Answers to Clinical Problems in Chaper 12: Exercise Physiology

1. Carbon dioxide production during aerobic metabolism comes from the chemical combination of carbohydrate or fatty acid with oxygen and the consequent production of carbon dioxide and water (see Fig. 12­1). During anaerobic metabolism, carbon dioxide is produced from the buffering of lactic acid. When anaerobic metabolism occurs along with aerobic metabolism, such as during the graded exercise test, lactate­generated carbon dioxide adds to the carbon dioxide from aerobic metabolism. At this point (anaerobic threshold), the total carbon dioxide load presented to the lungs increases, as can be appreciated from the rise in slope of VCO₂ (Fig. 12­1) .

2. You are asked to determine alveolar and arterial PO₂ of a well­trained jogger who has been running on a treadmill. Resting PetCO2 was 40 mm Hg and RQ was 0.8; after 5 minutes on the treadmill, the patient's RQ is still 0.8 (VCO₂ = 800; VO₂ = 1000), but minute ventilation has increased to 30 L/min. Despite the fivefold increase in VE, PetCO₂ is essentially unchanged at 30 mm Hg. PetCO₂ reflects PaCO₂, which in turn reflects PaCO₂ (see Chapter 4). Despite the large increase in minute ventilation, the jogger's PaCO₂ is thus unchanged, and he is not hyperventilating.

3. This 40­year­old man had the following predicted and achieved VO2 max and heart rate:

He achieved a VO2 max and a maximal heart rate close to his predicted values and was pronounced physically fit for the expedition.

4.Patient A has low PaO₂ and normal PaCO₂ at rest. During exercise, the patient's PaO₂ falls and PaCO₂ rises slightly; this suggests both diffusion impairment and severe ventilatory limitation and is compatible with severe emphysema. (Regardless of exercise level, alveolar ventilation normally rises to match carbon dioxide production, so PaCO₂ should normally never rise.) The severely emphysematous patient has lost pulmonary capillary vessels and so has less membrane area for diffusion. The severe airways obstruction of emphysema makes the patient unable to augment minute (and hence alveolar) ventilation to meet exercise needs.

Patient B has a slightly low PaO₂ and a normal PaCO₂ at rest. During exercise, the patient's PaCO₂ is unchanged (a normal finding), and his PaO₂ has increased by 6 mm Hg. Normally, PaO₂ remains fairly constant during exercise. An increase of PaO₂ over a low resting value without a change in PaCO₂ indicates improvement in ventilation­perfusion distribution within the lungs. Such improvement is commonly seen during exercise in patients with chronic bronchitis.

Patient C has a low normal PaO₂ and a reduced PaCO₂ at rest. During exercise, the patient's PaO₂ drops 15 mm Hg, and PaCO₂ also falls slightly indicating further hyperventilation. The drop in PaO₂ is best explained by a severe diffusion impairment, such as occurs from interstitial fibrosis. As pulmonary blood flow increases, there is less time for equilibration of oxygen, so PaO₂ falls.

5. This case exemplifies a common problem for which patients are referred for exercise testing. The patient has mild heart disease but not enough to cause symptoms at rest. He also has airways obstruction. What causes his dyspnea?

a. Respiratory quotient is VCO2 divided by VO2. O2­pulse is oxygen uptake in cc/min divided by heart rate; units are cc O2/heart beat. RQ and O₂­pulse are given below.

	Rest	2 mph 0% grade	2.5 mph 0% grade	3 mph 5% grade	3 mph 10% grade
RQ	0.86	0.75	0.80	0.83	0.86
O2-pulse	4.86	8.62	9.60	10.19	11.97

b. One way anaerobic threshold (AT) can be determined is by measuring the rise in blood lactate, but lactate was not measured in this patient. Another way of determining AT is by comparing the rise in minute ventilation (VE) to the rise in carbon dioxide production (VCO2); when the rise in VE exceeds that for VCO2, AT has been reached. In this patient, minute ventilation and carbon dioxide production each increased fourfold, so anaerobic threshold was not achieved.

How about ventilatory limitation? His MVV at rest was 50.5 L/min; shortly before he quit exercising, total minute ventilation was up to 48 L/min. Normally, maximal exercise ventilation reaches approximately 65% of the resting ventilatory capacity (MVV), leaving approximately 33% in reserve. This patient's exercise ventilation was over 90% of his MVV. Thus one can assume that ventilatory limitation was the reason he quit exercising.

c. The patient quit exercising because of dyspnea, which was likely related to ventilatory limitation. His heart rate increased appropriately, as did his O₂­pulse. He did not reach his predicted maximal heart rate and showed no evidence of a cardiac limitation to exercise. His dyspnea on exertion is most likely related to ventilatory impairment and not to any heart problem.

6. This patient had been seen by several physicians in the past but had not had formal exercise testing. His resting pulmonary function studies were normal. However, he had a clear history of dyspnea during exertion.

a. METS are multiples of the resting oxygen uptake. VD/VT is calculated from the Bohr equation (see Chapter 4):

The calculated METS and VD/VT follow:

	1 mph	2 mph	2.5 mph	3 mph	3.5 mph
METS	2.7	3.9	4.8	5.5	5.8
VD/VT	0.27	0.21	0.20	0.20	0.19

b. This patient came close to anaerobic threshold but did not reach it; there was no fall in PaCO₂, and RQ did not go above 1. Also, the patient maintained a steady pH, and bicarbonate did not fall. There was no ventilatory limitation; his MVV at rest was 112 L/min, and maximal exercise ventilation was only 38.5 L, well below his MVV. His heart rate increased appropriately, and there was no wheezing after the completion of exercise.

c. This test was interpreted as showing poor fitness caused by obesity and a sedentary life style. He had neither ventilatory nor cardiac limitation to exercise, but he simply could not continue after 10 minutes because of fatigue and dyspnea. In the final analysis, he had no industrially­related problem that could account for his symptoms.

TRUE - FALSE ANSWERS