Response of ventilatory and lactate thresholds to continuous and interval training DAVID C. POOLE AND Department of Kinesiology,
A. GAESSER of California,
POOLE, DAVID C., AND GLENN A. GAESSER.Responseof ventilatory and lactate thresholds to continuous and interval training. J. Appl. Physiol. 58(4): 1115-1121, 1985.-The purpose of this study was to evaluate the effects of continuous and interval training on changes in lactate and ventilatory thresholds during incremental exercise. Seventeen males were assigned to one of three training groups: group 1: 55 min continuous exercise at -50% maximum O2 consumption (V02 ,,,); group 2: 35 min continuous exercise at -70% VO, max;andgroup 3: 10 x 2-min intervals at -105% vozrnaxinterspersed with rest intervals of 2 min. All of the subjects were tested and trained on a cycle ergometer 3 day/wk for 8 wk. Lactate threshold (LT) and ventilatory threshold (VT) ( in addition to maximal exercise measures) were determined using a standard incremental exercise test before and after 4 and 8 wk of training. vogrnax increased significantly in all groups with no statistically significant differences between the groups. Increases (ME) in LT (ml Oz. min-‘) for group 1 (569 t 158), group 2 (584 k, 125), and group 3 (533 t 88) were significant (P < 0.05) and of the same magnitude. VT also increased significantly (P < 0.05) in each group. However, the increase in VT (ml Oz. min-‘) for group 3 (699 t 85) was significantly greater (P < 0.05) than the increases in VT for group 1 (224 t 52) and group 2 (404 t 85). For group 1, the posttraining increase in LT was significantly greater than the increase in VT (P < 0.05). We conclude that both continuous and interval training were equally effective in augmenting LT, but interval training was more effective in elevating VT. The marked dissociation between the changes in LT and VT after training in group 1 suggests that LT and VT are regulated by different mechanisms. Our results demonstrate that LT and VT cannot be used interchangeably as indices of training adaptations. exertion;
Los Angeles, California
(i.e., below LT and VT) and long duration (20). To our knowledge, the influence of high-intensity interval exercise training on either VT or LT has not been reported. Consequently, it is not known which type of training (i.e., continuous or interval) is most effective in altering either VT or LT. Because skeletal muscle has a greater capacity for adaptation than is reflected by changes in . vo 2max(15), it is feasible that training of a very high intensity will delay the accumulation of lactate in blood to a greater extent by increasing the oxidative capacity of a greater number of muscle fibers. Both LT and VT have been reported to be significantly correlated to muscle oxidative capacity (17, 23). Biochemical adaptations in skeletal muscle are dependent predominantly on training intensity (6, 11, 12). In rats (6, 11) and in humans (12) it has been demonstrated that “continuous” training at intensities between 50 and 80% of VO zrnaxis most effective in augmenting the oxidative capacity of type I fibers, whereas “interval” training employing work bouts at intensities calculated to elicit &O zrnax is most effective in augmenting the oxidative capacity of type II fibers. Therefore, we were interested in studying the influence of continuous exercise training, at intensities which induce adaptations primarily in type I fibers (6, 12), and interval exercise training, designed to induce adaptations in type II fibers (12), on LT and VT during incremental exercise. We used two continuous exercise protocols and one interval exercise protocol. Specifically, we evaluated the effects of the. three training protocols on changes in LT, VT, and VOW maxafter 4 and 8 wk of training. METHODS
SEVERAL GROUPS of investigators have reported that endurance training results in increases in either the lactate threshold (LT) or ventilation threshold (VT) observed during incremental exercise (3, 4, 24, 27, 32). In each of these studies the training protocols could be characterized as continuous exercise at a constant intensity. Although in one investigation (24) evidence was provided which indicated that for continuous exercise protocols a high training intensity [80% maximum O2 consumption (VO2 max)] was more effective than a low training intensity (40% Tjozmax) in elevating VT, crosssectional studies which have compared middle-distance athletes with marathon runners suggest that the accumulation of blood lactate during exercise might be delayed best by training at a low-to-moderate intensity 0161-7567/85
0 1985 the American
Subjects. Twenty-four sedentary young males volunteered as subjects for this study. Each subject was informed of all risks and stresses associated with this project and gave written consent to participate in this study. Seventeen subjects completed the training. Four subjects failed to complete the training program for personal reasons, and three more were deemed unsuitable due to their unsatisfactory compliance with the training. Accordingly, the data for a total of 17 subjects are presented. The pretraining mean (ME) weights of the subjects were 78.8 t 3.4, 74.9 t 3.6, and 77.0 t 3.3 kg for groups 1,2, and 3, respectively. The mean (ME) ages of the subjects were 24.6 t 3.0, 23.8 t 1.5, and 23.5 t 1.2 yr for groups 1, 2, and 3 (for a description of the groups see below). 1115
D. C. POOLE
Training. Following pretraining testing the subjects were randomly assigned to one of three training groups: group 1 (n = 5): 55 min of continuous exercise at -50% . vo 2 max; initial exercise training blood lactate 52 mM. group 2 (n = 6): 35 min of continuous exercise at -70% vo 2 max;initial exercise training blood lactate ~4 mM. group 3 (n = 10 repetitions of 2min intervals interspersed with .in at rest. The work load was calculated to elicit 105% V02max. The duration of the exercise sessions for groups 1 and 2 were chosen to keep the total energy expenditure during the training sessions approximately the same for these groups. The interval exercise protocol of group 3 was selected to ensure recruitment of type II fibers (12) and to result in a total energy expenditure approximately equal to that of groups 1 and 2. All training programs lasted 8 wk; the subjects trained 3 day/wk. The initial exercise-training blood lactate levels in groups 1 and 2 were determined from finger stick samples taken after 20 min of exercise during the first and second sessions of the first week of training. In all but two subjects (one in group 1 and one in group 2) the blood lactate levels were 52 mM in group 1 and between 4 and 8 mM in group 2. Appropriate work-load adjustments were made for these subjects to bring exercise blood lactate levels within the . desired ranges. The V02max and heart rate responses to training are essentially complete after 3-4 wk of training at a given intensity (13, unpublished observations). Therefore, at the end of the 4th wk of training the subjects performed an incremental test, and the training work load of each subject was increased (depending on his improvement) to maintain each subject’s adjusted training intensity at the same percentage of VO zmaxas he trained at during the first 4 wk of the study. The training intensity remained constant during the final 4 wk of the study. All of the training and testing were performed on a Monark (model 668) cycle ergometer. Measurements. Each subject performed a minimum of two pretra ining maxi ma1 incremental exercise tests on the cycle ergometer with a period of at least 1 day between tests. All exercise tests throughout the study were identical in format. These tests were performed with the subject in the postabsorptive state. Food intake was stan.dardized for 24 h immediately preceding these tests by means of dietary records. Pedaling at a constant 50 rpm, the tests began with a 4-min period of unloaded cycling (0 W). After this initial period the work rate was increased by 24 W every minute until the point was reached at which the subject could no longer move the pedals on the cycle ergometer. Vozmax was taken to be the highest VO, obtained on either of the pretraining incremental tests. The leveling off criterion was used to establish that a cycle ergometer V9grnax had been achieved. In fact, in many cases the Vo2 value at the final test condition was slightly lower than that of the preceding condition due to the pedaling rate approaching zero. During the incremental exercise tests, ventilatory and gas exchange responses were measured breath-by-breath using an integrated computerized system (Medical
G. A. GAESSER
Graphics, System 2000) which is based on that previously described by Beaver et al. (1). Subjects breathed through a low-resistance breathing valve (Hans-Rudolph, dead space 120 ml). Exercise airflow was measured by use of a pneumotachograph (Hans-Rudolph, 3800) which was attached to the outflow port of a 30-liter condensation chamber (maintained at room temperature) and connected to a variable-reluctance pressure transducer (Validyne, MP45). The pneumotachograph was maintained at a constant temperature of 37°C by a thermal feedback device. Calibration was performed by inputting known volumes of room air at several mean flows with various flow profiles. The partial pressures of CO2 and O2 (Pco~ and Po2, respectively) in respired gas were monitored continuously by rapidly responding CO2 (CD-101, Datex) S3A.) analyzers and O2 (Applied Electra-chemistry, which sa.mpled gas from the mouthpiece at 18 ml/s. Precision-analyzed gas mixtures were used for calibration of the gas analyzers. The electrical signals from these devices underwent analog-to-digital conversion, appropriate time alignment, and computer analysis (Tektronix, 4052) for the on-line breath-by-breath determination of expired ventilation (VE), CO2 output ([email protected]
), O2 uptake (VO,), respiratory exchange ratio (R), ventilatory equivalents for Co2 and 02 (VE/k02, vE/'T;T02), and end-tidal Pco2 and Po2 (PETIT, and PETE,, respectively). In addition to breath-by-breath determination of these variables, computer-calculated average values for each minute of the exercise test were obtained on the basis of data collected during the last 30 s of each minute of the exercise test. The ventilation and gas exchange algorithms were validated by means of independent analysis of mixed expired gas collected during the steady state of several different work rates (rest, 50 W, 100 W, 150 W). During three of the incremental exercise tests (pretraining session and after 4 and 8 wk of training), blood was sampled from a nonheparinized Ugauge indwelling catheter which was inserted into an antecubital vein. Samples (1 ml) were taken at rest, during unloaded pedaling, and at l-min intervals thereafter. The blood was immediately deproteinized in ice cold 8% perchloric acid and stored at -5°C until analysis for lactate (14). LT was calculated as the Vo2 associated with the work load prior to that at which the venous lactate concentration increased above resting values (17). This corresponded with the onset of an exponential rise in blood lactate. VT was determined as the vo2 at which iTE/v02 displayed a systematic increase without a simultaneous increase in TjE/h02. This criterion has been reported to be the most sensitive indicator of VT (2, 3, 26). Both investigators determined VT for each of the 68 exercise tests (17 subjects; 2 pretraining tests, 4 wk, 8 wk) using the following data: 1) computer printout plot of the breath-by-breath i7E/v02 and TjE/vC02 as a function of 7j02 and 2) mean values at each work rate for vE/v02, vE/k02, and vo2 obtained by computer averaging of all breaths during the last 30 s of each work rate during the exercise test (Fig. 1 and Table 1). The VT determinations bY each investigator were made using coded photocopies of the data, thus having no knowledge of subject, group,
or date of test. The average of the two independent determinations was taken to be VT. The differences between the independent observations were in 41 cases (60.3%)
y= .92x + 104
ir0, tml=min-‘I FIG. 2. Test-retest correlation for ventilatory 1 and Test 2 refer to two pretraining incremental
groups. Additionally, when expressed as a percentage of . vo 2 max9 all groups increased LT significantly (P < 0.05). Figure 3 shows the breath-by-breath plots of i7E/7jO2 as a function of X70, and of blood lactate as a function of Tjo2 during the incremental tests pre- and posttraining for a selected subject from each group. For the subject from group 1, LT increased by 980 ml, whereas VT for this subject increased by only 335 ml after 8 wk of training. This is representative of the results obtained in group 1 in which the average posttraining increase in LT (568 ml) was over 2.5 times the increase in VT (224 ml). Further, a t test comparison of the changes in VT and LT after 8 wk of training indicated that for group 1 the increase in LT was significantly greater than the increase in VT (P < 0.05). The subject from group 2 increased LT by 1,120 ml and VT by 460 ml. By comparison, the subject from group 3 increased LT by 480 ml in contrast with a larger increase in VT (875 ml). Although the responses of the subjects selected from groups 2 and 3
The results of this study show that both continuous and interval exercise training will significantly increase VT and LT. This is the first study which has demonstrated the different responses of LT and VT to continuous and interval training. Although the three training protocols resulted in similar increases in LT (Table 3), the increase in VT after training varied substantially between groups. Whereas in groups 2 and 3 the posttraining increases in LT and VT were not significantly different from one another, this was not the case for group 1 in which the increase in LT was over 2.5 times the increase in VT. These data suggest that alterations in VT and LT are regulated by different mechanisms. Further support for this conclusion is the fact that the correlation between pre- vs. posttraining changes in VT and LT was a very low -0.13 (P > 0.05). If the two were causally linked, one would expect a much stronger correlation between the increases in VT and LT. Both LT and VT have been used as indices of a socalled “anaerobic threshold.” Problems with this term have been addressed by others (9, 10, 16, 18, 25, 26, 31), and it is evident that controversy exists with respect to both the actual determination of this physiological phenomenon as well as the very concept of an anaerobic threshold. Irrespective of both the controversy surrounding the concept of the anaerobic threshold and of arguments over nomenclature, the terms associated with the socalled anaerobic threshold (i.e., LT and VT) have proved useful in clinical exercise testing (18, 28) and as determinants of aerobic endurance performance (4,15,17,19, 20, 23). However, an important question that can be raised [and has been previously (9, 10, 16, 18, 25, 31)] is whether the two phenomena (i.e., LT and VT) are causally linked. Crucial to the anaerobic threshold model of Wasserman and co-workers (28) is the cause-effect
3. Comparison of lactate and ventilatory
LT Vo2, ml. min-l % hmax
VT Vo2, ml - min-l %
thresholds pre- and posttraining
1,464 rtr93 48.8 t3.6
1,684” t141 47.7 k3.3
2,033” 2135 58.3* t2.7
1,481 *lo2 46.2 t2.0
1,960” t136 55.2* k4.4
2,065* 286 53.4* 22.4
1,852 *168 49.4 24.1
2,168” 2218 49.8 t4.8
2,385” t136 55.4* t3.5
1,459” +80 42.2 t5.0
1,415” &60 41.1 t3.0
1,418 t147 43.7 t2.5
1,680” 2153 46.6 t2.5
1,822” tlll 47.2 t1.8
1,528 t145 40.9 t4.4
1,905” t148 44.1 t3.8
2,227*-f +155 51.3”? k3.9~
Values are means t SE (n = 5 for group 1; n = 6 for group 2; n = 6 for group 3). vo2, ventilatory O2 uptake. pretraining value. (P < 0.05). t Posttraining increase significantly greater than groups 1 and 2 (P c 0.05). .
B . 7CI =t
0 . 0 In 1
* l oQ 8 QQQ0 “A.
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*. ..‘2. . E I’.-.:
bo, [ml- m/m-’I . ..’ *. . . .. . . . I
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. . . . .
:. *. *: . : . ...:
i .-. -.
. . .*.. . ‘: .* .’ .. * . ., :.. . _’ . . - *. . t . .*.s. . .. . . . . .* . . . ‘. ’ . * *
225t 902 (mbmin-‘)
. . ‘;
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.:.* *. . . .* . .’ . .. . ‘I . . “0.. -. : .. . . ‘, . .
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. .: -.. . : .\ z ’ . * . . .s . *:. .. . .
225t [ mhnidl
25.8 [ mhnin-‘1
FIG. 3. Changes in lactate threshold and ventilatory threshold after 8 wk of training for subject selected from each of 3 training groups. For each subject, top graph is a plot of blood lactate response to incremental exercise pretraining (0) and posttraining (a). Lactate thresholds are indicated with arrows. Middle (pretraining) and bottom (posttraining)
are breath-by-breath plots of ventilatory equivalents for 02 (V$ iTo2) as a function of ventilatory O2 uptake (VO,) during the pre- and posttraining incremental exercise tests. Ventilatory thresholds are indicated by vertical lines. (See Results for further explanation and discussion.)
relationship between LT (cause) and VT (effect). Previous studies have reported that the Vo2 at which VT and LT occur are in close agreement (17, 28, 32). However, the precise nature of this relationship has recently been challenged (9, 10, 16, 25, 31). Scheen et al. (25) found that the Vo2 at which the VT was detected differed
substantially from the TO, at which the LT was determined. Hagberg et al. (10) reported that McArdle’s disease patients (who lack muscle phosphorylase) demonstrate a VT during exercise but do not exhibit a LT, thus showing that (at least in these patients) hyperventilation during exercise can occur with no increase in blood
1120 lactate levels or plasma [H+] [actually a decrease in plasma [H’] was observed]. Furthermore, there is evidence to suggest that the agreement between VT and LT is dependent upon dietary status. When incremental ergometry was performed with subjects in a glycogendepleted condition, Hughes et al. (16) reported a marked dissociation between LT and VT. Compared with normal glycogen conditions, VT decreased to a lower work load, whereas LT increased to a higher work load during exercise in the glycogen-depleted condition. The results of our group 1 provide an additional example of a dissociation between LT and VT. The data suggest that the causes of LT and VT are not the same, and when the two occur at the same work rate (VO,) it may be only coincidental. Lactic acidosis is but one of a number of factors which could influence pulmonary ventilation and hence be a cause of VT (18, 29). Increased ventilation during exercise may result from nonhumoral stimuli originating in active muscle or in the brain, thus having a neurogenic origin (10, 29). It is beyond the purpose of this paper to address the complex range of possible mechanisms associated with the control of ventilation. However, our results indicate that noninvasive ventilatory parameters (VT) cannot always be used to reflect accurately the onset of blood lactate accumulation (LT). Furthermore, our results demonstrate that VT and LT cannot be used interchangeably as indices of training adaptations. There are several possible mechanisms by which LT could be increased as a result of endurance training. Included among these are 1) enhanced O2 delivery to working skeletal muscle fibers, 2) biochemical alterations within skeletal muscle which would enhance oxidation of pyruvate and reduce lactate formation (l5), 3) increased rate of lactate clearance from the blood during exercise (5), and 4) diminished catecholamine release during submaximal exercise intensities after training (30), which would decrease stimulation of glycogenolysis during exercise (22). Both LT (17) and VT (23) have been reported to be significantly correlated with muscle oxidative capacity. It is known that the biochemical adaptations in slowtwitch and fast-twitch muscle fibers are not the same for continuous and interval exercise traini .ng (6, 12). Studies on rats indicate that interval training increases the oxidative capacity of slow-twitch and fast-twitch fibers (6). In one study o n humans, Henricks son and Reitman (1.2) reported that interval training of a similar protocol to that used in this study did not result in adaptation in slow-twitch fibers but did increase the oxidative capacity of the fast-twitch fibers. Since all groups increased LT to a similar extent, and because it is probable that skeletal muscle bioch .emical adaptations were different in the three groups (6, 12), it is likely that the elevation in LT observed in our subjects was due to factors other than, or in addition to, alterations in skeletal muscle oxidative capacity. Another alternative .for explaining the similar training-induced adaptations in LT among the three groups is that a similar reduction in catecholamine-induced glycogenolysis may have occurred in the three groups.
D. C. POOLE
G. A. GAESSER
Glycogenolysis in skeletal muscle is stimulated by epinephrine (22), which also enhances the release of lactate from muscle to blood (22). Since the catecholamine response to submaximal exercise is decreased by >50% within the initial 3 wk of exercise training (30), it is possible that a diminished catecholamine response at submaximal exercise intensities may be partially responsible for the delayed blood lactate response to incremental work following training which we observed in this study. However, it is not likely that the increase in LT could be attributed entirely to a diminished catecholamine response. In the study of Winder et al. (30), a lower posttraining exercise blood lactate level was associated with a reduced catecholamine respon .se at a given absolute work rate, whereas at the same relative work rate significantly higher catecholamine levels were associated with an unchanged blood lactate (compared with pretraining). The influences of exercise-training intensity, duration, and frequency on alterations .n the catecholamine responses to exercise are unknown The speculation that the alterations in LT which we observed in our subjects after training could be due in part to changes in a catecholamine threshold during exercise remains to be established. Although LT was not further enhanced by training at high intensities (which presumably results in recruitment of more fast-twitch fibers), this was not the case for VT. Although LT may be determined primarily by metabolic factors regulating lactate production and removal (5, 15, 17, 22), VT may be regulated by factors of both metabolic and neurogenic origin (29). However, the precise nature of the interplay between neural and humoral factors and their con .trol of the exerci .se hyperpnea is currently undetermined (29 ). Therefore, the postulation of any neural mechanism by which the recruitment and training of fast-twitch fibers could affect VT would be mere speculation. It has been reported that the improvement of aerobic capacity with training is related to the intensity and duration of the training sessions (21). However, the finding of a similar increase in Tjozrnax with groups of subjects who trained at markedly different exercise intensities is not without precedent (8). The substantial increase in VO 2maxin group 3 (570 ml 02. min-l) contrasts with the data of Henricksson and Reitman (12), who reported that 8 wk of interval training (5 X 4 min at -100% vo2 max, 3 days/wk) did not increase Vo2max. However, there were only four subjects in their interval training group, and two of the subjects had very high initial aerobic capacities. Our data are in agreement with Fox (7) and indicate that interval training (as described herein) is just as effective as continuous training in elevating V02 max. The fact that in the present study all three groups increased VO 2max and LT significantly, and to approximately the same extent, challenges the suggestion of Kindermann et al. (19, p. 32) that “the optimal load intensity for endurance training should be in the range of the ‘aerobic-anaerobic threshold’ of 4 mmol/l lactate.” Our data demonstrate that low-intensity training, which results in minimal elevation in blood lactate during ex-
ercise (52 ml), is sufficient to significantly improve . vo 2 max9 LT, and VT. Interval training, which undoubtedly results in exercise blood lactate concentrations in the range of lo-20 mM, also results in substantial improvements in vO2 max, LT, and VT. Thus we find little evidence to suggest that optimal load intensities for endurance exercise may be determined on the basis of the blood lactate response during the training sessions. In conclusion, our data indicate that with respect to endurance exercise-training protocols (as described herein), interval training is more effective than continuous training in augmenting VT, but both types of training appear to be equally effective in altering LT. That training can induce a greater increase in LT than VT
(group I) suggests that these two physiological phenomena are subject to regulation by different mechanisms. Finally, our data demonstrate that LT and VT cannot be used interchangeably as indices of training adaptations. The authors thank B. Gardner, L. Havicon, P. McDonald, and R. Rich for technical assistance and V. Reggie Edgerton for his critique of the manuscript. We extend a special note of thanks to Dr. Susan Ward and the Dept. of Anesthesiology, UCLA, for support and for use of laboratory space. This research was supported in part by a grant-in-aid from the American Heart Association, California Affiliate. Received
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