Comprehensive Physiology Wiley Online Library

Respiratory Control During Exercise

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 New Techniques for Studying Exercise Hyperpnea
1.1 Computerized Data Analysis
1.2 Systems Analysis of Dynamic Work‐Rate Forcings
2 Behavior of Ventilatory Control System
2.1 Ventilatory Response to Incremental Exercise
2.2 Ventilatory Response to Constant‐Load Exercise
2.3 Factors Affecting Ventilatory Response to Constant‐Load Exercise
3 Conceptual Development of Ventilatory Control Hypotheses
3.1 Central Neurogenic Drive
3.2 Peripheral Neurogenic Drive
3.3 Neurohumoral Drive
3.4 Humoral Concepts
3.5 Cardiovascular Linkages
4 Conclusion
Figure 1. Figure 1.

Breath‐by‐breath measurement of end‐tidal partial pressure of CO2 and O2 ( and ), minute expiratory ventilation (), CO2 output (), O2 uptake (), and, at times indicated by points, arterial and pH measurements for a 1‐min incremental‐work test on a cycle ergometer in a normal subject. Isocapnic buffering, period when and increase curvilinearly at the same rate, keeping constant but increasing . Respiratory compensation (Resp Comp), period when starts to decrease.

Adapted from Wasserman 225
Figure 2. Figure 2.

General scheme of ventilation during exercise and recovery. Phase I identifies period of abrupt change during transition between rest and exercise. Phase II identifies period of slow change to steady state (phase III).

Figure 3. Figure 3.

Continuous measurement of ventilation and gas exchange for 1 subject during exercise performed from rest to 50 W and 150 W (avg of breath‐by‐breath studies done 8 times at each work rate). Vertical bars, ±1 SEM; HR, heart rate; R, gas exchange ratio. Subject starts on command at 0 time and is ordered to stop at 4 min. Flywheel of cycle is at 60 rpm when subject starts so no load is added at onset beyond that needed to maintain the work. Fraction of total ventilatory response attributable to phase I is decreased at higher work rate. Also , , and R are unchanged during transition from rest to exercise. Note transient undershoot in R and starting at τ20 s.

Figure 4. Figure 4.

Changes in , breathing frequency (f), tidal volume (Vt), and during cycle ergometer exercise and recovery in 1 subject (8‐breath avg). Left panel, performance at a work rate below subject's anaerobic threshold (AT). Right panel, results of same subject above his anaerobic threshold. Work rate started at base line of unloaded cycling and increased at times indicated.

Figure 5. Figure 5.

Effect of prolonged constant‐work‐rate exercise on partial pressures of O2 () and CO2 () in arterial blood (A and B, respectively) and pH (C) for moderate, heavy, and very heavy work. Each point, average of 10 subjects.

From Wasserman et al. 226
Figure 6. Figure 6.

Arterial pH, , , and lactate during recovery from very heavy work (0 time is value within 1 min before stopping exercise). Outer horizontal dashed lines, range of control values for arterial pH, , and . Inner dashed lines, range of normal, resting lactate concentration. Each point, average of 4 subjects physically stressed to the same degree. Plots for each subject conform to average. Note that pH corrects first. Lactate, , and recover in parallel.

Figure 7. Figure 7.

Comparison of time constants (τ) for and (left panel) and for and (right panel) from onset of constant‐work‐rate exercise from rest (Δ), transition from 25 W to subject's anaerobic threshold while pedaling at a constant rate (•), and same work‐rate transition from 25 W to subject's anaerobic threshold but while increasing pedal rate from 40 to 80 rpm (○). All points are above the line of identity, indicating that ventilatory kinetics are slower than kinetics for and . Ventilatory kinetics are closely correlated with kinetics but weakly correlated with kinetics.

Adapted from Diamond, Casaburi, Wasserman, and Whipp 68
Figure 8. Figure 8.

Measurements of (btps), (stpd), and for sinusoidally varying work rate between 25 and 120 W performed by a normal subject breathing air (left panel) and 100% O2 (right panel).

From Casaburi, Whipp, Wasserman, et al. 32
Figure 9. Figure 9.

Ventilatory response to 90‐W exercise from an unloaded cycling base line. Kinetics (time constant) are clearly affected by inspired O2 concentration.

Figure 10. Figure 10.

Amplitude and phase relations (Φ, phase lag) for sinusoidally varying work rate at periods of 10, 4, and 2 min for a normal subject. Points, average responses for 2, 6, and 10 sinusoidal cycles, respectively. Curves are sine waves of best fit to response data.

From Casaburi, Whipp, Wasserman, et al. 34
Figure 11. Figure 11.

Relationship of to (A) and (B) in 10 normal subjects. Each curve is determined from at least six 4‐min work‐rate increments with 4th‐min values plotted.

From Wasserman et al. 226
Figure 12. Figure 12.

Computed isometabolic curves as related to . Lower curve, for resting (0.2 liters/min) and 0.33 dead space‐tidal volume ratio (Vds/Vt). Upper curve, for exercise (2.0 liters/min) and Vds/Vt (0.2). Length of vertical dashed lines indicates increase in when going from rest to exercise when set point is 40 mmHg (right) and 30 mmHg (left).

Figure 13. Figure 13.

Effect of changing inspired O2 concentration on ventilation for work rates above (left panel) and below (right panel) anaerobic threshold (AT) for 1 subject. Top panel, inspiratory gas was switched from air to O2; bottom panel, gas was switched from O2 to air. Note effect of the switch on and .

From Wasserman, Whipp, Casaburi, et al. 231
Figure 14. Figure 14.

Effect of partial diversion of venous return from right atrium to lower aorta during exercise in 2 anesthetized dogs. Upgoing black arrow, when stimulation of the hindlimb muscles started in order to induce muscular exercise; downgoing black arrow, when stimulus was removed. White arrows, when bypass flow from exchanger was increased from 0.5 liter/min to 3 liters/min and then decreased back to 0.5 liter/min. Dog A weighed 40.5 kg; dog B weighed 47 kg. Note abruptness of change in during diversion in A with only small transient decrease in before returning to prediversion value. Also note that in B actually increased during diversion. , expiratory airflow; PRV, right ventricular pressure; BP, systemic arterial blood pressure.

Figure 15. Figure 15.

Hypotheses of breathing control during exercise.



Figure 1.

Breath‐by‐breath measurement of end‐tidal partial pressure of CO2 and O2 ( and ), minute expiratory ventilation (), CO2 output (), O2 uptake (), and, at times indicated by points, arterial and pH measurements for a 1‐min incremental‐work test on a cycle ergometer in a normal subject. Isocapnic buffering, period when and increase curvilinearly at the same rate, keeping constant but increasing . Respiratory compensation (Resp Comp), period when starts to decrease.

Adapted from Wasserman 225


Figure 2.

General scheme of ventilation during exercise and recovery. Phase I identifies period of abrupt change during transition between rest and exercise. Phase II identifies period of slow change to steady state (phase III).



Figure 3.

Continuous measurement of ventilation and gas exchange for 1 subject during exercise performed from rest to 50 W and 150 W (avg of breath‐by‐breath studies done 8 times at each work rate). Vertical bars, ±1 SEM; HR, heart rate; R, gas exchange ratio. Subject starts on command at 0 time and is ordered to stop at 4 min. Flywheel of cycle is at 60 rpm when subject starts so no load is added at onset beyond that needed to maintain the work. Fraction of total ventilatory response attributable to phase I is decreased at higher work rate. Also , , and R are unchanged during transition from rest to exercise. Note transient undershoot in R and starting at τ20 s.



Figure 4.

Changes in , breathing frequency (f), tidal volume (Vt), and during cycle ergometer exercise and recovery in 1 subject (8‐breath avg). Left panel, performance at a work rate below subject's anaerobic threshold (AT). Right panel, results of same subject above his anaerobic threshold. Work rate started at base line of unloaded cycling and increased at times indicated.



Figure 5.

Effect of prolonged constant‐work‐rate exercise on partial pressures of O2 () and CO2 () in arterial blood (A and B, respectively) and pH (C) for moderate, heavy, and very heavy work. Each point, average of 10 subjects.

From Wasserman et al. 226


Figure 6.

Arterial pH, , , and lactate during recovery from very heavy work (0 time is value within 1 min before stopping exercise). Outer horizontal dashed lines, range of control values for arterial pH, , and . Inner dashed lines, range of normal, resting lactate concentration. Each point, average of 4 subjects physically stressed to the same degree. Plots for each subject conform to average. Note that pH corrects first. Lactate, , and recover in parallel.



Figure 7.

Comparison of time constants (τ) for and (left panel) and for and (right panel) from onset of constant‐work‐rate exercise from rest (Δ), transition from 25 W to subject's anaerobic threshold while pedaling at a constant rate (•), and same work‐rate transition from 25 W to subject's anaerobic threshold but while increasing pedal rate from 40 to 80 rpm (○). All points are above the line of identity, indicating that ventilatory kinetics are slower than kinetics for and . Ventilatory kinetics are closely correlated with kinetics but weakly correlated with kinetics.

Adapted from Diamond, Casaburi, Wasserman, and Whipp 68


Figure 8.

Measurements of (btps), (stpd), and for sinusoidally varying work rate between 25 and 120 W performed by a normal subject breathing air (left panel) and 100% O2 (right panel).

From Casaburi, Whipp, Wasserman, et al. 32


Figure 9.

Ventilatory response to 90‐W exercise from an unloaded cycling base line. Kinetics (time constant) are clearly affected by inspired O2 concentration.



Figure 10.

Amplitude and phase relations (Φ, phase lag) for sinusoidally varying work rate at periods of 10, 4, and 2 min for a normal subject. Points, average responses for 2, 6, and 10 sinusoidal cycles, respectively. Curves are sine waves of best fit to response data.

From Casaburi, Whipp, Wasserman, et al. 34


Figure 11.

Relationship of to (A) and (B) in 10 normal subjects. Each curve is determined from at least six 4‐min work‐rate increments with 4th‐min values plotted.

From Wasserman et al. 226


Figure 12.

Computed isometabolic curves as related to . Lower curve, for resting (0.2 liters/min) and 0.33 dead space‐tidal volume ratio (Vds/Vt). Upper curve, for exercise (2.0 liters/min) and Vds/Vt (0.2). Length of vertical dashed lines indicates increase in when going from rest to exercise when set point is 40 mmHg (right) and 30 mmHg (left).



Figure 13.

Effect of changing inspired O2 concentration on ventilation for work rates above (left panel) and below (right panel) anaerobic threshold (AT) for 1 subject. Top panel, inspiratory gas was switched from air to O2; bottom panel, gas was switched from O2 to air. Note effect of the switch on and .

From Wasserman, Whipp, Casaburi, et al. 231


Figure 14.

Effect of partial diversion of venous return from right atrium to lower aorta during exercise in 2 anesthetized dogs. Upgoing black arrow, when stimulation of the hindlimb muscles started in order to induce muscular exercise; downgoing black arrow, when stimulus was removed. White arrows, when bypass flow from exchanger was increased from 0.5 liter/min to 3 liters/min and then decreased back to 0.5 liter/min. Dog A weighed 40.5 kg; dog B weighed 47 kg. Note abruptness of change in during diversion in A with only small transient decrease in before returning to prediversion value. Also note that in B actually increased during diversion. , expiratory airflow; PRV, right ventricular pressure; BP, systemic arterial blood pressure.



Figure 15.

Hypotheses of breathing control during exercise.

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Karlman Wasserman, Brian J. Whipp, Richard Casaburi. Respiratory Control During Exercise. Compr Physiol 2011, Supplement 11: Handbook of Physiology, The Respiratory System, Control of Breathing: 595-619. First published in print 1986. doi: 10.1002/cphy.cp030217