Azmy Faisal

Prior moderate and heavy exercise accelerate oxygen uptake and cardiac output kinetics in endurance athletes

Cardiorespiratory interactions at the onset of dynamic cycling exercise are modified by warm-up exercises. We tested the hypotheses that oxygen uptake (Vo(2)) and cardiac output (Q) kinetics would be accelerated at the onset of heavy and moderate cycling exercise by warm-up. Nine male endurance athletes (peak Vo(2): 60.5 +/- 3.2 ml.min(-1).kg(-1)) performed multiple rides of two different 36-min cycling protocols, involving 6-min bouts at moderate and heavy intensities. Breath-by-breath Vo(2) and beat-by-beat stroke volume (SV) and Q, estimated by Modelflow from the finger pulse, were measured simultaneously with kinetics quantified from the phase II time constant (tau(2)). One novel finding was that both moderate (M) and heavy (H) warm-up bouts accelerated phase II Vo(2) kinetics during a subsequent bout of heavy exercise (tau(2): after M = 22.5 +/- 2.7 s, after H = 22.1 +/- 2.9 vs. 26.2 +/- 3.2 s; P < 0.01). Q kinetics in heavy exercise were accelerated by both warm-up intensities (tau(2): M = 22.0 +/- 4.1 s, H = 23.8 +/- 5.6 s vs. 27.4 +/- 7.2 s; P < 0.05). During moderate exercise, prior heavy-intensity warm-up (one or two bouts) accelerated Vo(2) kinetics and elevated Q at exercise onset, with no changes in Q kinetics. A second novel finding was a significant overshoot in the estimate of SV from Modelflow in the first minutes of each moderate and heavy exercise bout. These findings suggest that the acceleration of Vo(2) kinetics during heavy exercise was enabled by the acceleration of Q kinetics, and that rapid increases in Q at the onset of moderate and heavy exercise might result, in part, from an overshoot of SV.

Mechanisms of exertional dyspnoea in symptomatic smokers without COPD.

Dyspnoea and activity limitation can occur in smokers who do not meet spirometric criteria for chronic obstructive pulmonary disease (COPD) but the underlying mechanisms are unknown. Detailed pulmonary function tests and sensory–mechanical relationships during incremental exercise with respiratory pressure measurements and diaphragmatic electromyography (EMGdi) were compared in 20 smokers without spirometric COPD and 20 age-matched healthy controls. Smokers (mean±sd post-bronchodilator forced expiratory volume in 1u2005s (FEV1)/forced vital capacity 75±4%, mean±sd FEV1 104±14% predicted) had greater activity-related dyspnoea, poorer health status and lower physical activity than controls. Smokers had peripheral airway dysfunction: higher phase-III nitrogen slopes (3.8±1.8 versus 2.6±1.1%·L−1) and airway resistance (difference between airway resistance measured at 5u2005Hz and 20u2005Hz 19±11 versus 12±7% at 5u2005Hz) than controls (p<0.05). Smokers had significantly (p<0.05) lower peak oxygen uptake (78±40 versus 107±45% predicted) and ventilation (61±26 versus 97±29u2005L·min−1). Exercise ventilatory requirements, operating lung volumes and cardio-circulatory responses were similar. However, submaximal dyspnoea ratings, resistive and total work of breathing were increased in smokers compared with controls (p<0.05); diaphragmatic effort (transdiaphragmatic pressure/maximumal transdiaphragmatic pressure) and fractional inspiratory neural drive to the diaphragm (EMGdi/maximal EMGdi) were also increased (p<0.05) mainly reflecting the reduced denominator. Symptomatic smokers at risk for COPD had greater exertional dyspnoea and lower exercise tolerance compared with healthy controls in association with greater airways resistance, contractile diaphragmatic effort and fractional inspiratory neural drive to the diaphragm. Exertional dyspnoea in smokers without COPD is linked to higher inspiratory neural drive to the crural diaphragm http://ow.ly/e9Z7302uFM6

O2 uptake and blood pressure regulation at the onset of exercise: interaction of circadian rhythm and priming exercise

Circadian rhythm has an influence on several physiological functions that contribute to athletic performance. We tested the hypothesis that circadian rhythm would affect blood pressure (BP) responses but not O(2) uptake (Vo(2)) kinetics during the transitions to moderate and heavy cycling exercises. Nine male athletes (peak Vo(2): 60.5 ± 3.2 ml·kg(-1)·min(-1)) performed multiple rides of two different cycling protocols involving sequences of 6-min bouts at moderate or heavy intensities interspersed by a 20-W baseline in the morning (7 AM) and evening (5 PM). Breath-by-breath Vo(2) and beat-by-beat BP estimated by finger cuff plethysmography were measured simultaneously throughout the protocols. Circadian rhythm did not affect Vo(2) onset kinetics determined from the phase II time constant (τ(2)) during either moderate or heavy exercise bouts with no prior priming exercise (τ(2) moderate exercise: morning 22.5 ± 4.6 s vs. evening 22.2 ± 4.6 s and τ(2) heavy exercise: morning 26.0 ± 2.7 s vs. evening 26.2 ± 2.6 s, P > 0.05). Priming exercise induced the same robust acceleration in Vo(2) kinetics during subsequent moderate and heavy exercise in the morning and evening. A novel finding was an overshoot in BP (estimated from finger cuff plethysmography) in the first minutes of each moderate and heavy exercise bout. After the initial overshoot, BP declined in association with increased skin blood flow between the third and sixth minute of the exercise bout. Priming exercise showed a greater effect in modulating the BP responses in the evening. These findings suggest that circadian rhythm interacts with priming exercise to lower BP during exercise after an initial overshoot with a greater influence in the evening associated with increased skin blood flow.

Effective Bronchoscopic Lung Volume Reduction Accelerates Exercise Oxygen Uptake Kinetics in Emphysema

BACKGROUNDnThe impact of bronchoscopic lung volume reduction (BLVR) on physiologic responses to exercise in patients with advanced emphysema remains incompletely understood. We hypothesized that effective BLVR (e-BLVR), defined as a reduction in residual volume > 350 mL, would improve cardiovascular responses to exercise and accelerate oxygen uptake (Vo₂) kinetics.nnnMETHODSnThirty-one patients (FEV1, 36% ± 9% predicted; residual volume, 219% ± 57% predicted) underwent a constant intensity exercise test at 70% peak work rate to the limit of tolerance before and after treatment bronchoscopy (n = 24) or sham bronchoscopy (n = 7). Physiologic responses in patients who had e-BLVR (n = 16) were compared with control subjects (ineffective BLVR or sham bronchoscopy; n = 15).nnnRESULTSne-BLVR reduced residual volume (-1.1 ± 0.5 L, P = .001), improved lung diffusing capacity by 12% ± 13% (P = .001), and increased exercise tolerance by 181 ± 214 s (P = .004). Vo₂ kinetics were accelerated in the e-BLVR group but remained unchanged in control subjects (Δ mean response time, -20% ± 29% vs 1% ± 25%, P = .04). Acceleration of Vo₂ kinetics was associated with reductions in heart rate and oxygen pulse response half-times by 8% (84 ± 14 to 76 ± 15 s, P = .04) and 20% (49 ± 16 to 34 ± 16 s, P = .01), respectively. There were also increases in heart rate and oxygen pulse amplitudes during the cardiodynamic phase post e-BLVR. Faster Vo₂ kinetics in the e-BLVR group were significantly correlated with reductions in residual volume (r = 0.66, P = .005) and improvements in inspiratory reserve volume (r = 0.56, P = .024) and exercise tolerance (r = 0.63, P = .008).nnnCONCLUSIONSnLung deflation induced by e-BLVR accelerated exercise Vo₂ kinetics in patients with emphysema. This beneficial effect appears to be related mechanistically to an enhanced cardiovascular response to exercise, which may contribute to improved functional capacity.

Exertional dyspnoea in COPD: the clinical utility of cardiopulmonary exercise testing.

Activity-related dyspnoea is often the most distressing symptom experienced by patients with chronic obstructive pulmonary disease (COPD) and can persist despite comprehensive medical management. It is now clear that dyspnoea during physical activity occurs across the spectrum of disease severity, even in those with mild airway obstruction. Our understanding of the nature and source of dyspnoea is incomplete, but current aetiological concepts emphasise the importance of increased central neural drive to breathe in the setting of a reduced ability of the respiratory system to appropriately respond. Since dyspnoea is provoked or aggravated by physical activity, its concurrent measurement during standardised laboratory exercise testing is clearly important. Combining measurement of perceptual and physiological responses during exercise can provide valuable insights into symptom severity and its pathophysiological underpinnings. This review summarises the abnormal physiological responses to exercise in COPD, as these form the basis for modern constructs of the neurobiology of exertional dyspnoea. The main objectives are: 1) to examine the role of cardiopulmonary exercise testing (CPET) in uncovering the physiological mechanisms of exertional dyspnoea in patients with mild-to-moderate COPD; 2) to examine the escalating negative sensory consequences of progressive respiratory impairment with disease advancement; and 3) to build a physiological rationale for individualised treatment optimisation based on CPET. Measurement of symptom intensity, ventilatory control and mechanics during exercise exposes mechanisms of dyspnoea http://ow.ly/6OXQ3020tEA

Effect of age-related ventilatory inefficiency on respiratory sensation during exercise

To examine the effect of age-related respiratory function impairment on exertional dyspnea, we compared ventilatory and perceptual responses to incremental exercise under control (CTRL) and added dead space (DS) loading conditions in healthy fit older (55-79 years) and younger (20-39 years) men. Older individuals had higher ventilatory equivalents for CO2 throughout exercise (p<0.05) suggesting greater ventilatory inefficiency but operating lung volumes were similar compared to younger individuals. With added DS compared to CTRL, both groups similarly increased tidal volume (by 0.3-0.6 L) and ventilation (by 8-13 L/min) at submaximal work rates (each p<0.05). At peak exercise with DS, both groups failed to further increase ventilation and had small reductions in peak work rate (p<0.05). Increases in dyspnea intensity ratings with the addition of DS were similar at standardized submaximal work rates in older and younger groups. We conclude that, despite differences in ventilatory efficiency, the respiratory-mechanical and sensory responses to added chemostimulation during exercise were similar in fit older and younger individuals.

Resting Physiological Correlates of Reduced Exercise Capacity in Smokers with Mild Airway Obstruction

ABSTRACT Smokers with minor spirometric abnormalities can experience persistent activity-related dyspnea and exercise intolerance. Additional resting tests can expose heterogeneous physiological abnormalities, but their relevance and association with clinical outcomes remain uncertain. Subjects included sixty-two smokers (≥20 pack-years), with cough and/or dyspnea and minor airway obstruction [forced expiratory volume in one-second (FEV1) ≥80% predicted and >5th percentile lower limit of normal (LLN) (i.e., z-score >−1.64) using the 2012-Global Lung Function Initiative equations]. They underwent spirometry, plethysmography, oscillometry, single-breath nitrogen washout, and symptom-limited incremental cycle exercise tests. Thirty-two age-matched nonsmoking controls were also studied. Thirty-three (53%) of smokers had chronic obstructive pulmonary disease by LLN criteria. In smokers [n = 62; age 65 ± 11 years; smoking history 43 ± 19 pack-years; post-bronchodilator FEV1 z-score −0.60 ± 0.72 and FEV1/FVC z-score −1.56 ± 0.87 (mean ± SD)] versus controls, peak oxygen uptake (̇VO2) was 21 ± 7 vs. 32 ± 9 ml/kg/min, and dyspnea/̇VO2 slopes were elevated (both p < 0.0001). Smokers had evidence of peripheral airway dysfunction and maldistribution of ventilation when compared to controls. In smokers versus controls: lung diffusing capacity for carbon monoxide (DLCO) was 85 ± 22 vs. 105 ± 17% predicted, and residual volume (RV)/total lung capacity (TLC) was 36 ± 8 vs. 31 ± 6% (both p < 0.01). The strongest correlates of peak ̇VO2 were DLCO% predicted (r = 0.487, p < 0.0005) and RV/TLC% (r = −0.389, p = 0.002). DLCO% predicted was also the strongest correlate of dyspnea/̇VO2 slope (r = −0.352, p = 0.005). In smokers with mild airway obstruction, associations between resting tests of mechanics and pulmonary gas exchange and exercise performance parameters were weak, albeit consistent. Among these, DLCO showed the strongest association with important outcomes such as dyspnea and exercise intolerance measured during standardized incremental exercise tests.

Increased respiratory neural drive and work of breathing in exercise-induced laryngeal obstruction

Exercise-induced laryngeal obstruction (EILO), a phenomenon in which the larynx closes inappropriately during physical activity, is a prevalent cause of exertional dyspnea in young individuals. The physiological ventilatory impact of EILO and its relationship to dyspnea are poorly understood. The objective of this study was to evaluate exercise-related changes in laryngeal aperture on ventilation, pulmonary mechanics, and respiratory neural drive. We prospectively evaluated 12 subjects (6 with EILO and 6 healthy age- and gender-matched controls). Subjects underwent baseline spirometry and a symptom-limited incremental exercise test with simultaneous and synchronized recording of endoscopic video and gastric, esophageal, and transdiaphragmatic pressures, diaphragm electromyography, and respiratory airflow. The EILO and control groups had similar peak work rates and minute ventilation (V̇e) (work rate: 227 ± 35 vs. 237 ± 35 W; V̇e: 103 ± 20 vs. 98 ± 23 l/min; P > 0.05). At submaximal work rates (140-240 W), subjects with EILO demonstrated increased work of breathing ( P < 0.05) and respiratory neural drive ( P < 0.05), developing in close temporal association with onset of endoscopic evidence of laryngeal closure ( P < 0.05). Unexpectedly, a ventilatory increase ( P < 0.05), driven by augmented tidal volume ( P < 0.05), was seen in subjects with EILO before the onset of laryngeal closure; there were however no differences in dyspnea intensity between groups. Using simultaneous measurements of respiratory mechanics and diaphragm electromyography with endoscopic video, we demonstrate, for the first time, increased work of breathing and respiratory neural drive in association with the development of EILO. Future detailed investigations are now needed to understand the role of upper airway closure in causing exertional dyspnea and exercise limitation. NEW & NOTEWORTHY Exercise-induced laryngeal obstruction is a prevalent cause of exertional dyspnea in young individuals; yet, how laryngeal closure affects breathing is unknown. In this study we synchronized endoscopic video with respiratory physiological measurements, thus providing the first detailed commensurate assessment of respiratory mechanics and neural drive in relation to laryngeal closure. Laryngeal closure was associated with increased work of breathing and respiratory neural drive preceded by an augmented tidal volume and a rise in minute ventilation.

Unraveling the Cause of Severe Exertional Dyspnea in a Heavy Smoker

Unraveling the Cause of Severe Exertional Dyspnea in a Heavy Smoker Amany F. Elbehairy, Karlo Hockmann, Casey E. Ciavaglia, Azmy Faisal, Elizabeth Hill, Katherine A. Webb, J. Alberto Neder, and Denis E. O’Donnell Department of Medicine, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada; Department of Chest Diseases, Faculty of Medicine, and Faculty of Physical Education for Men, Alexandria University, Alexandria, Egypt; and School of Health, Sport and Bioscience, University of East London, London, United Kingdom