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European Journal of Heart Failure 2007 9(8):834-838; doi:10.1016/j.ejheart.2007.05.004
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© 2007 European Society of Cardiology

Biomechanical efficiency is impaired in patients with chronic heart failure{star}

Klaus K. Wittea,*, Wayne C. Levyb, Kenneth A. Lindsayc and Andrew L. Clarkd

a Department of Cardiology, Leeds General Infirmary, Great George Street Leeds, LS1 3EX, UK
b University of Washington Seattle, USA
c Department of Mathematics, Glasgow University UK
d Department of Cardiology, University of Hull UK

* Corresponding author. Tel.: +44 113 3926000; fax: +44 113 2787206 E-mail address: klauswitte{at}hotmail.com.


   Abstract
Top
 Notes
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Introduction: Patients with chronic heart failure (CHF) have a lower peak oxygen consumption (pVO2) than normal subjects, and for a given quantity of work, have a lower total oxygen consumption (VO2) than controls. This apparent increase in biomechanical efficiency (BE) might be due to a higher proportion of anaerobic metabolism which, although leading to lower VO2 during steady state exercise, must be compensated for during recovery.

Methods: 13 patients with stable CHF and 12 controls underwent peak cycle exercise testing followed by three separate steady state exercise tests at 15%, 25% and 50% of the peak workload in random order. Oxygen consumption at steady state, deficit (during onset) and debt (during recovery) were calculated. BE was estimated as the total oxygen required to perform a given quantity of work.

Results: Patients had lower pVO2 and peak workload than control subjects. Absolute oxygen deficit and debt as a percentage of total oxygen consumed during the steady state tests was the same in both groups. However, once controlled for workload, VO2 deficit, debt and uptake at steady state were greater in patients than controls for the tests at 15% and 25% of peak. BE was inversely related to peak oxygen consumption in controls and patients.

Conclusions: Patients with CHF have impaired BE at low work loads when compared with normal subjects.

Key Words: Oxygen consumption • Exercise capacity • Heart failure

Received October 26, 2006; Revised February 24, 2007; Accepted May 3, 2007


   1. Introduction
Top
 Notes
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Chronic heart failure (CHF) patients suffer exercise intolerance due to breathlessness and fatigue. Patients with CHF have lower peak oxygen consumption and greater ventilatory response to exercise, represented by an increase in the slope relating carbon dioxide (VCO2) to ventilation (VE) (VE/VCO2 slope), than normal subjects during exercise testing with metabolic gas exchange [1]. Patients with CHF take longer to reach steady state metabolic gas exchange in response to a constant work load, and longer to return to baseline at the end of such exercise, than normals [2].

Previous reports examining oxygen consumption during steady state exercise have suggested that for a given amount of work, patients with CHF have a lower oxygen consumption than control subjects [3-5]. This has been interpreted as an increase in biomechanical efficiency in CHF subjects. In contrast, magnetic resonance spectroscopy data have suggested that for a given unit of work patients with heart failure have higher skeletal muscle ATP consumption, suggesting decreased metabolic efficiency [6]. Earlier reports of oxygen consumption during steady state exercise to obtain oxygen consumption per unit of work did not include data collected during the onset and offset of exercise. It is therefore possible that the apparent increase in biomechanical efficiency is a reflection of a higher proportion of anaerobic work with increased lactate production, which although leading to lower oxygen consumption during exercise, must be compensated for during recovery (oxygen debt). Two recent publications using peak exercise tests and fixed workload steady state tests have supported this suggestion [7,8]. Both studies used total oxygen consumption over the entire test; the sum of oxygen debt, the measured oxygen consumption during the test and the oxygen uptake during recovery. Using this method, patients with heart failure have a higher oxygen requirement per unit work than controls.

However, the kinetics of the metabolic gases at onset and offset are affected by workload [2]. This might affect the measures of calculated oxygen uptake and hence measures of biomechanical efficiency. The present analysis was performed to investigate biomechanical efficiency in patients with CHF compared with control subjects. We used multiple submaximal workloads related to the individuals' peak work rather than absolute fixed values as previously [7,8].


   2. Methods
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
The methods employed have been presented elsewhere [1,2]. Briefly, 13 male patients with stable CHF (no change in therapy or hospital admission for 3 months) and 12 male controls underwent echocardiography and peak exercise testing on a stationary electronically braked cycle (Rehcor, Cardiokinetics, Salford, UK) with metabolic gas exchange (Oxycon Record, Jaeger, Germany). All patients were on optimal medical therapy including β-blockers. The controls were selected randomly from the lists of local general practitioners and none had symptoms or signs of cardiovascular disease, or were taking any regular medication. For the peak test, a respiratory exchange ratio (RER), (VCO2/VO2) greater than 1 was taken as evidence of maximal effort. Standard spirometry (FEV1 and FVC) was also performed. Peak VO2 and the anaerobic threshold (AT), using the VCO2/VO2 slope method [9], were determined. The VE/VCO2 slope was calculated by linear regression.

In order to examine patients at similar degrees of relative work, we exercised subjects at percentages of their pre-determined peak capacity rather than at identical absolute workloads. After the initial visit, each individual returned at 1 week to perform three separate steady state exercise tests at 15%, 25% and 50% of the workload achieved at the peak test. The order of these tests was randomised, and each test was separated by 30-min rest. Metabolic gas exchange measurements were made for 3 min of rest, the duration of exercise, and for at least 5 min following the cessation of exercise or until oxygen consumption values had returned to pre-test levels whichever was the longest. Steady state was assumed to have been achieved during the sub-maximal tests when no further changes in ventilatory or oxygen intake had occurred for at least 1 min [10]. Exercise was continued for 3 min after this.

The calculation of oxygen consumption is illustrated in Fig. 1. As previously described, curves were mathematically fitted to the raw breath-by-breath oxygen uptake data. Oxygen deficit (during onset of exercise) (area D) and debt (recovery) (area C) were calculated for peak and each submaximal test [2,11]. Exercise oxygen consumption was estimated from areas A and B. Subsequently, the areas A, B and C were calculated to estimate total oxygen uptake above the resting level (area E) for the total work undertaken. We calculated oxygen deficit and debt as percentages of total oxygen taken up per unit of time during the test; D/[(A+B+C)/exercise time] and debt, C/[(A+B+C)/exercise time].


Figure 01
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  		Fig. 1 Absolute and relative oxygen consumption during a steady state test. Area A is oxygen consumption during onset of exercise. Area is D is previously defined oxygen deficit which is made up during recovery. Area C is oxygen debt. Area B is oxygen consumption during steady state. Area E is resting oxygen consumption which is assumed to continue during the test.

 
Total energy expended (joules) was calculated as the product of work performed (watt) and time. Using these data, biomechanical efficiency was then estimated by calculating the oxygen required to perform work for the time of exercise (exercise VO2/watt areas A+B); for recovery (area C) (recovery VO2/watt); and for the whole exercise session including recovery (areas A, B, and C), (total VO2/watt). Using these data, and the time of exercise duration, we then calculated average oxygen consumption per joule of work performed. We also compared total oxygen consumption for exercise (areas A, B and C - the debt method) with total oxygen consumption using the deficit method (areas A, B and the interpolated value for D).

We used unpaired Student's t-test for between group comparisons. Least squares linear regression was used to explore the relation between peak oxygen consumption and biomechanical efficiency for the whole population and the two groups. A p-value of < 0.05 was taken to be significant.


   3. Results
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
Table 1 shows the baseline variables for patients (n=12) and control subjects (n=9) in whom reliable modelling of the steady state curves was achievable. Those excluded (1 patient and 3 control subjects) were not significantly different in terms of exercise tolerance, but were rejected because of poor signal to noise ratio. Subjects in the two groups were well matched for age, height and weight. Patients had impaired ventricular function, and significantly lower peak oxygen consumption and peak workload, and steeper VE/VCO2 slope than control subjects.


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  		Table 1 Subject characteristics

 
Results from the steady state tests for oxygen are shown in Table 2. Workloads at 15%, 25% and 50% of maximal were significantly greater in control subjects than patients and despite our attempt to adjust the work performed during the submaximal tests according to the workload achieved during the peak test, RER values were higher in patients than controls for each of the steady state tests.


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  		Table 2 Oxygen uptake data in patients and controls for submaximal tests

 
Absolute oxygen deficit and debt as a percentage of total oxygen consumed per minute during the steady state tests were not greater in controls than patients. However, once controlled for workload, the three variables of O2 deficit, debt and uptake at steady state were greater in patients than controls for each of the lower workload tests. For the higher workload test, there were no differences between patients and controls.

The data on total oxygen consumption during exercise calculated using the debt or deficit methods gave very similar results (r=0.99). Mean difference between the two was 3.1% (4.3%). We have presented the debt method (area C) for further calculations, since this is an actual measurement and area D is an interpolated assumption, although the results were similar if the deficit method was employed.

Biomechanical efficiency (total oxygen uptake per joule) for the 15% and 25% steady state tests was inversely related to peak oxygen consumption (ml/kg/min) for the whole population (r=0.49, p<0.05 for 15% and r=0.44, p<0.05 for 25%) (Figs. 2a and b). There was no relationship between the peak oxygen consumption and biomechanical efficiency at the highest workload (r=0.21, p=0.35) (Fig. 2c). The relationships were non-significant when split between the control and patient populations. There was a relation between absolute workload and biomechanical efficiency in both control subjects and patients (Fig. 3), significantly different between the groups (p<0.001). Figs. 2a, b and c also suggest an optimal efficiency of 0.25, which is reached earlier at lower workloads by patients (Fig. 3).


Figure 02
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  		Fig. 2 a-c: Biomechanical efficiency (calculated from submaximal tests) related to peak oxygen consumption for patients (unfilled circles) and controls (filled circles) for 15% (a), for 25% (b), and for 50% (c) of peak. In subjects with a greater impairment of peak exercise capacity, the amount of oxygen needed to perform a single joule of work increases. Patients with chronic heart failure have a lower biomechanical efficiency during low workloads than control subjects, and appear higher on the Y-axis (higher oxygen/joule of work) than controls.

 


Figure 03
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  		Fig. 3 Biomechanical efficiency related to workload in patients (unfilled circles and dashed line: r=0.66; p<0.0001) and control subjects (solid circles and trend line: r=0.46; p<0.02).

 

   4. Discussion
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
During daily living, patients perform activities at a similar percentage of peak exercise as control subjects, but at a lower absolute level [12]. Our data are the first to demonstrate that at low workloads matched as a percentage of peak exercise, patients have higher oxygen requirement for a given work than controls, suggesting reduced biomechanical efficiency.

Absolute oxygen deficit and debt for the 15% and 25% tests were not different between patients and control subjects. At the highest workload, oxygen deficit and debt were greater in the control population, presumably as a result of their greater absolute workload. When corrected for workload, however, patients had significantly greater oxygen deficit and debt at the two low levels of work than control subjects. Furthermore, during steady state, patients had a higher oxygen uptake for a given workload than controls. As a result, patients had a higher total oxygen requirement per unit work performed than controls at low levels of exercise at low workloads. At higher workloads, the differences in biomechanical efficiency between patients and controls were no longer significant. The suggestion that patients with CHF might be less efficient at lower workloads than at higher workloads is novel and may reflect the fact that at lower workloads, resting oxygen consumption forms a higher proportion of total oxygen consumption, which becomes less important at higher levels of exercise. There may also be delays in adaptation of skeletal musculature metabolism and recruitment of blood vessels, which are less stimulated at lower workloads. Our data suggest an ideal biomechanical efficiency of 0.25 which is reached earlier by patients at lower workloads than controls.

The fact that the respiratory exchange ratios measured during the steady state tests are higher in patients even when the workload is matched to the patients' peak capacity, confirms for the first time that at workloads well below anaerobic threshold, patients are more ‘anaerobic’ than control subjects. This supports the concept that an earlier and more extensive shift to anaerobic metabolism occurs in patients with CHF. We and others have previously demonstrated prolonged recovery times with extended time constants for both metabolic gases in patients with CHF related to the severity of the condition [13]. With this analysis, we speculate that at least some of the delay in recovery of the metabolic gases might be due to higher levels of anaerobic metabolism seen in CHF patients even during low levels of exercise.

The reduced biomechanical efficiency demonstrated by our analysis at low workloads and the prolonged recovery kinetics of the metabolic gases may be a consequence of changes in skeletal muscle ultrastructure in CHF, with a shift from muscle fibre types capable of prolonged aerobic metabolism (type I fibres) to those with a lower mitochondrial density (type IIb fibres) [14-16]. Type II fibres have twice the requirement of oxygen and higher ATP consumption for a given workload [6,17,18], which leads to an increased dependence upon anaerobic metabolism and greater lactic acid production during exercise [19].

Our demonstration of reduced biomechanical efficiency is contrary to previous data which failed to include recovery kinetics [3,4], but supports more recent data demonstrating reduced work for a given oxygen uptake when recovery kinetics are taken into account [8]. We were also able to demonstrate a correlation of our biomechanical efficiency to peak oxygen consumption suggesting that the implied skeletal muscle changes are related to the severity of the condition.

Taken together our findings suggest that since patients perform daily activities at lower absolute levels of work [12], during which they are particularly inefficient, patients with CHF spend more of their time repaying an oxygen debt and thus may begin the next period of work before recovering fully from the last.


   5. Conclusions
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
The present analysis confirms that patients with CHF have impaired biomechanical efficiency at low levels of work when compared with control subjects. They require more oxygen to perform similar levels of exercise relative to the severity of the heart failure. Our data also suggest that even at low levels of exercise, patients with CHF are already more anaerobic than control subjects implying an anaerobic shift in metabolism earlier during exercise in skeletal muscle. The combination of these factors might contribute importantly to fatigue and a sensation of breathlessness even at low workloads in patients with CHF.


   Notes
Top
 Notes
Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
{star} Financial support: Dr. Witte has received educational funding from Guidant (Canada) and Medtronic (UK). Back


   References
Top
 Notes
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

  1. Witte K.K., Clark A.L. Is the elevated slope relating ventilation to carbon dioxide production in chronic heart failure a consequence of slow metabolic gas kinetics? Eur J Heart Fail (2002) 4:469–472.[Abstract/Free Full Text]
  2. Witte K.K., Thackray S.D., Lindsay K.A., Cleland J.G., Clark A.L. Metabolic gas kinetics depend upon the level of exercise performed. Eur J Heart Fail (2005) 7:991–996.[Abstract/Free Full Text]
  3. Itoh H., Taniguchi K., Koike A., Doi M. Evaluation of severity of heart failure using ventilatory gas analysis. Circulation (1990) 81(1 Suppl):II31–II37.[Medline]
  4. Solal A.C., Chabernaud J.M., Gourgon R. Comparison of oxygen uptake during bicycle exercise in patients with chronic heart failure and in normal subjects. J Am Coll Cardiol (1990) 16:80–85.[Abstract]
  5. Itoh H., Nakamura M., Ikeda C., et al. Changes in oxygen uptake-work rate relationship as a compensatory mechanism in patients with heart failure. Jpn Circ J (1992) 56:504–508.[Medline]
  6. Massie B.M., Conway M., Rajagopalan B., et al. Skeletal muscle metabolism during exercise under ischemic conditions in congestive heart failure. Evidence for abnormalities unrelated to blood flow. Circulation (1988) 78:320–326.[Abstract/Free Full Text]
  7. Levy W.C., Maichel B.A., Steele N.P., Leclerc K.M., Stratton J.R. Biomechanical efficiency is decreased in heart failure during low-level steady state and maximal ramp exercise. Eur J Heart Fail (2004) 6:917–926.[Abstract/Free Full Text]
  8. Mitchell S.H., Steele N.P., Leclerc K.M., Sullivan M., Levy W.C. Oxygen cost of exercise is increased in heart failure after accounting for recovery costs. Chest (2003) 124:572–579.[Abstract/Free Full Text]
  9. Beaver W.L., Wasserman K., Whipp B.J. A new method for detecting the anaerobic threshold by gas exchange. J Appl Physiol (1986) 60:2020–2027.[Abstract/Free Full Text]
  10. Sietsema K.E., Daly J.A., Wasserman K. Early dynamics of O2 uptake and heart rate as affected by exercise work rate. J Appl Physiol (1989) 67:2535–2541.[Abstract/Free Full Text]
  11. Picozzi N.M., Clark A.L., Lindsay K.A., et al. Responses to constant work exercise in patients with chronic heart failure. Heart (1999) 82:482–485.[Abstract/Free Full Text]
  12. Clark A.L., Rafferty D., Arbuthnott K. Exercise dynamics at submaximal workloads in patients with chronic heart failure. J Card Fail (1997) 3:15–19.[CrossRef][Medline]
  13. Nanas S., Nanas J., Kassiotis C., et al. Early recovery of oxygen kinetics after submaximal exercise test predicts functional capacity in patients with chronic heart failure. Eur J Heart Fail (2001) 3:685–692.[Abstract/Free Full Text]
  14. Clark A.L., Poole-Wilson P.A., Coats A.J. Exercise limitation in chronic heart failure: central role of the periphery. J Am Coll Cardiol (1996) 28:1092–1102.[Abstract]
  15. Sullivan M.J., Green H.J., Cobb F.R. Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. Circulation (1990) 81:518–527.[Abstract/Free Full Text]
  16. Mancini D.M., Coyle E., Coggan A., et al. Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure. Circulation (1989) 80:1338–1346.[Abstract/Free Full Text]
  17. Awan M.Z., Goldspink G. Energy utilization by mammalian fast and slow muscle in doing external work. Biochim Biophys Acta (1970) 216:229–230.[Medline]
  18. Coyle E.F., Sidossis L.S., Horowitz J.F., Beltz J.D. Cycling efficiency is related to the percentage of type I muscle fibers. Med Sci Sports Exerc (1992) 24:782–788.[Web of Science][Medline]
  19. Kemp G.J., Thompson C.H., Stratton J.R., et al. Abnormalities in exercising skeletal muscle in congestive heart failure can be explained in terms of decreased mitochondrial ATP synthesis, reduced metabolic efficiency, and increased glycogenolysis. Heart (1996) 76:35–41.[Abstract/Free Full Text]

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Is exercise efficiency really impaired in heart failure patients?
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