ORIGINAL ARTICLE

A. Vinet á D. Le Gallais á P.L. Bernard á M. PoulainA. Varray á J. Mercier á J.P. Micallef

Aerobic metabolism and cardioventilatory responsesin paraplegic athletes during an incremental wheelchair exercise

Accepted: 22 April 1997

Abstract The aims of the present study were: (1) toassess aerobic metabolism in paraplegic (P) athletes(spinal lesion level, T4±L3) by means of peak oxygenuptake ( _V O2peak) and ventilatory threshold (VT), and (2)to determine the nature of exercise limitation in theseathletes by means of cardioventilatory responses at peakexercise. Eight P athletes underwent conventionalspirographic measurements and then performed an in-cremental wheelchair exercise on an adapted treadmill.Ventilatory data were collected every minute using anautomated metabolic system: ventilation (l á min)1),oxygen uptake ( _V O2, l á min)1, ml á min)1 á kg)1), car-bon dioxide production ( _V CO2, ml á min)1), respiratoryexchange ratio, breathing frequency and tidal volume.Heart rate (HR, beats á min)1) was collected with the aidof a standard electrocardiogram. _V O2peak was determinedusing conventional criteria. VT was determined by thebreakpoint in the _V CO2 ÿ _V O2 relationship, and is ex-pressed as the absolute VT ( _V O2, ml á min)1 á kg)1) andrelative VT (percentage of _V O2peak). Spirometric valuesand cardioventilatory responses at rest and at peak ex-ercise allowed the measurement of ventilatory reserve(VR), heart rate reserve (HRr), heart rate response(HRR), and O2 pulse (O2 P). Results showed a _V O2peak

value of 40.6 (2.5) ml á min)1 á kg)1, an absolute VTdetected at 23.1 (1.5) ml á min)1 á kg)1 _V O2 and a rela-

tive VT at 56.4 (2.2)% _V O2peak. HRr [15.8 (3.2) beatsá min)1], HRR [48.6 (4.3) beat á l)1], and O2 P [0.23(0.02) ml á kg)1 á beat)1] were normal, whereas VR atpeak exercise [42.7 (2.4)%] was increased. As wheelchairexercise excluded the use of an able-bodied (AB) controlgroup, we compared our _V O2peak and VT results withthose for other P subjects and AB controls reported inthe literature, and we compared our cardioventilatoryresponses with those for respiratory and cardiac pa-tients. The low _V O2peak values obtained compared withsubject values obtained during an arm-crank exercisemay be due to a reduced active muscle mass. AbsoluteVT was somewhat comparable to that of AB subjects,mainly due to the similar muscle mass involved inwheelchair and arm-crank exercise by P and AB sub-jects, respectively. The increased VR, as reported inpatients with chronic heart failure, suggested that Pathletes exhibited cardiac limitation at peak exercise,and this contributed to the lower _V O2peak measured inthese subjects.

Key words Incremental test á Peak oxygen uptakeSpinal cord injury á Ventilatory thresholdWheelchair exercise

Introduction

In recent years, wheelchair sports have increased inpopularity, with many spinal cord injured (SCI) individ-uals now participating in recreational and competitivephysical activities (Coutts et al. 1983). This has led to anincrease in training programs speci®c for wheelchair-de-pendent athletes, particularly in endurance sports such aswheelchair racing (Steadward and Walsh 1986). In orderto improve the standards of performance, endurancetraining programs have been based on the development ofaerobic metabolism as assessed by peak oxygen uptake( _V O2peak) and ventilatory threshold (VT), since these twoaerobic parameters are highly correlated with long-dis-

Eur J Appl Physiol (1997) 76: 455±461 Ó Springer-Verlag 1997

A. Vinet (&) áM. Poulain áA. VarrayLaboratoire ``Sport, Sante , De veloppement'', UFR STAPS,700 avenue du Pic Saint Loup, F-34100 Montpellier, France

D. Le Gallais á J. MercierLaboratoire de Physiologie des Interactions,CHU Arnaud de Villeneuve, 371 avenue Doyen Gaston Giraud,F-34095 Montpellier Cedex 5, France

P.L. BernardLaboratoire de Biome canique et de Biologie de l'exercise,UFR STAPS, 261 route de Grenoble,F-06200 Nice, France

J.P. MicallefINSERM U103, 395 avenue des Moulins,F-34090 Montpellier, France

tance race performance in able-bodied (AB) subjects(Yoshida et al. 1987). The aerobic metabolism charac-teristics of paraplegic (P) athletes have been extensivelystudied using _V O2peak as a way of assessing aerobic powerand physical aptitude, in the laboratory (Veeger et al.1991; Cooper et al. 1992; Hartung et al. 1993; Rascheet al. 1993; Bhambani et al. 1994 ) and on the ®eld (Vinetet al. 1996). Similarly, VT, which can be used to assessaerobic capacity and to give an indication of endurancelevels in AB subjects, has beenwidely studied in P subjects(Flandrois et al. 1986; Lakomy et al. 1987; Lin et al. 1993;Rotstein et al. 1994; Bhambani et al. 1995; Coutts andMcKenzie 1995). _V O2peak values have been reported to belower in P than in AB subjects due to reduced activemuscle mass in the former (Van Loan et al. 1987; Burkettet al. 1990), whereas absolute VT, expressed in l á min)1

and ml á min)1 á kg)1 of _V O2, has been reported to besimilar (Flandrois et al. 1986; Lin et al. 1993). RelativeVT, expressed as a percentage of _V O2peak (VT%), hasbeen reported to be higher in P subjects due to their lower_V O2peak. These _V O2peak and VT values suggest that Pathletes had a lower physical aptitude ( _V O2peak) butsimilar or higher levels of endurance (absolute VT andrelative VT, respectively) than AB subjects (Flandrois etal. 1986). Thus, _V O2peak and particularly VT values mayhave a speci®c pathophysiological signi®cance in SCIsubjects.

Recently, heart rate reserve (HRr), heart rate re-sponse (HRR), ventilatory reserve (VR) and O2 pulse(O2 P) at maximal exercise were found to be usefuldeterminants of cardiac or pulmonary exercise limita-tions in patients with chronic heart failure (CHF) andchronic obstructive lung disease (COLD) (Messner-Pellenc et al. 1994). The aims of the present study were:(1) to determine _V O2peak and VT values in P athletes,based on a wheelchair incremental exercise on anadapted treadmill, and (2) to assess the cardioventila-tory responses of P athletes at maximal exercise in orderto compare them with those of other disabled patientsdescribed in the literature and to assess the origin oftheir maximal exercise limitation as expressed in termsof _V O2peak.

Methods

Subjects

Eight male P athletes, aged 28.3 (3.9) years (range: 24±35 years),provided informed written consent before participating in thisstudy. All of the subjects had lower-limb disability for at least 2years prior to the study: in six of the subjects paraplegia was due totraumatic SCI, with disability levels from T8 to L3, one due to spinabi®da at L5, and one subject was post-poliomyelitic with paralysis ofthe lower limbs. The subjects included students, a computer scien-tist, a doctor, and administrative managers. They used theirwheelchairs in their daily activities and at work. All subjects prac-ticed sports for at least 7 (2.5) h per week: four subjects practicedwheelchair racing and four subjects practiced tennis. All of thesubjects were considered to have good control of their wheelchairs,which was essential for the study. According to the InternationalStoke Mandeville Games (ISMG) functional classi®cation, threesubjects were in class III (T6±T10) and three subjects were in class IV(T11±L3). The two non-traumatic P subjects were in class V, whichcorresponds to the motor and sensibility disabilities of traumatic Psubjects with lesions at L3-S2 (McCann 1984). The anthropometricdata and general characteristics of P athletes are given in Table 1.

Protocol

Before testing, a medical examination was performed that includedclinical examination (height, body mass, body fat), blood pressure,conventional spirographic measurements (Pulmonet III, Sensor-Medics, Bilthoven, The Netherlands), cardiopulmonary auscultat-ion, and a resting 12-lead electrocardiogram (ECG). Height wasdetermined while the subject was in a supine position, body masswas determined using a scale designed for weighing P patients in asitting position (SECA, model D720, Germany), and body fat wasestimated by using the Durnin and Womersley equation (1974)which uses the sum of four skinfold measurements (biceps, triceps,subscapularis and suprailiac), gender and age (Table 1). All resultswere normal and did not contraindicate maximal exercise testing inany of the subjects. The subjects then performed an incrementalexercise test with their own well-adjusted, general purpose wheel-chairs. They were given verbal encouragement to reach maximale�ort. At the end of exercise the P athletes were asked about theirfunctional ventilatory state, e.g. whether they were dyspnoeic. Thetest was performed using an adapted treadmill (Sopur, Malsche,Germany). The protocol was a maximal continuous multistageexercise (Cooper et al. 1992; Veeger et al. 1991). After a 2-min rest,the subjects warmed up for a 3-min period at 4 km á h)1, the speedwas then increased by 1 km á h)1 every minute until exhaustion;recovery was monitored for 5 min. Ventilatory data were collected

Table 1 Characteristics of the paraplegic athletes. C complete, F ¯accid, I incomplete, ISMG International Stoke Mandeville Games,L lumbar, S spastic, T thoracic

Subject Age(years)

Body mass(kg)

Height(cm)

Body fata

(%)Lesion level(L-T)

Lesionclassi®cation

Lesion type(I-C-S-F)

Sport Trainingvolume

(ISMG) (h á week)1)

1 28 72 180 22.9 L3 IV I/F Tennis 62 24 66 165 23.1 Spina L5 V ± Racing 103 31 82 184 27.3 T10 III C/S Racing 104 33 50 161 17.7 Polio V ± Racing 105 24 67 175 24.3 T8-T9 III C/S Tennis 46 25 60 170 22.5 T12 IV I/- Tennis 47 27 62 180 12.6 T12-L1 IV I/F Racing 78 35 72 176 31.4 T8 III C/S Tennis 5

Mean 28.3 66.3 174 22.7 ± ± ± ± 7SEM (1.5) (3.4) (2.8) (2.0) ± ± ± ± (1)

a according to Durnin and Womersley (1974)

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every minute using a breath-by-breath automated metabolic system(CPX, Medical Graphics, Minnesota, USA). Brie¯y, expiratoryair¯ow was measured using a Pitot ¯owmeter tube and expiredgases were analysed for O2 with a zirconia solid electrolyte O2 an-alyser, and for CO2 with an infrared analyser. Before each test, thevolume was calibrated using ®ve inspiratory strokes with a 3-lpump; each gas analysis was calibrated using room air (20.96% O2,0.03% CO2) and with a standard certi®ed commercial gas prepa-ration (12% O2, 5% CO2). A 12-lead ECG (Medical Graphics) wasmonitored continuously to collect HR data. Minute ventilation ( _VE,l á min)1), oxygen uptake ( _V O2, ml á min)1 á kg)1), and carbon di-oxide production ( _V CO2, ml á min)1) were collected every minuteas the average of the last 20 s of every stage. The observation of atleast three of the four following criteria was necessary to considerthat the subjects had reached their _V O2peak: (1) the stability of _V O2

in spite of the speed increment, (2) HR near the predicted maximumHRmax (210±0.65 ´ age) (Lange-Anderson et al. 1971), (3) a respi-ratory exchange ratio (R) above 1.1, and (4) the inability of theathlete to maintain the imposed speed.

VT was determined using the V-slope method of Beaver et al.(1986). This method involves analysis of the behaviour of _V CO2 asa function of _V O2, and assumes that VT corresponds to thebreakpoint in the _V CO2) _V O2 relationship. VT was determinedautomatically using an IBM computer and breakpoint determina-tion was veri®ed by two experienced investigators. HRr and HRRwere calculated as follows: HRr = predicted HRmax)HRpeak, andHRR = (HRpeak)HRrest)/( _V O2peak) _V O2rest), where HRpeak is thepeak HR, HRrest is the resting HR, and _V O2rest is the resting _V O2.HRr represents the potential to increase HR at peak exercise and isgenerally used for the di�erential diagnosis between cardiac andrespiratory limitations during exercise. HRR can be used to assessthe HR and _V O2 increases during exercise. In heart disease, HRincreases more than _V O2, thus HRR is higher in these subjects thanin normal subjects. The ventilatory reserve (VR) at peak exercisewas calculated as follows: 100)(100 ´ measured _VEpeak/predicted_VEmax), where predicted _VEmax= measured forced expiratory vol-ume in l s (FEV1) ´ 35 (Jones and Campbell 1982) and _VEpeak is thepeak _VE. VR represents the potential to increase _VE at peak exercise.An increased VR suggests that _VE could still rise above that at-tained at peak exercise and therefore that the increase in _VE doesnot contribute to limitation at peak exercise. The O2 P at peakexercise ( _V O2peak=HRpeak) is expressed in ml á kg)1 á beat)1. The_V O2peak and VT values recorded in our P athletes were compared tothose of other P athletes and non-athletes reported in the literature(Flandrois et al. 1986; Lin et al. 1993; Coutts and McKenzie 1995),

as well as to those of AB controls performing arm-crank exercise(Flandrois et al. 1986; Lin et al. 1993). Cardioventilatory responseswere compared to data reported in AB control subjects and inCOLD and CHF patients (Messner-Pellenc et al. 1994).

Statistical analysis

All values are reported as means (SEM). Comparisons were madeusing a t-test for independent groups to compare: (1) _V O2peak andVT values in the P athletes with those of P subjects with similarlevels of injury and training performing a similar exercise test, (2)the means of breathing frequency �f � and _VE at peak exercise tomaximal theoretical values (35 for f and theoretical _VEmax), and(3) the percentage of spirometric values to the theoretical 100%values.

Results

Resting spirometric values were 4.76 (0.63) l for FEV1

[corresponding to 118 (4)% of the theoretical value],5.60 (0.92) 1 for vital capacity (VC) [corresponding to113 (24)% of the theoretical value], and 0.53 (0.04) l fortidal volume (Vt). The maximal speed reached at the endof the incremental test was 9.4 (1.5) km á h)1, corre-sponding to a test duration of 8 min 50 s (1 min 24 s),which was within the time span recommended by Bu-chfuhrer et al. (1983), i.e. 8±12 min to reach _V O2max.HRpeak values [173.5 (2.9) beats á min)1] were higherthan 90% of the predicted HRmax, and R values [1.35(0.04)] were higher than 1.1. Absolute VT was detectedat 1.53 (0.14) l á min)1, i.e. 23.1 (1.53) ml á min)1 á kg)1

_V O2. Relative VT was found to be 56.4 (2.2)% _V O2peak.HR and R values at VT were 127.3 (1.74) beats á min)1

[73.5 (1.7)% HRpeak] and 0.92 (0.04), respectively._V O2peak values were 2.67 (0.15) l á min)1, correspondingto 40.6 (2.5) ml á min)1 á kg)1. The _V O2 kinetics wereassessed throughout the nine 1-min stages of the incre-mental test performed by all subjects (Fig. 1). Car-

Fig. 1 Oxygen uptake � _V O2,ml á min)1) kinetics in paraple-gic athletes throughout the in-cremental test. R1, R2 recovery(min). Stage 4 corresponds tothe mean of the 3-min warm-upat 4 km á h)1

457

dioventilatory values for _V O2; _V CO2; _VE; _VE= _V O2;_VE= _V CO2; f ; Vt and HR, at peak exercise and at VT,are given in Table 2. The breathing pattern was repre-sented by an f of 49.7 (11.9) breaths á min)1, and a Vt of1954.8 (153.6) ml. None of the P athletes complained ofdyspnoea at peak exercise.

Comparisons of _V O2peak data with those in theliterature showed that the _V O2peak values reached bythe P athletes were not statistically di�erent from thosereported by Cooper et al. (1992) using the same testprotocol in 11 P wheelchair road-racers with comparabledisabilities. In contrast, the mean _V O2peak valuerecorded in the present study was signi®cantly higherthan that reported by Rasche et al. (1993) [29.8 (4.3)ml á min)1 á kg)1] and Martel et al. (1991) [1.90 (0.63)ml á min)1 á kg)1] in trained P subjects with spinal lesionlevels T7±L2 and T3±L5, respectively, practicing teamsports. The absolute VT was signi®cantly lower thanthat reported by Coutts and McKenzie (1995) in class IIIathletes who performed an incremental wheelchair ex-ercise. Values for HRr, HRR, VR and O2 P at maximalexercise are given in Table 3. Comparisons with theseparameters in CHF, COLD and AB subjects (Messner-Pellenc et al. 1994) showed that P athletes had increasedVR values, as was reported in CHF patients, whichsuggests that they exhibited similar cardiac limitations atpeak exercise.

Discussion

Eight P wheelchair athletes were tested using an incre-mental test in a wheelchair mounted on an adaptedtreadmill. All showed _V O2peak, absolute VT and relativeVT values comparable to those reported previously inthe literature for this type of population. Moreover, withrespect to their increased VR values at peak exercise, theP athletes exhibited exercise limitations similar to thosereported for patients with CHF. This suggests the role ofa cardiac limitation in the decreased _V O2peak measuredin these athletes.

Inherent problems arise when attempts are made tocompare _V O2peak among SCI individuals because ofdiscrepancies in the levels of injury, anthropometriccharacteristics, the exercise protocols and the individualtraining states of the subjects. The e�ect of SCI levelupon aerobic metabolism has been assessed by com-paring _V O2peak in AB subjects to high-lesion versus low-lesion P and tetraplegic subjects (Coutts et al. 1983; VanLoan et al. 1987). As expected, AB subjects reachedhigher _V O2peak values than SCI subjects, and the higherthe lesion level, the lower _V O2peak (Coutts et al. 1983;Van Loan et al. 1987). This reduced _V O2peak with higherlesion levels is usually attributed to a lower availablefunctional muscle mass (Coutts et al. 1983). In addition,the role of impaired cardiac stimulation has been re-ported by Jehl et al. (1991), and Davis and Shephard(1988) reported that impaired cardiovascular functionmay be the primary cause of the lower _V O2peak andpoorer physical performance seen in P compared to ABsubjects. The e�ect of the exercise protocol upon aerobicmetabolism has been assessed by Lasko-McCarthey andDavis (1991) for di�erent workloads and duration in-crements. High-power (8 W á min)1) and long-duration(2-min) increments induced lower _V O2peak values. Thee�ect of training and conditioning level upon _V O2peak inSCI subjects has been demonstrated by Zwiren andBarOr (1975) and Davis and Shephard (1988). As ex-pected, these authors concluded that trained and highlyactive SCI subjects reached a signi®cantly higher_V O2peak than less active and sedentary SCI subjects. Inthe present study we compared our results with those ofsimilar studies in terms of level of injury, training level ofP subjects and test protocol. The signi®cantly higher_V O2peak values recorded in the present study, compared

Table 2 Physiological variables at peak exercise and ventilatorythreshold of the paraplegic (P) athletes. Values are reported asmeans (SEM). ( _V E Minute ventilation, _V O2 oxygen consumption,_V CO2 carbon dioxide output, R respiratory exchange ratio, HRheart rate, _V E= _V O2 ventilatory exchange ratio for O2, _V E= _V CO2

ventilatory exchange ratio for CO2, f breathing frequency,Vt tidal volume; VT ventilatory threshold)

Parameters VT Peak value

_V E (l á min)1) 39.7 (5.7) 104.4 (10.8)_V O2 (l á min)1) 1.53 (0.14) 2.67 (0.15)_V O2 (ml á min)1ákg)1) 23.1 (1.53) 40.6 (2.5)_V CO2 (ml á min)1) 1280 (103) 3500 (146)R 0.92 (0.04) 1.35 (0.11)HR (beats á min)1) 127.3 (1.74) 173.5 (2.87)_VE= _V O2 25.3 (1.89) 38.1 (1.94)_VE= _V CO2 28.1 (1.75) 28.6 (1.37)f (breaths á min)1) 29.2 (1.5) 49.7 (11.9)_Vt (l) 1.33 (0.23) 1.95 (0.15)

Table 3 Exercise parameters at peak exercise in P athletes, cardiac heart failure (CHF) patients, chronic obstructive lung disease (COLD)patients and able-bodied control subjects reported in the literature. Values are reported as means (SEM). (HRr heart rate reserve, HRRheart rate response, VR ventilatory reserve, O2P oxygen pulse)

Parameters P athletesn = 8

CHFa

n = 15COLDa

n = 15Controlsa

n = 10

HRr (beats á min)1) 15.8 � 3.2 48.9 � 4.4 35.2 � 5.2 16.1 � 4.0HRR (beats á l)1) 48.6 � 4.3 65.7 � 1.0 55.7 � 6.5 45.6 � 1.4VR (%) 42.0 � 2.4 49.7 � 3.2 8.4 � 5.8 35.9 � 4.4O2 P (ml á kg)1 á beats)1) 0.230 � 0.02 0.103 � 0.006 0.119 � 0.007 0.164 � 0.005

a Messner-Pellenc et al. (1994)

458

with those of Rasche et al. (1993) and Martel et al.(1991), can be attributed to the practice of team sportsrather than endurance sports, as already noted byVeeger et al. (1991). In agreement with this observation,the _V O2peak of the four wheelchair racers recorded in thepresent study was signi®cantly higher than that of thefour tennis players: 46.4 versus 34.8 ml á min)1 á kg)1,respectively. On the other hand, the _V O2peak was similarin wheelchair racers and tennis players when expressedwith respect to lean body mass [58.4 (7) ml á min)1

á kg)1 versus 46.7 (4) ml á min)1 á kg)1]. Thus, in thepresent study _V O2peak di�erences between wheelchairracers and tennis players can be attributed to higherlevels of body fat in the tennis players than in thewheelchair racers [25.3 (4.1)% versus 20.2 (6.4)%].

The absolute VT reached by the P athletes in thepresent study was 1.53 (0.14) l á min)1. This value wassimilar to that reported by Coutts and McKenzie (1995)using a di�erent exercise protocol and similar VT de-termination in athletes of classes II±IV performing awheelchair exercise, but was higher than that reportedby Lin et al. (1993) in non-athletic P subjects performingan arm-crank exercise. This di�erence may be attributedto the use of di�erent ergometers and/or to the di�erencein the training level of the subjects. The use of VT is areliable endurance index in AB subjects (Vago et al.1987) and has recently been shown to be detectable inSCI subjects (Bhambani et al. 1995). Comparisons ofanaerobic threshold (AT) in SCI and AB subjects havebeen assessed by numerous authors (Flandrois et al.1986; Lin et al. 1993; Coutts and McKenzie 1995). Ab-solute AT was found to be similar in P versus AB sub-jects by Flandrois et al. (1986). This agrees with the®nding of similar aerobic exercise responses in low-levellesion P versus AB subjects during the submaximal ex-ercise stages of a graded arm-crank test (Coutts et al.1985). The relative VT reached by P athletes in thepresent study was 56.4 (2.2)% _V O2peak. This value waslower than that reported by Lin et al. (1993), who noteda VT% at 74 and 63% of _V O2peak in non-athletic classIII and IV P subjects. This di�erence may be related tothe training level of those P subjects. The hypothesis thattraining induces a higher increase in _V O2peak than inabsolute VT, and thus a decrease in VT% in P subjects,was con®rmed by Bhambani et al. (1995) in tetraplegics.These di�erent training adaptations lead to the conclu-sion that the exercise and training adaptations in Psubjects are not similar to those in AB subjects, and thata reduced muscle mass is not su�cient to explain thesedi�erences. In the present study relative VT was alsosigni®cantly lower than that observed by Coutts andMcKenzie (1995) in trained class II±V P athletesthroughout an incremental wheelchair exercise andsimilar VT determination (69% _V O2peak). This di�erencemay be attributed to the class II athletes who reached alower _V O2peak in their study. In fact, relative VT wasfound to be related to the spinal lesion level in SCIsubjects, with a higher VT% occurring in tetraplegicversus P subjects, and a higher VT% occurring in class

III versus classes IV and V subjects (Coutts andMcKenzie 1995; Lin et al. 1993).

Medical advances in the acute management of SCIhave reduced early mortality. Owing to this increasedlife expectancy, cardiovascular disease has become amajor cause of death in this population (Dearwater et al.1986). Attention should thus be focused upon whetherthe exercise limitation in SCI subjects is of cardiovas-cular origin. Hjeltnes (1977) and Davis and Shephard(1988) reported a reduced cardiac output and lowerstroke volume in P subjects, in contrast to Hopman et al.(1992, 1993) and Jehl et al. (1991), who respectively re-ported similar and higher cardiac outputs in P versus ABsubjects at a given _V O2. The lower stroke volume wasexplained by the loss of central sympathetic vasomotorout¯ow and the loss of a muscle pump below the level ofinjury, inducing a venous pooling of blood. This ``hy-pokinetic circulation'' leads to an inadequate muscleblood ¯ow. These authors also noted that this impairedcardiovascular function was the primary cause of thelower _V O2peak reported for SCI subjects. Furthermore,Messner-Pellenc et al. (1994) showed that VR at ex-haustion of incremental exercise can be used to predictcardiac or pulmonary limitations in CHF and COLDpatients. In order to assess the origin of these exerciselimitations in P athletes, we measured HRr, HRR, VRand O2 P in these P athletes at peak exercise, andcompared these values with those of CHF and COLDpatients and control subjects at similar levels of incre-mental exercise (Messner-Pellenc et al. 1994). Messner-Pellenc et al. (1994) have shown that CHF patients ex-hibit an increased VR during symptom-limited exercise,whereas COLD patients exhibit a decreased VR at asimilar level of exercise. HRr and HRR were reported tobe signi®cantly di�erent in COLD and CHF patientsversus control subjects, but not in COLD versus CHFpatients. In the present study, the VR values in P ath-letes [42.7 (2.4)%] were found to be increased, as re-ported in the CHF patients. HRr and HRR values [15.8(3.2) beats á min)1 and 48.6 (4.3) beats á l)1, respectively]were close to those reported for AB controls [16.1 (4.0)beats á min)1 and 45.6 (1.4) beats á l)1, respectively], andO2 P values [0.23 (0.02) ml á kg)1 á beats)1] were higherin P athletes than in CHF and COLD patients andcontrols (Table 3). Thus, P athletes may present an ex-ercise limitation similar to that of CHF patients, at leastin terms of their increased VR values at peak exercise.Nevertheless, the cardiac limitation in P athletes, sug-gested in the present study by the increased VR, must beinterpreted carefully because of: (1) the di�erence in ageand training level between our P athletes and the pa-tients in the study of Messner-Pellenc et al. (1994), (2)the di�erent types of exercise, arm versus leg exercise,used in the two studies, (3) the normal HRr and HRRvalues reported for the P athletes, showing that theyreached their HRmax and indicating a normal nor-adrenaline response to exercise, (4) the high O2 P valuesin the P athletes indicating a good O2 transport system,and (5) the absence of dyspnoea in the P athletes in

459

contrast with that usually reported in CHF patientsduring symptom-limited exercise. Moreover, the in-creased VR values observed for the P athletes of thepresent study resulted in a high maximum predicted_VE�FEV1 � 35� and a low measured _VE at peak exercise.The former resulted from a signi®cantly higher FEV1

compared with the theoretical value [118 (4)%], andcould be the consequence of the training state andcompetitive activity of the P athletes. The latter has beenreported to be lower in arm versus leg exercise at max-imal intensity in AB subjects (Louhevaara et al. 1990).The _VE at peak exercise has also been reported to belower in P than in AB subjects by Flandrois et al. (1986)and Hooker et al. (1993), and is thought to be related toan impaired innervation of some of the respiratorymuscles. The low _VEpeak recorded for the P athletes in thepresent study was unexpected since they exhibited highFEV1 values [4760 (240) ml] and a normal FEV1=VCratio [103.8 (3.01)% of the theoretical value]. The lowerblood lactate concentration observed in P athletes dur-ing exercise could explain their lower measured _VEpeak.Unfortunately, we did not take blood lactate measure-ments, and Flandrois et al. (1986) reported normalblood lactate concentrations in P athletes during peakincremental exercise. The breathing pattern at peak ex-ercise could explain the low _VEpeak. The high f values[49.7 (11.9) breaths á min)1] may be linked with the arm-wheelchair propulsion rhythm. In turn, these high fvalues associated with the forward ¯exion of the trunkduring the wheelchair propulsion could have generatedlow Vt values [1954 (153) ml] and a low _VEpeak [104.4(10.8) l á min)1].

In conclusion, the results of the present study showthat the relationship between _V O2peak and absolute andrelative VT in P wheelchair athletes remains speci®c tothese subjects, and is linked with the spinal lesion leveland training state. Moreover, these athletes exhibited anincreased VR at peak exercise. Given the fact that anincreased VR is a potentially valid indicator of cardiaclimitation, this suggests a cardiac limitation in P athletesat peak exercise, as expressed by their limited _V O2peak.This cardiac limitation must be taken into account interms of development of rehabilitation programs for SCIpatients, the management of increased risks for cardio-vascular disease in sedentary SCI subjects, and speci®ctraining programs for SCI athletes. Further researchinto the validity of VR seems merited in this population.

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