Acta Physiol Scand 1981, 112: 215-217

Onset of blood lactate accumulation after prolonged exercise

IRA JACOBS, BERTIL SJODIN,’ PETER KAISER and JAN KARLSSON Laboratory for Human Performance, Department of Clinical Physiology, Karolinska Hospital, Stockholm and ‘National Defense Research Institute (FOA 545). Stockholm

The performance of submaximal exercise in a con- tinuously step-wise increasing manner enables the determination of the “onset of blood lactate ac- cumulation” (OBLA) (Mader et al. 1976, Kinder- mann, Simon & Keul 1979, Sjodin & Jacobs 1981). OBLA depends upon a number of factors including muscle fiber type distribution, the capacity of the circulatory apparati, capillary density (Farrell et al. 1979, Ivy et al. 1980, Sjodin & Jacobs 1981) enzyme activities (authors’ pers. comm.) and the response of these factors to training.

Significantly lower blood lactate concentrations, compared to a control situation, have been re- peatedly observed when high intensity exercise is performed subsequent to prolonged exercise (As- trand et al. 1963, Saltin & Hermansen 1967, Karlsson 1971). A similar observation has been re- cently reported regarding muscle lactate (Jacobs 1981). In this regard markedly reduced intramuscu- lar glycogen stores and/or an increased oxidation of lactate have been implicated. In an attempt to clarify factors which may influence OBLA, 7 male runners were examined 1 week before, immediately (within 60 min) after, and 2 weeks following their participation and completion of the Stockholm Marathon, 1980. Their age, height, weight, maximal oxygen consumption (VO, max) during treadmill running, muscle fibre type distribution in m. vastus lateralis and mean marathon time averaged (range) respectively: 34.7 (2742) yrs, 176 (170-183) cm, 65.5 (55-71) kg, 62.5 (55-71) ml O,xkg-’xmin-’, 40.9 (28-64)% FT, 3.28 (2.54.4) h.

During each visit the exercise intensity at OBLA was determined as previously described (Sjodin & Jacobs 1981). Briefly, following a warm-up subjects ran for 4 min at each of 4 different velocities. During the last minute at each velocity expired gases were collected (Douglas bag procedure) and analyzed for the determination of oxygen consumption and the

ventilatory exchange ratio (R). During the last 30 s at each velocity finger-tip blood was sampled for blood lactate determination (Strom 1949). The rela- tionship between blood lactate concentration and treadmill running velocity was used to calculate the velocity at which a blood lactate concentration of 4 mmolxl-’ would occur (VOBLA). The changes in VoBI.A are depicted in Fig. 1. Subjects were not able to raise blood lactate levels when the test protocol was administered immediately after the marathon. Perceived exertion at the initial running velocities was higher than during the control experiments, thus the entire protocol could not be completed nor could OBLA be determined. Two weeks following the marathon the lactate-velocity curve was shifted to the right. A significantly greater running velocity was required to elicit the OBLA as compared to before the marathon (4.31 k0.47 vs. 4.17f0.54 mxs-’, meankS.D., p<O.OI). The difference exhibited in Fig. 1 is typical of differences as- sociated with training status (MacDougall 1977) and would seem to indicate an improved endurance capacity two weeks after the marathon. Usually such differences are considered to be reflective of an enhanced fat combustion at higher absolute exercise levels therebye inducing a “glycogen spar- ing” effect. The respiratory R was reduced only immediately after the marathon but was higher two weeks later as compared to the pre-marathon values (Fig. I ) . These lower blood lactate levels taken together with the increased respiratory R two weeks after the marathon may be explained on the basis of an increased utilization of blood lactate. In this manner blood lactate concentration would be reduced in spite of an increased relative contribu- tion of carbohydrates to the metabolic demands of the exercise.

Reduced lactate production and/or accumulation when high intensity exercise is performed im-

216 I . Jacobs et al.

5 1 I

10 -

0 d

3 ‘ (19- K

Bdora 1 Irnrndiotaly oftar 0 Two waahs oftar

I 1 I 35 ko 4.5

i, Vetocity. m us-’

Fig. 1 . Upper panel: The relationship of blood lactate concentration to treadmill running velocity before (0- 0). immediately after (x-x), and two weeks after ( 0 4 ) a marathon competition. The velocity corresponding to a lactate concentration of 4 mmolx 1 - I (VoSu) is indicated (*p<0.02). Values are expressed as the mean (S.D.) of 7 subjects. Lower panel: The ventilatory exchange ratio (R) at two running velocities before, immediately after, and 2 weeks after (legends as above) a marathon competition. Values are expressed as means (S.D.). The “immediately after” and “two weeks after” values are significantly dif- ferent (p<0.05) from the control values only at the slower velocity.

mediately after prolonged exercise, is well estab- lished. A similar phenomenon was observed in the present study even two weeks following a marathon race and this has not been previously reported to our knowledge. The acute effects of prolonged exercise include a greater relative energy derivation from fat combustion (Pernow & Saltin 1971) and possibly, as discussed above, an increased utiliza- tion of blood-borne lactate when subsequent exer- cise is performed. Gollnick et al. (1981) have ob- served that lactate is extracted from blood by a leg

Actcr Physiol Sccrnd I I2

with depleted glycogen stores during exercise even 24 h after the depletion. As the decrements in blood lactate concentrations in the present study were observed over a two week duration it is difficult to suggest that a decreased glycolytic potential is im- plicated. However, this may be valid with regard to the inability to raise blood lactate concentrations immediately after the race. In this situation it can be assumed that muscle glycogen concentrations are extremely depleted (Costill et al. 1971) and this may directly or indirectly affect lactate production (As- mussen et al. 1974, Jacobs 1981). There is a paucity of data presently available in support of our hypothesis of an increased lactate utilization during exercise subsequent to prolonged exercise. The present data, however, are interpreted as being in- dicative of such a phenomenon.

The technical assistence of Dr Angela Smith and K. Elwin is gratefully acknowledged. This study was supported par- tially by a grant from the Research Council of the Swedish Sports Federation, the Swedish Medical Research Council (No. 4251), and by a grant from the Swedish National Defense Research Institute (570-5056:2 & 01G-5197:4) to Prof. G. Borg.

REFERENCES ASMUSSEN, E., KLAUSEN, K., NIELSEN. L.,

TECHOW, 0. I& TONDER, P. 1974. Lactate produc- tion and anaerobic work capacity after prolonged exercise. Acta Physiol Scand 90: 731-742.

ASTRAND, P.-0.. HALLBACK, I., HEDMAN, R. & SALTIN, B. 1%3. Blood lactates after prolonged se- vere exercise. J Appl Physiol 18: 619-622.

COSTILL, D. L., BOWERS, R., GRANAM, G. & SPARKS, K. 1971. Muscle glycogen utilization during prolonged exercise on successive days. J Appl Physiol 31: 834-838.

LING, J. & COSTILL, D. L. 1979. Plasma lactate accumulation and distance running performance. Med Sci Sports 11: 338-344.

GOLLNICK, P. D., PERNOW, B., ESSkN, B., JANSSON, E. & SALTIN, B. 1981. Availability of glycogen and plasma FFA for substrate utilization in leg muscle of man during exercise. Clin Physiol 1 : 27- 42.

IVY, J., WITHERS, R., VAN HANDEL, P., ELGER, D. & COSTILL, D. L. 1980. Muscle respiratory capacity and fiber type as determinants of the lactate threshold. J Appl Physiol: Respirat Environ Exercise Physiol

JACOBS, I. 1981. Lactate concentrations after short, maximal exercise at various glycogen levels. Acta Physiol Scand 1 1 1 : 465469.

KARLSSON, J. 1971. Lactate in working muscles after prolonged exercise. Acta Physiol Scand 82: 123-130.

FARRELL, P. A., WILMORE, J., COYLE, E., BIL-

48: 523-527.

Blood lactate after prolonged exercise 217

KINDERMANN, W., SIMON, G. & KEUL, J. 1979. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endur- ance training. Eur J Appl Physiol 42: 25-34.

McDOUGALL, J. D. 1977. The anaerobic threshold: its significance for the endurance athlete. Can J Appl Sport Sci 2: 137-140.

MADER, A., LIESEN, H., PHILIPPI, H., ROST, R., SCHURCH, P. & HOLLMAN, W. 1976. Zur Beur- teilung der sportartspezifischen Ausdauerleis- tungsfahigheit im Labor. Sportarzt Sportmed 27: 80- 88.

PERNOW, B. & SALTIN, B. 1971. Availability of sub- strates and capacity for prolonged heavy exercise for man. J Appl Physiol31: 416-422.

SALTIN, B. & HERMANSEN, L. 1%7. Glycogen stores and prolonged severe exercise. In: Symposia of the Swedish Nutrition Foundation V (ed. G. Blix), vol. V, pp. 32-46. Almqvist & Wiksell, Uppsala.

SJODIN, B. & JACOBS, I. 1981. Onset of blood lactate accumulation and marathon running performance. Int J Sports Med 2: 23-26.

STROM, G. 1949. The influence of anoxia on lactate utilization in man after prolonged muscular work. Acta Physiol Scand 17: 440-451,

Arlcr Physiol Scund 112