A Steady-state Hr Is Two Consecutive Hr Readings Within Bpm of Each Other.

Symptom-limited incremental do tests accept long been used to approximate the severity of cardiovascular disease and the patient's daily activity.^{ane two iii 4} Oxygen uptake (V̇o ₂) at maximal exercise (peak V̇o ₂) is a noninvasive parameter of cardiac reserve. Withal, data obtained at maximal do may not be reproducible⁵ because of factors such equally the subject's motivation and the criteria used by the physician to terminate the exercise test. Thus, cardiologists are interested in obtaining objective data based on submaximal rather than maximal exercise.^{4 half-dozen}

While at the onset of exercise the oxygen requirement of muscle increases approximately exponentially, only a pocket-size amount of oxygen is bachelor from intracellular sources.⁷ Since the ability to apace increase the commitment of oxygen is essential for cellular homeostasis, the ability to match the V̇o _two to the cellular oxygen requirement depends on cardiac and circulatory function. Thus, patients with cardiovascular illness may take a lower uptake of oxygen (a slowing of V̇o _ii kinetics) at the onset of exercise as compared with normal subjects.

We hypothesized that a decrease in maximal exercise chapters can be estimated from V̇o ₂ kinetics at the onset of exercise. We therefore measured the time abiding of V̇o ₂ during the onset of l West of constant piece of work rate exercise and compared it with data obtained during maximal exercise in incremental do testing conducted in patients with a variety of cardiovascular diseases and in normal subjects. We too compared the time abiding of V̇o ₂ during recovery from 50 West of constant work rate exercise with data on do chapters in these subjects.

Methods

Subjects

Xxx-four consecutive patients with cardiovascular affliction classified as New York Centre Association functional class I or II were studied between May 1992 and August 1993 (Table 1). Xiv healthy subjects who were recruited from a medical screening clinic during this flow and determined to be costless of any pregnant affliction on the footing of history, concrete examination, chest radiograph, 12-lead ECG, and other routine laboratory tests were as well studied (Table 1). These fourteen subjects had a normal ECG response on a screening maximal ergometer exercise. Diagnoses of the patients included previous myocardial infarction (13 patients), coronary artery disease without myocardial infarction (7 patients), valvular heart disease (half dozen patients), dilated cardiomyopathy (5 patients), hypertensive heart disease (1 patient), and other heart disease (2 patients). We excluded from the study those with pure mitral stenosis, aortic stenosis, unstable angina, heart failure classified equally functional class 3 or IV, and documented lung disease. No patient had a myocardial infarction inside the month earlier enrollment in the report. All patients were clinically stable at the fourth dimension of the study. A β-blocker was withheld for seven days. A slow-release nitrate or calcium antagonist was withheld for 48 hours. All the other medications were withheld for at least 24 hours earlier the report. The nature and purpose of the written report was explained to the subjects, and after being and so informed, each consented voluntarily to participate in the study.

Practise Protocol

An upright, electromagnetically braked cycle ergometer (Siemens-Elema 930, Siemens Elema AB) was used in the exercise test. On the twenty-four hours of the study, each subject performed the 50-W constant work rate test for six minutes starting from rest and so performed an incremental exercise examination to the symptom-limited maximum. The incremental exercise exam began with a 3-infinitesimal warm-up at twenty Westward and 60 rpm; the load so was increased incrementally by one Due west every 6 seconds. The interval between the two tests was approximately 60 minutes. A 12-lead ECG was obtained every minute using a Case 2 Stress Organization (Marquette Electronics). Cuff blood pressure was determined every infinitesimal with an automatic indirect manometer (STBP-680F, Collin Denshi). The finish point of the incremental practice test was breast pain in 3 patients who had coronary artery disease; it was leg fatigue or dyspnea in the remaining subjects.

Measurements of V̇o _two During Exercise

V̇o _ii was measured with the subject at rest, seated on the ergometer, and throughout the do period, using an Aeromonitor AE-280 (Minato Medical Science).^eight This system consists of a microcomputer, a hot-wire flowmeter, and oxygen and carbon dioxide gas analyzers (zirconium element–based oxygen analyzer and infra-red carbon dioxide analyzer). Gas was sampled at the rate of 220 mL/min through a filter by a suction pump through the analyzers. The Aeromonitor AE-280 calculated the breath-by-breath V̇o ₂ based on the mathematical analysis described past Beaver et al.^ix The organization was calibrated before each study.

Information Analysis

Resting V̇o _ii was determined as the boilerplate of ii minutes with the subject sitting on the ergometer earlier starting exercise. The V̇o ₂ at 6 minutes was determined every bit the average between 330 to 360 seconds during 50-Due west practice. Peak V̇o ₂ was defined equally the highest V̇o ₂ that was attained over a ten-second flow during incremental do.

A five-point moving boilerplate of the breath-by-jiff data was used to evaluate V̇o _ii kinetics during the fifty-W constant work rate exercise. The time constant of V̇o ₂ kinetics was determined by fitting a monoexponential part to the V̇o ₂ response starting at exercise onset, assuming the resting value of V̇o ₂ as its baseline.^{10 eleven} The fourth dimension constant was derived by nonlinear regression by using least-squares and iterative techniques^{10 11} with a bmdp statistical software package.¹² The time constant of V̇o ₂ during recovery from the 50-W exercise was determined similarly in all subjects except for subject 17 (Tabular array i), whose respiratory gases could non be obtained during recovery.

Statistical Analysis

Data are reported every bit hateful±SD. Comparisons of variables between normal subjects and patients with cardiovascular disease were fabricated by unpaired t tests. The comparison of the fourth dimension constant of V̇o ₂ during practise with that of recovery was made by paired t tests. Linear regression assay was used to correlate the time constant of V̇o _two and other variables. Differences were considered statistically significant at P<.05.

Results

Table two shows the mean maximum work rate and the peak V̇o ₂ as determined in the incremental practise tests in the cardiac patients and in the normal subjects. Differences in both variables between the two groups were statistically significant.

Fig 1 shows the changes in V̇o ₂ during l W of constant piece of work charge per unit practice and during recovery, forth with the computer-derived line of the all-time fit to a single exponential model of the V̇o _ii response, for a representative normal subject (subject v in Tabular array 1). After the onset of exercise, V̇o ₂ increased exponentially and reached a steady state inside approximately iii minutes of practice in the normal subject. The kinetics of V̇o _ii during recovery from exercise were similar to that during do; the calculated time constants of V̇o _ii during exercise and recovery were 39.9 and 39.7 seconds, respectively.

The time constant of V̇o _two response during 50 W of exercise was determined in all subjects. The kinetics of V̇o ₂ during exercise tended to exist slower in the patients with cardiovascular disease, showing a significantly longer time constant as compared with the normal subjects (61.iv±15.ii versus 48.eight±x.4 seconds, P=.008). The mean time constant during recovery also was significantly longer in the patients with cardiovascular disease than that of normal subjects (58.7±12.six versus 49.4±11.7 seconds, P=.02).

The relation betwixt the time abiding of V̇o ₂ during 50-W exercise and the parameters for exercise capacity obtained during incremental practise testing appears for all subjects in Fig ii. The time abiding of V̇o ₂ increased with a decrease in peak V̇o _two, with a pregnant negative correlation observed betwixt the two variables (r=−.67). There also was a pregnant negative correlation between the time abiding of V̇o ₂ and the maximum work rate (r=−.66). Similarly, the time constant of V̇o _two during recovery showed a meaning negative correlation with the peak V̇o _two (r=−.63) and the maximum piece of work rate (r=−.54) in all subjects (Fig 3).

Even in the patient population excluding normal subjects, the time abiding of V̇o ₂ during l-W exercise showed a significant negative correlation with peak V̇o ₂ (r=−.57) and the maximum work rate (r=−.59). The time constant of V̇o ₂ during recovery from 50-W exercise too showed a significant negative correlation with peak V̇o _ii (r=−.56) and the maximum piece of work charge per unit (r=−.40) in this population.

The time constant of V̇o ₂ during exercise at l W of constant piece of work rate and that of recovery showed a significant positive correlation (r=.53) (Fig 4). The difference betwixt the fourth dimension constant of V̇o ₂ during exercise and that of recovery was not pregnant by the paired t test.

The time constant of V̇o ₂ during exercise became longer with age in normal subjects (y=0.50ten+26.eight, r=.71); the time constant of V̇o ₂ during recovery also tended to be longer with age (y=0.33x+34.8, r=.42).

Give-and-take

The V̇o ₂ response during constant work charge per unit exercise is postulated to accept three phases¹³ : phase I, an firsthand increase at the offset of practise lasting approximately 20 seconds; phase Two, a subsequent exponential increase that lasts 2 to three minutes; and phase III, a steady-state level or slow drift stage that starts at approximately 3 minutes. If the exercise at a constant piece of work charge per unit is mild or moderate, V̇o _ii usually reaches a steady state within 3 minutes. However, at piece of work rates associated with increased blood lactate, V̇o ₂ continues to increment beyond 3 minutes. Although nosotros did not measure out the blood lactate concentration, the time constant of V̇o _two is positively correlated with claret lactate level during exercise.¹¹

If the work rate is sufficiently high, the stage I increase in V̇o _two is relatively small. The overall increase in V̇o _two during abiding piece of work charge per unit exercise is determined mainly by increases in phase II and phase III. However, if the work rate is very low (15 or 20 Westward), the full V̇o _two increase during six minutes of do is determined mainly by the increase in phase I within the start 20 seconds.¹⁰ In this case, the increase in V̇o ₂ during phase Two is modest, making it hard to approximate V̇o ₂ kinetics during this period. From our experience,¹⁴ most patients with functional grade I or Ii tin comfortably sustain 50 W of constant piece of work rate exercise for half dozen minutes. Nosotros therefore used a abiding work rate exercise of 50 W in all subjects studied. In some patients, 50 West may be as well high to exist sustained for 6 minutes, specially those with severe centre failure classified as functional class III or 4 or astringent myocardial ischemia. However, the mean middle rate in our patients at 6 minutes at l-W practise was not very high (116±25 beats per minute; Table two). We therefore believe that this practice tin can be performed safely by most patients with cardiovascular disease.

Nosotros used a unmarried exponential equation to narrate the overall kinetics of the increase in V̇o _two. Although the slowed V̇o _two kinetics seen in cardiac patients may have been better fitted to a double exponential equation,^xv the methodology of this fitting would be too circuitous to obtain a clinical parameter for practise chapters. Still, a single exponential model is reported to characterize the increase in V̇o ₂ even during exercise associated with an increase in blood lactate.¹¹ The V̇o ₂ during recovery from exercise is also known to decrease exponentially.¹⁶ Therefore, we used the same exponential model for the decreasing V̇o _ii kinetics during recovery.

An oxygen deficit is defined as the divergence between the predicted corporeality of oxygen required to perform the exercise (steady-state V̇o _ii×duration of practise) and the actual cumulative consumption of oxygen.¹⁷ Oxygen debt is the deviation betwixt that consumed during recovery and the production of the preexercise resting V̇o ₂ and the duration of recovery.¹⁷ The oxygen deficit can be accounted for past existing chemic energy stores in the muscle besides as in tissue and blood, and, ultimately, the formation of ATP by the nonoxidative metabolism of saccharide substrates.^{7 10 eighteen} The oxygen deficit and oxygen debt will be equal if the elapsing of exercise is long enough for the V̇o ₂ to accomplish a steady state.¹⁹ The time constant of V̇o ₂ during exercise and recovery can exist calculated from the post-obit equations.^{20 21}

Therefore, if the work rate is moderate and the duration of exercise and recovery are long plenty to attain a steady state, the time constant of V̇o _two during recovery would theoretically be identical to that of exercise, equally we noted in this study.

The fourth dimension constants of V̇o ₂ during exercise and recovery were both significantly prolonged in patients with cardiovascular disease as compared with normal subjects despite our finding of no difference in hemodynamic variables either at residue or at 6 minutes of exercise (Table 2). Hughson and Smyth²² and Petersen et al²³ reported that β-blockade slows the V̇o ₂ increase during submaximal practice in normal subjects. Sietsema et al²⁴ demonstrated that patients with cyanotic congenital center disease exhibited prolonged V̇o ₂ response kinetics. The V̇o _ii response also has been slowed by experimentally decreasing the blood oxygen content in normal subjects.^xi These previous findings are consequent with our observations, although the normal subjects of the present study were not historic period-matched with the patients, and the time constant of V̇o ₂ was institute to be influenced by historic period.

Because the pulmonary V̇o _ii kinetics closely reflect muscular V̇o ₂ during the onset of abiding work rate practise, the slowed pulmonary V̇o ₂ kinetics probably are due to a decrease in oxygen availability at the exercising muscles. Therefore, the longer time constant of V̇o ₂ during exercise seen in cardiac patients with decreased exercise capacity must partly be related to their slower increase in cardiac output, as recently reported.^{25 26} Although the mechanism underlying V̇o ₂ kinetics during recovery is not well understood, the time course of cardiac output during recovery, which probably is slower in patients with cardiovascular disease,²⁷ might have influenced recovery V̇o ₂ kinetics. Withal, the V̇o _two kinetics too are related to peripheral oxygen commitment and metabolic utilization at the exercising muscles. Therefore, the abnormal V̇o ₂ kinetics may not exist specific for cardiovascular disease.

Maximal V̇o ₂, a plateau of V̇o _two despite further increases in the piece of work charge per unit, has been used as a useful parameter to evaluate maximal exercise capacity. Although maximal V̇o ₂ is more often than not adamant by maximal cardiac output and the potential for oxygen extraction by the exercising muscles,^{13 28} this parameter is often hard to obtain in patients with cardiovascular disease because of limitations such as breast hurting or leg discomfort before attaining the target work rate. On the other mitt, elevation V̇o ₂, which is simply the highest V̇o _two attained during the incremental do, is easily influenced by the patient's willingness to do as well every bit the subjective evaluation of the physician who has the responsibility to terminate the exercise exam.

In patients with coronary artery illness, maximal exercise capacity may be artificially limited due to onset of angina, which may not be present at submaximal levels. Thus, there is a considerable amount of interest in obtaining objective and submaximal measurements of aerobic office. The fourth dimension abiding of V̇o ₂ during the initiation and recovery from the submaximal practise is contained from maximal exercise attempt and may be a better reflection of exercise limitations at a daily action level compared with the maximal or peak V̇o ₂.

The present study used a Siemens Elema 930 ergometer, which requires approximately 10 seconds to accomplish the established work rate afterwards the outset of practice. Therefore, the actual work rate was less than 50 Westward in the showtime 10 seconds. The characteristics of the work rate at the start of practise may have influenced the phase I increment in V̇o ₂ and partly affected the calculated time constant of V̇o _two. This influence would be more marked at a very low piece of work rate, in which the magnitude of the increase in V̇o _ii during the 6 minutes of exercise is determined mainly during the first xx seconds. Even so, these characteristics did non impact the time constant of V̇o ₂ during recovery.

The fourth dimension constants of V̇o ₂ during both the initiation of and the recovery from exercise showed significant negative correlations with peak V̇o ₂ and maximal piece of work rate over a wide range of exercise capacity in our subjects. Although the factors that determine V̇o _ii kinetics, especially during the recovery from exercise, remain to exist clarified, we believe that the time constant of V̇o ₂ both during fifty W of constant piece of work rate exercise and during recovery from this exercise, which does non crave the subject'southward maximal effort, is a useful parameter for objectively evaluating the exercise capacity of patients with mild to moderate cardiovascular illness.

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Figure 1. Plot of changes in oxygen uptake (V̇o ₂) during 50 W of constant work charge per unit practise and during recovery, along with the computer-derived line of the all-time fit to a single exponential model of the V̇o ₂ response, for a representative normal subject (subject 5 in Tabular array i). τ indicates time constant of V̇o ₂.

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Effigy 2. Scatterplots show A, relation of the fourth dimension abiding of oxygen uptake (V . o _ii) during 50-W do to peak V . o ₂, and B, maximal work rate (WR) obtained during the incremental exercise tests in all subjects.

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Figure iii. Scatterplots testify A, relation of time constant of oxygen uptake (V̇o ₂) during recovery from 50-West exercise to acme V̇o _ii, and B, maximal work charge per unit (WR) obtained during the incremental exercise tests in all subjects.

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Figure iv. Scatterplot shows relation betwixt time constant of oxygen uptake during fifty-West exercise and that of recovery in all subjects. The line of identity is shown.

Tabular array i. Physical Characteristics, Diagnosis, and Maximum Work Rate in All Subjects Tested

	Sex	Age, y	Meridian, cm	Weight, kg	Cardiac Lesion	Maximum Work Rate, Watts
Normal subjects (northward=14)
one	F	69	147	44		66
2	M	41	174	73		155
3	Thousand	43	167	62		112
4	M	49	166	54		108
5	1000	43	167	63		143
6	F	68	157	72		83
7	M	23	175	62		172
8	F	44	152	71		107
nine	G	24	174	59		148
ten	F	59	146	51		75
xi	F	48	160	60		101
12	M	17	172	68		227
xiii	Thou	41	177	85		188
14	M	51	164	74		127
Mean±SD		44±fifteen	164±ten	64 ±x		129±44
Patients with cardiovascular disease (northward=34)
xv	M	65	154	59	CAD	73
xvi	M	48	164	72	OMI	127
17	One thousand	57	169	75	CAD	100
18	Chiliad	67	168	68	CAD	100
19	Thousand	53	164	58	CAD	116
20	Thou	68	158	59	OMI	94
21	M	69	153	53	MR	63
22	F	44	160	61	MR	78
23	F	64	153	52	DCM	63
24	Chiliad	59	167	54	DCM	75
25	M	41	171	71	CAD	120
26	Grand	threescore	150	45	DCM	83
27	M	30	157	62	DCM	117
28	M	65	160	56	HHD	66
29	M	69	163	45	DCM	88
30	Thou	67	170	64	CAD	82
31	F	72	152	46	OMI	57
32	Thousand	65	151	64	VSD	79
33	F	69	147	54	OMI	73
34	G	71	154	63	OMI	81
35	One thousand	57	169	64	OMI	92
36	M	75	154	55	AR	111
37	K	49	165	61	OMI	125
38	M	60	163	60	OMI	91
39	Yard	58	161	53	OMI	72
40	M	57	165	68	OMI	106
41	M	70	168	57	CAD	80
42	M	58	176	72	AR	103
43	Thousand	69	156	50	AR	101
44	M	69	161	63	AR	112
45	Thousand	63	168	65	OMI	85
46	F	71	156	53	OMI	76
47	Yard	48	180	95	OMI	142
48	F	59	155	48	HCM	80
Hateful±SD		61±x	161±8	60 ±10		92±21

Table 2. Hemodynamic Information at Residue, at 6 Minutes of fifty-Westward Constant Exercise, and at Peak Do During Incremental Exercise Testing

Condition	Normal Subjects (n=14)	Cardiac Patients (north=34)	P
Residue
Heart rate, bpm	seventy ±nine	70±11	NS
Systolic claret pressure, mm Hg	135 ±xiii	137±21	NS
Diastolic blood pressure, mm Hg	77 ±10	78±thirteen	NS
Oxygen uptake, mL/min	308±49	283 ±44	NS
Oxygen uptake, mL/min/kg	4.8±0.half-dozen	iv.7 ±0.vi	NS
6 Minutes of fifty-W practise
Heart rate, bpm	116 ±14	116±25	NS
Systolic blood pressure, mm Hg	183 ±19	182±26	NS
Diastolic blood pressure, mm Hg	88 ±15	88±xx	NS
Oxygen uptake, mL/min	1176±100	1095 ±98	<.05
Oxygen uptake, mL/min/kg	18.viii±3.1	xviii.6±2.ix	NS
Peak exercise
Work rate, W	129±44	92 ±21	<.001
Center rate, bpm	154 ±15	133±24	<.005
Systolic blood force per unit area, mm Hg	210±22	193±27	NS
Diastolic claret pressure, mm Hg	92±22	95±22	NS
Oxygen uptake, mL/min	2098±658	1494±345	<.001
Oxygen uptake, mL/min/kg	32.vi±8.4	24.nine ±4.ix	<.001

Presented in part at the annual meeting of Experimental Biology, Anaheim, Calif, April 1994.

Footnotes

Correspondence to Akira Koike, MD, 2nd Department of Internal Medicine, Tokyo Medical and Dental Academy, 5-45 Yushima one-chome, Bunkyo-ku, Tokyo 113, Japan.

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Source: https://www.ahajournals.org/doi/10.1161/01.CIR.91.6.1719

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