Ventilation and Acid Base

Figure 2 shows the time course of changes in ventilation during a constant level of submaximal exercise. A rapid initial increase is followed by a slower increase until a steady state is achieved. Current theories for exercise hyperpnea, defined as the increase in ventilation during exercise, involve a combination of feedforward mechanisms and feedback from the chemoreceptor and mecha-noreceptor reflexes. Feedforward mechanisms (also called central command) are neural inputs from higher centers in the brain that directly stimulate the respiratory centers. For example, signals from the motor cortex or hypothalamus to move a muscle can also stimulate ventilation. Feedforward mechanisms have essentially no delay and can explain the rapid increase in ventilation at the onset of exercise. The slower, secondary increase in ventilation is explained by neural mechanisms, such as second-messenger systems activated by neurotransmit-ters, changes in intracellular calcium that stimulate neurons, and possibly such changes in chemical stimuli to sensory nerves as potassium ions in muscle.

Figure 1 showed how alveolar ventilation increases in perfect proportion to CO2 production, so PaCO2 is maintained at the normal resting value during submaximal steady-state exercise. Because arterial blood gases

Rest m

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