Recovery from maximal effort exercise: lactate disappearance and subsequent performance.

Recovery from maximal effort exercise: lactate disappearance and subsequent performance ARTHUR Exercise

WELTMAN, BRYANT A. STAMFORD, AND CHARLES FULCO Physiology Laboratory, University of Louisville, Louisville, Kentucky 40206

WELTMAN,ARTHUR,BRYANT A. STAMFORD,AND CHARLES Recovev from maximal effort exercise: Lactate disappearance and subsequent performance. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47(4): 677-682, 1979.-The effects of differing recovery patterns following maximal exercise on blood lactate disappearance and subsequent performance were examined. Nine subjects completed four randomly assigned experimental sessions. Each session consisted of a 5-min maximal effort performance test conducted on a Monark bicycle ergometer (T1) followed by 20 min of recovery and a second 5 min maximal effort performance test (T2). Blood lactate levels were measured during min 5,10,15, and 20 of recovery. Recovery patterns consisted of passive recovery (PR), active recovery below anaerobic threshold (AR c AT), active recovery above anaerobic threshold (AR > AT), and active recovery above anaerobic threshold while breathing 100% oxygen (AR > AT + 02). Blood lactate levels prior to T2 were significantly different across treatments (P < 0.05). Comparison among treatments and between T1 and T2 revealed no significant differences in work output. It was concluded that while lactate disappearance following severe exercise can be affected by varying the recovery pattern, elevated levels of blood lactate exert no demonstrable effect on maximal effort performance of 5-min duration. FULCO.

work drop-off; anaerobic ergy metabolism

threshold;

maximal

performance;

en-

RESULTS OBTAINED from several investigations suggest that work performance may be adversely affected by elevated blood lactate levels (12, 15, 21, 22). Because intense muscular exercise results in the production of lactic acid (7), which may inhibit the rate of glycolysis (8, 13) as well as the mobilization of free fatty acids (lo), removal of lactate from the blood after high-intensity exercise is thought to be critical for subsequent performance. As a result, numerous reports have appeared concerning the effects of various recovery protocols on blood lactate disappearance following maximal exercise (1,2,5, 7, 20). Unfortunately, these studies have failed to examine the effects of varying degrees of blood lactate disappearance on subsequent performance. The purpose of the present investigation was to determine the efficacy of various recovery protocols with respect to blood lactate disappearance and subsequent performance of maximal effort exercise. METHODS

Nine males volunteered as subjects. Mean age was 25.8 OlSl-7567/79/0000-OOOO$O1.25

Copyright

0 1979 the American

Physiological

t 4.7 yr and mean height and weight were 179.7 t 9.8 cm and 81.9 t 12.5 kg, respectively. Each subject completed a discontinuous maximal oxygen uptake (Vo, max)test on the bicycle ergometer. Pedaling rate was maintained at 60 rpm and resistance was progressively increased. An alternating 3-min work and 3-min rest regimen was continued until the subject could not complete a given work bout. A plateau in oxygen uptake (Voz) between progressive loads indicated that ~oZ maxhad been reached (23). During each rest period an antecubital venous blood sample was taken. The samples were analyzed later for lactate concentration using an enzymatic technique (9) so that the anaerobic threshold (AT) could be determined (4, 26). AT was defined as a significant elevation of blood lactate above resting level during the incremental VO2 maxtest. The highest work rate attained on the bicycle ergometer during the VOW maxtest was recorded for each subject. On four separate occasions subjects completed two maximal 5-min work tests (Tl, Ta) at the above work rate on the Monark friction-type bicycle ergometer. Each test was separated by randomly assigned 20-min recovery protocols. Blood samples for determination of lactate concentration were taken at rest, prior to initiation of testing, and at min 5, 10, 15, and 20 of recovery. The recovery patterns consisted of the following. I) Passive recovery (PR), sitting quietly on a chair at bike level. 2) Active recovery below AT (AR c AT), pedaling at a work rate not associated with significant elevation in blood lactate concentration above the resting concentration of 1.3 mM (approx 40% Tj02 max). Base-line blood lactate concentration at this work rate was 1.9 mM. Baseline blood lactate concentration was determined on separate days from 20 min of work at the prescribed recovery rate, without prior exercise. 3) Active recovery above AT (AT > AT), pedaling at a work rate associated with significant elevation in blood lactate concentration above resting concentration (approx 65% VO2 max).B ase-line blood lactate concentration at this work rate was 3.5 mM. 4) Active recovery above AT with oxygen (AR > AT + 02), pedaling at the same work rate as AR > AT while breathing 100% oxygen. Base-line blood lactate concentration at this work rate (1.9 mM) was not significantly different from resting blood lactate concentration. Subjects were naive concerning the gas mixtures utilized during the recovery periods. The gas breathed during all recovery conditions was directed to the subject from a Society

677

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678

WELTMAN,

Tissot tank and gas tanks used were kept out of view of the subject. Subjects performed active recovery sessions on an electric bicycle. The electric bicycle was utilized during recovery to ensure the fact that work rate was maintained at the proper level without the confounding effects of inaccurate pedaling rates. Experimental sessions were conducted at the same hour of the day for each individual subject with 1 wk allowed between each session. The maximal performance test was modified from the maximal effort model for measuring endurance performance first presented by Henry and Kleeberger (6). This technique requires subjects to attempt to maintain some predetermined work rate for a constant duration. In the present study the initial work rate was the highest attained on the Vo2 maxtest and the duration was 5 min. As individual subjects are forced to reduce pedaling rate during the performance, those who reduce pedaling rate the most will accomplish the least amount of work and hence be lowest in endurance. Because all subjects perform work for the same predetermined duration, the total amount of work done by each subject is the mathematical integral under the work performance or drop-off curve (Fig. 1). For example, line AB represents 100%endurance whereas lines AC and AD represent varying amounts of work drop-off. Significant decreases in pedaling rate, using the above protocol, were expected based on previous data using a similar test procedure (29). Test-retest reliability of endurance scores (total work output) using this model has been reported to be r = 0.87 (14). A microswitch mounted to the frame of the bicycle counted pedal revolutions and allowed calculation of work output. Pedaling rate was initiated at 75 rpm and each subject was instructed to maintain the initial pedaling rate set by a metronome for the full duration of the test. The proper resistance was set within 2 s from the command “go.” When the subject dropped below the prescribed pedaling rate he was exhorted to increase the rate. \ioz, ventilation (\jE at BTPS), respiratory exchange ratio (R), carbon dioxide output (hoz), heart rate (HR), and pedal revolutions were measured during all maximal performance tests. Open-circuit spirometry methods were utilized for the collection of metabolic data. Inspired ventilatory volume was measured via a dry gas meter (Parkinson-Cowan CD4) that had been previously calibrated against a 600-liter Tissot gasometer. Expired air

TIME 1. Measurement performance. See text FIG.

of endurance for d .etails.

using

a maximal

effort

model

of

STAMFORD,

AND

FULCO

was channeled from a breathing valve (Collins triple J) through low-resistance plastic tubing to a 5-liter gas mixing chamber. Samples of expired gas were pumped via a high-speed varistaltic pump (Manostat) from a Costill- Wilmore gas collection apparatus to oxygen (Beckman OM-11) and carbon dioxide (Beckman LB-2) gas analyzers. Analyzers were frequently calibrated with commercially prepared gas mixtures verified with the Lloyd-Haldane gas analyzer. HR response was recorded electrocardiographically. Separate 4 X 5 X 9 factorial analysis of variance (ANOVA) with repeated measures on the last two factors was used to determine statistical significance (P < 0.05) for the dependent variables pre- and postrecovery. The factors examined were the four recovery patterns and five levels of time (min-by-min for 5 min) within nine subjects. Paired t tests were utilized to determine significant differences between T1 and Tz dependent variables for the two maximal performance tests. Blood lactate data were analyzed by a 4 x 4 x 9 (time (5, 10, 15, and 20 min of recovery) x condition x subject) factorial ANOVA with repeated measures on the last two factors. The Scheffe contrast method was used for post hoc analysis. RESULTS

For the analyses of lactate disappearance and subsequent performance to be meaningful, all initial (Tl) maximal performance tasks must be similar in terms of work performed. This was the case as no significant differences in minute-by-minute (Fig. 2) or total pedal revolutions, and therefore, external work were found. Figure 2 also shows the min-by-min pedal revolution scores for the second maximal effort test (Tz). There were no significant differences in minute-by-minute or total pedal revolutions among the treatment groups during Tz. Comparison of T1 and Tz pedal revolution scores revealed no significant differences in either min-by-min or total pedal revolution scores. The highest observed SE was only k3.6 revolutions. Therefore, the lack of statistical significance was not due to high variability. The only significant main effect observed was a drop-off in pedal revolutions over time. Total drop-off through the 5-min work period was 10.2 and 11.1% for T1 and Tz, respectively. Blood lactate concentration significantly decreased with time during recovery (Fig. 3). Main treatment effects revealed recovery during hyperoxia (AR > AT + 02) resulted in significantly greater lactate disappearance than did PR and AR > AT. AR < AT was not significantly different from the other three treatments. A significant interaction between time and conditions also existed. At min 5, the AR > AT + 02 treatment resulted in significantly lower blood lactate levels than all other treatments with the exception of PR. At min 10 the AR > AT + 02 condition resulted in significantly lower blood lactate levels than all other treatments. At min 15 and 20 all treatment comparisons for blood lactate with the exception of AR < AT vs. AR > AT + 02 were significantly different. VoZ data for the first and second performance tests are presented in Fig. 4. Comparisons within T1 and Tz re-


BLOOD

LACTATE

DISAPPEARANCE

AND

MAXIMAL

679

PERFORMANCE

2. Mean T1 and T2 min-by-min 9. Highest observed SE was t3.6

FIG. n=

revolution revolutions.

scores;

60 I I

PRE- RECOVERY

TIME

(MINUTES)

I 2

POST-

I

I

I

3

4

5

RECOVERY

vealed an increase in Voz over time. During T1 significant differences in v02 over time were evident at all levels with the exception of min 4 vs. 5. During T2 only the v02 value for min 1 was significantly lower than all other v02 values. Comparison of the T1 vs. T2 ~oZ values revealed significantly higher Vo2 values during min 1 and 2 of the second test. From min 3 on, no significant differences were observed. Comparison of total Voz revealed no significant differences among treatments during either T1 or Tz. Examination of T1 vs. T:! cumulative Vop revealed significantly greater cumulative oxygen consumption during TZ (T1 = 14.38 liters 02, T2 = 15.46 liters 02, P < 0.05). No significant differences existed between the highest ~oZ attained during each of the eight T1 and T2 tests and VOW maxattained initially with the discontinuous protocol. During T1 the only significant differences found for Vcoz, TE, R, and HR were increases over time (Fig. 5). During Tz significant increases in all the above variables over time as well as treatment effects were observed. Vcoz, VE, and R during PR were significantly lower during min 3, 4, and 5 of Tz. Cumulative VCO~ was also significantly lower during T2. VE was significantly higher during min 1 of Tz. From min 2 on, no significant differences in VE were noted between T1 and Tz. Comparison of T1 vs. Tz R values indicated that at each minute the second performance test resulted in significantly lower R values. HR values were significantly higher at each time interval during TZ as compared to T1. DISCUSSION

The major finding association between formance. Although sulted in significantly to Tz (Fig. 3), there minute or total work

of the present study was the lack of blood lactate concentration and perthe four recovery treatments redifferent blood lactate levels prior were no differences in minute-byoutput (Fig. 2). Further, minute-by-

\\\8 f 4

,-*

= PR

,m-+= ---4 B-v--.+

--l-I

AR
AT =AR>AT+

5

IO TIME

FIG.

recovery

r\;I. .IMean treatments

02

I-5

2-o

(MINUTES)

-+ SE differences in blood over time; n = 9.

lactate

levels

during

four

minute and total work output attained during T2 were not significantly different from T1 (Fig. 2). These data indicate that elevated blood lactate concentration is not detrimental to maximal effort performance. Similar findings have been reported for anaerobic work performance of l-min duration (30). The present data contradict several previous studies


680

WELTMAN,

STAMFORD,

AND

FULCO

4--,

B

t D

3 -:

FIG.

#

Highest

4. Mean observed

TI and Tg min-by-min SE was k0.16 liter.

$kz values;

n = 9.

+ =PR Q = AR AT * =AR>AT+

I

I

I PRE-

I

2

02

I

3

RECOVERY

I

I

4

5 TIME

(MINUTES)

I

2

3

4

5

POST-RECOVERY

that indicate that work performance is inhibited when blood lactate levels are elevated due to severe prior exercise (12, 15, 21, 22). The previous studies used fixed work rate testing to measure performance. During fixed work rate testing subjects are limited by their inability to maintain the prescribed rate. It is difficult to compare results using fixed work rate testing with the present findings because drop-off was permitted in the present study. Further, recovery times used in the fixed work rate studies were much shorter than 20 min. Data of the present study indicate that lactate disappearance was enhanced when exercise was imposed during recovery (Fig. 3). These data are in agreement with studies from our laboratory (20, 30) as well as several other reports (1, 2, 5, 7). While the mechanism for enhanced lactate disappearance during activ -e recovery from strenuous exercise is unknown, it seemsreasonable that an important mechanism for lactate disappearance is the oxidation of lactate in skeletal muscle. Data supporting this hypothesis come from studies of in situ dog muscle preparations (18, 28), intact rats (3), and exercising humans (11). The present data reveal that exercise recovery at a work level below anaerobic threshold (AR < AT) is more effective, with respect to lactate disappearance, than exercise recovery above anaerobic threshold (AR > AT). This occurred even though muscle blood flow was presumably higher above AT. Differences observed between AR conditions below and above anaerobic threshold may be explained by expected differences in base-line lactate production and splanchnic blood flow. The base-line blood lactate concentration for the AT treatment (3.5 mM) was significantly greater than the resting concentration. These differences in base-line blood lactate levels may have affected lactate disappearance. Splanchnic

blood flow must also be considered. It is known that splanchnic blood flow decreases with physical exercise (16). Further, this reduction of splanchnic blood flow is related to the intensity (%Vo, max)of exercise. Because the splanchnic region represents an important lactate removal site (17), reduction of splanchnic blood flow could be detrimental to lactate disappearance. The most effective lactate disappearance pattern was exercise recovery above the anaerobic threshold while breathing oxygen (AR > AT + 02). Recent data have indicated that oxygen inhalation does not increase oxygen delivery to exercising muscles (27). As such, hyperoxia should not affect lactate disappearance at the actively recovering muscles. Therefore, it is postulated that hyperoxia increased lactate removal in the splanchnic region and in the nonactively working muscles. The findings of increased cumulative Voz during Tz were primarily due to increased VO, during min 1 and 2 (Fig. 3). This may be due to an increased base-line v02 as a result of severe prior exercise and/or imposed recovery patterns. The greater VOWduring T2 may suggest a higher aerobic component when compared to T1. However, total energy cost of the two tests cannot be determine d from Vo2 and bl.ood lactate concentration. Expected alterations in gas exchange characteristics as a result of elevated blood lactate did not occur. Wasserman and Whipp (24, 25) suggest that buffering of lactic acid by bicarbonate will produce CO* in addition to that produced metabolically and that this increased COa delivery to the lung increases ho2 and drives VE. In the present study \j~ was not different for T1 vs. T2. However, ho2 and R were both significantly reduced during Tz (Fig. 5). Because the acid-base status of the subjects was not measured we can only speculate a.sto the mechanism responsible for these findings. Lactic acid produced during T1 was most likely buffered by bicarbonate, thus reducing the bicarbonate stores. During T2 not as much bicarbonate would be available for buffering additional


BLOOD

LACTATE

DISAPPEARANCE

AND

MAXIMAL

PERFORMANCE

(Sella) NOllV7llN3A

+.

* +a

*m* +

** **

*

5. Mean T1 and Tz min-by-min VE, for VE, &OZ, HR, and R, respectively.

FIG.

units

+ *+ .

%k02,

HR,

and R; n = 9. Highest

observed

SE were

t7.3

liters,

to.17

liter,

t3.4

beats,

and ~10.06 R


682 lactic acid. Therefore, less nonmetabolic CO2 would be produced and ho2 and R would be reduced. The subject would however, be more acidotic, which would stimulate ventilation. This could effect, when comparing T1 and TP, a decrease in VCO~ and R without any change in VE, a result consistent with our observations (Fig. 5). In summary, the present results indicate 1) elevated blood lactate levels have little effect on maximal effort exercise of 5-min duration; 2) exercise recovery following severe exercise will result in enhanced lactate disappearance; 3) exercise recovery below AT is more effective for

WELTMAN,

STAMFORD,

AND

FULCO

lactate disappearance than exercise recovery above AT; and 4) exercise recovery in hyperoxia performed above AT significantly enhances lactate disappearance. The authors scientific review

manu?ript* This research Arts

and Sciences

Received

thank Drs. L. B. Gladden and of this research and their helpful

R. Stremel suggestions

was supported in part by a University Faculty Research Grant.

26 October

1978; accepted

in final

form

10 May

for their with the

of Louisville

1979.

REFERENCES 1. BELCASTRO, A. N., AND A. BONEN. Lactic acid removal rates during controlled and uncontrolled recovery exercise. J. Appl. PhysioZ. 39: 932-936, 1975. 2. BONEN, A., AND A. N. BELCASTRO. Comparison of self-selected recovery methods on lactic acid removal rates. Med. Sci. Sports 8: 176-178, 1976. 3. BROOKS, G. A., K. E. BRAUNER, AND R. G. CASSENS. Glycogen synthesis and metabolism of lactic acid after exercise. Am. J. PhysioZ. 224: 1162-l 168, 1973. 4. DAVIS, J. A., P. VODAK, J. H. WILMORE, I. VODAK, AND P. KURTZ. Anaerobic threshold and maximal aerobic power for three modes of exercise. J. Appl. Physiol. 41: 544-550, 1976. 5. GISOLFI, C., S. ROBINSON, AND E. S. TURRELL. Effects of aerobic work performed during recovery from exhausting work. J. AppZ. Physiol. 21: 1767-1772, 1966. 6. HENRY, F. M., AND F. N. KLEEBERGER. The validity of the pulseratio test of cardiac efficiency. Res. Q. Am. Assoc. HeaZth Phys. Educ. Retreat. 9: 32-46, 1938. 7. HERMANSEN, L., AND I. STENSVOLD. Production and removal of lactate during exercise in man. Acta Physiol. Stand. 86: 191-201, 1972. 8. HILL, D. K. Anaerobic recovery of heat. J. Physiol. London 98: 460-467, 1940. 9. HOHORST, H. J. Laktat Bestimmung mit Laktat-dehydrogenase und DPN. In: Methods of Enzymatic Analysis. Weinheim: Verlag Chemie, 1962, p. 266. 10. ISSEKUTZ, B., JR., AND H. I. MILLER. Plasma free fatty acids during exercise and the effect of lactic acid. Proc. Sot. Exp. BioZ. Med. 100: 237-243, 1962. 11. JORFELDT, L. Metabolism of L (+) lactate in human skeletal muscle during exercise. Acta Physiol. Stand. Suppl. 338, 1970. 12. KARLSSON, J., F. BONDE-PETERSON, J. HENRIKSSON, AND H. G. KNUTTGEN. Effects of previous exercise with arms or legs on metabolism and performance in exhaustive exercise. J. AppZ. PhysioZ. 38: 763-767, 1975. 13. KARLSSON, J., L. D. NORDESJO, L. JORFELDT, AND B. SALTIN. Muscle lactate, ATP, and CP levels during exercise after physical training in man. J. AppZ. Physiol. 33: 199-203, 1972. 14. KATCH, V. L., AND F. I. KATCH. Reliability, individual differences and intravariation of endurance performance on the bicycle ergometer. Res. Q. Am. Assoc. HeaZth Phys. Educ. Retreat., 43: 31-38, 1972. 15. KLAUSEN, K., H. G. KNUTTGEN, AND H. FORSTER. Effect of preexisting high blood lactate concentration on maximal exercise performance. Stand. J. CZin. Lab. Inuest. 30: 415-419, 1972. 16. ROWELL, L. B., J. R. BLACKMAN, AND R. A. BRUCE. Indocyanine green clearance and estimated hepatic blood flow during mild to

17.

18. 19.

20.

21.

22.

23.

24. 25. 26.

27.

28.

29.

30.

maximal exercise in upright man. J. CZin. Invest. 43: 1677-1690, 1964. ROWELL, L. B., K. KRANING, T. EVANS, J. KENNEDY, J. R. BLACKMON, AND F. KUSUMI. Splanchnic removal of lactate and pyruvate during prolonged exercise in man. J. AppZ. Physiol. 21: 1773-1783, 1966. STAINSBY, W. N., AND H. WELCH. Lactate metabolism of contracting dog skeletal muscle in situ. Am. J. PhysioZ. 211: 177-183, 1966. STAMFORD, B. A. Step increment versus constant load tests for determination of maximal oxygen uptake. Eur. J. AppZ. Physiol. Occup. Physiot. 35: 89-93, 1976. STAMFORD, B. A., R. J. MOFFATT, A. WELTMAN, C. MALDONADO, AND M. CURTIS. Blood lactate disappearance following supramaximal one-legged exercise. J. AppZ. Physiol.: Respirat. Environ. Exercise PhysioZ. 45: 244-248, 1978. STAMFORD, B. A., R. ROWLAND, AND R. J. MOFFATT. Effects of severe prior exercise on assessment of maximal oxygen uptake. J. AppZ. Physiol.: Respirat. Environ. Exercise Physiol. 44: 559-563, 1978. STAMFORD, B. A., A. WELTMAN, R. J. MOFFATT, AND C. FULCO. Effects of severe prior exercise on assessment of maximal oxygen uptake during one versus two-legged cycling. Res. Q. Am. Assoc. HeaZth Phys. Educ. Retreat. 47: 363-371, 1978. TAYLOR, H. L., E. R. BUSKIRK, AND A. HENSCHEL. Maximal oxygen intake as an objective measure of cardio-respiratory performance. J. AppZ. PhysioZ. 8: 73-80, 1955. WASSERMAN, K. Breathing during exercise. N. EngZ. J. Med. 298: 780-785, 1978. WASSERMAN, K., AND B. J. WHIPP. Exercise physiology in health and disease. Am. Rev. Respir. Dis. 112: 219-249, 1975. WASSERMAN, K., B. J. WHIPP, S. N. KOYAL, AND W. L. BEAVER. Anaerobic threshold and respiratory gas exchange during exercise. J. AppZ. PhysioZ. 35: 236-243, 1973. WELCH, H. G., F. BONDE-PETERSEN, T. GRAHAM, K. KLAUSEN, AND N. SECHER. Effects of hyperoxia on leg blood flow and metabolism during exercise. J. AppZ. Physiol.: Respirat. Environ. Enercise Physiol. 42: 385-390, 1977. WELCH, H. G., AND W. N. STAINSBY. Oxygen debt in contracting dog skeletal muscle in situ. Respir. Physiol. 3: 229-242, 1967. WELTMAN, A., V. KATCH, AND S. SADY. Effects of increasing oxygen availability on bicycle ergometer endurance performance. Ergonomics 21:427-438, 1978. WELTMAN, A., B. A. STAMFORD, R. J. MOFFATT, AND V. L. KATCH. Exercise recovery, lactate removal, and subsequent high intensity exercise performance. Res. Q. Am. Assoc. HeaZth Phys. Educ. Retreat. 48: 786-796, 1977.


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