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New Findings: What is the central question of this study?To what extent are the mechanical‐ventilatory responses to upper‐body exercise influenced by task‐specific locomotor mechanics?What is the main finding and its importance?When compared with lower‐body exercise performed at similar ventilations, upper‐body exercise was characterized by tidal volume constraint, dynamic lung hyperinflation and an increased propensity towards neuromechanical uncoupling of the respiratory system. Importantly, these responses were independent of respiratory dysfunction and flow limitation. Thus, the mechanical ventilatory responses to upper‐body exercise are attributable, in part, to task‐specific locomotor mechanics (i.e. non‐respiratory loading of the thorax). The aim of this study was to determine the extent to which the mechanical ventilatory responses to upper‐body exercise are influenced by task‐specific locomotor mechanics. Eight healthy men (mean ± SD: age, 24 ± 5 years; mass, 74 ± 11 kg; and stature, 1.79 ± 0.07 m) completed two maximal exercise tests, on separate days, comprising 4 min stepwise increments of 15 W during upper‐body exercise (arm‐cranking) or 30 W during lower‐body exercise (leg‐cycling). The tests were repeated at work rates calculated to elicit 20, 40, 60, 80 and 100% of the peak ventilation achieved during arm‐cranking (V̇E, UBE). Exercise measures included pulmonary ventilation and gas exchange, oesophageal pressure‐derived indices of respiratory mechanics, operating lung volumes and expiratory flow limitation. Subjects exhibited normal resting pulmonary function. Arm‐crank exercise elicited significantly lower peak values for work rate, O2 uptake, CO2 output, minute ventilation and tidal volume (p < 0.05). At matched ventilations, arm‐crank exercise restricted tidal volume expansion relative to leg‐cycling exercise at 60% V̇E, UBE (1.74 ± 0.61 versus 2.27 ± 0.68 l, p < 0.001), 80% V̇E, UBE (2.07 ± 0.70 versus 2.52 ± 0.67 l, p < 0.001) and 100% V̇E, UBE (1.97 ± 0.85 versus 2.55 ± 0.72 l, p = 0.002). Despite minimal evidence of expiratory flow limitation, expiratory reserve volume was significantly higher during arm‐cranking versus leg‐cycling exercise at 100% V̇E, UBE (39 ± 8 versus 29 ± 8% of vital capacity, p = 0.002). At any given ventilation, arm‐cranking elicited greater inspiratory effort (oesophageal pressure) relative to thoracic displacement (tidal volume). Arm‐cranking exercise is sufficient to provoke respiratory mechanical derangements (restricted tidal volume expansion, dynamic hyperinflation and neuromechanical uncoupling) in subjects with normal pulmonary function and expiratory flow reserve. These responses are likely to be attributable to task‐specific locomotor mechanics (i.e. non‐respiratory loading of the thorax). [ABSTRACT FROM AUTHOR]

Key points: The perceived intensity of exertional breathlessness (i.e. dyspnoea) is higher in older women than in older men, possibly as a result of sex‐differences in respiratory system morphology.During exercise at a given absolute intensity or minute ventilation, older women have a greater degree of mechanical ventilatory constraint (i.e. work of breathing and expiratory flow limitation) than their male counterparts, which may lead to a greater perceived intensity of dyspnoea.Using a single‐blind randomized study design, we experimentally manipulated the magnitude of mechanical ventilatory constraint during moderate‐intensity exercise at ventilatory threshold in healthy older men and women. We found that changes in the magnitude of mechanical ventilatory constraint within the physiological range had no effect on dyspnoea in healthy older adults.When older men and women perform moderate intensity exercise, mechanical ventilatory constraint does not contribute significantly to the sensation of dyspnoea. We aimed to determine the effect of manipulating mechanical ventilatory constraint during submaximal exercise on dyspnoea in older men and women. Eighteen healthy subjects (aged 60–80 years; nine men and nine women) completed two days of testing. On day 1, subjects were assessed for pulmonary function and performed a maximal incremental cycle exercise test. On day 2, subjects performed three 6‐min bouts of cycling at ventilatory threshold, in a single‐blind randomized manner, while breathing: (i) normoxic helium‐oxygen (HEL) to reduce the work of breathing (Wb) and alleviate expiratory flow limitation (EFL); (ii) through an inspiratory resistance (RES) of ∼5 cmH2O L−1 s−1 to increase Wb; and (iii) ambient air as a control (CON). Oesophageal pressure, diaphragm electromyography, and sensory responses (category‐ratio 10 Borg scale) were monitored throughout exercise. During the HEL condition, there was a significant decrease in Wb (men: –21 ± 6%, women: –17 ± 10%) relative to CON (both P < 0.01). Moreover, if EFL was present during CON (four men and five women), it was alleviated during HEL. Conversely, during the RES condition, Wb (men: 42 ± 19%, women: 50 ± 16%) significantly increased relative to CON (both P < 0.01). There was no main effect of sex on Wb (P = 0.59). Across conditions, women reported significantly higher dyspnoea intensity than men (2.9 ± 0.9 vs. 1.9 ± 0.8 Borg scale units, P < 0.05). Despite significant differences in the degree of mechanical ventilatory constraint between conditions, the intensity of dyspnoea was unaffected, independent of sex (P = 0.46). When older men and women perform moderate intensity exercise, mechanical ventilatory constraint does not contribute significantly to the sensation of dyspnoea. Key points: The perceived intensity of exertional breathlessness (i.e. dyspnoea) is higher in older women than in older men, possibly as a result of sex‐differences in respiratory system morphology.During exercise at a given absolute intensity or minute ventilation, older women have a greater degree of mechanical ventilatory constraint (i.e. work of breathing and expiratory flow limitation) than their male counterparts, which may lead to a greater perceived intensity of dyspnoea.Using a single‐blind randomized study design, we experimentally manipulated the magnitude of mechanical ventilatory constraint during moderate‐intensity exercise at ventilatory threshold in healthy older men and women. We found that changes in the magnitude of mechanical ventilatory constraint within the physiological range had no effect on dyspnoea in healthy older adults.When older men and women perform moderate intensity exercise, mechanical ventilatory constraint does not contribute significantly to the sensation of dyspnoea. [ABSTRACT FROM AUTHOR]

Neuromuscular fatigue compromises exercise performance and is determined by central and peripheral mechanisms. Interactions between the two components of fatigue can occur via neural pathways, including feedback and feedforward processes. This brief review discusses the influence of feedback and feedforward mechanisms on exercise limitation. In terms of feedback mechanisms, particular attention is given to group III/IV sensory neurons which link limb muscle with the central nervous system. Central corollary discharge, a copy of the neural drive from the brain to the working muscles, provides a signal from the motor system to sensory systems and is considered a feedforward mechanism that might influence fatigue and consequently exercise performance. We highlight findings from studies supporting the existence of a ‘critical threshold of peripheral fatigue’, a previously proposed hypothesis based on the idea that a negative feedback loop operates to protect the exercising limb muscle from severe threats to homeostasis during whole-body exercise. While the threshold theory remains to be disproven within a given task, it is not generalisable across different exercise modalities. The ‘sensory tolerance limit’, a more theoretical concept, may address this issue and explain exercise tolerance in more global terms and across exercise modalities. The ‘sensory tolerance limit’ can be viewed as a negative feedback loop which accounts for the sum of all feedback (locomotor muscles, respiratory muscles, organs, and muscles not directly involved in exercise) and feedforward signals processed within the central nervous system with the purpose of regulating the intensity of exercise to ensure that voluntary activity remains tolerable. [ABSTRACT FROM PUBLISHER]

Fatigue of the respiratory muscles during intense exercise might compromise leg blood flow, thereby constraining oxygen uptake (V̇o2) and limiting exercise tolerance. We tested the hypothesis that inspiratory muscle training (IMT) would reduce inspiratory muscle fatigue, speed V̇o2 kinetics and enhance exercise tolerance. Sixteen recreationally active subjects (mean ± SD, age 22 ± 4 yr) were randomly assigned to receive 4 wk of either pressure threshold IMT [30 breaths twice daily at ~50% of maximum inspiratory pressure (MIP)] or sham treatment (60 breaths once daily at ~15% of MIP). The subjects completed moderate-, severe- and maximal-intensity "step" exercise transitions on a cycle ergometer before (Pre) and after (Post) the 4-wk intervention period for determination of V̇o2 kinetics and exercise tolerance. There were no significant changes in the physiological variables of interest after Sham. After IMT, baseline MIP was significantly increased (Pre vs. Post: 155 ± 22 vs. 181 ± 21 cmH2O; P < 0.001), and the degree of inspiratory muscle fatigue was reduced after severe- and maximal-intensity exercise. During severe exercise, the V̇o2 slow component was reduced (Pre vs. Post: 0.60 ± 0.20 vs. 0.53 ± 0.24 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 765 ± 249 vs. 1,061 ± 304 s; P < 0.01). Similarly, during maximal exercise, the V̇o2 slow component was reduced (Pre vs. Post: 0.28 ± 0.14 vs. 0.18 ± 0.07 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 177 ± 24 vs. 208 ± 37 s; P < 0.01). Four weeks of IMT, which reduced inspiratory muscle fatigue, resulted in a reduced V̇o2 slow-component amplitude and an improved exercise tolerance during severe- and maximal-intensity exercise. The results indicate that the enhanced exercise tolerance observed after IMT might be related, at least in part, to improved V̇o2 dynamics, presumably as a consequence of increased blood flow to the exercising limbs. [ABSTRACT FROM AUTHOR]

We have demonstrated that 50-μm-diameter artenovenous pathways exist in isolated, healthy human and baboon lungs, ventilated and perfused under physiological pressures. These findings have been confirmed and extended by demonstrating the passage of 25-μm microspheres through the lungs of exercising dogs, but not at rest. Determination of blood flow through these large-diameter intrapulmonary arteriovenous pathways would be an important first step to establish a physiological role for these vessels. Currently, we sought to estimate blood flow through these arteriovenous pathways using technetium-99m (99mTc) labeled macroaggregated albumin (MAA) in healthy humans at rest and during maximal treadmill exercise. We hypothesized that the percentage of 99mTc MAA able to traverse the pulmonary circulation (%transpulmonary passage) would increase during exercise. Seven male subjects without patent foramen ovale were injected with 99mTc MAA at rest on 1 day and during maximal treadmill exercise on a separate day (>6 days). Within 5 mm after injection, subjects began whole body imaging in the supine position. Six of the seven subjects showed an increase in transpulmonary passage of MAA with maximal exercise. Using two separate analysis methods, percent transpulmonary passage significantly increased with exercise from baseline to absolute values of 1.2 ± 0.8% (P = 0.008) and 1.3 ± 1.0% (P = 0.016), respectively (means ± SD; paired t-test). We conclude that MAA may be traversing the pulmonary circulation via large-diameter intrapulmonary arteriovenous conduits in healthy humans during exercise. Recruitment of these pathways may divert blood flow away from pulmonary capillaries during exercise and compromise the lung's function as a biological filter. [ABSTRACT FROM AUTHOR]

AbstractPurposeMaterials and methodsResultsConclusions\nIMPLICATIONS FOR REHABILITATIONTo evaluate the validity of a consumer-grade wearable for estimating energy expenditure, sedentary behaviour, and physical activity in manual wheelchair users with spinal cord injury (SCI).Fifteen manual wheelchair users with SCI (C5-L1, four female) completed activities of daily living and wheelchair propulsion (2–8 km·h−1). Wrist-worn accelerometry data were collected using consumer-grade (z-Track) and research-grade (ActiGraph GT9X) devices. Energy expenditure was measured via indirect calorimetry. Linear regression was used to evaluate the prediction of criterion metabolic equivalent of task (MET) by each accelerometer’s vector magnitude (VM). Area under the receiver operating characteristic curve (ROC-AUC) evaluated the accuracy of VM for discriminating between physical activity intensities and for identifying accelerometer cut-points.Standardised β-coefficients for the association between z-Track and ActiGraph VM for criterion MET were 0.791 (p < 0.001) and 0.774 (p < 0.001), respectively. The z-Track had excellent accuracy for classifying time in sedentary behaviour (ROC-AUC = 0.95) and moderate-to-vigorous physical activity (ROC-AUC = 0.93); similar values to the ActiGraph (ROC-AUC = 0.96 and 0.88, respectively). Cut-points for the z-Track were ≤37 g·min−1 for sedentary behaviour and ≥222 g·min−1 for moderate-to-vigorous physical activity.This study supports the validity of a consumer-grade wearable to measure sedentary time and physical activity in manual wheelchair users with SCI.A consumer-grade wearable device provides valid estimations of sedentary time and physical activity in manual wheelchair users with spinal cord injury.Commercially available consumer-grade wearables may enable accurate self-monitoring in this population and, therefore, have potential for supporting behaviour change.A consumer-grade wearable device provides valid estimations of sedentary time and physical activity in manual wheelchair users with spinal cord injury.Commercially available consumer-grade wearables may enable accurate self-monitoring in this population and, therefore, have potential for supporting behaviour change. [ABSTRACT FROM AUTHOR]

We have demonstrated that 50-mum-diameter arteriovenous pathways exist in isolated, healthy human and baboon lungs, ventilated and perfused under physiological pressures. These findings have been confirmed and extended by demonstrating the passage of 25-microm microspheres through the lungs of exercising dogs, but not at rest. Determination of blood flow through these large-diameter intrapulmonary arteriovenous pathways would be an important first step to establish a physiological role for these vessels. Currently, we sought to estimate blood flow through these arteriovenous pathways using technetium-99m ((99m)Tc)-labeled macroaggregated albumin (MAA) in healthy humans at rest and during maximal treadmill exercise. We hypothesized that the percentage of (99m)Tc MAA able to traverse the pulmonary circulation (%transpulmonary passage) would increase during exercise. Seven male subjects without patent foramen ovale were injected with (99m)Tc MAA at rest on 1 day and during maximal treadmill exercise on a separate day (>6 days). Within 5 min after injection, subjects began whole body imaging in the supine position. Six of the seven subjects showed an increase in transpulmonary passage of MAA with maximal exercise. Using two separate analysis methods, percent transpulmonary passage significantly increased with exercise from baseline to absolute values of 1.2 +/- 0.8% (P = 0.008) and 1.3 +/- 1.0% (P = 0.016), respectively (means +/- SD; paired t-test). We conclude that MAA may be traversing the pulmonary circulation via large-diameter intrapulmonary arteriovenous conduits in healthy humans during exercise. Recruitment of these pathways may divert blood flow away from pulmonary capillaries during exercise and compromise the lung's function as a biological filter.

Reductions in arterial O2 saturation (-5 to -10% SaO2 < rest) occur over time during sustained heavy intensity exercise in a normoxic environment, due primarily to the effects of acid pH and increased temperature on the position of the HbO2 dissociation curve. We prevented the desaturation via increased F1O2 (.23 to .29) and showed that exercise time to exhaustion was increased. We used supramaximal magnetic stimulation (1 - 100 Hz) of the femoral nerve to test for quadriceps fatigue. We used mildly hyperoxic inspirates (F1O2 .23 to .29) to prevent O2 desaturation. We then compared the amount of quadriceps fatigue incurred following cycling exercise at SaO2 98% vs. 91% with each trial carried out at equal exercise intensities (90% Max) and for equal durations. Preventing the normal exercise-induced O2 desaturation prevented about one-half the amount of exercise-induced quadriceps fatigue; plasma lactate and effort perception were also reduced. We conclude that the normal exercise-induced O2 desaturation during heavy intensity endurance exercise contributes significantly to exercise performance limitation in part because of its effect on locomotor muscle fatigue. These effects of EIAH were confirmed in mild environmental hypoxia (FIO2 .17, SaO2 88%) which significantly augmented the magnitude of exercise-induced quadriceps fatigue observed in normoxia.