Incremental Ramp Research Articles

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.

Bilateral arm power imbalance in swim bench exercise to exhaustion

We examined the supposition that swimmers may exhibit an imbalance in bilateral arm power output during simulated swimming exercise. Ten competitive front crawl swimmers (5 males, 5 females; age 20.5 - 2.3 years; height 1.74 - 0.09 m; body mass 72.0 - 16.7 kg; 400 m freestyle swim time 278 - 20.5 s; mean - s ) performed four incremental (10 W·min -1 ) swim ramp tests on a computer-interfaced biokinetic swim bench ergometer. External power output from each arm was measured continuously to exhaustion. The results showed that, throughout the course of the simulated swim, external power output clearly favoured the left arm ( F 1,9 = 12.5, P = 0.006). This was especially evident in the final 30 s to exhaustion, when 54.0 - 3.87% of external power output was derived from the left arm versus 46.0 - 3.87% from the right arm. The disparity in external power output was further highlighted when the participants were grouped into unilateral and bilateral breathers. Unilateral breathers ( n = 5) produced 57.1 - 2.62% of external power output from the left arm versus 42.9 - 2.62% from the right arm ( P = 0.001). Bilateral breathers ( n = 5) exhibited a more balanced external power output of 51.0 - 1.82% from the left arm and 49.0 - 1.82% from the right arm ( P = 0.177). Evidence of power imbalance in the simulated swimming stroke may have important implications for optimizing swim performance. The observed power imbalance may be reduced when a bilateral breathing technique is adopted.

A novel rating scale to predict maximal exercise capacity.

To predict maximal exercise capacity, we have developed the rating of perceived capacity (RPC) scale, based on metabolic equivalents (METs). MET values from 1 to 20 were listed on a progressive scale and linked to physical activities. Test subjects rated their perceived capacity by choosing the most strenuous activity and the corresponding MET value that they could sustain for 30 min. In order to validate the RPC, 87 healthy women participated in the study (age range 21-79 years). The capacity rated from the scale (MET(RPC)) was compared with the actual work capacity in a maximal incremental ramp cycle test. The maximal load achieved at the cycle test (in W), was transformed into the unit MET (MET(test)). The mean difference between MET(RPC) and MET(test) was -1.4 (3.18) (2SD). Multiple linear regression showed that MET(test) depended significantly on MET(RPC) and age. Extended regression analysis suggested that a nonlinear correction was most appropriate in order to improve the prediction. The maximal predicted capacity was given by: MET(pred) = (5.08 + 0.70 x MET(RPC))/[1+(e(0.059 (age-87.2)))]. After this correction, the mean difference between MET(pred) and MET(test) was reduced to 0.0 (2.62) (2SD). Reference values for MET(pred) and MET(test) were also obtained. In conclusion, the RPC combined with an age correction was shown to predict accurately maximal exercise capacity; it is also quick and easy to use. Thus, RPC may be a valuable tool in the prescription of exercise and in monitoring the effects of exercise and rehabilitation.

Peak power output, the lactate threshold, and time trial performance in cyclists

To determine the relationship between maximum workload (W(peak)), the workload at the onset of blood lactate accumulation (W(OBLA)), the lactate threshold (W(LTlog)) and the D(max) lactate threshold, and the average power output obtained during a 90-min (W(90-min)) and a 20-min (W(20-min)) time trial (TT) in a group of well-trained cyclists. Nine male cyclists (.VO(2max) 62.7 +/- 0.8 mL.kg(-1).min(-1)) who were competing regularly in triathlon or cycle TT were recruited for the study. Each cyclist performed four tests on an SRM isokinetic cycle ergometer over a 2-wk period. The tests comprised 1) a continuous incremental ramp test for determination of maximal oxygen uptake (.VO(2max) (L.min(-1) and mL.kg(-1).min(-1)); 2) a continuous incremental lactate test to measure W(peak), W(OBLA), W(LTlog), and the D(max) lactate threshold; and 3) a 20-min TT and 4) a 90-min TT, both to determine the average power output (in watts). The average power output during the 90-min TT (W(90-min)) was significantly (P < 0.01) correlated with W(peak) (r = 0.91), W(LTlog) (r = 0.91), and the D(max) lactate threshold (r = 0.77, P < 0.05). In contrast, W(20-min) was significantly (P < 0.05) related to .VO(2max) (L.min(-1)) (r = 0.69) and W(LTlog) (r = 0.67). The D(max) lactate threshold was not significantly correlated to W(20-min) (r = 0.45). Furthermore, W(OBLA) was not correlated to W(90-min) (r = 0.54) or W(20-min) (r = 0.23). In addition, .VO(2max) (mL.kg(-1).min(-1)) was not significantly related to W(90-min) (r = 0.11) or W(20-min) (r = 0.47). The results of this study demonstrate that in subelite cyclists the relationship between maximum power output and the power output at the lactate threshold, obtained during an incremental exercise test, may change depending on the length of the TT that is completed.

Prolonged stage duration during incremental cycle exercise: effects on the lactate threshold and onset of blood lactate accumulation.

The aim of this study was to investigate whether increasing the duration of workloads from 3 min to 8 min during incremental exercise would influence workload (W), oxygen consumption (VO2) and heart rate (HR) at the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA). Two groups of six male cyclists were assigned to a well-trained (WT) and recreational (REC) group on the basis of their performance in a maximal incremental ramp test. Each subject then performed two incremental lactate tests (EXT) consisting of six workloads of either 3 min (EXT3-min) or 8 min (EXT8-min) duration. At the completion of each workload whole capillary blood samples were obtained for the determination of blood lactate (BLa) concentration (mM). Power output (Watts, W), HR and VO2 were averaged in the final minute of each workload as well as in the third minute of the EXT8-min. The workload, HR and VO2 at the LT and OBLA were subsequently determined from the data of EXT3-min and EXT8-min. The results demonstrate that workload and VO2, but not HR, at the LT and OBLA were higher in the WT cyclists. At the same time, the workload at the LT obtained from the results of the EXT3-min was significantly (P < 0.05) higher then the value obtained in the EXT8-min in the WT subjects but not the REC subjects. However, the workload, VO2 and HR at the OBLA, together with the VO2 and HR at the LT were not significantly different when calculated from data obtained from EXT3-min or EXT8-min. The data obtained in this study suggest that incremental exercise protocols using workloads of duration longer than 3 min have the effect of increasing the workload at the LT in well-trained cyclists. However, the OBLA determined in exercise tests using stage increments of either 3 min or 8 min is similar in cyclists of different training status.

PEAK POWER OUTPUT, THE LACTATE THRESHOLD AND 90-MIN TIME TRIAL PERFORMANCE IN WELL TRAINED CYCLISTS

Presently there is limited data examining the relationship between physiological variables obtained during incremental exercise tests and cycle time trial performance over distances greater than 60-min. The purpose of this study was to determine the relationship between peak power output (Wpeak), the workload at the lactate threshold (WLT) and the average power output obtained during a 90-min (W90-min) cycle time trial (TT). Nine male welltrained cyclists (Age 32.1 ± 3.0 yrs) with a Wpeak of > 4 W/kg were recruited for the investigation. Each cyclist performed three tests over a two-week period. The tests included (1) a continuous incremental ramp test for determination of maximal oxygen uptake (VO2max; L/min); (2) a continuous incremental lactate test to measure W peak (W) and WLT (W); and (3) a 90-min TT to obtain the W90-min (W). The W90-min was significantly (p < 0.01) correlated with Wpeak (r = 0.91) and WLT (r = 0.91). However W90-min was not significantly related to VO2max (r = 0.38). In addition, Wpeak was highly related to WLT (r = 0.86; p < 0.01) but not significantly related to VO2max (r = 0.51; p = 0.16). The results of this study demonstrate that the maximum workload and the workload at the lactate threshold obtained during an incremental exercise test are highly related to 90-min TT performance in well-trained cyclists. The results also suggest that delaying blood lactate accumulation influences the maximum workload obtained during incremental cycle exercise. In contrast to other physiological variables, the WLT and Wpeak should be used to assess changes in cycling performance in highly trained athletes.

VO2 PLATEAU DETECTION IN CYCLE ERGOMETRY

Recently, the presence of a plateau in VO2 at maximal work rates has been questioned (Noakes, MSSE 1997). Currently, there is no consensus regarding the appropriate criteria for detecting a plateau, and criteria based on absolute changes in VO2 (e.g., 150 ml/min) are problematic considering differences in workload increments and body size. In addition, the time interval over which to evaluate changes in VO2 (breath-by-breath (BxB) vs. various time averages) is not established. To avoid these concerns, we applied signal processing techniques common in biomechanics to examine the presence of the plateau. Twenty subjects (10 males) performed two individualized incremental ramp protocols to exhaustion (pedal rpm < 40) on an electrically braked cycle ergometer interfaced with a metabolic cart (Max 1, Physio Dyne). The first test was for subject familiarization, while the results of the second test were analyzed. To create evenly spaced data points, each BxB VO2 signal was interpolated (cubic spline), re-sampled at 60 Hz, normalized (to the highest 15 sec. average), and smoothed (Butterworth low pass filter, cutoff = 0.02 Hz). The first derivative (FD) signal was calculated (mean of means = 0.12 [0.01] %max/sec) and FD minima (FDM; criteria = 2 SD below mean FD) were identified. Of the 20 trials, 12 had one FDM and 8 had two. All FDM nadirs were < 0.0 (−0.82 [0.41]). Sixteen trials had FDM occur within the last 5% of the ride (0.6 [1.2] %), indicating changes in VO2 indicative of a plateau. (This was supported by visual examination in all cases.) These were easily distinguished from the 8 FDM not associated with plateaus because their positions were 41.5 [16.8]% from the end of the ride (end = 100%). These results indicate that: a) the plateau is evident in most trials (16 of 20), and b) the FDM criterion may be useful in objectively identifying the VO2 plateau.

Influence of Muscle Fibre Type and Fitness on the Oxygen Uptake/Power Output Slope During Incremental Exercise in Humans

We recently reported that a higher percentage of type I fibres in vastus lateralis and a greater peak oxygen uptake (O2) were associated with a greater initial rise in O2 (O2 /W, where W is work rate) following the onset of heavy constant power output exercise (above the lactate threshold, LT). It was unclear if these results were true only for heavy exercise, or if the association between fibre type and/or fitness and O2 /W would also be seen for moderate (< LT) exercise. The purpose of the present study was to compare the relationships between fibre type or peak O2 and O2 /W determined for moderate (< LT) and heavy (> LT) exercise intensities during incremental exercise. Nine healthy subjects performed an incremental ramp test on a cycle ergometer. The O2 /Wslope was calculated for the domain of power outputs up to the LT (S1), from the LT towards peak O2 (S2), and over the entire linear portion of the O2 /W response (ST), and compared to fibre type distribution determined from biopsy of the vastus lateralis, and to peak O2 (as ml kg-1 min-1). Significant correlations between O2 /W and the proportion of type I fibres were found for each exercise domain (r is 0.69, 0.71 and 0.84 for S1, S2 and ST, respectively, P < 0.05). S1 ranged between about 9 ml min-1 W-1 for a low proportion of type I fibres and 11 ml min-1 W-1 for a high proportion of type I fibres. Similar correlations were also found between S2 (r = 0.70) and ST (r = 0.76) and peak O2. These results are consistent with our previous findings during > LT constant power output exercise, and suggest that the proportion of type I fibres, and possibly fitness as indicated by peak O2, is associated with greater O2 /W during the initial adjustment to < LT as well as > LT exercise. These results do not appear to be explained by classical descriptions of the kinetics of adjustment of O2 following the onset of ramp or constant power output exercise. They might reflect enhanced motor unit recruitment in subjects with a greater percentage of type I fibres, and/or who are more aerobically fit. However, the underlying mechanism for these findings must await further study.

Improvement in exercise tolerance in isovaleric acidaemia with L-carnitine therapy.

The effect of 4 weeks' treatment with oral-L-carnitine (100 mg/kg per day) on carnitine status and metabolic parameters during an incremental ramp exercise test in a 12-year-old girl with isovaleric acidaemia was examined to determine its possible therapeutic role. The maximum work rate achieved increased from 110 to 120 watts; oxygen consumption at anaerobic threshold from 600 to 800 L/min; peak oxygen consumption from 1270 to 1450 L/min; and oxygen pulse, a measure of cardiac output, from 7.0 to 8.1 L/beat. These changes were associated with increases in plasma and urinary free and acyl carnitine concentrations but no change in physical activity. This observed effect of L-carnitine on exercise performance may be on cardiac or skeletal muscle function or both. We conclude that, in this single patient with isovaleric acid-aemia, L-carnitine supplementation had objective benefits and further studies on more patients are warranted.

Exhaled Nitric Oxide During Exercise in Primary Pulmonary Hypertension and Pulmonary Fibrosis

Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of humans. We wished to quantify NO production in patients with abnormalities of the pulmonary circulation. Nine patients with primary pulmonary hypertension (PPH), six with pulmonary fibrosis (PF), and 20 normal volunteers were studied. All subjects were studied at rest and during continuous incremental (ramp) cycle ergometry exercise. All patients with PPH and nine matched normal volunteers also performed constant exercise at equal absolute work rates. The concentration of NO was measured continuously in mixed expired air, and the rate of NO production (VNO) calculated. Peak exercise capacity was markedly impaired in both patient groups. VNO was similar at rest in the PPH patients (142 +/- 84 nL/min) and the normal subjects (117 +/- 45 nL/min), but lower in the PF patients (66 +/- 13 nL/min; p < 0.05; analysis of variance with Bonferonni correction). While VNO in normal subjects more than doubled by peak exercise to 268 +/- 85 nL/min, there was no significant rise with exercise in either patient group (PPH, 155 +/- 81 nL/min; PF, 91 +/- 67 nL/min). Constant work rate exercise induced a significant rise in VNO in the normal subjects (rest, 101 +/- 68 nL/min; exercise, 147 +/- 87 nL/min; p < 0.001) but no significant change in the PPH patients (rest, 127 +/- 111 nL/min; exercise, 68 +/- 65 nL/min). We conclude that the low resting VNO in PF may be due to loss of normal functional pulmonary capillary bed. The increase in VNO seen in normal subjects may be associated with dilatation and recruitment of the pulmonary capillary bed during exercise, and failure to increase VNO during exercise in disease states may reflect an inability to recruit the capillary bed.

RELATIONSHIP BETWEEN PEAK ??Vo2 AND RECOVERY ??Vo2 KINETICS IN HIGH SCHOOL AGE GIRLS 708

Both peak ˙Vo2 and the kinetics of ˙Vo2 during submaximal exercise have been used as indices of cardiorespiratory fitness. Further, these variables are inversely related when healthy subjects and CHF patients are compared together (Cohen-Solal et al, Circ. 91:2924, 1995). Determining these variables requires two different exercise tests--incremental and constant work rate. We wondered if the kinetics of ˙Vo2 in recovery from incremental, maximal exercise would demonstrate a similar inverse relationship to peak ˙Vo2. We examined these relationships in 19 high school girls (age 15-17). Each girl performed an incremental (ramp) test to volitional fatigue on an upright cycle ergometer. ˙Vo2 was determined breath-by-breath during exercise and for 6 min of recovery.˙Vo2 kinetics were determined by fitting the recovery response following the ramp test to a three exponential decay function. A mean response time (MRT) was calculated as the sum of the amplitude-weighted (time constant+ time delay) for each exponential term. Peak ˙Vo2 averaged 1.30±0.56 L/min (22.7±7.9 ml/min/kg), while MRT was 51.9±23.4 sec. The MRT is significantly faster than that found by Cohen-Solal for middle-aged healthy men (80±11 sec, P<0.001). Peak˙Vo2 (L/min) was significantly correlated with body weight(r=0.60,P<0.005), while MRT was weakly related (r=0.44, P<0.05). In contrast to our hypothesis, there was no significant correlation between MRT and peak ˙Vo2 (as ml/kg/min)(r=0.20). In conclusion, MRT following maximal exercise is sensitive to age, body mass and possibly gender. However, MRT does not relate to peak ˙Vo2 in healthy post-pubertal girls.

A model analysis of asymmetrical response of pulmonary VO2 during incremental and decremental ramp exercise.

The responses of gas exchange and ventilatory variables exhibit obvious asymmetry between the incremental and decremental phases of trapezoidal ramp exercise (29). Computer simulation was performed to explore the possible mechanisms producing this asymmetry of pulmonary O2 uptake (VO2) dynamics. The model consisted of three compartments (the lungs, the exercising muscles, and the other organs and tissues), which were perfused by respective regional circulations. Exercise was simulated by increasing the pulmonary blood flow (Q) and the muscle. VO2 in proportion to work rate. The dynamic responses of Q and the muscle VO2 were assumed to obey first-order linear kinetics. The ratio of blood flow in the muscle compartment to total cardiac output was assumed to increase linearly with work rate. Our simulation demonstrated that the muscle blood flow and mixed venous O2 content exhibited significant asymmetry between the incremental and decremental phases of exercise. The model suggested that the asymmetry of VO2 between incremental and decremental ramp exercise was dependent on the redistribution ratio of blood flow to the working muscles. The validity of the model was then evaluated by comparing the simulated results with experimental data obtained.

Effects of base line changes in work rate on cardiorespiratory dynamics in incremental and decremental ramp exercise.

The kinetics of ventilatory and gas exchange responses during the decremental (off) phase of trapezoidal and triangular ramp exercise in healthy subjects has been found to be significantly faster than those during the incremental (on) phase (1, 2). As an aid in exploring the mechanisms governing the on-off asymmetry of \( \dot V{O_2} \) dynamics, a model analysis has been presented by Niizeki et al. (3). They suggested that the redistribution of blood flow during exercise would play a dominant role in producing the asymmetry of gas exchange response, assuming that the blood flow ratio of active muscles to total cardiac output increases linearly with the work intensity. Therefore, we tested the hypothesis that the asymmetrical response of gas exchange could be modulated by altering the absolute baseline of cardiac output. The dynamic properties of pulmonary gas exchange responses to trapezoidal ramp exercise in the upright position starting from two different baselines of 30- and 50-W were studied in five healthy men.

Ventilatory Responses during Incremental Exercise in Men under Hyperoxic Conditions.

The aim of the present study was to explore the role of the carotid chemoreceptors in the regulation of breathing during incremental ramp exercise. We measured minute ventilation (VE), oxygen uptake (VO2), carbon dioxide output (VCO2), end-tidal PO2 and PCO2 (PETO2 and PETCO2), and heart rate (HR) during incremental exercise in healthy young men breathing air and 50% O2. During incremental exercise (15 W/min, from 0 to 300 W) VCO2 in hyperoxia did not differ from the normoxic response, but VE in hyperoxia increased more linearly with an increasing load in comparison to the curvilinear rise of normoxic VE. The isocapnic buffering of PETCO2 observed in normoxia at the transition from moderate to heavy work did not appear in hyperoxia until a very heavy work load had been attained. This agrees with the observation that normoxic VE/VCO2 that was consistently falling with load and became flat near the isocapnic point and then turned upward with a further increase in work load, while VE/VCO2 in hyperoxia decreased continuously during heavy exercise. These results would suggest the delayed onset of anaerobic metabolism and the depression of VE under hyperoxic conditions. However, we found that VE and HR increased from a specific work rate with a steeper slope during incremental exercise under both normoxic and hyperoxic conditions. There was a significant correlation between the work rates at which the inflection points of the VE and HR slopes were observed. These findings suggest that factors unrelated to peripheral chemoreceptor activity and affecting both the ventilatory and circulatory systems may be responsible for hyperpnea during heavy exercise.

Dynamics of ventilation, circulation, and gas exchange to incremental and decremental ramp exercise

Transient responses of minute volume (VE), O2 uptake (VO2), CO2 output (VCO2), heart rate (HR), and cardiac output (Q) to a step change and ramp changes with slopes ranging from 33.3 to 14.3 W/min were studied in five healthy human subjects over the load range from 25 to 125 W. The ramp responses were fitted to a first-order model with a pure time delay (td) and a time constant (TC), while most of the step responses fitted better to a second-order model, consisting of a fast and a slow component. No significant asymmetry was observed between the on- and off-responses to step forcing. The mean response time (MRT = td+TC) of the incremental ramp response was prolonged, whereas the MRT of the decremental ramp response was shortened or unchanged, with decreasing ramp slope. The asymmetry was commonly observed in respiratory and gas exchange variables and, to a lesser extent, also in circulatory variables. Neural and humoral factors that might be responsible for this phenomenon are discussed.

Asymmetries of oxygen uptake transients at the on‐ and offset of heavy exercise in humans.

1. At work rates which do not result in a sustained increase in blood lactate ([L-]), oxygen uptake (VO2) approaches the steady state with first-order kinetics. However, when [L-] is increased, at least two kinetic components are required to characterize the VO2 response dynamics. The purpose of the present investigation was to determine whether these more-complex kinetics are best represented as: (a) two components which operate throughout the exercise or (b) a delayed slow component which is consequent to the lactic acidaemia and which does not influence the early development of the O2 deficit. 2. Six healthy subjects underwent an incremental ramp test on a cycle ergometer, to the limit of tolerance, for determination of the maximum VO2 (micro VO2) and and estimation [symbol: see text] of the threshold for lactic acidaemia (theta L) non-invasively. Subjects then performed, on different days, two to four repetitions of square-wave exercise from a baseline of unloaded pedalling ('O' Watts (W)) to work rates (WR) less than theta L (90% theta L) and greater than theta L (half-way between theta L and micro VO2). Ventilatory and pulmonary gas exchange variables were determined breath-by-breath. For each subject, the VO2 transitions were averaged prior to fitting a least-squares algorithm to the on- and off-transient responses. 3. The less than theta L test resulted in a mono-exponential VO2 response, with a time constant of 31.3 and 31.5 s for the on- and off-transients, respectively. 4. The VO2 responses to the greater than theta L test were fitted to three competing models: (a) a single exponential for the entire period; (b) a double exponential for the entire period; and (c) an initial single exponential with a subsequent phase of delayed onset. Model (c) yielded a significantly lower residual mean-squares error than methods (a) and (b), with a time constant for the initial component of 40.2 s for the on-transient and 32.9 s for the off-transient and a subsequent phase of VO2 increase for the on-transient which averaged 230 ml min-1. The delta VO2/delta WR for the early kinetics of the greater than theta L test were not different from the less than theta L test (9.6 and 9.5 ml min-1 W-1, respectively). 5. These data suggest that the slow phase of the greater than theta L VO2 kinetics is a delayed-onset process. This being the case, the O2 deficit during heavy exercise, as conventionally estimated, would be overestimated.

Linking in accessory pathways. Functional loss of antegrade preexcitation.

Concealed retrograde activation has been proposed as a mechanism for antegrade conduction block in the bundle branches and atrioventricular accessory pathways. We studied this hypothesis (linking) in 10 patients with the Wolff-Parkinson-White syndrome in whom antegrade preexcitation could be persistently blocked by overdrive atrial pacing. An atrial pacing protocol, with a decremental ramp followed by an incremental ramp, defined a range of atrial paced cycle lengths (linking window) associated with both persistent conduction and block in the accessory pathway. Within the limits of the linking window, the ability of an atrial impulse to conduct over the accessory pathway was dependent on the preceding state (i.e., conduction or block). The observed linking window ranged from 70 to 290 msec (mean, 185 +/- 68 msec) and closely approximated the measured delay in retrograde activation of the accessory pathway during persistent antegrade block. The mean antegrade effective refractory period of the accessory pathways was long (486 +/- 156 msec), and in each case, it exceeded the antegrade refractory period of the normal atrioventricular pathway. Critically timed premature ventricular extrastimuli, delivered while linking was maintained in the accessory pathway, were able to interrupt the linking and restore antegrade accessory pathway conduction. These observations suggest that accessory pathway linking is associated with bidirectional block in the accessory pathway. The ability to initiate linking (and the stability of the phenomenon) depends on a critical relation between antegrade accessory pathway refractoriness and the magnitude of retrograde accessory pathway activation delay.

Daily Bedside Electrophysiological Testing Following Surgery for the WPW Syndrome

A simple technique is described that allows daily bedside evaluation of the results of surgery for the Wolff-Parkinson-White (WPW) syndrome, using standard postoperative myocardial wires, a single-channel ECG machine, and a temporary pacer capable of rapid stimulation. Rate incremental atrial and ventricular ramp pacing was performed daily in 40 postoperative WPW patients. This technique, together with underdrive pacing in some individuals permits quick assessment of anterograde and retrograde conduction. Two surgical failures were identified in early postoperative days, and promptly returned to the operating room for successful reoperation. No additional failures were identified at formal predischarge electrophysiological testing or following discharge. The technique permits reassurance on a daily basis to apparent successes and early identification in the event of failure, permitting prompt intervention.

Comparison of Ramp and Stepwise Incremental Pacing in Assessment of Antegrade and Retrograde Conduction

Conventional assessment of antegrade (AV) and retrograde (VA) conduction involves stepwise increments in pacing rates until block in conduction is observed. This study was designed to establish the comparative characteristics of ramp pacing, in which the rate is continuously and smoothly incremented until block occurs. Two hundred and ten patients participated in portions of this study. Stepwise pacing was performed in 10 beat/minute steps, with the rate held for at least 15 seconds at each step; if marked prolongation or variability in conduction was observed, the rate was held constant for up to 60 seconds to allow for accommodation. With ramp pacing, the rate was gradually increased at a steady 2-4 beats/minute/second. Whenever possible, both stepwise and ramp pacing were performed for assessment of both antegrade and retrograde conduction. All patients had conducted sinus rhythm as their baseline mechanism. Antegrade conduction was similar using incremental stepwise and ramp pacing. The AH interval at a cycle length (CL) of 500 ms, the maximum AH increment, the cycle length at AV block were all remarkably similar (p = NS). Assessment of retrograde conduction produced similar results, with insignificant differences between maximum conducted VA intervals, and cycle length at VA block using the two pacing techniques. Ramp pacing provides a useful and rapid alternative to conventional stepwise incremental pacing in the assessment of antegrade and retrograde conduction in patients using both normal and accessory pathways. Ramp pacing was better tolerated, and some correlations between antegrade and retrograde conduction were stronger with the ramp pacing technique.