Arterial pH, PCO2, standard bicarbonate, lactate, and ventilation were measured with a high sampling density during rest, exercise, and recovery in normal subjects performing upright cycle ergometer exercise. Three 6-min constant-work exercise tests (moderate, heavy, and very heavy) were performed by each subject. We found a small respiratory acidosis during the moderate-intensity exercise and an early respiratory acidosis followed by a metabolic acidosis for the heavy- and very-heavy-intensity exercise. During recovery, arterial pH rapidly returned to the preexercise value for the moderate-intensity work. However, arterial pH decreased further during the first 2 min of recovery for the heavy- and very-heavy-intensity work, before a slower return toward the resting values. We conclude that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this acidosis is blunted but not eliminated by the ventilatory response. During recovery, the return to resting arterial pH and PCO2 and standard bicarbonate appears to be determined by the rate of lactate decline.

Cardiopulmonary exercise testing (CPET) is under-utilized in assessing patients with prominent complaints of dyspnea or exercise limitation and should be one of the early tests used to assess exercise intolerance. The standard 12-lead ECG treadmill stress test focuses on coronary artery disease and is inadequate to assess the various subsystems (i.e., heart, lung, pulmonary vascular, peripheral vascular, muscle and psychological motivation) that can contribute individually, or more commonly in an interrelated fashion, to cause exercise limitation. The additional gas exchange information from CPET is very helpful in the identification of a more precise diagnosis, assessment of the severity of the impairment, determination of response to treatment and prediction of mortality. This special report will highlight some of the recent important applications of CPET to clinical medicine with specific references to heart failure, preoperative risk assessment, and regenerative and rehabilitative medicine, and the evidence that currently exists in the medical literature to support routine CPET use. It will also detail the recent evidence regarding the association of VO2max and survival in health and disease.

Chronic obstructive pulmonary disease (COPD) is a common multisystem inflammatory disease with ramifications involving essentially all organ systems. Pulmonary rehabilitation is a comprehensive program designed to prevent and mitigate these disparate systemic effects and improve patient quality of life, functional status, and social functioning. Although initial patient assessment is a prominent component of any pulmonary rehabilitation (PR) program, cardiopulmonary exercise testing (CPET) is not regularly performed as a screening physiologic test prior to PR in COPD patients. Further, CPET is not often used to assess or document the improvement in exercise capacity related to completion of PR. In this review we will describe the classic physiologic abnormalities related to COPD on CPET parameters, the role of CPET in Risk Stratification/Safety prior to PR, the physiologic changes that occur in CPET parameters with PR, and the literature regarding the use of CPET to assess PR results. Finally, we will compare CPET to 6MW in COPD PR, the common minimal clinically important difference (MCID) is associated with CPET, and the potential future roles of CPET in PR and Research.

Oxygen uptake (V.o2) measured at the mouth, which is equal to the cardiac output (CO) times the arterial–venous oxygen content difference [C(a–v)O2], increases more than 10- to 20-fold in normal subjects during exercise. To achieve this substantial increase in oxygen uptake [V.o2 = CO × C(a–v)O2] both CO and the arterial–venous difference must simultaneously increase. Although this occurs in normal subjects, patients with heart failure cannot achieve significant increases in cardiac output and must rely primarily on changes in the arterial–venous difference to increase V.o2 during exercise. Inadequate oxygen delivery to the tissue during exercise in heart failure results in tissue anaerobiosis, lactic acid accumulation, and reduction in exercise tolerance. H+ is an important regulatory and feedback mechanism to facilitate additional oxygen delivery to the tissue (Bohr effect) and further aerobic production of ATP when tissue anaerobic metabolism increases the production of lactate (anaerobic threshold). This H+ production in the muscle capillary promotes the continued unloading of oxygen (oxyhemoglobin desaturation) while maintaining the muscle capillary Po2 (Fick principle) at a sufficient level to facilitate aerobic metabolism and overcome the diffusion barriers from capillary to mitochondria (“critical capillary Po2,” 15–20 mm Hg). This mechanism is especially important during exercise in heart failure where cardiac output increase is severely constrained. Several compensatory mechanisms facilitate peripheral oxygen delivery during exercise in both normal persons and patients with heart failure.