Which one of the following statements about monitoring exercise heart rate is true?

Maximal Oxygen Uptake

Maximal oxygen uptake (

Plateau in Oxygen Uptake.

Maximal oxygen uptake is considered the best index of aerobic capacity and maximal cardiorespiratory function. By defining the limits of the cardiopulmonary system, it has been an invaluable measurement clinically for assessing the efficacy of drugs, exercise training, or invasive procedures. No other measure of work is as accurate, reliable, or reproducible as ventilatory maximal oxygen uptake. The collection and analysis of an expired gas sample taken during the last period of an exercise test has generally been used to determine maximal oxygen uptake. From early studies using interrupted protocols, a test was considered “maximal” only when there was no further increase in oxygen uptake despite further increases in workload. Conversely, oxygen uptake has been considered “peak” when the subject reaches a point of fatigue where no plateau in oxygen uptake was observed. Unfortunately, the many problems associated with the determination and criteria for the “plateau” in oxygen uptake make these definitions more semantic than physiologic. A brief history of this concept and its inherent problems follows.

In 1955 Taylor et al96 established the criteria of plateauing as a failure to increase oxygen uptake more than 150 mL/min, or 2.1 mL/kg/min, with an increase in workload. Their original research was done using interrupted progressive treadmill protocols. With interrupted protocols, stages of exercise could be separated by rest periods ranging from minutes to days. Taylor et al96 found that 75% of their subjects fulfilled these criteria. Using continuous treadmill protocols, Pollock et al97 found that 69%, 69%, 59%, and 80% of subjects plateaued when tested using the Balke, Bruce, Ellestad, and Astrand protocols, respectively. Froelicher et al98 found that only 33%, 17%, and 7% of healthy subjects met these criteria during testing with the Taylor, Balke, and Bruce protocols, respectively, despite the fact that there were no significant differences between the protocols in maximal heart rate, VO2 max, or blood pressure. Taylor et al later reported that plateauing did not occur when using continuous treadmill protocols. Subsequent studies, using a variety of empirical criteria, report the occurrence of a plateau ranging from 7% to 90% of tests.

The plateau concept has been subjected to many interpretations and criteria. The newer, automated gas exchange systems, which allow breath-by-breath or any specified sampling interval, have raised new questions regarding the interpretation of a plateau. Although the definitions of plateauing vary greatly, all focus on the concept that oxygen uptake at some point will fail to continue to rise as work increases. Using ramp treadmill testing, in which work increases constantly at an individualized rate, we measured the slope of the change in work versus the change in oxygen uptake at different sampling intervals.22,99 In this way, if oxygen uptake were no longer increasing (while work was increasing continuously) the slope of the relationship between the two variables would equal, or not differ from, zero. To increase the possibility of observing a plateau, a large sampling interval of 30 consecutive eight-breath averages was used. We observed that patients plateau on several occasions submaximally, even when some subjects do not meet these criteria at maximal exercise. This is because the slope of the relationship between oxygen uptake and work rate varies greatly, despite a constant, continuous change in external work and the use of large, averaged samples. In addition, it was found that this response was poorly reproducible, and that the occurrence of a plateau depended greatly upon which definition of a plateau was used and how the data were sampled (e.g., 30-second samples, various breath-averaging techniques, etc.). These observations would appear to preclude the determination of a plateau by common definitions.

The plateau concept is long ingrained in exercise physiology. Intuitively, it is known that the body's respiratory and metabolic systems must reach some finite limit beyond which oxygen uptake can no longer increase, and some subjects who are highly motivated may exhibit a plateau. However, the occurrence of a plateau depends as much on the criteria applied, the sampling interval, and methodology as on the subjects' health, fitness, and motivation. Studies performed in our laboratory22,99 and others100–103 suggest that the plateau concept has limitations for general application during standard exercise testing.

Use of Nomograms to Express Exercise Capacity

One of the most important results of the exercise test is to determine an individual's exercise capacity relative to a “normal” value. This is particularly important in light of the many recent studies demonstrating the prognostic power of exercise capacity. Determining what constitutes normal can be a difficult undertaking. For example, many protocols have been developed to assess various patient populations. Rapidly advanced protocols may be suited to screening younger or more active individuals (e.g., Bruce, Ellestad), whereas more moderate ones are appropriate for older or deconditioned patients (e.g., Ramp, Naughton, Balke-Ware, United States Air Force School of Aerospace Medicine [USAFSAM]). The main disadvantage to having so many techniques has been determining equivalent workloads between them (e.g., what does 5 minutes on a modified Bruce protocol mean relative to a Balke-Ware protocol or in terms of real-life activities such as hiking or grocery shopping?).

It has been well established that maximal oxygen uptake (VO2) can be reasonably estimated from the workload achieved on a given protocol, although there are notable limitations in doing so. The widely used equations to estimate METs come from the American College of Sports Medicine guidelines:

Estimated METs based on treadmill/speed and grade: METs = (mph × 26.8) [0.1 + (grade × .018) + 3.5]/3.5

Estimated METs based on cycle ergometer workload: METs = [(Watts × 12/Body weight in Kg) + 7]/3.5

As mentioned earlier, the term metabolic equivalent (MET) has been commonly used to describe the quantity of oxygen consumed by the body from inspired air under basal conditions. The MET is equal on average to 3.5 ml O2kg/min.13 A multiple of the basal metabolic rate, or MET, is a useful clinical expression of a patient's exercise capacity. Directly measured VO2 is translated into METs by dividing by 3.5, thus providing a unitless and convenient method for expressing a patient's exercise capacity.

Because VO2 depends on age, gender, activity status, and disease states, tables that consider these factors must be referred to in order to accurately categorize a certain MET value as either normal or abnormal. We developed a nomogram in order to make it more convenient for physicians to translate an MET level into a percentage of normal exercise capacity for males based on age and activity status.14 We retrospectively reviewed the exercise test results of 3583 male patients referred to our laboratory for the evaluation of possible or probable CAD. Simple univariate linear regression was performed, with age as the independent variable and METs achieved as the dependent variable. This was done separately for the entire group, as well as for the “sedentary” and “active” groups. The nomograms derived from estimated MET levels are presented in Figures 3-3 and 3-4 for males, and a nomogram for females is presented in Figure 3-5.15

Note that there have been numerous regression equations developed in various populations; determining a “normal” value for exercise capacity relative to age is population specific. Some of the different regression equations from the literature are presented in Table 3-2. For example, the greater slope in the Veterans Administration (VA) population is consistent with a faster decline in exercise capacity with age than that found in previous studies. Regression equations can vary because of population differences, including age, activity status, state of health, definition of normal or healthy individuals, and gender. The decline in maximal heart rate with age is also steeper in our referrals, paralleling that for the slope in VO2. Thus maximal heart rate decreased with age at a greater rate than in prior studies,16 which could be attributed to a submaximal effort or complicating illnesses in older patients, or it may simply be due to the wide scatter that has been observed for this measurement in past studies.

One must also consider differences in methodology when examining divergent results. Few such studies have used measured VO2 in developing normal values. Additionally, the treadmill protocols were quite different, and it has been demonstrated that some protocols are more accurate than others when estimating METs. For instance, more gradual protocols may favor the elderly and thus alter the regression line. Nevertheless, the mean MET levels for age in our study agree quite well with those of prior investigations (Table 3-3). It would be difficult to sort out which study has produced the most “universal” regression equations, because all have weaknesses in either population selection or methodology.

The upward shift in the slope of the nomogram scale among volunteers whose oxygen uptake was determined directly from ventilatory gas exchange analysis is because estimating MET levels from treadmill work results in an overestimation of exercise capacity.17 Thus the approximately 1 to 1.5 higher predicted MET values for any given age among referred patients whose exercise capacity was estimated from treadmill workload is expected.

Key Points:

Establishing a patient's exercise capacity relative to a normal standard is an important result of the exercise test and should be included in the test report.

Normal exercise capacity tables/graphs/scales are population specific.

Although measured oxygen uptake is the more precise measure of work, normal standards are also specific to whether oxygen uptake was measured or estimated.

An estimation of maximal ventilatory oxygen uptake from treadmill or cycle ergometer workload during dynamic exercise (expressed as METs) has been the common language with which investigators and clinicians communicate when assessing these widely different exercise protocols and everyday physical activities of their patients (Table 3-4)

Aerobic capacity and endurance.

Aerobic capacity is commonly described by the

Exercise testing in a laboratory typically involves progressive and incremental increases in exercise intensity while the patient is walking on a treadmill or riding a bicycle ergometer. The Bruce and Balke treadmill protocols are two commonly employed progressive exercise testing protocols. The Bruce approach uses six stages of work, each of 3 minutes' duration. The first stage begins with a treadmill speed of 1.7 miles per hour (mph) at a grade of 10%. Subsequent stages increase both speed and grade until stage VI requires 6.0 mph at a grade of 20%. Nomograms by which to determine functional impairment are available for the Bruce protocol. The Balke protocol, another commonly used approach, requires that the patient begin at a fast speed of 3.3 mph but on a level surface. The incline or grade is added gradually so that a “steady-state” exercise regimen is replicated. Steady-state testing is often used in development of a training regimen baseline. Well-supported bicycle ergometer protocols are also available.

When this type of equipment is not available, a 6- or 12-minute timed walking test, a shuttle walking test, or a step test are simple alternatives.

Exercise testing sites should have the capacity for continuous electrocardiographic monitoring, periodic heart rate and blood pressure measurement, cutaneous oximetry and arterial blood gas determination, and expired gas analysis; they should also have an oxygen source. In addition, a cardiac defibrillator, other emergency equipment and supplies, and proper personnel for their use must be immediately available in case of cardiopulmonary emergency. Maximal and submaximal testing may be performed. A complete discussion of aerobic testing may be found in Chapter 3.

Physical Performance

GH replacement improves exercise capacity in parallel with an increase in maximal oxygen uptake in GH-deficient adults113,146 (Fig. 11-10). The improvement occurs within 6 months of therapy.147 The anaerobic threshold, a measure of submaximal exercise performance, increases significantly during GH treatment, suggesting that physical activities of daily living may be accomplished with less metabolic stress and subjective perception of effort.148 Maximal workload and oxygen consumption increased progressively over a 5-year period of GH treatment.141 Many factors may contribute to an improvement in exercise performance. These include enhanced cardiac function, increased red cell mass, and improved heat dissipation through increased sweating. The data supporting a positive effect of GH on cardiac function are strong. Stroke volume, cardiac output, and diastolic function improve during GH treatment.113,149

Studies on muscle strength have revealed that improvements emerge late. Most studies over 6 months have failed to show a benefit compared to placebo treatment.147 The majority of studies assessing GH effects beyond 12 months report significant improvement in muscle strength, although these are uncontrolled.9,150 The results of most studies suggest that the increased muscle strength in response to GH replacement is due to increased muscle mass and not to intrinsic changes in the contractile function.114 Long-term observation of treatment over 10 years shows that muscle strength increased gradually over the first 5 years and thereafter protects against the normal age-related decline in neuromuscular function, resulting in approximately normalized muscle strength.151

MAXIMAL CARDIAC OUTPUT

Maximal cardiac output has long been considered the major factor limiting maximal oxygen uptake; numerous studies have demonstrated a linear relation between cardiac output and oxygen uptake during exercise. The rate of increase in cardiac output is commonly judged to be roughly 6 L per 1 L increase in oxygen uptake. However, there is a wide biologic scatter between maximal cardiac output and VO2 max in healthy persons, even when age, gender, and activity status are considered. Because both maximal cardiac output and maximal oxygen uptake decline with age, the effects of age and disease are usually difficult to separate.

McDonough et al35 measured maximal cardiac output in a group of patients and found a decline in maximal cardiac output to be the major hemodynamic consequence of symptomatic CAD and one that resulted in exercise impairment. Reductions in left ventricular performance at high levels of exercise, manifested by decreasing stroke volume and increasing pulmonary artery pressure, appeared to be the mechanism limiting cardiac output. Hossack et al36 studied 100 patients with coronary disease (89 men, 11 women) to characterize their aerobic and hemodynamic profiles at rest and during upright treadmill exercise. The mean maximal cardiac output, measured using the direct Fick equation, was 57 ± 14% of average normal values. The reduction in maximal heart rate (63 ± 13% of normal) was a greater factor influencing the reduction in cardiac output than stroke volume (88 ± 16% of normal). Peak VO2 was 48 ± 15% of normal, and the greater reduction in peak VO2 compared with cardiac output was due to lower peripheral extraction in the patients with CAD. Variables that correlated with maximal cardiac output in a univariate analysis included angina severity (r = −0.45), peak VO2 (r = 0.67), maximal heart rate (r = −0.31), degree of left ventricular dysfunction (r = −0.45), maximal SBP (r = −0.31), and number of vessels with 50% or greater diameter reduction (r = −0.30). Resting EF did not correlate with maximal cardiac output using a multivariate analysis, but four variables correlated significantly (r = 0.77) with maximal cardiac output in the following order: VO2 max, number of vessels with 50% or greater stenosis, magnitude of ST depression, and gender. These data were used to estimate limits of maximal cardiac output and stroke volume in normal subjects, and these normal standards were then used to evaluate the results in the patients. Patients with an EF of less than 50% had significantly impaired age-adjusted cardiac output and stroke volume.

Many similar studies were performed during the 1980s and 1990s, and while they varied greatly in terms of populations and methods used to measure cardiac output (echocardiographic, nuclear, impedence cardiography, or direct Fick), collectively they confirm that cardiac output is the major hemodynamic factor influencing exercise capacity. Therefore, a disruption in any of the factors that define cardiac output (e.g., maximal heart rate achieved, stroke volume, filling pressure, ventricular compliance, contractility, or afterload) will limit exercise tolerance.

Cardiovascular training

If an endurance programme is applied to young healthy children, any gains in maximal oxygen uptake will be less than those seen where an endurance training programme is applied to young adolescents or adults. The reasons for this are not clear and may be linked to the fact that children are usually active by nature so training programmes are not as effective or because of the hormonal changes which happen at puberty. Where children are hypoactive, for example those with chronic diseases, cardiovascular training may produce improvements in the child’s ability to carry out functional activities.

Monitoring of exercise in patients with Type II diabetes mellitus

Exercise intensity is typically prescribed and monitored using heart rate or a percentage of the maximal oxygen uptake (VO2), which can be initially established during the exercise stress test. However, some patients can develop autonomic neuropathy which can affect the cardiovascular response to exercise and in such patients, exercise intensity can also be measured by rating of perceived exertion.

Blood glucose monitoring should be performed before and after physical activity to monitor the effect of the exercise on blood glucose concentration.

Supplemental carbohydrates are generally not needed in the patients with Type II diabetes; however, if patients are prone to hypoglycemia, they may require additional carbohydrates during and following exercise. A total of 1 h of exercise will require an additional 15 g of carbohydrate either before or after exercise. If exercise is vigorous or of longer duration, an additional 15–30 g of carbohydrate per hour may be required.

Adaptations to Submaximal/Endurance Exercise Training

Submaximal exercise generally refers to an intensity of exercise that requires less than an individual's maximal oxygen uptake. Submaximal exercise challenges the body to deliver and utilize an increased amount of oxygen in the resynthesis of ATP. With training, changes occur that increase the body's ability to utilize oxygen. For simplicity, the adaptations to submaximal exercise training have been grouped according to the site at which they occur.

Central adaptations to regular submaximal exercise include alterations in the morphology and function of the heart and circulatory systems that allow greater delivery of oxygen to the working muscle. Modest cardiac hypertrophy characterized by an increase in left ventricular volume occurs in response to training. This adaptation allows an increase in stroke volume, leading to a reduction in heart rate at rest and during submaximal workloads and an increased cardiac output during maximal workloads. An increase in total plasma volume and an increase in the total amount of hemoglobin have been observed in response to submaximal endurance training.

Peripheral adaptations to regular submaximal exercise include changes in the structure and function of skeletal muscle that enhance its ability to use oxygen to produce energy aerobically. A consequence of endurance training is an augmented blood supply to the working muscle. This is achieved by an increased capillarization in trained muscles, greater vasodilation in existing muscle capillaries, and a more effective redistribution of cardiac output to the working muscle. Increases in both the activity of aerobic enzymes and mitochondrial volume density (approximately 4–8%) within trained muscle have been noted. These are coupled with greater glycogen storage within the muscle and augmented fat mobilization allowing a higher rate of aerobic ATP resynthesis from free fatty acids and glucose.