Maximal aerobic power describes the functional capacity of the cardiorespiratory system and is defined as the maximum rate at which oxygen can be used during a specified period, usually during intense exercise. It is a function both of cardiorespiratory performance and the maximum ability to remove and use oxygen from the blood. The higher the measured cardiorespiratory fitness level, the more oxygen has been transported to and used by exercising muscles, resulting in a higher level of exercise intensity that is able to be achieved. Because regular physical activity is required to maintain cardiovascular health and improve athletic performance, its measurement continues to be a focus in the health and clinical setting. Because of its underlying value as a health indicator across a variety of clinical populations, maximal aerobic power often is used as a primary or secondary end point in many research trials (10). This article will discuss the measurement of maximal aerobic power and the use of this measurement in various clinical settings, particularly as it relates to cardiovascular disease.
FACTORS AFFECTING MAXIMAL AEROBIC POWER
Maximal aerobic power has been shown to provide important prognostic and diagnostic information in a variety of patient populations. It provides the foundation for many clinical and research applications and can be measured directly or estimated from physiological responses to submaximal or maximal exercise tests. Direct measurement of maximal aerobic power often is expressed as maximal oxygen consumption (V˙O2max), which is the product of cardiac output and arteriovenous oxygen (AV O2) difference and defines the ability of an individual to perform aerobic work. Maximal aerobic power also can be expressed in metabolic equivalents (METs) to allow for intersubject comparison relative to body weight because one MET approximates 3.5 mL O2/kg body weight per minute (10). Maximal aerobic power can be affected by age, conditioning status, the presence of disease, or medication regimen. Typically, the average V˙O2max in men is 10% to 20% greater than that in women, related largely to a greater muscle mass, higher hemoglobin concentration, and greater stroke volume (10). Regular endurance exercise has been associated with an increase in V˙O2max of 10% to 30%, because of enhanced AV O2 difference and increased maximal stroke volume, which can help attenuate the reduction in aerobic capacity that occurs over time, often declining by 8% to10% per decade in nonathletic subjects (9). These declines often are the result of a decrease in maximal heart rate and AV O2 difference (9).
Because few activities of daily living require maximal effort, tests done to measure V˙O2max often includes measurement of the ventilatory threshold (VT). VT is a submaximal value that is identified as the point during which ventilation increases exponentially relative to the increase in oxygen consumption. The VT is linked to the rising lactic acid level in the blood, which is, in turn, related to an increased recruitment of fast twitch muscle fibers, higher levels of epinephrine and a decreased rate of removal of lactate by the liver. The increased lactic acid accumulation, and subsequent conversion to lactate, results in increased carbon dioxide production and an increased ventilatory response to the exercise (21). The VT usually occurs between 47% and 64% of V˙O2max in most healthy individuals but occurs at a higher percentage in trained endurance athletes (5,13). Additional variables measured during cardiopulmonary exercise testing are presented in the Table.
Direct measurement of VO2 is the most accurate and reliable method for determining maximal aerobic power, yet it can prove very difficult to find outside traditional exercise physiology laboratories. Expensive and sophisticated equipment, along with highly trained staff, is required for testing. In addition, many patients are unable or unwilling to exercise to a truly maximal VO2. In such instances, maximal aerobic power may need to be estimated using regression equations derived from submaximal or maximal exercise protocols. Although it is important to note that direct measures of VO2 are more reproducible and are used to minimize the standard deviation of the measurement, regression equations can provide reasonable estimations of aerobic capacity from steady state exercise protocols. However, care must be taken to eliminate variables that could alter the accuracy of the regression equations.
In addition to traditional testing measures, a timed walking test (6- or 12-minute walk test) can be used to estimate maximal aerobic power and assess the risk for cardiopulmonary morbidity and mortality in various patient populations (8,15). These tests possess administration benefits over maximal exercise tests, are well tolerated in many clinical populations, and have demonstrated significant correlation with maximal oxygen consumption tests (11,14). Although both methods provide advantages in safety and ease of use, the potential for error in estimating functional capacity should be recognized in a clinical setting.
When evaluating maximal aerobic power, protocol selection is very important to ensure accurate outcomes are achieved. In the United States, testing is typically completed using a motorized treadmill or cycle ergometer, although treadmill is the preferred mode because of greater familiarity. Arm ergometer testing is typically avoided as a testing modality because of an inability to achieve and maintain high work rates as a result of a smaller muscle mass being used. Avoidance of protocols that involve large work rate increments is recommended, instead focusing on protocols that allow for smaller MET increments per stage (i.e., Balke and Ware (1) or Naughton et al. (20) protocols). Regardless of the protocol selected, the test should be tailored to each patient to yield fatigue-limited exercise duration of approximately 10 minutes (19).
AEROBIC CAPACITY MEASUREMENT IN PATIENTS WITH CARDIOVASCULAR DISEASE
Decreased maximal aerobic power, as a measure of cardiorespiratory fitness, is associated with increased cardiovascular disease and all-cause mortality (7). Low cardiorespiratory fitness increases the relative risk of death to a similar level as tobacco abuse, hypertension, and/or diabetes (2,16). Maximal aerobic power also has significant prognostic capabilities in patients with known or suspected cardiovascular disease. In particular, when using the standard Bruce protocol during graded exercise testing, a maximal aerobic power exceeding 14 METs was associated with a reduced probability for severe coronary artery disease and an improved 4-year survival rate when compared with those with less than a 5 MET maximal aerobic power (18). Additionally, in coronary artery disease patients undergoing preoperative evaluations before noncardiac surgery, the ability to achieve a high exercise workload was consistent with a low postoperative cardiac risk, regardless of associated symptoms or ST-segment changes (6). In patients entering cardiac rehabilitation, maximal aerobic power measurements provide the necessary information for developing an appropriate exercise prescription and for evaluating the results of an exercise training regimen.
In patients with chronic heart failure, estimates of maximal aerobic power are less reliable than the direct measurement of gas exchange (3). Thus, in this patient population, cardiopulmonary gas exchange measurements have become standard for the assessment of maximal aerobic power. In particular, measurements of peak VO2 and VT are highly reproducible and recommended for this patient population (4). Markedly impaired exercise tolerance places the heart failure patient in a high-risk category for a poor outcome. For instance, a peak VO2 of less than 10 to 12 mL O2/kg body weight per minute identifies a poor 1-year prognosis, whereas a peak VO2 of greater than 14 mL O2/kg body weight per minute demonstrate a more favorable outcome (17).
Evaluation of peak VO2 also can be beneficial in patients with other cardiovascular diseases. In those with valvular or congenital heart disease, measuring maximal aerobic power can assist in identifying candidates in need of early surgical intervention (12). Additionally, using maximal aerobic power measurements in those with peripheral arterial disease can assist in the development of an exercise prescription and evaluate the overall response to exercise training (10).
OPPORTUNITIES FOR THE CLINICAL EXERCISE PROFESSIONAL
Data support the use of maximal aerobic power in clinical populations, particularly in those with cardiovascular disease, to help guide treatment and evaluate interventions. Exercise professionals, particularly those with clinical backgrounds, are uniquely qualified to assist with research and testing in this area. These individuals can play a significant role in the coordination of oxygen consumption testing to ensure protocol optimization and data collection. Although directly measured VO2 is primarily used in patients with cardiovascular disease and in athletes, the use of estimated V˙O2max is a regular part of fitness evaluations. Thus, clinical exercise professionals who are adept at exercise testing, including in the measurement of VO2, can play an important role in the use and interpretation of these important clinical measures.
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