They increase due to metabolic acidosis

They increase due to CO₂ retention

They decrease due to hyperventilation

They remain unchanged

To reduce oxygen uptake

To maintain or increase minute ventilation

To compensate for reduced cardiac output

Because of increased airway resistance

Insulin

Aldosterone

Angiotensin II

Vasopressin

It increases proportionally with tidal volume

It decreases due to bronchodilation

It remains constant regardless of exercise intensity

It increases, but less than tidal volume, improving gas exchange efficiency

Promote water reabsorption

Stimulate aldosterone release

Increase sodium excretion

Decrease blood pressure

Is reduced by over 50% due to sympathetic vasoconstriction

Remains constant at 25% of cardiac output

Decreases slightly due to passive effects

Increases due to sympathetic vasodilation

Decreases aortic pressure

Reduces heart rate

Increases stroke volume in response to increased end-diastolic volume

 Increases norepinephrine release

Stroke volume is higher in untrained trained individuals than trained individuals

Stroke volume is the same in both trained and untrained individuals 

Stroke volume will decrease in trained individuals during exercise 

Stroke volume is higher in trained individuals than untrained individuals

It generates 3 ATP and 3 NADH molecules per acetyl CoA molecule

It occurs in the cytoplasm

It is the final step of the cellular respiration process

It is inhibited by ATP

Decreased alveolar ventilation

Bronchial hyperresponsiveness

Stiffening of lung tissue reducing expansion

Increased airway resistance