants then performed a cycle test to exhaustion. Heart rate, blood pressure, and blood flow responses during IHG and PECO were similar between the COPD group and healthy controls (p > 0.05). There was no association between disease severity or exercise capacity and the magnitude of the muscle metaboreflex. We observed a preserved muscle metaboreflex in mild-to-severe COPD, suggesting the metaboreflex is not a contributing factor to the development of exercise intolerance in this population.

The focus of this symposium is on the physiological demands of exercise in hypoxia. The study of hypoxia by exercise physiologists has a strong tradition and many questions first asked over 100 years ago continue to be relevant, yet still unsatisfactorily answered. The primary theme of the following papers is how different models of hypoxia allow different questions to be asked. The first paper addresses questions of exercise ventilatory control using intermittent, rather than continuous, hypoxia. The second manuscript attempts to understand the hypoxic exercise responses using a population-level approach (i.e., generations spanning millennia). Lastly, the third paper uses acute hypoxia to better understand cardio-pulmonary interactions during exercise. Collectively, these reviews are intended to stimulate additional study and debate.

Exposure to chronic or intermittent hypoxia produces alterations in the ventilatory response to hypoxia. These adaptations can differ depending on the severity of the hypoxic stimulus, its duration, its pattern, and the presence or absence of other chemical stimuli. As such, there are significant differences between the responses to intermittent versus continuous hypoxia. Intermittent hypoxia (IH) has been shown to elicit significant changes in the peripheral chemoresponse, but the functional implications of these changes for resting and exercise ventilation are not clear. We summarize the impact of IH on resting chemosensitivity and discuss the use of IH to better understand ventilatory control during exercise. We also suggest future directions for this relatively young field, including potential clinical applications of IH research.

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.

The purpose of this study was to determine which upper-limb muscle exhibits the greatest change in muscle deoxygenation during arm-cranking exercise (ACE). We hypothesized that the biceps brachii (BB) would show the greatest change in muscle deoxygenation during progressive ACE to exhaustion relative to triceps brachii (TR), brachioradialis (BR), and anterior deltoid (AD). Healthy young men (n = 11; age = 27 +/- 1 y; mean +/- SEM) performed an incremental ACE test to exhaustion. Near-infrared spectroscopy (NIRS) was used to monitor the relative concentration changes in oxy- (O2Hb), deoxy- (HHb), and total hemoglobin (Hbtot), as well as tissue oxygenation index (TOI) in each of the 4 muscles. During submaximal arm exercise, we found that changes to NIRS-derived measurements were not different between the 4 muscles studied (p > 0.05). At maximal exercise HHb was significantly higher in the BB compared with AD (p < 0.05). Relative to the other 3 muscles, BB exhibited the greatest decrease in O2Hb and TOI (p < 0.05). Our investigation provides two new and important findings: (i) during submaximal ACE the BB, TR, BR, and AD exhibit similar changes in muscle deoxygenation and (ii) during maximal ACE the BB exhibits the greatest change in intramuscular O2 status.

Studies examining pulmonary gas exchange during exercise have primarily focused on young healthy men, whereas the female response to exercise has received limited attention. Evidence is accumulating that the response of the lungs, airways, and (or) respiratory muscles to exercise is less than ideal and this may significantly compromise oxygen transport in certain groups of otherwise healthy, fit, active, male subjects. Women may be even more susceptible to exercise-induced pulmonary limitations than height-matched men, by virtue of their smaller lung volumes, lower maximal expiratory flow rates, and smaller diffusion surface areas. We have recently shown that exercise-induced arterial hypoxaemia (EIAH) is more prevalent and occurs at relatively lower fitness levels in females than in males. Despite this finding, few physiologically based mechanisms have been identified to explain why women may be more susceptible to EIAH than men. Potential mechanisms of EIAH include relative alveolar hypoventilation, ventilation-perfusion inequality, and diffusion limitation. Whether these mechanisms are different between sexes remains controversial. The primary purpose of this review is to summarize the available data on EIAH in women and to discuss potential sex-based mechanisms for gas exchange impairment. Furthermore, we discuss unresolved questions dealing with pulmonary system limitations during exercise in women.

Respiratory muscle training (RMT) has been proposed as an effective means to increase the strength of the inspiratory muscles and improve exercise performance. The purpose of this study was to examine the effect of RMT on cycling time to exhaustion (TTE) and to determine any potential sex effect. We hypothesized that RMT would improve maximal inspiratory pressure (MIP) and TTE to a similar degree in men and women. Males (n = 7; mean (+/- SD) age, 22.1 +/- 1.5 y) and females (n = 8; mean (+/- SD) 24.5 +/- 4.9 y) performed an incremental cycle test to determine maximal oxygen consumption ((.)VO(2) (max)) (day 1), followed by a familiarization TTE (day 2) and baseline TTE (day 3) at 80% maximal work achieved during the ((.)VO(2) (max)) test. Subjects then completed 5 weeks of respiratory muscle training (RMT) (5 d/week, 2 sets of 30 inspirations against 50% MIP). Four training sessions per week were performed at home and the 5th was supervised, during which the threshold load was increased if necessary. Following RMT, subjects completed 2 TTE tests (days 4 and 5). MIP increased in each subject (37% +/- 18%, P < 0.05). There was no difference between men (pre = -100 +/- 20 vs. post = -140 +/- 29 cmH(2)O) and women (pre = -90 +/- 28 vs. post = -117 +/- 28 cmH(2)O). Baseline TTE (male = 301 +/- 122 s; female = 338 +/- 98 s) was shorter in comparison with the best of the 2 TTE-post tests (male = 353 +/- 68 s; female = 416 +/- 116 s; P < 0.01), but not when compared with days 4 or 5 (P > 0.05). RMT increases MIP and may improve exercise performance; however, improvements are variable with no differences between men and women.