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Arterial po2 will not change because it's almost at maximum already. Venous po2 will decrease due to increased oxygen consumption by respiring muscle. Venous and arterial pCo2 will actually either stay the same or fall due to the increased ventilation stimulated by the increased Co2 production by respiring muscles. The increased pCO2 is detected by central and peripheral chemoreceptors and leads to increased ventilation, resulting in increased ventilation - causing pCo2 to remain normal or decrease. This mechanism cannot be used to explain the ventilation increase in light exercise because pCo2 hardly rises at all during light exercise, therefore the chemoreceptors may not be responsible for the mechanism resulting in increased ventilation,

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Q: How does exercise affect pO2 in the muscle cell?
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