science 2017-03-28T22:21:17+00:00

Back in the day, many of us were taught lactic acid is only “a caustic waste product”. That’s not what they teach these days. New York Times health writer Gina Kolata’s May 2006 article, “Lactic Acid Is Not Muscles’ Foe, It’s Fuel” will help bring you up to date. She quotes University of California, Berkeley’s Dr. George Brooks and Auburn University’s Dr. Bruce Gladden, the top minds on the subject in the U.S., if not the world. You’ll see these names again in several of the clinical research citations below.

Lactate, commonly called lactic acid, is turning out to be seriously amazing stuff. Science no longer regards it as a waste product of anaerobic exercise, as was thought for most of the 20th century. Lactate is now recognized as a key carbohydrate muscle fuel source which muscles produce, exchange and consume both at rest and during exercise. And it’s the primary ingredient in SportLegs. What’s alternately termed the Lactate System or Lactic Acid System is now recognized as the primary source of energy for short-term “sprint” activities. Since most competitive sports are sequences of sprint activities, lactate remains a focus of current research. For instance, it’s recently been proven that lactate can surpass glucose as muscles’ primary fuel during intense exercise (20). At rest and during light exercise, your muscles balance lactate production and consumption, producing just as much lactate as they consume (21). But kicking up the pace upsets the balance:

When you start serious exercise, muscles produce more lactate than they consume (1,2,3,4,5), particularly at altitude (2,6), which is why skiers and mountain bike racers suffer more “burn” than most. This continues until the concentration of lactate in your blood rises enough to signal muscles to stop producing excess lactate (7,8,9,10,11,12,13). Until this happens, a domino effect begins which limits your subsequent performance: Lactate accumulates in muscles; limbs “pump up” and feel heavier. The harder you exercise, the more lactate accumulates (14). Lactate accumulated from flow imbalance quickly becomes acidic (14,15) and even less mobile (16), further exacerbating accumulation. This “Lactic Acidosis” is classically associated with reduced Lactate Threshold, reaching the “burn point” at a lower level of exertion. Muscular strength plummets as well (17,18,19).

How taking SportLegs first helps performance: SportLegs uses lactate, your body’s primary high-exertion muscle fuel, to signal muscles not to overproduce lactate before you even begin exercise. Muscles switch from lactate overproduction to net lactate consumption in response to a rise in blood lactate concentration, regardless of whether blood lactate is raised naturally or from exogenous infusion (7,8,9,10,11,12,13). That’s precisely what SportLegs accomplishes. It’s 86.4% lactate. Taken an hour before exercise, SportLegs raises blood lactate, so you experience exercise with less limb “pump” and heaviness, and improved lactate transfer facilitates a noticeably higher Lactate Threshold. Reduced lactate accumulation means less retention of free radicals and other metabolic wastes in muscle tissues, for faster recovery and less next-day soreness.

How taking SportLegs afterward helps recovery: “Because lactate is combusted [metabolized] as an acid (C3H6O3), not an anion (C3H5O3), the combustion of an externally supplied salt of lactic acid (CHO3H5O3+H++3O2 → 3H2O+3CO2) effects the removal of the proton taken up during endogenous lactic acid production (Gladden, L. B. and J. W. Yates, J Appl Physiol 54:1254-1260, 1983). A side benefit of alkalizing the plasma by feeding lactate would be to enhance movement (efflux) of lactic acid from active muscles into plasma, a process which is inhibited by low (relative to muscle) blood pH. (Brooks, G. A. and D. A. Roth, Med Sci Sports Exerc 21(2):S35-207, 1989; Roth, D. A. and G. A. Brooks, Med Sci Sports Exerc 21(2):S35-206, 1989). Moreover, maintenance of a more normal blood pH during strenuous exercise would decrease the performer’s perceived level of exertion. The conversion of lactate to glucose in the liver and kidneys also has alkalizing effects by removing two protons for each glucose molecule formed, 2C3H5O3 + 2H+ C6H12O6. Thus, whether by oxidation or conversion to glucose, clearance of exogenously supplied lactate lowers the body concentration of H+, raising pH.”(22)

  1. Ahlborg, G. Mechanism of glycogenolysis in nonexercising human muscle during and after exercise. Am J Physiol. 248(5 Pt 1):E540-5, 1985
  2. Brooks, G. A., G. E. Butterfield, R. R. Wolfe, et al. Decreased reliance on lactate during exercise after acclimatization to 4,300 m. J Appl Physiol 71:333-341, 1991.
  3. Brooks, G. A., E. E. Wolfel, G. E. Butterfield et al. Poor relationship between arterial lactate and leg net release during steady-state exercise at 4,300 m altitude. J Appl Physiol 275:R1192-R1201, 1998.
  4. Richter, E. A., B. Kiens, B. Saltin, N. J. Christensen and G. Savard. Skeletal muscle glucose uptake during dynamic exercise in humans: role of muscle mass. Am J Physiol 254:E555-E561, 1988.
  5. Wahren, J., P. Felig, G. Ahlborg and L. Jorfeldt. Glucose metabolism during leg exercise in man. J Clin Invest 50:2715-2725, 1971.
  6. Brooks, G. A., E. E. Wolfel, B. M. Groves, et al. Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m. J Appl Physiol 72:2435-2445, 1992.
  7. Freyschuss U, Strandell T (1967) Limb circulation during arm and leg exercise in supine position. J Appl Physiol, 23:163-170
  8. Ahlborg G, Hagenfeldt L, Wahren J (1975) Substrate utilization by the inactive leg during one-leg or arm exercise. J Appl Physiol, 39:718-723
  9. Ahlborg G, Hagenfeldt L, Wahren J (1976) Influence of lactate infusion on glucose and FFA metabolism in man. Scan J Clin Lab Invest, 36:193-201
  10. Poortmans JR, Bossche JD-V, Leclercq R (1978) Lactate uptake by inactive forearm during progressive leg exercise. J Appl Physiol, 45:835-839
  11. Stamford BA, Moffatt RJ, Weltman A, Maldonado C, Curtis M (1978) Blood lactate disappearance after supramaximal one-legged exercise. J Appl Physiol 45:244-248
  12. Dodd S, Powers SK, Callender T, Brooks E (1984) Blood lactate disappearance at various intensities of recovery exercise. J Appl Physiol 57:1462-1465
  13. Mazzeo RS, Brooks GA, Schoeller DA, Budinger TF (1986) Disposal of blood [1-13C] lactate in humans during rest and exercise. J Appl Physiol, 60:232-241
  14. Gladden, L. B. Lactate metabolism: a new paradigm for the third millennium. J Physiol 558.1:5-30, 2004.
  15. Brooks, G. A., T. D. Fahey, T. P. White, K. M. Baldwin. In Exercise Physiology. Human Bioenergetics and its Applications. 3rd edn. pp804-805. Mayfield Publishing Company, 2000.
  16. Roth, D. A. The sarcolemmal lactate transporter: transmembrane determinants of lactate flux. Med Sci Sports Exerc 23:925-934, 1991.
  17. Fitts, R. H. Mechanisms of muscular fatigue. In Principles of Exercise Biochemistry, 3rd edn. Ed. Poortmans, J. R., pp279-300. Karger, Basel.
  18. Hermansen, L. Effect of metabolic changes on force generation in skeletal muscle during maximal exercise. In CIBA Foundation Symposium 82. Human Muscle Fatigue: Physiological Mechanisms, ed. Porter, R. & Whelan, J., pp75-88. Pitman Medical, London 1981.
  19. Sahlin, K. Metabolic factors in fatigue. Sports Med 13:99-107, 1992.
  20. Brooks, G. A. Intra and extra-cellular lactate shuttles. Med Sci Sports Exerc 32:790-799, 2000.
  21. Brooks, G. A., T. D. Fahey, T. P. White, K. M. Baldwin. In Exercise Physiology. Human Bioenergetics and its Applications. 3rd edn. p210. Mayfield Publishing Company, 2000.
  22. Brooks, G. A. Method and composition for energy source supplementation during exercise and recovery. U. S. Patent #5,420,107, May 30, 1995.