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Ventilation and Respiratory Mechanics

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Abstract

During dynamic exercise, the healthy pulmonary system faces several major challenges, including decreases in mixed venous oxygen content and increases in mixed venous carbon dioxide. As such, the ventilatory demand is increased, while the rising cardiac output means that blood will have considerably less time in the pulmonary capillaries to accomplish gas exchange. Blood gas homeostasis must be accomplished by precise regulation of alveolar ventilation via medullary neural networks and sensory reflex mechanisms. It is equally important that cardiovascular and pulmonary system responses to exercise be precisely matched to the increase in metabolic requirements, and that the substantial gas transport needs of both respiratory and locomotor muscles be considered. Our article addresses each of these topics with emphasis on the healthy, young adult exercising in normoxia. We review recent evidence concerning how exercise hyperpnea influences sympathetic vasoconstrictor outflow and the effect this might have on the ability to perform muscular work. We also review sex‐based differences in lung mechanics. © 2012 American Physiological Society. Compr Physiol 2:1093‐1142, 2012.

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Figure 1. Figure 1.

Schematic example of the ventilatory responses to progressive increases in cycling work rate in a healthy young subject. Note the initial rise in tidal volume, which then plateaus. After this, further increases in ventilation are accomplished by increases in breathing frequency.

Figure 2. Figure 2.

Ventilatory response and hemoglobin saturation (SpO2) during the final minute of leg cycling exercise at four different workloads with (Fentanyl, gray bars) and without (Placebo, black bars) partially blocked somatosensory neural feedback from the working locomotor muscles. The P value indicates the overall main effect of fentanyl. *P < 0.05; 1P = 0.08. From Amann et al. 23.

Reprinted with permission of the American Physiological Society.
Figure 3. Figure 3.

The solid line represents the estimated relationship between the work of breathing and exercise ventilation based on a regression equation from Aaron et al. 3, where the work of breathing = −80.041 + 1.459 (VE) + 0.011 (VE)2. The dotted line represents the estimated relationship between the respiratory muscle oxygen cost and exercise ventilation based on a regression equation from Aaron et al. 5, where the respiratory muscle o2 = 0.081 + 0.001 (exercise Wv – resting Wv), where Wv = the work of breathing.

Figure 4. Figure 4.

Relative effects of changing work of breathing on leg blood flow ( legs; A) and leg oxygen consumption (o2legs; B). Note that as the work of breathing is reduced (proportional assist ventilator) or increased (graded resistive loads) there is a corresponding increase and decrease in  legs and o2legs, respectively. Also note that the increased  legs with unloading occurs in the face of a reduced stroke volume and cardiac output.

Adapted, with permission, from Harms et al. 210. Reprinted with permission of the American Physiological Society.
Figure 5. Figure 5.

Respiratory muscle indocyanine green dye (ICG) response measured by near‐infrared spectroscopy (NIRS) at four different ventilatory loads in a single representative subject. There is a progressive increase in slope and peak ICG concentration with increasing levels of , indicating a faster rate of dye accumulation and therefore a higher blood flow response. Actual blood flow values at 20, 42, 85, and 121 liter/min were 10.2, 23.5, 32.9, and 76.0 mL/100 mL/min, respectively.

Adapted, with permission, from Guenette et al. 197. Reprinted with permission of the American Physiological Society.
Figure 6. Figure 6.

Raw data traces showing arterial and venous blood velocity, blood pressure, esophageal (Pes) and gastric pressure (Pga), calf force, and airflow during mild contraction conditions. The shaded areas and a downward deflection in the airflow trace denote inspiration. Note that arterial inflow remains unaffected by the type of breathing pattern used by the subject, and is also relatively unaffected by the calf contraction cycle. However, significant respiratory modulation of femoral venous outflow persists in the face of mild calf contraction during both ribcage and diaphragm breathing, as the phasic increases in venous return associated with the calf muscle pump are most pronounced during a ribcage inspiration (denoted by upward arrows). In contrast, during a diaphragmatic inspiration, anterograde femoral venous blood flow occurs exclusively during the calf contraction phase (denoted by downward arrows).

Adapted, with permission, from Miller et al. 369. Reprinted with permission.
Figure 7. Figure 7.

A working hypothesis for the neurophysiological underpinnings of perceived respiratory discomfort (breathlessness) during exercise in healthy humans: a working hypothesis. Refer to text for details. o2 and , metabolic rates of oxygen consumption and carbon dioxide output; Type III and IV mechano‐ and metabosensitive afferents in the peripheral locomotor (and respiratory) muscles and their vasculature; SARs, slowly adapting receptors; RARs, rapidly adapting receptors; C‐fibers, bronchopulmonary C‐fibers; J‐receptors, juxtapulmonary capillary receptors; GTOs, Golgi tendon organs; PCO2, partial pressure of carbon dioxide; [H+], hydrogen ion concentration; [La], lactate ion concentration; Pao2, arterial partial pressure of oxygen; SaO2, arterial blood oxygen saturation.

Adapted, with permission, from Jensen et al. 243. Reprinted with permission.
Figure 8. Figure 8.

Thickness of tenascin immunoreactive band in subepithelial basement membrane zone in controls, elite cross‐country skiers with and without bronchial hyperresponsiveness (BHR), and asthmatic subjects. Horizontal bar = median value.

Adapted, with permission, from Karjalainen et al. 266. Reprinted with permission of the American Thoracic Society. Copyright(c) American Thoracic Society. Karjalainen EM, Laitinen A, Sue‐Chu M, Altraja A, Bjermer L, and Laitnen LA. 2000. Evidence of airway inflammation and remodeling in ski athletes with and without bronchial hyperresponsiveness to methacholine. American Journal of Respiratory and Crtical Care Medicine. 161:2086‐2091. Official journal of the American Thoracic Society.
Figure 9. Figure 9.

Typical responses of esophageal (Pes), gastric (Pga), and transdiaphragmatic (Pdi) pressures and diaphragm EMG (i.e., M‐waves) to 10‐Hz bilateral phrenic nerve stimulation before and immediately after whole‐body exercise at 90% o2 max. Pdi was significantly reduced following the whole‐body exercise. There was no change in the M‐wave response of the diaphragm to the supramaximal stimulation.

Adapted, with permission, from Johnson et al. 246. Reprinted with permission of Wiley‐Blackwell, copyright 1993.
Figure 10. Figure 10.

Abdominal muscle fatigue in response to dynamic exercise. (A) Group (n = 11) mean gastric pressure (Pga) in response to magnetic stimulation at 1 Hz (single twitch) through 25 Hz (tetanic stimulation) before, and up to 30 min after whole‐body exercise. At all frequencies of stimulation, Pga immediately postexercise was reduced below baseline values. (B) Identity plot for thoracic nerve stimulation at 1‐25 Hz. *P < 0.05; **P < 0.01, values less than 1‐min postexercise significantly different from preexercise values at the same stimulation frequency. *P < 0.05; **P < 0.01, values 30‐min postexercise significantly different from preexercise values at the same stimulation frequency.

Adapted, with permission, from Taylor et al. 516. Reprinted with permission of the American Physiological Society.
Figure 11. Figure 11.

Schematic of the proposed respiratory muscle metaboreflex and its effects. The metaboreflex is initiated by fatigue of the respiratory muscles, mediated supraspinally via group III/IV afferents, leading to sympathetically mediated vasoconstriction of limb locomotor muscle vasculature, exacerbating peripheral fatigue of working limb muscles, and (via feedback) intensifying effort perceptions, thereby contributing to limitation of heavy‐intensity endurance exercise performance.

Adapted, with permission, from Dempsey et al. 131 as published in Romer and Polkey 454. Reprinted with permission of the American Physiological Society.
Figure 12. Figure 12.

Effects of fatiguing the diaphragm on muscle sympathetic nerve activity (MSNA). Note that MSNA remains relatively unchanged at the onset of high levels of inspiratory muscle force output, but increased gradually over time in both frequency and amplitude.

Adapted, with permission, from St. Croix et al. 493. Reprinted with permission.
Figure 13. Figure 13.

Summary of effects of increasing and decreasing inspiratory muscle work on quadriceps muscle fatigue. Percent twitch force (Qtw) represents the reduction in the average quadriceps force output determined across four stimulation frequencies (1‐100 Hz) and compared between baseline (preexercise) and 2.5 min postexercise. Control versus respiratory muscle unloading (via mechanical ventilation) effects on quadriceps muscle fatigue were compared at equal cycle ergometer work rates and durations (the durations being determined by the time to exhaustion under control conditions). Control versus respiratory muscle resistive loading effects on quadriceps muscle fatigue were also compared at equal cycle work rates and durations (the duration being determined by the time to exhaustion under loaded conditions). Force output of the inspiratory muscles was measured as the time integral of the average esophageal pressure multiplied by breathing frequency and for the diaphragm was measured as the average transdiaphragmatic pressure time integral multiplied by breathing frequency. Differences in Qtw were significant (*P < 0.01) between control and unload, and control and load.

Data taken, with permission, from Romer et al. 449, figure as published in Romer and Polkey 454. Reprinted with permission of the American Physiological Society.
Figure 14. Figure 14.

Raw data from an individual subject during resistive breathing. Resistive breathing consisted of breathing at 60% of maximal inspiratory pressure, a prolonged duty cycle of 0.70 and a breathing frequency of 15 breath/min. Shown are values at baseline (A) and following 5 weeks of inspiratory muscle training (B). Note the attenuation of the blood pressure response following inspiratory muscle training.

Adapted, with permission, from Witt et al. 575. Reprinted with permission.
Figure 15. Figure 15.

Shown in (A) [adapted from reference 251] is the flow‐volume response to exercise in the average fit healthy young adult during incremental exercise plotted within the maximum flow volume loop. Note that in this population, end‐expiratory lung volume (EELV) progressively decreases with exercise, and expiratory flow limitation (EFL) is only present near EELV over a small portion of the tidal volume. Considerable room exists to increase ventilation even at peak exercise. Similar responses are also shown for the fit aged adult [(B); adapted from reference 250] and the young endurance athlete [(C); adapted from reference 251]. The older adult represents a group of subjects with a mild decline in lung function but maintenance of a high ventilatory demand. Flow limitation occurs at a low work intensity and ventilatory demand (40 liter/min) and EILV at peak exercise reaches a higher percent of TLC. This group has significant ventilatory constraint at peak exercise. The fit young athlete (C) represents a group of subjects with normal lung function but excessive ventilatory demands. EELV initially decreases during exercise like the average fit adult, but increases as significant expiratory flow limitation occurs. By peak exercise in the majority of these subjects, significant ventilatory constraint is observed similar to the aged, fit adult.

Figure as published in Johnson et al. 253. Reprinted with permission.
Figure 16. Figure 16.

Airway tree with assigned labels. Labels refer to segments but are assigned to terminating branchpoint of respective segment. Definition of abbreviations: LMB, left main bronchus; LUL, left upper lobe; LB, left bronchus; LLB, left lower lobe; RMB, right main bronchus; RUL, right upper lobe; RB, right bronchus; BRONINT, intermediate bronchus; RLL, right lower lobe. * indicates significant differences between men and women of varying body size (P < 0.05). † indicates significant differences between of subjects matched for lung size (P < 0.05).

Adapted, with permission, from Sheel et al. 475. Reprinted with permission of the American Physiological Society.
Figure 17. Figure 17.

Mean curve relating the work of breathing versus minute ventilation in men (thin line) and women (thick line). Each curve has been extrapolated to 200 liter/min for theoretical purposes only.

Adapted, with permission, from Guenette et al. 198. Reprinted with permission.
Figure 18. Figure 18.

Modified Campbell diagrams of an individual male and female subject matched approximately for absolute minute ventilation [100 vs. 101 liter/min, respectively] tidal volume (2.1 vs. 2.2 liters, respectively) and breathing frequency (52 vs. 49 breath/min). Oblique hatching represents the inspiratory resistive work of breathing (Ir). Horizontal hatching represents the inspiratory elastic work of breathing (Ie). Stippling represents the expiratory resistive work of breathing (Er). Vertical hatching represents the expiratory elastic work of breathing (Ee). Cl, dynamic lung compliance; Ccw, chest wall compliance. Upward arrow represents inspiration and downward arrow represents expiration. Small open circles represent zero flow points.

Adapted, with permission, from Guenette et al. 195. Reprinted with permission of the American Physiological Society.
Figure 19. Figure 19.

Individual tidal flow‐volume loops during the final stage of exercise in women (A; n = 10) and men (B; n = 8). Dark lines represent the control breath and thin lines represent the negative expiratory pressure (NEP) breath. Subjects were considered flow limited if part of the NEP breath overlapped the preceding control breath. One male subject (subject 3) was excluded in the analysis of expiratory flow limitation because the NEP caused a sustained decrease in expiratory flow. Expiratory flow limitation was observed three of the seven male subjects and nine of the ten female subjects during the final stage of exercise. Subject 3 was the only female that did not develop expiratory flow limitation. Of all female subjects she also had the largest lungs (134% predicted FVC) and the lowest work of breathing.

Adapted, with permission, from Guenette et al. 198. Reprinted with permission.
Figure 20. Figure 20.

Breathlessness/oxygen uptake (o2) slopes showed a significant aging effect with no significant sex‐related effect: slopes were greater in 60‐ to 80‐year‐old women [old female (OF) group] compared with 40‐ to 59‐year‐old women [young female (YF) group] but not in 60‐ to 80‐year‐old men [old male (OM) group] compared with 40‐ to 59‐year‐old men [young male (YM) group]. Breathlessness/ventilation () slopes showed a significant sex‐related effect only, such that women had steeper slopes than men. * indicates that ratings of dyspnea intensity at a standardized O2 of 20 mL/kg/min showed a significant age effect, as well as a significant interaction between aging and sex‐related effects: the age‐related increase in dyspnea ratings was greater in women.

Adapted, with permission, from Ofir et al. 400. Reprinted with permission of the American Physiological Society.


Figure 1.

Schematic example of the ventilatory responses to progressive increases in cycling work rate in a healthy young subject. Note the initial rise in tidal volume, which then plateaus. After this, further increases in ventilation are accomplished by increases in breathing frequency.



Figure 2.

Ventilatory response and hemoglobin saturation (SpO2) during the final minute of leg cycling exercise at four different workloads with (Fentanyl, gray bars) and without (Placebo, black bars) partially blocked somatosensory neural feedback from the working locomotor muscles. The P value indicates the overall main effect of fentanyl. *P < 0.05; 1P = 0.08. From Amann et al. 23.

Reprinted with permission of the American Physiological Society.


Figure 3.

The solid line represents the estimated relationship between the work of breathing and exercise ventilation based on a regression equation from Aaron et al. 3, where the work of breathing = −80.041 + 1.459 (VE) + 0.011 (VE)2. The dotted line represents the estimated relationship between the respiratory muscle oxygen cost and exercise ventilation based on a regression equation from Aaron et al. 5, where the respiratory muscle o2 = 0.081 + 0.001 (exercise Wv – resting Wv), where Wv = the work of breathing.



Figure 4.

Relative effects of changing work of breathing on leg blood flow ( legs; A) and leg oxygen consumption (o2legs; B). Note that as the work of breathing is reduced (proportional assist ventilator) or increased (graded resistive loads) there is a corresponding increase and decrease in  legs and o2legs, respectively. Also note that the increased  legs with unloading occurs in the face of a reduced stroke volume and cardiac output.

Adapted, with permission, from Harms et al. 210. Reprinted with permission of the American Physiological Society.


Figure 5.

Respiratory muscle indocyanine green dye (ICG) response measured by near‐infrared spectroscopy (NIRS) at four different ventilatory loads in a single representative subject. There is a progressive increase in slope and peak ICG concentration with increasing levels of , indicating a faster rate of dye accumulation and therefore a higher blood flow response. Actual blood flow values at 20, 42, 85, and 121 liter/min were 10.2, 23.5, 32.9, and 76.0 mL/100 mL/min, respectively.

Adapted, with permission, from Guenette et al. 197. Reprinted with permission of the American Physiological Society.


Figure 6.

Raw data traces showing arterial and venous blood velocity, blood pressure, esophageal (Pes) and gastric pressure (Pga), calf force, and airflow during mild contraction conditions. The shaded areas and a downward deflection in the airflow trace denote inspiration. Note that arterial inflow remains unaffected by the type of breathing pattern used by the subject, and is also relatively unaffected by the calf contraction cycle. However, significant respiratory modulation of femoral venous outflow persists in the face of mild calf contraction during both ribcage and diaphragm breathing, as the phasic increases in venous return associated with the calf muscle pump are most pronounced during a ribcage inspiration (denoted by upward arrows). In contrast, during a diaphragmatic inspiration, anterograde femoral venous blood flow occurs exclusively during the calf contraction phase (denoted by downward arrows).

Adapted, with permission, from Miller et al. 369. Reprinted with permission.


Figure 7.

A working hypothesis for the neurophysiological underpinnings of perceived respiratory discomfort (breathlessness) during exercise in healthy humans: a working hypothesis. Refer to text for details. o2 and , metabolic rates of oxygen consumption and carbon dioxide output; Type III and IV mechano‐ and metabosensitive afferents in the peripheral locomotor (and respiratory) muscles and their vasculature; SARs, slowly adapting receptors; RARs, rapidly adapting receptors; C‐fibers, bronchopulmonary C‐fibers; J‐receptors, juxtapulmonary capillary receptors; GTOs, Golgi tendon organs; PCO2, partial pressure of carbon dioxide; [H+], hydrogen ion concentration; [La], lactate ion concentration; Pao2, arterial partial pressure of oxygen; SaO2, arterial blood oxygen saturation.

Adapted, with permission, from Jensen et al. 243. Reprinted with permission.


Figure 8.

Thickness of tenascin immunoreactive band in subepithelial basement membrane zone in controls, elite cross‐country skiers with and without bronchial hyperresponsiveness (BHR), and asthmatic subjects. Horizontal bar = median value.

Adapted, with permission, from Karjalainen et al. 266. Reprinted with permission of the American Thoracic Society. Copyright(c) American Thoracic Society. Karjalainen EM, Laitinen A, Sue‐Chu M, Altraja A, Bjermer L, and Laitnen LA. 2000. Evidence of airway inflammation and remodeling in ski athletes with and without bronchial hyperresponsiveness to methacholine. American Journal of Respiratory and Crtical Care Medicine. 161:2086‐2091. Official journal of the American Thoracic Society.


Figure 9.

Typical responses of esophageal (Pes), gastric (Pga), and transdiaphragmatic (Pdi) pressures and diaphragm EMG (i.e., M‐waves) to 10‐Hz bilateral phrenic nerve stimulation before and immediately after whole‐body exercise at 90% o2 max. Pdi was significantly reduced following the whole‐body exercise. There was no change in the M‐wave response of the diaphragm to the supramaximal stimulation.

Adapted, with permission, from Johnson et al. 246. Reprinted with permission of Wiley‐Blackwell, copyright 1993.


Figure 10.

Abdominal muscle fatigue in response to dynamic exercise. (A) Group (n = 11) mean gastric pressure (Pga) in response to magnetic stimulation at 1 Hz (single twitch) through 25 Hz (tetanic stimulation) before, and up to 30 min after whole‐body exercise. At all frequencies of stimulation, Pga immediately postexercise was reduced below baseline values. (B) Identity plot for thoracic nerve stimulation at 1‐25 Hz. *P < 0.05; **P < 0.01, values less than 1‐min postexercise significantly different from preexercise values at the same stimulation frequency. *P < 0.05; **P < 0.01, values 30‐min postexercise significantly different from preexercise values at the same stimulation frequency.

Adapted, with permission, from Taylor et al. 516. Reprinted with permission of the American Physiological Society.


Figure 11.

Schematic of the proposed respiratory muscle metaboreflex and its effects. The metaboreflex is initiated by fatigue of the respiratory muscles, mediated supraspinally via group III/IV afferents, leading to sympathetically mediated vasoconstriction of limb locomotor muscle vasculature, exacerbating peripheral fatigue of working limb muscles, and (via feedback) intensifying effort perceptions, thereby contributing to limitation of heavy‐intensity endurance exercise performance.

Adapted, with permission, from Dempsey et al. 131 as published in Romer and Polkey 454. Reprinted with permission of the American Physiological Society.


Figure 12.

Effects of fatiguing the diaphragm on muscle sympathetic nerve activity (MSNA). Note that MSNA remains relatively unchanged at the onset of high levels of inspiratory muscle force output, but increased gradually over time in both frequency and amplitude.

Adapted, with permission, from St. Croix et al. 493. Reprinted with permission.


Figure 13.

Summary of effects of increasing and decreasing inspiratory muscle work on quadriceps muscle fatigue. Percent twitch force (Qtw) represents the reduction in the average quadriceps force output determined across four stimulation frequencies (1‐100 Hz) and compared between baseline (preexercise) and 2.5 min postexercise. Control versus respiratory muscle unloading (via mechanical ventilation) effects on quadriceps muscle fatigue were compared at equal cycle ergometer work rates and durations (the durations being determined by the time to exhaustion under control conditions). Control versus respiratory muscle resistive loading effects on quadriceps muscle fatigue were also compared at equal cycle work rates and durations (the duration being determined by the time to exhaustion under loaded conditions). Force output of the inspiratory muscles was measured as the time integral of the average esophageal pressure multiplied by breathing frequency and for the diaphragm was measured as the average transdiaphragmatic pressure time integral multiplied by breathing frequency. Differences in Qtw were significant (*P < 0.01) between control and unload, and control and load.

Data taken, with permission, from Romer et al. 449, figure as published in Romer and Polkey 454. Reprinted with permission of the American Physiological Society.


Figure 14.

Raw data from an individual subject during resistive breathing. Resistive breathing consisted of breathing at 60% of maximal inspiratory pressure, a prolonged duty cycle of 0.70 and a breathing frequency of 15 breath/min. Shown are values at baseline (A) and following 5 weeks of inspiratory muscle training (B). Note the attenuation of the blood pressure response following inspiratory muscle training.

Adapted, with permission, from Witt et al. 575. Reprinted with permission.


Figure 15.

Shown in (A) [adapted from reference 251] is the flow‐volume response to exercise in the average fit healthy young adult during incremental exercise plotted within the maximum flow volume loop. Note that in this population, end‐expiratory lung volume (EELV) progressively decreases with exercise, and expiratory flow limitation (EFL) is only present near EELV over a small portion of the tidal volume. Considerable room exists to increase ventilation even at peak exercise. Similar responses are also shown for the fit aged adult [(B); adapted from reference 250] and the young endurance athlete [(C); adapted from reference 251]. The older adult represents a group of subjects with a mild decline in lung function but maintenance of a high ventilatory demand. Flow limitation occurs at a low work intensity and ventilatory demand (40 liter/min) and EILV at peak exercise reaches a higher percent of TLC. This group has significant ventilatory constraint at peak exercise. The fit young athlete (C) represents a group of subjects with normal lung function but excessive ventilatory demands. EELV initially decreases during exercise like the average fit adult, but increases as significant expiratory flow limitation occurs. By peak exercise in the majority of these subjects, significant ventilatory constraint is observed similar to the aged, fit adult.

Figure as published in Johnson et al. 253. Reprinted with permission.


Figure 16.

Airway tree with assigned labels. Labels refer to segments but are assigned to terminating branchpoint of respective segment. Definition of abbreviations: LMB, left main bronchus; LUL, left upper lobe; LB, left bronchus; LLB, left lower lobe; RMB, right main bronchus; RUL, right upper lobe; RB, right bronchus; BRONINT, intermediate bronchus; RLL, right lower lobe. * indicates significant differences between men and women of varying body size (P < 0.05). † indicates significant differences between of subjects matched for lung size (P < 0.05).

Adapted, with permission, from Sheel et al. 475. Reprinted with permission of the American Physiological Society.


Figure 17.

Mean curve relating the work of breathing versus minute ventilation in men (thin line) and women (thick line). Each curve has been extrapolated to 200 liter/min for theoretical purposes only.

Adapted, with permission, from Guenette et al. 198. Reprinted with permission.


Figure 18.

Modified Campbell diagrams of an individual male and female subject matched approximately for absolute minute ventilation [100 vs. 101 liter/min, respectively] tidal volume (2.1 vs. 2.2 liters, respectively) and breathing frequency (52 vs. 49 breath/min). Oblique hatching represents the inspiratory resistive work of breathing (Ir). Horizontal hatching represents the inspiratory elastic work of breathing (Ie). Stippling represents the expiratory resistive work of breathing (Er). Vertical hatching represents the expiratory elastic work of breathing (Ee). Cl, dynamic lung compliance; Ccw, chest wall compliance. Upward arrow represents inspiration and downward arrow represents expiration. Small open circles represent zero flow points.

Adapted, with permission, from Guenette et al. 195. Reprinted with permission of the American Physiological Society.


Figure 19.

Individual tidal flow‐volume loops during the final stage of exercise in women (A; n = 10) and men (B; n = 8). Dark lines represent the control breath and thin lines represent the negative expiratory pressure (NEP) breath. Subjects were considered flow limited if part of the NEP breath overlapped the preceding control breath. One male subject (subject 3) was excluded in the analysis of expiratory flow limitation because the NEP caused a sustained decrease in expiratory flow. Expiratory flow limitation was observed three of the seven male subjects and nine of the ten female subjects during the final stage of exercise. Subject 3 was the only female that did not develop expiratory flow limitation. Of all female subjects she also had the largest lungs (134% predicted FVC) and the lowest work of breathing.

Adapted, with permission, from Guenette et al. 198. Reprinted with permission.


Figure 20.

Breathlessness/oxygen uptake (o2) slopes showed a significant aging effect with no significant sex‐related effect: slopes were greater in 60‐ to 80‐year‐old women [old female (OF) group] compared with 40‐ to 59‐year‐old women [young female (YF) group] but not in 60‐ to 80‐year‐old men [old male (OM) group] compared with 40‐ to 59‐year‐old men [young male (YM) group]. Breathlessness/ventilation () slopes showed a significant sex‐related effect only, such that women had steeper slopes than men. * indicates that ratings of dyspnea intensity at a standardized O2 of 20 mL/kg/min showed a significant age effect, as well as a significant interaction between aging and sex‐related effects: the age‐related increase in dyspnea ratings was greater in women.

Adapted, with permission, from Ofir et al. 400. Reprinted with permission of the American Physiological Society.
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Further Reading
 1.The thorax. Roussos C, editor. Lung Biology in Health and Disease. Lenfant C, series editor. New York: Marcel Dekker, 1995.
 2.The Lung: Scientific Foundations. Crystal RG, West JB, Weibel ER, Barnes PJ, editors. Philadelphia: Lippincott‐Raven, 1997.
 3.West JB. Respiratory Physiology – The Essentials (8th ed). Baltimore: Lippincott Williams and Wilkins, 2008.
 4.Physiological Basis of Respiratory Disease. Hamid Q, Shannon J, Martin J, editors. Hamilton, ON: BC Dekker Inc, 2005.

Further Reading

The Thorax. Roussos C (Ed).  Lung Biology in Health and Disease. C. Lenfant (Series Ed).  New York: Marcel Dekker, 1995.

The Lung: Scientific Foundations. Crystal RG, West JB, Weibel ER and Barnes PJ.  Philadelphia: Lippincott-Raven, 1997.

West JB. Respiratory Physiology – The Essentials (8th Edition).  Baltimore: Lippincott Williams and Wilkins, 2008.

Physiological basis of respiratory disease.  Hamid Q, Shannon J and Martin J (Eds).  Hamilton, ON: BC Dekker Inc, 2005.

 


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Andrew William Sheel, Lee M. Romer. Ventilation and Respiratory Mechanics. Compr Physiol 2012, 2: 1093-1142. doi: 10.1002/cphy.c100046