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Lactate and Lactic Acid

Lactate, also known as lactic acid, has a bad reputation. It's commonly viewed as a waste product that causes fatigue, burning muscles, and Delayed Onset Muscle Soreness (DOMS). In reality, Lactate is an intermediary in the metabolism of carbohydrates, and is a fuel source that is preferred by working muscles over glucose. A crude analogy would be a steam train, where the coal (carbohydrate) is burnt to form steam (Lactate), and the steam is used to turn the wheels (muscles). This is a flawed analogy, as the creation of lactate from glucose provides direct energy for the muscles, and of course muscles have other fuel sources such as fat, but hopefully you get to the gist.

Contents

1 Lactate Production

At one time it was believed that Lactate was a waste product that indicated insufficient oxygen being supplied to the muscles, but this view has changed. Because Lactate is produced by metabolism in the absence of oxygen[1], the natural conclusion was that the presence of Lactate indicates insufficient oxygen and therefore anaerobic metabolism[2][3]. However, more recent studies have that Lactate production is related to exercise intensity, not insufficient oxygen supply[4][5][6]. Lactate levels appear to depend on many factors, including the metabolism of glucose (to pyruvate), Lactate removal, fast twitch fiber recruitment, and energy demand (ADP/ATP ratio, which is in turn dependent on oxygen levels)[7].

2 Lactate and Fatigue

Initial studies have indicated that that acidity may reduce force production in muscles[8] or reduce the rate of glucose metabolism[9], leading to fatigue, and of course of Lactate is Lactic Acid in the blood. However, more recent studies have shown that the effects of acidity are not seen in more realistic situations[10][11]. A study of isolated rat muscles showed Lactate can protect against fatigue[12]. However, more research into the role of Lactate and fatigue are required[7].

3 Lactate as a Fuel

The view of Lactate as a waste product has changed over time, and Lactate has been shown to be a mechanism for distributing carbohydrate (AKA the "Lactate Shuttle"[13]. During prolonged low-moderate intensity exercise, muscles that initially released Lactate into the blood can become net importers[14][15]. At higher intensities, the working muscles extract and metabolize Lactate, even while being a net Lactate producer[16]. There is some evidence that muscles at rest will absorb and store Lactate[17], while at exercise the majority of absorbed Lactate is metabolized by the working muscles[17][18]. Lactate is a preferred fuel source for working muscles, as extra Lactate injected will be metabolized in place of glucose[19]. A low intensities, Lactate will be converted back to Glucose (AKA Gluconeogenesis)[20]. When performing Interval Training, lactate clearance during the recovery period depends on the exercise intensity, so complete rest will not metabolize the lactate as effectively as active recovery[21].

4 Lactate Threshold

Main article: Lactate Threshold

In the spite of all of the myths around Lactate and lactic acid, the concept of Lactate Threshold is both valid and important. Lactate Threshold is a good predictor of athletic performance, especially in runners.

5 Lactate and Wound Healing

It's been known since the 1960 that lactate is an important part of wound healing, with collagen synthesis almost doubled when Lactate is increased to 15 mmol/l in cultures[22]. When you're used to looking at Lactate levels during exercise this seems ridiculously high, but values of 10-15 mmol/l are commonly seen in healing wounds[23], and this does not appear to be due to low oxygen levels[24]. In fact, oxygen levels seem to have little impact on lactate levels[25][26]. It's possible that the beneficial effects of Lactate may be in stimulating vascular growth (angiogenesis)[25] and/or increased oxygen supply to the wound through vasodilation[27][24].

6 References

  1. ↑ A. V. Hill, H. Lupton, Muscular Exercise, Lactic Acid, and the Supply and Utilization of Oxygen, QJM, volume os-16, issue 62, 1923, pages 135–171, ISSN 1460-2725, doi 10.1093/qjmed/os-16.62.135
  2. ↑ K. Wasserman, The anaerobic threshold measurement to evaluate exercise performance., Am Rev Respir Dis, volume 129, issue 2 Pt 2, pages S35-40, Feb 1984, PMID 6421216
  3. ↑ BA. Mizock, JL. Falk, Lactic acidosis in critical illness., Crit Care Med, volume 20, issue 1, pages 80-93, Jan 1992, PMID 1309494
  4. ↑ RJ. Connett, TE. Gayeski, CR. Honig, Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ., J Appl Physiol (1985), volume 61, issue 2, pages 402-8, Aug 1986, PMID 3745033
  5. ↑ RS. Richardson, EA. Noyszewski, JS. Leigh, PD. Wagner, Lactate efflux from exercising human skeletal muscle: role of intracellular PO2., J Appl Physiol (1985), volume 85, issue 2, pages 627-34, Aug 1998, PMID 9688741
  6. ↑ GA. Brooks, Anaerobic threshold: review of the concept and directions for future research., Med Sci Sports Exerc, volume 17, issue 1, pages 22-34, Feb 1985, PMID 3884959
  7. ↑ 7.0 7.1 LB. Gladden, Lactate metabolism: a new paradigm for the third millennium., J Physiol, volume 558, issue Pt 1, pages 5-30, Jul 2004, doi 10.1113/jphysiol.2003.058701, PMID 15131240
  8. ↑ L. Hermansen, Effect of metabolic changes on force generation in skeletal muscle during maximal exercise., Ciba Found Symp, volume 82, pages 75-88, 1981, PMID 6913479
  9. ↑ K. Sahlin, Metabolic factors in fatigue., Sports Med, volume 13, issue 2, pages 99-107, Feb 1992, PMID 1561513
  10. ↑ H. Westerblad, DG. Allen, J. Lännergren, Muscle fatigue: lactic acid or inorganic phosphate the major cause?, News Physiol Sci, volume 17, pages 17-21, Feb 2002, PMID 11821531
  11. ↑ J. Bangsbo, K. Madsen, B. Kiens, EA. Richter, Effect of muscle acidity on muscle metabolism and fatigue during intense exercise in man., J Physiol, volume 495 ( Pt 2), pages 587-96, Sep 1996, PMID 8887768
  12. ↑ OB. Nielsen, F. de Paoli, K. Overgaard, Protective effects of lactic acid on force production in rat skeletal muscle., J Physiol, volume 536, issue Pt 1, pages 161-6, Oct 2001, PMID 11579166
  13. ↑ GA. Brooks, Intra- and extra-cellular lactate shuttles., Med Sci Sports Exerc, volume 32, issue 4, pages 790-9, Apr 2000, PMID 10776898
  14. ↑ WN. Stainsby, HG. Welch, Lactate metabolism of contracting dog skeletal muscle in situ., Am J Physiol, volume 211, issue 1, pages 177-83, Jul 1966, PMID 5911036
  15. ↑ LB. Gladden, Net lactate uptake during progressive steady-level contractions in canine skeletal muscle., J Appl Physiol (1985), volume 71, issue 2, pages 514-20, Aug 1991, PMID 1938723
  16. ↑ WC. Stanley, EW. Gertz, JA. Wisneski, RA. Neese, DL. Morris, GA. Brooks, Lactate extraction during net lactate release in legs of humans during exercise., J Appl Physiol (1985), volume 60, issue 4, pages 1116-20, Apr 1986, PMID 3084443
  17. ↑ 17.0 17.1 KM. Kelley, JJ. Hamann, C. Navarre, LB. Gladden, Lactate metabolism in resting and contracting canine skeletal muscle with elevated lactate concentration., J Appl Physiol (1985), volume 93, issue 3, pages 865-72, Sep 2002, doi 10.1152/japplphysiol.01119.2001, PMID 12183479
  18. ↑ RS. Mazzeo, GA. Brooks, DA. Schoeller, TF. Budinger, Disposal of blood [1-13C]lactate in humans during rest and exercise., J Appl Physiol (1985), volume 60, issue 1, pages 232-41, Jan 1986, PMID 3080398
  19. ↑ BF. Miller, JA. Fattor, KA. Jacobs, MA. Horning, F. Navazio, MI. Lindinger, GA. Brooks, Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion., J Physiol, volume 544, issue Pt 3, pages 963-75, Nov 2002, PMID 12411539
  20. ↑ MJ. Roef, K. de Meer, SC. Kalhan, H. Straver, R. Berger, DJ. Reijngoud, Gluconeogenesis in humans with induced hyperlactatemia during low-intensity exercise., Am J Physiol Endocrinol Metab, volume 284, issue 6, pages E1162-71, Jun 2003, doi 10.1152/ajpendo.00425.2002, PMID 12604505
  21. ↑ P. Menzies, C. Menzies, L. McIntyre, P. Paterson, J. Wilson, OJ. Kemi, Blood lactate clearance during active recovery after an intense running bout depends on the intensity of the active recovery., J Sports Sci, volume 28, issue 9, pages 975-82, Jul 2010, doi 10.1080/02640414.2010.481721, PMID 20544484
  22. ↑ H. GREEN, B. GOLDBERG, COLLAGEN AND CELL PROTEIN SYNTHESIS BY AN ESTABLISHED MAMMALIAN FIBROBLAST LINE., Nature, volume 204, pages 347-9, Oct 1964, PMID 14228868
  23. ↑ TK. Hunt, WB. Conolly, SB. Aronson, P. Goldstein, Anaerobic metabolism and wound healing: an hypothesis for the initiation and cessation of collagen synthesis in wounds., Am J Surg, volume 135, issue 3, pages 328-32, Mar 1978, PMID 626315
  24. ↑ 24.0 24.1 O. Trabold, S. Wagner, C. Wicke, H. Scheuenstuhl, MZ. Hussain, N. Rosen, A. Seremetiev, HD. Becker, TK. Hunt, Lactate and oxygen constitute a fundamental regulatory mechanism in wound healing., Wound Repair Regen, volume 11, issue 6, pages 504-9, PMID 14617293
  25. ↑ 25.0 25.1 JS. Constant, JJ. Feng, DD. Zabel, H. Yuan, DY. Suh, H. Scheuenstuhl, TK. Hunt, MZ. Hussain, Lactate elicits vascular endothelial growth factor from macrophages: a possible alternative to hypoxia., Wound Repair Regen, volume 8, issue 5, pages 353-60, PMID 11115148
  26. ↑ AY. Sheikh, JJ. Gibson, MD. Rollins, HW. Hopf, Z. Hussain, TK. Hunt, Effect of hyperoxia on vascular endothelial growth factor levels in a wound model., Arch Surg, volume 135, issue 11, pages 1293-7, Nov 2000, PMID 11074883
  27. ↑ K. Mori, Y. Nakaya, S. Sakamoto, Y. Hayabuchi, S. Matsuoka, Y. Kuroda, Lactate-induced vascular relaxation in porcine coronary arteries is mediated by Ca2+-activated K+ channels., J Mol Cell Cardiol, volume 30, issue 2, pages 349-56, Feb 1998, doi 10.1006/jmcc.1997.0598, PMID 9515011
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Last edited on 16 August 2015, at 16:10