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1Department of Physiology and Pharmacology, Karolinska Institute, Stockholm; 2Åstrand Laboratory of Work Physiology and the Swedish School of Sport and Health Sciences, Stockholm; and 3Department of Laboratory Medicine, Section of Clinical Physiology, Karolinska Institute, Stockholm, Sweden
Submitted 19 May 2006 ; accepted in final form 17 October 2006
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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O2 max). We measured cardiac output (
) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting O2 max. Eight well-trained men (age 24.4 ± 2.8 yr, weight 81.3 ± 7.8 kg, and O2 max 59.1 ± 2.0 ml·min–1·kg–1) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured O2 max, maximal , and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently O2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic. central governor; error of the method; maximal exercise; oxygen uptake
O2 max) is of vital importance for both physical performance and health in general. That is why questions regarding this important physiological parameter have been researched since 1923, when Hill and Lupton showed that the oxygen uptake did not continue to increase with increasing rate of work (17). Despite more than 80 years of scientific investigation of O2 max, there is still no clear consensus regarding the fundamental question: What sets the upper limit for O2 max during exercise with a large muscle mass included?
Over the years, several theories have been proposed as limitation(s) factors to O2 max, e.g., skeletal muscle oxidative capacity, mainly total mitochondrial volume (peripheral limitation) (27), vasodilatation in relation to cardiac output () (7), symmorphosis theory where there is no single limiting factor for O2 max (28, 32), partly revised to different links in the oxygen transport system chain during severe dynamic exercise as resistances in Ohm's law (8, 9).
According to our view, this theory of a harmonized oxygen transport system chain during maximal exercise is in line with the one in which the volume of oxygen transported from the left ventricle to the periphery [ times oxygen content of arterial blood (Ca
)] is the basic determinant for O2 max (11, 12). In this thinking, changes in different factors within the oxygen transport system chain, such as variations in hemoglobin concentration, oxygen content of inspired air, arterial oxygen saturation, or type of exercise, may only modify the O2 max obtained under optimal conditions.
However, another theory has been introduced into this discussion (22–24). The basis for this theory is that the central nervous system (a central governor) controls the circulation during severe exercise. No experimental data are presented, which could have supported the theory, but the author states that there is sufficient evidence for the opinion that the central nervous system moderates the central circulation during maximal exercise. By doing so, the circulation is primarily hindered to utilize its whole capacity to protect the heart muscle from becoming ischemic. Thus, according to the central governor theory, O2 max is only a consequence of the amount of work that the heart is allowed to perform and not vice versa, i.e., that the total volume of oxygen transported from the heart to the periphery has reached its maximum during maximal exercise with large muscle groups.
This central governor theory has been both supported (25) and rejected (5, 31). Since no consensus has been obtained and no earlier study has specifically addressed this question, the aim of the present investigation was to study the central circulation during different maximal work rates. It is acknowledged that the double product of blood pressure (BP) times and BP times heart rate (HR) reflects the myocardial oxygen uptake (MO2) (20, 21). Our aim was therefore to measure BP and at two maximal work rates, differing in a range of 
10–15% in watts (W). The work time had to be long enough to create O2 max in both tests.
The hypothesis for this study was that, during maximal and supramaximal exercise with the use of large muscle groups in well trained subjects, a higher rate of work would create a higher BP than the lower one; at the same time, the HR, , and O2 max would be equal in the two maximal tests. Therefore, the heart during the higher maximal work rate should have produced more mechanical work than during the lower one. Thus, if this is the case, the work of the heart would not have been hindered by the central nervous system at the lower maximal work rate.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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O2 max 59.1 ± 2.0 ml·min–1·kg–1, volunteered to participate in this study. To avoid any training effect as a consequence of the study, the subjects had to be fairly well trained, since the study included several preexperimental maximal exercises to secure peak values of O2 on several maximal rates of work, and two maximal exercises had to be carried out within 2 h in the main experiment. Therefore, the subjects were selected according to the following criteria: 1) a O2 max of 
55 ml·min–1·kg–1, 2) training history of >5 yr of endurance training, and 3) current training frequency of 4 times/wk. The protocol was explained to the subjects before they had given their written, informed consent to participate in this study. The study was approved by the Regional Ethics Committee of Stockholm, Sweden. All experimental tests were performed within a 6-wk period. The subjects performed the tests at about the same time of the day (±2 h). There was >48 h between individual maximal tests, except in the main experiment, during which only 1 h elapsed between two maximal tests. The subjects were asked to eat a small meal no less than 4 h before each test, to avoid caffeine-enriched beverages during this 4-h period, and not to be on medication during the test period.
All tests were carried out using a combined arm and leg ergometer system, which consisted of two mechanically braked cycle ergometers (Monark 839E, Monark, Vansbro, Sweden). One of these was used as an ordinary leg cycle ergometer, whereas the other was placed on an aluminium frame and used as an arm ergometer, with handgrips mounted on the cranks. The subjects were seated behind the arm ergometer, with the height of the saddle adjusted so that the arms, when extended, were just below heart level.
The ratio between arm and leg work in all tests was 20:80% to 25:75% of the total rate of work. The cadence was set to 80 rpm. The cadence figures, one for legs and the other for arms, were available on two computer screens. If the subject lost his cadence within reasonable limits, the Monark 839E system corrected the braking force so that the work intensity set for the test would be maintained.
An important part in this study was to establish a clear leveling off of O2 vs. rate of work to create a situation with different demands on the heart while O2 max was the same. This was done through an extensive pretest program in which several submaximal and maximal combined arm and leg exercises were carried out. From the results of these tests, an individual leveling-off configuration of O2, in relation to increasing rate of work, could be established in all subjects, and from this figure the lowest rate of work (L) that elicited O2 max was chosen. The L work rate was used in the main test with catheters indwelled, and the data obtained were compared with data from an 10% higher maximal rate of work (H). O2 max was reached according to Åstrand and Rodahl (3a) when 1) total work time was >5 min, 2) leveling off of O2 vs. rate of work with O2 on the highest work rate being within 150 ml/min from previous highest obtained value in the test (29), 3) subjective rate of perceived exertion of >16, and 4) and blood lactate concentrations above 8 mM.
We had to perform the L and H maximal tests on the same day. However, no difference was observed in O2 values between the two maximal tests during the pretests. Furthermore, there were no differences between obtained values of O2 and HR for the L rate of work with and without catheters indwelled. We also used well-trained subjects who were familiar with repeated maximal exercises during normal training sessions. Thus there are no reasons to believe that the test procedure during the main test influenced the conclusions of this study (see DISCUSSION).
O2 was measured continuously using an ergospirometry system (AMIS 2001, Innovision, Odense, Denmark) based on the mixed expired method with an inspiratory flowmeter. Averaged values of O2 data of 10-s averages were available on the computer screen. For the gas analyzer calibration, high precision gases (16.00 ± 0.04% O2 and 4.00 ± 0.1% CO2, Air Liquide, Kungsängen, Sweden) and normal air were used. Before each test, the ambient conditions were measured, and gas analyzers and inspiring flowmeter were calibrated. The calibration of the flowmeter was performed with a 3.0-liter air syringe (Hans Rudolph) at a low, medium, and high flow velocity. This system's accuracy has been validated against the Douglas bag technique (18). HR was continuously measured using a HR monitor (model Polar S610, Polar Electro) integrated with the AMIS 2001.
A thin catheter was introduced in the brachial artery for sampling of blood and measurement of intra-arterial BP. A balloon-tipped catheter was inserted percutaneously via an antecubital vein and advanced under fluoroscopic control to a branch of the pulmonary artery for sampling of blood. The hemoglobin concentration and blood O2 saturation was measured by an automatic spectrophotometric method (ABL 520 Radiometer) radiometer in blood drawn from the brachial and pulmonary artery. was determined by the Fick's principle, based on O2 and the difference in O2 content in arterial (arteria brachialis) and mixed venous (arteria pulmonalis) blood.
Determinations of blood lactate concentrations were done on samples of blood (20 µl) obtained on fingertip blood and analyzed on Biosen 5140 (EKF, Diagnostic, Magdeburg, Germany). Calibration of the blood lactate analyzer was performed before each test and checked by using a lactate standard of 12 mM. Calibration results within ±0.1 mM were accepted. The voltage was checked by a control solution of 4.8–6.4 mM. RPE was evaluated using the 6–20 RPE scale, according to Borg (6), applied on central (dyspnoea, tachycardia) and local (active muscle) fatigue (10).
Main test.
The preparation and procedure for each test was the same for every subject. In the morning of the experimental day, the catheters were inserted. After arrival to the exercise test room, saddle height was adjusted, 11 ECG electrodes were applied, and the first submaximal rate of work (200 W) was carried out for 4 min. O2 and HR were measured continuously with the AMIS 2001 and the ECG. At the end of the submaximal work period, BP was recorded from the brachial artery. Thereafter blood samples for determination of CaO2 and mixed venous O2 concentration were simultaneously obtained from the brachial and pulmonary artery catheters, respectively. After a short rest and 2 min of warm-up at 50% of final work rate, the L maximal rate of work was performed. The subjects worked until subjective exhaustion or until they could not keep the cadence. O2 and HR were measured continuously. At 2 min from start of the L maximal rate of work, BP in the brachial artery was recorded for the first time and then at least another three times. On each occasion, at least 25 BP curves were recorded, and average values were calculated. After the first BP recording, blood samples for determination of Ca and mixed venous O2 concentration were simultaneously drawn from the brachial and pulmonary artery catheters, respectively. At least three pairs of blood samples were obtained during the L maximal test.
After the subject had rested for 1 h, resting values of O2, HR, and BP were recorded, and blood samples were drawn from the two catheters for determination of while sitting on the cycle ergometer. Thereafter, using the same experimental protocol as in the first exercise session, the 200-Wsubmaximal and the H maximal exercise were carried out. However, since the H maximal rate of work was higher, the work time became shorter. Therefore, after the first recording of BP and at 2 min, only another 1 or 2 values of and BP could be obtained until the subject was exhausted (Fig. 1).
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Shapiro-Wilk's W-test was applied to examine the normality in the distribution of data. To detect differences between the L and the H trials, paired t-tests were used. Significance of differences was determined at P < 0.05, and data are reported as means ± SD, unless otherwise stated. Mean BP was calculated from diastolic BP + 1/3 of the difference between systolic and diastolic BP.
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RESULTS |
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O2 max and peak HR in the L combined arm and leg work between the two pretests were 0.06 l/min and 1.8 beats/min (P < 0.03 and P < 0.22, respectively). Between the two pretests and the L trial, the differences in O2 max and peak HR were 0.01 and 0.04 l/min and 2.8 and 1.0 beats/min (P = 0.95 and 0.81 and P = 0.11 and 0.53, respectively). Between the two pretests and the H trial, the differences in O2 max and peak HR were 0.01 and 0.07 l/min and 3.5 and 1.8 beats/min (P = 0.97 and 0.74 and P = 0.04 and 0.46, respectively). Average peak blood lactate concentration after the final pretest was 13 ± 2 mM. All results and relevant statistics for the main experiment are presented in Table 1 and Figs. 2 and 3.
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O2 max, , and HR values in the L and H tests, the 95% CI of the differences included a zero. The H maximal work load generated a higher systolic, diastolic, and calculated mean arterial BP than the L maximal work. In these BP measurements, the 95% CI for the differences did not include zero.
Since the HR was the same during the H and L maximal exercise, the average product of HR times systolic and HR times mean BP was 12% and 8% higher in the H than in the L maximal exercise, respectively. Since was the same during the H and L maximal exercise (24.7 and 25.0 l/min, respectively), the increase in times systolic and times mean BP during the H compared with the L maximal exercise was 14% and 10%, respectively. In all these increases, the 95% CI for the differences did not include zero.
For values obtained during the two submaximal exercises, the 95% CI for the differences included zero only in HR measurement.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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O2 max is only a consequence of the amount of work that the heart is allowed to perform and not vice versa. This theory has been forwarded without any experimental scientific support. Since the early works of Hill and others, many theories on the limitation(s) to O2 max have come forward, but no one has been definitively and indisputably proven and accepted by all exercise physiologists. According to our view, O2 max is mainly a result of the amount of oxygen offered to the periphery from the left ventricle ( x Ca) during maximal exercise. This is supported by the results of previous experiments (2, 11, 12, 26).
In the present study, the double product for HR times both systolic and mean BP and times both systolic and mean BP was higher in the H than the L maximal exercise, whereas the O2 max was the same. According to Kitamura et al. (20) and Nelson et al. (21), the double product for HR times BP flow is a satisfactory predictor of MO2 and coronary blood flow in normal young subjects exercising. They observed a close correlation of HR times BP with MO2 and coronary blood flow. This would suppose that the heart is able to perform more mechanical work during the H than the L maximal exercise. This can also be confirmed by a recent study where 35 male and 16 female well-trained distance runners had identical O2 max on a treadmill between a maximal and a supramaximal exercise (30% above incremental O2 max) (16).
This indicates that the limitation of the central circulation during the L maximal exercise must be discussed in other terms, i.e., in relation to flow limitations rather than a central nervous inhibition as it was suggested in the "central governor" theory. As mentioned in the introduction and above, when different relevant aspects regarding this topic are discussed, i.e., in (2, 4, 14, 15, 19, 26, 30), the volume of oxygen transported from the heart to the periphery seems to be the major determinant for maximal oxygen transport and utilization during severe prolonged dynamic exercise with large muscle groups involved. The results of the present study support this theory.
The higher product of or HR times BP at the H compared with the L maximal work rate indicates that the energetic cost of the work of the heart is increased during the H maximal work. The 8–12% increase in pressure-rate product in this study should increase myocardial oxygen consumption by about equal amount (21). Also, the 9% higher pulmonary ventilation on the H maximal work rate costs more oxygen (1, 3). Thus, since O2 and at the H and the L maximal work sessions were equal, it can be speculated that part of the average 1 min 10 s shorter time to exhaustion at the H maximal work could be attributed to the increased oxygen cost of the heart and the ventilation, since, evidently, less volume of oxygen is available for the working skeletal muscles. The order of the L and H tests was not randomized for methodological reasons. We had to perform the L trial before the H trial; otherwise, we would never have known what caused the effects on either the L or the H trial. A lower BP during the L trial after the H trial could have been interpreted as a consequence of the H trial. With this order, we have the reversed situation. If anything, the higher BP during the H trial could only have been a consequence from the H work.
In a recent review article, Vella and Robergs discussed different stroke volume (SV) responses to incremental exercise (33). In a great number of articles published, SV continues to increase from a medium submaximal exercise level up to maximal exercise, whereas in an about equal amount of studies SV remains unchanged during the same part of the exercise spectrum. Even a decrease in SV at peak exercise has been reported. In the present study, the SV was 108 ml while sitting on the ergometer. During the two submaximal exercises, SV increased to 139 and 132 ml, respectively, but remained unchanged during further exercise or to 131 and 132 ml at the H and L experiments, respectively. Thus, in this study, SV increased from rest to submaximal exercise but was unchanged from 60–65% to 100% of O2 max in both the L and H part of the study, which is in line with the comment forwarded in relation to the Vella and Robergs article (9a). Early literature indicates an error in a single determination of of 5% (13).
The variation in measurement of during submaximal exercise was 0.06 l/min (limit of agreement –3.11 to 3.22). The variation during maximal exercise, using the last values of the L and H tests, was 0.32 l/min (limit of agreement –2.81 to 3.45). During the L trial, one of the subjects had his pulmonary artery catheter removed from its location due to technical reasons. This gave us very limited data during this measurement, and we decided to exclude this subject's and SV data from this calculation (see Table 1; 
n = 7). Using the last two measurements done during the last minutes of both the 7 L and 8 H maximal exercises, when O2 max was stable, the variation was 0.12 l/min (limit of agreement –2.21 to 2.46). These figures indicate that the variation in measurement of with the direct Fick method is fairly small, which is important in the discussion of factors limiting O2 max. We used only well-trained subjects in this study, but there are no reasons to believe that the basic results and conclusions from this study cannot be applied to other types of healthy adult subjects such as female and untrained people. However, in patients with reduced cardiovascular function or in elderly people, changes in functions and structures may very well be of such importance that the conclusion from this study may not apply to them.
In conclusion, the H maximal work generated a higher systolic, diastolic, and calculated mean arterial BP than the L maximal work rates, whereas O2 max and were the same for the two different maximal work rates. The heart was able to perform more mechanical work during the H than the L maximal exercise. This study suggests that the limitation of the central circulation during maximal work must be discussed in other terms rather than a central nervous inhibition, as suggested in the central governor theory.
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ACKNOWLEDGMENTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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O2 max at the whole animal level. J Exp Biol 115: 319–331, 1985.O2 max. Exerc Sport Sci Rev 28: 10–14, 2000.[Medline]This article has been cited by other articles:
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  S. P. Mortensen, R. Damsgaard, E. A. Dawson, N. H. Secher, and J. Gonzalez-Alonso Restrictions in systemic and locomotor skeletal muscle perfusion, oxygen supply and VO2 during high-intensity whole-body exercise in humans J. Physiol., May 15, 2008; 586(10): 2621 - 2635. [Abstract] [Full Text] [PDF]
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 J. Gonzalez-Alonso Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individuals J Appl Physiol, January 1, 2008; 104(1): 275 - 276. [Full Text] [PDF]
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B. D. Levine : what do we know, and what do we still need to know? J. Physiol., January 1, 2008; 586(1): 25 - 34. [Abstract] [Full Text] [PDF]
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