Acute leg length discrepancy causes increased VO2

Acute leg length discrepancy causes increased VO2

ELSEVIER Gait & Posture 4 (1996) 108-I 11 Acute leg length discrepancy causes increased VO, Tommy Boone *, Raymond R. Hammons Department of Exercise...

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ELSEVIER

Gait & Posture 4 (1996) 108-I 11

Acute leg length discrepancy causes increased VO, Tommy Boone *, Raymond R. Hammons Department of Exercise Physiology. College of St. Scho&stica, Duluth, MN 55811. USA Received I1 April 1994, accepted 21 June 1995

Abstract

Oxygen consumption (VM is an accepted measure of an individual’s expenditure of energy. It is frequently determined by walking or running on a treadmill at a fixed workload in which VO, is generally constant and accurately reflects the individual’s physical effort. Under certain conditions, however, such as with a leg length discrepancy, VO, may be increased as well as related respiratory measures (Fb and V,). In that the increase in VO, is subject to changes in central (Q = HR x SV) and/or peripheral (a-voz diff) adjustments to physical effort, it is important to detetine the specific reason for the increase. In the case of an artificially created leg length discrepancy (31.8 nun) in this study, the subjects’ HR increased with a corresponding increase in Q to match the increased need for oxygen when walking with unequal leg lengths. This central adjustment wasnot accommodated by a peripheral adjustment, which would have allowed for a sharing of the responsibility for increasing VOW Moreover, the central adjustment was made specifically by the subjects’ HR with no change in SV. This adjustment is not as beneticial as when SV is the reason for the increase in Q. Hence, the data indicate that the acute leg length discrepancy predisposed the subjects to a slightly higher metabolic demand at the heart level (given the significant rise in HR and the correlation between HR and myocardial oxygen consumption). Keywords:Leg length discrepancy; Oxyen consumption; Cardiac output

1. Intraddoo Oxygen consumption (VOW) is a measure of an individual’s ability to take in and distribute oxygen to working muscles during increased physical activity 11). Hence, it is frequently considered as the best single indicator of an individual’s cardiorespiratory capacity. One way to determine this capacity is by exercising the individual on a treadmill. The end result is commonly a Voz response that is consistent with the individual’s central and/or peripheral circulatory responses for the increased need for oxygen. On occasion, though, given certain physical and/or environmental conditions, the Vq response may not be an accurate reflection of the test. For example, Delacerda and McCrory [2] found that the Voz response while exercising on the treadmill was persistently increased when the right leg was 28.6 mm shorter than the left leg. * Corresponding author. 09&6362/95/$09.50 0 1995 Elsevier Science B.V. All rights reserved SSDI 0966-6362(95)01038-B

Although the authors’ report was a case study of one subject, there is a large population of subjects with leg length asymmetry [3]. If a leg length discrepancy is not anticipated prior to a treadmill test to evaluate VO, and the subject’s general response to exercise, it may act as a confounding variable that interferes with the overall cardiorespiratory assessment. There is also the need to determine the reason for the increased need for oxygen (if that should be the case). One way to address the latter point is to measure cardiac output with and without equal leg lengths. This measurement would then allow for the determination of whether the increase in V$ occurred by a central adjustment (i.e. heart rate (HR) and/or stroke volume (SV)), or a peripheral adjustment (arteriovenous oxygen difference (a-v@ diff)), or whether both components of the V@ equation facilitated the response. The purpose of this study was, therefore, twofold: (1) to determine the effects of a leg length discrepancy on

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Vo2 during treadmill walking; and (2) to clarify the VOW response as a central and/or peripheral adjustment. 2. 2.1. subJk?cts Ten college males between the ages of 18 and 27 years vohmteered to participate in this study. All subjects were instructed in the risks and benefits of participation, and signed a written consent statement approved by the Human Research Review Committee. 2.2. Measurement of leg length differences In that there is no universally accepted clinical method for measuring leg length differences 141,we used the frequently described method of a tape measure to determine the distances from the ASISs to the medial malleoli [S-7]. All measurements were obtained by one person (RH). During each measurement, the subjects wore only a pair of jogging shorts. The subjects’ lower limbs were exposed from .sIightIy above the midthigh to their feet. The subjects were instructed to stand with their feet er. The subjects’ medial maIleoli were positioned touching so that they met in a plane that approximated the midsq$ttal line (or anatomical position) of the body. The examiner stood on the side of the limb he was measuring. A blank tape measure was held between his thumb and the first finger of the hand nearest the subject’s pelvis. Using the same hand, he used the thumb to palpate the subject’s ASIS at the site of the origin of the sartorius muscle. The examiner then guided the tape down the anteromedial aspect of the subject’s lower limb until he made contact with the medial malleolus, where the measurement was recorded. The same procedures were repeated on the subject’s opposite lower limb. FoBowing these procedures, it was determined that each subject had no leg length differences. This fmding was considered a prerequisite for subject participation, although any measurement that might not have been a 1000/o accurate reflection of leg length was minimized by the subjects acting as their own controls. 2.3. Data collection procedures Prior to collection of data, each subject was familiarized with the research laboratory and the metabolic equipment by walking on the treadmill for 5 min and breathing through the metabolic mouthpiece. The CO, rebreathing procedure (used to determine cardiac output) was practiced, questions were answered, and then the subject was scheduled for the second and final laboratory session. During the second session, the subject’s age and weight were recorded upon entering the laboratory. The subject was connected to the electrocardiograph, placed in a chair positioned on the treadmill where he rested in the upright sitting position for 5 min. Following stabilization of HR, the subject stood erect and began

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walking on the treadmill at 0% grade, 350’miles/h for 5 min. Using a random order approach to w&king with and without the artificially created leg length discrepancy, expired ventilation (V,), frequency of breaths (Fb), tidal volume (VT), respiratory exchange ratio (RER), volume of carbon dioxide produced (VCO~), and VOz were recorded during each minute of the 5-min treadmill walk. The last 3 min of each S-mm period were averaged and statistically analyzed. Cardiac output was determined during the last minute of walking using the Beckman Metabolic Measurement Cart (MMC). Arterial CO2 (P.&q) was derived from the end-tidal PC@ (PE$o~). Mixed venous Pco2 (P&O& was derived from the rebreathing procedure during which the subjects were disconnected from the non-breathing valve and connected to a bag tilled with 11.75% CQ in oxygen. A Beckman MMC recorder was used to graphically examine the CO, signal generated during the rebreathing to ensure that a satisfactory Pm2 equilibrium was achieved. Subsequent calculations of SV, mean arterial pressure (MAP), systemic vascu.Iar resistance (SVR), and a-v02 diff were performed The subjects then rested for ting position (as previously peated the same test, except this without the artificially created leg Each subject was tested at approxima each day, and the laboratory environmental conditions were the same for both treadmill tests. The treatment variable constituted the wearing of a shoe lift constructed of rubber to result in a leg length discrepancy of 3 1.8 mm. All subjects abstained from exercise 36 h prior to data collection. 2.4. Data analysis A dependent (two-tailed) t-test was used to statistically analyze the walking data with ad without the shoe lift. Alpha was set at the 0.05~level of significance. 3. ResnIts Table 1 shows values for all obtained during both without a leg length di al that the artiftily created resulted in a significant i and thus energy expended lation, Fb, V-r, VCO2, significantly increased (while SVR walking with the shoe lift. The lift had no e&ct RER, MAP, SV, and a-M)* diff.

on

4. Di!mmsh With current interest in exercise and re tation, it is important to identify factors (such as a leg length dis-

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Table 1 Oxygen consumption and cardiovascular data in response to walking at 3.5 miles/h on the treadmill with and without a shoe life of 31.8 mm in thickness (n = IO) Variable

Walking without lift

Walking with lift

f-ratio

P-value

V, (Ismin-‘) F, (breaths - min-‘) Vr (ml. breath) Voz (I -mm-‘) Vo2 (ml -kg-‘. mm-‘) Vcoz (1. mm-‘) RER HR (beats - mm-‘) SV (ml-beat) Q (I-mitt -I ) a-vo2 diff (ml. 100 ml-‘) MAP (mmHg) SVR (dyn - set - cmT5)

28.49 zt 5.08 24.40 f 3.76 1126.30 f 176.31 1.04 zt 0.18 13.80 f 1.79 0.83 f 0.15 0.79 f 0.06 102.30 f 16.72 82.90 EIZ12.94 8.37 f 1.43 12.45 -+ 1.69 85.20 f 10.54 805.00 f 98.77

32.75 zt 6.1 I 26.35 f 4.58 1252.50 f 142.72 1.27 zt 0.21 16.84 f 2.16 I.01 f 0.17 0.80 + 0.04 113.30 f 22.84 88.80 f II.44 9.89 EIZ1.44 12.77 zt I.14 83.30 f 13.70 672.50 f III.42

-3.138 -3.387 -3.769 -5.893 -5.815 -5.670 -0.236 -2.586 -1.441 -3.826 -0.732 0.523 4.183

0.012* 0.008* 0.005* 0.000* 0.000* 0.001* 0.812 0.028* 0.181 0.004’ 0.512 0.522 0.003*

‘P < 0.05.

crepancy) that may alter VO, and thus energy expended. It is equally important to understand the role of central and/or peripheral hemodynamic responses in the regulation of V02. The shoe lift resulted in a significant increase in V,, which corresponded to the significant increase in VO,. Both the rate (Fb) and depth (Vr) of breathing increased in accordance with the subjects’ increased ventilatory response. Although the mechanisms for regulating V, are not fully understood, the increase in metabolism (when walking with the shoe lift) resulted in an increase in carbon dioxide that plays a large part in determining plasma acidity. While the latter was not measured in this study, Vcoz was significantly increased which no doubt helped to enhance ventilation (given that it is an important respiratory stimulus) [8]. The increase in Vq (with respect to the Vo2 equation where oxygen consumption is the product of oxygen transport (Q = HR x SV) and oxygen utilization (avo2 diff)) was due to the significant increase in the subjects’ central adjustment (Q) with no change in the peripheral contribution (a-vo2 diff). The increase in Q was due to the significant increase in HR and not SV. This particular finding is somewhat of a concern because it suggests that the heart’s need for oxygen, given the high correlation of HR with myocardial oxygen consumption [9], was increased when walking with the lift. In this regard, the data suggest that subjects with unequal leg lengths, who fail to wear shoes designed to correct the discrepancy, may expect to perform a walking exercise with higher than necessary HRs and general body metabolism. The increased sympathetic adrenergic discharge (HR) is directly related to the subjects’ increased workload (when walking without the lift) and thus oxygen transport, which is consistent again with the increased Vo2. So, in effect, given that systemic arterial oxygen satur-

ation did not change and that a-vo2 diff did not widen (although more oxygen was taken up by the muscles over time given the increased flow), it is clear that the HR response increased Q so that a matching of blood flow to metabolic needs occurred during the treatment condition. When doing the same treadmill walk with equal leg lengths, HR was 11 beats/min lower (with the same SV response), thus allowing for a Q-response that was 1.52 l/mm less. The lower Q response was accompanied by less muscular exertion with less expenditure of energy. 5. coneIusIoll The central and peripheral hemodynamic changes that occurred as a result of the artificially created leg length discrepancy indicate rather clearly that Vo2 is not constant at a fmed workload. Oxygen consumption may vary with different treatment conditions. In this study, V02 varied in accordance with the workload (i.e. muscular effort), and in this case changed as a direct function of the unequal leg lengths. Heart rate and Q increased abruptly with the decrease in efftciency of walking, and SVR decreased accordingly. As a result of the decrease in afterload, the increase in blood flow was unhampered at the same MAP. References 111 Shaver LG. Essentials of Exercise Publishing Company, Minneapolis/MN,

Physiology. Burgess 1981 [21 Delacerda FG, McCrory ML. A case report: effect of a leg length differential on oxygen consumption. J Orthop Sports Phys Ther 1981; 3: 17-20 [31 Pearson WM. Progressive structural study of school children. J Am Osfeop Assoc 1951; 61: 155-167 141 Ingram AI. Anterior poliomyelitis. In: Edmonson AS, Crenshaw AH, editors. Campbell’s Operative Orthopaedics, ed. 6, C.V. Mosby Company, St. Louis/MO, 1980

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[S] Clarke OR. Unequal leg length: an accurate method of detection and some clinical results. Rhewnatol Phys Med 1972; 11: 385-390 (61 Nichols PJR, Bailey MTJ. The accuracy of measuring leg-length differences. Br Med J 1955; 25: 1247-1248 [7] Beattie P, Rothstein JM, Kopriva L. The clinical reliability of measuring leg length [abstract]. Phys Ther 1988; 68: 588

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WD, Katch FI, Katch VL. Erercke P&&&gy: and Human Perfrmame, ed. 3, Lea & Febiger, PhiladclphialLondon, 199 1 [9] Kitamura K, Jorgensen CR, Gobel FL et al. Hemodynamk correlates of myocardial oxygen consumption during upright exercise. J Appl Physiol 1972; 32: 516-522 Energy,

Nuttition,