Lactic Acid
Article by Brad Hiskins
Lactic acid has been the focus of sports massage therapists for many an athletic season. History tells us that massage ‘rids’ the body of that evil, muscle ravaging soreness provoking chemical, leaving the body ‘recovered’ and ready for another exercise bout. However, it should be asked… what exactly is lactic acid? Does it really cause muscle soreness? Does it really sit in the blood stream and muscles for prolonged periods of time after exercise and finally, the all important question; does ‘massage’ make an iota of difference?
The Energy Systems
Before describing lactic acid, it is important to have an understanding of the energy systems the body uses to supply energy to the working muscles. For muscles to contract, they require energy, which is supplied to the muscle cells as molecules of energy called ATP. There are three methods the body uses to supply energy in the form of ATP. Two of these methods, called the ATP/alactic system and the glycolytic/lactate system, are both considered to be anaerobic systems because they do not require oxygen immediately for their chemical processes. The third system is considered aerobic as it relies on a steady supply of oxygen to regenerate the ATP energy molecule. The type of exercise an athlete endures, will determine which of the three energy systems the athlete will use and hence whether lactic acid will be a factor.
ATP/alactic energy system
- Power athletes (ex: weightlifters, 100meter sprinters)
- No lactic acid formed
A power athlete such a weightlifter will use the ATP/alactic system for energy. ATP is a molecule found inside muscle cells that when broken down, provides fast and large amounts of energy for muscles to do work. As ATP is broken down, it is simultaneously reformed via a substance called Creatine Phosphate. Throwing, jumping and 100 metre sprints are all events that rely on this ATP-Creatine Phosphate system. A major drawback of this pathway, however, is that it can only produce continuous energy for up to 15 seconds of muscle activity due to a very limited quantity of ATP and Creatine Phosphate being stored within the muscles. If strenuous exercise is to continue beyond this brief period of 15 seconds, the means of replacing lost ATP must come via the second anaerobic system, the glycolysis/lactate system.
This system does not produce lactic acid as a part of its cycle and hence athletes using this energy system will not suffer from excess lactic acid production.
Glycolytic/lactate system.
- Intense amount of muscle activity beyond approximately 15 secs and up to 3 minutes (ex: 100 meter swimming, 400 meter running)
- No oxygen necessary for energy production
- Glucose converted to energy with Pyruvic acid as end product
- Lactic acid produced as bi-product if formation of pyruvic acid is more than its removal – exercise intensity too prolonged for our physiological capacity to cope (see ‘when is lactic acid formed’ below)
A 400m runner and a 100m swimmer are typical athletes who would rely heavily on glycolysis/lactate system. At this distance requiring an intense amount of muscle activity, the ATP present in the muscle cells would have been almost used up at the start of the race, and now the lactate system has kicked into gear and contributing significantly to the energy required to complete the event. The fuels for glycolysis comes from the molecule glucose that has been circulating in the blood or that have been stored in another form called glycogen in the muscles and liver in the body. These forms of glucose are broken down via a series of ten different chemical reactions into a substance called pyruvic acid. Whilst the energy or ATP released from these reactions is extremely rapid and does not require oxygen, only a small amount of ATP is resynthesised. Consequently in events such as the marathon, soccer games and endurance cycling, the pyruvic acid must be shunted into the third energy system to keep providing energy – the aerobic system – described below.
The Aerobic Energy System.
- Prolonged muscle activity beyond approximately 3minutes (ex: marathon)
- Oxygen necessary
The Aerobic System is required for any athletic event that extends beyond about 3 minutes in duration, such as a 5km run, 800m swim, or a soccer match. This final and virtually limitless supply of energy will provide for more than 90% of the energy required for such activities (Anderson, 1997). However the rate of maximal energy production from this system is not as high as from the anaerobic systems and so aerobic events like the marathon are run at a considerably slower pace then a 400m run.
Why is lactic acid formed?
The rate at which the glycolytic/lactate system burns to provide energy in the form of ATP, is critical to the development and maintenance of high power outputs or speed. However, a problem can arise if the product of glycolysis (pyruvic acid) is not being removed and funneled into the aerobic system for further metabolism, as fast as it is being produced by glycolysis. If the concentration of pyruvic acid becomes too high it will bring glycolysis to a halt – and the energy it provides. To avoid this dilemma, an enzyme called lactate dehydrogenase steps in and converts some of the pyruvic acid to lactic acid (removing pyruvic acid and half of the free H+ ions produced during glycolysis) and hence ‘buys some time’ to allow glycolysis to continue to reform the ATP molecule.
Once lactic acid has been formed in the working muscle cells, it immediately breaks down into a salt called lactate and hydrogen ions, which are then transported out of the muscle cells and diffuse into the blood and surrounding tissues. The constant formation of lactic acid in the blood, and then its removal by various tissues, means that lactic acid levels in both the muscles and blood can remain at constant levels without adverse effects on cell metabolism for long periods of exercise. Lactate can later be reconverted into pyruvate, acting as a fuel source to tissues not working as hard.
For this reason, an athlete such as a marathon runner, will have near resting levels of lactic acid in their blood following a race, due to a balance between the lactic acid that is released into the blood and the rate it is removed from the blood. In addition, because this event relies predominately on the aerobic energy system and oxygen is readily available to allow flow through the aerobic system, very little pyruvic acid is allowed to accumulate due to its removal into the aerobic system rather than being converted to lactic acid.
When does the lactic acid become a problem?
At some point of exercise intensity between 55 and 90 percent of VO2 max (intense muscle activity such as 800 meter running), the ‘lactate threshold’ is passed. Up until this point the lactate is being used by the aerobic system at the same rate is being produced. Now due to physiological shortages (oxygen availability to cells, certain enzymes, or lack of cell mitochondria (the energy houses in cells)) the utilisation of lactate as an energy source is overwhelmed by its production. Blood lactate levels increase rapidly acidifying the blood (lowering pH) which in turn overwhelm natural ph buffers and eventually block the rate of the glycolytic/lactate system. It is at this stage that lactic acid becomes a problem for the athlete as energy production is decreased and the effects of low pH levels in the blood take effect – the lactic acid ‘burn’.
Hence the only type of athlete that will experience excessive lactic acid levels are those that compete in sports that demand high intensity exercise for prolonged periods of time. Furthermore, these athletes tend to train this glycolytic/lactic system (increased mitochondria, enzyme levels an oxygen supplies) enabling a greater ability to withstand high levels of lactic acid and therefore not be effected as much as we might assume.
What happens to these excessive levels of lactic acid?
Scientific evidence has shown that approximately 70% of the lactic acid formed during any intensity of exercise is converted back to pyruvic acid and is used as a substrate by the heart and skeletal muscle. The efficient action of the body’s circulatory system results in lactic acid concentration in the blood being almost at resting levels 30-60 minutes following all intensities and durations of athletic events (Dodd, Powers, Callender & Brooks, 1984). That is, lactic acid levels in the muscle and blood are at physiological resting levels after 60 minutes of rest. Physiologically after intense exercise, excess lactate is reconverted back to glucose in the liver. This newly made glucose can be used to resynthesise glycogen that is depleted during exercise. It takes approximately 20-60 minutes to fully remove lactic acid (lactate and hydrogen ions) produced during maximal exercise.
Given this fact, those sore achy muscles that occur the following day after an especially tough exercise session can hardly be blamed on lactic acid, which is well at resting levels by this time. Muscle soreness that occurs 24-72 hours after exercise is most likely to be delayed onset muscle soreness which is not effected by lactic acid levels.
Does massage help remove blood lactate?
What we have seen so far is that lactic acid only affects a small proportion of athletic performance and hence most athletes that present to us will not be affected by excessive levels. Secondly, the normal levels of lactic acid are a good source of energy and a necessary part of the energy production process. Not quite the wicked chemical we make it out to be. But what about those athletes that do break that lactic acid barrier and endure excessive levels? Does recovery massage help?
Several studies have shown massage to be no more effective for speeding up lactic acid removal from the blood than simply resting after exercise (Dolgener & Morien, 1993; Hemmings et al., 2000, Gupta et al., 1996). The failure of massage to benefit lactic acid removal is thought to be because massage like passive recovery, fails to effect any significant change to the volume or rate of blood flow that enters and leaves muscles. (Shoemaker, Tiidus & Mader, 1997). However it has been widely acknowledged that blood lactate is removed more quickly during active recovery because blood flow remains elevated through the active muscle, which in turn is believed to enhance lactate removal from the muscle cell (Wilmore, 1994).
Quite simply, if blood lactate levels are back to normal levels one hour post exercise no matter what the athlete does post exercise, of course recovery massage does not make a difference to this physiology. So what does recovery massage do?
So what does recovery massage do?
So if blood lactic acid removal is unlikely to be one of the benefits of recovery massage post exercise , then what does it do? There are many possible effects, all of which need further study to substantiate what we are trying to achieve with recovery massage. Possibilities:
- It is possible that massage leads to an enhanced rate in the exchange of fluids situated around the cells although as described previously, this is unlikely to occur via an increase in blood flow.
- Normalizing hypertonicity
- Decreasing metabolic rate (possibly decreasing fuel usage and metabolic waste production)
- Relaxed muscle decreases pressure on surrounding tissues (possibly improving local circulation and lymphatic drainage)
- neurological calming affects
- reducing hypersensitivity of nerve ending posts exercise
- alleviating pain-spasm-pain reflexes
- release a cascade of chemical messengers associated with parasympathetic responses
A study comparing the effects of passive recovery versus massage to 11 male subjects did demonstrate that mechanical massage applied for 20 minutes by a modified pneumatic intermittent device improved duration of cycling on a subsequent exercise cycling bout (Zelikovski, Kaye and Fink, 1993) and several studies have also confirmed that during the application of massage to the triceps surae muscle group, there is a decrease in muscle tone as measured by a decrease in the H-reflex amplitude, a measure of motor nerve excitability (Morelli et al., 1990, Morelli et al., 1991; Sullivan et al., 1991) However, these H-reflex amplitudes returned to normal immediately on termination of the massage, so the lasting effects of this tone reduction have yet to be studied.
Whilst there are numerous anecdotal accounts attesting to the positive affect of massage on psychological well being, empirical evidence is scarce and hampered by poor experimental designs and sample sizes. One study has shown massage to have an affect on positive mood state, synonymous with decrease tension, anger, anxiety and depression in physical education students (Weinberg, Jackson & Kodny, 1988). Further, various massage techniques applied to the hamstring muscles has been shown to cause a measurable increase in hip flexion range in (Crossman et al 1984).Massage therapy has also been shown to increase neck extension range and shoulder abduction in a group of university dancers (Leivadi et al 1999) and shoulder joint internal rotation range in swimmers (Blanch et al 1995).
In conclusion
From the above it can be concluded that lactic acid is not the nasty chemical we make it out to be and even when it does create problems to athletes (when in excess) it is quickly restored to resting levels without any intervention. Our challenge as soft tissue therapists is to search for more probable effects that recovery massage no doubt has and hence enable us to explain to the athletes what we actually are trying to achieve. Undoubtedly, athlete feedback has provided vast (overwhelming?) anecdotal evidence supporting recovery massage. However, our challenge as Soft Tissue Therapists is to discover, understand and impart what is actually physiologically achieved (affected) through application of recovery techniques. In addition, it is necessary to support these claims, and moreover squash ill founded beliefs, through scientific evidence.
References
Ahmaidi, S., Granier, P., and Tasutaou, J.M. (1996). Effects of active recovery on plasma lactate and anaerobic power following repeated intensive exercise. Medicine and Science in Sports and Exercise, 28:450-456.
Anderson, O. (1997). Things your mom forgot to tell you about blood lactate. Running Research News, 13 (10).
Astrand, P., and Rodahl, K. (1986). Textbook of work physiology. New York: McGraw Hill.
Bale, P., and James, H. (1991). Massage, Warm down and rest as recuperative measures after short term intense exercise. Physiotherapy in sport, 13:4-7.
Belcastro, A.N and Bonen, A. (1975). Lactic acid removal rates during controlled and uncontrolled recovery exercise. Journal of Applied Physiology. 39;932-936.
Blanch PD, Clews W, Popov V and Matley K (1995) The effect of massage on the isolated active glenohumeral internal range of swimmers. Proceedings, Australian Conference of Science and Medicine in Sport, Hobart
Bonen, A. and Belcastro, A.N (1976). Comparison of self-selected recovery methods on lactic acid removal rates. Medicine and Science in Sports and Exercise. 8; 176-178.
Brooks,G.A. (1991).Current concepts in lactate exchange. Medicine and Science in Sports and Exercise, 23:895-906
Brooks, G.A., and Gaesser, G.A. (1980). End points of lactate and glucose metabolism after exhausting exercise. Journal of Applied Physiology, 49: 1057- 1069.
Dodd, S., Powers, S.K., Callender, T., and Brooks, E. (1984). Blood lactate disappearance at various intensities of recovery exercise. Journal of Applied Physiology, 57:1462-1465.
Dolgener, F., Morien, A. (1993). The effect of massage on lactate disappearance. Journal of Strength and Conditioning Research, 7:159-162.
Dubrovsky, V.I (1983). Changes in muscle and venous blood flow after massage. Soviet Sports Review, 18,3:134-135.
Gupta, S., Goswarni, A., and Sadhukhan, K. (1996). Comparative study of lactate removal in short term massage of extremities, active recovery and a passive recovery period after supramaximal exercise sessions. International Journal of Sports Medicine 17:106-110.
Hemmings, B., Smith, M., Graydon, J., and Dyson, R. (2000). Effects of massage on physiological restoration, perceived recovery and repeated sports performance. British Journal of Sports Medicine, 34; 109-115.
Hermansen, L. (1981). Effect of metabolic changes on force generation in skeletal muscle during maximal exercise. In: Human muscle fatigue: physiological mechanisms. (Eds. R Porter & J Whelan) pp 75-88. London: Pitman Medical.
Hernandez-Reif M, Field T, Krasneger J and Theakston H. (2001). Lower back pain is reduced and range of motion increased after massage. International Journal of Neuroscience 106:131-145.
MacClaren, D., Gibson, H., Parry-Billings, M. (1989). Review of the metabolic and physiological factors in fatigue. In: Pandolf K, ed. Exercise and sport sciences reviews. Baltimore: Williams and Wilkins,
Martin, N., Zoeller, R., Robertson, R., and Lephart, S. (1998). The comparative effects of sport massage, active recovery and rest in promoting blood lactate clearance after supramaximal leg exercise. Journal of Athletic training, 33 (1), 30-35.
Morelli, M., Seaborne, D.E., Sullivan, J. (1990). Changes in H-reflex amplitude during massage of triceps surae in healthy subjects. Journal of Orthpaedic and Sports Physical Therapy, 12:55-59.
Morelli, m., Seaborne, D.E., Sullivan, J. (1991). H-reflex modulation during manual muscle massage of human triceps surae. Archives of Physical Medicine and rehabilitation. 72: 915-919.
Preyde M (2000). Effectiveness of massage therapy for sub acute low-back pain: a randomised controlled trial. Canadian Medical Association Journal 162 (13)
Rontoyannis, G.P. (1988). Lactate elimination from the blood during active recovery. Journal of Sports Medicine and Physical Fitness. 28; 115-123
Ross, M. (1999). Delayed-Onset Muscle soreness. Work out now, pay later? The Physician and Sports Medicine. Retrieved on 15th April 2002 from the World Wide Web. http://www.physsportsmed.com/issues/1999/01_99/muscle.htm
Sejersted, O.M., Vollestad, N.K., Medbo, J.I. (1986). Muscle fluid electrolyte balance during and following exercise. Acta Physiologica Scadinavia, 128 (Supp 556):119-127.
Shoemaker, K.J., Tiidus, P., Mader, R. (1997). Failure of manual massage to alter limb blood flow: measures by Doppler ultrasound. Medicine and Science in Sports and Exercise. 29; (5), 610-614
Stamford, B.A., Weltman,A., Moffatt, R and Sady, S. (1981). Exercise recovery above and below anaerobic threshold following maximal work. Journal of Applied Physiology, 51;840-844.
Sullivan, J., Williams, L., Seaborne, D., Morelli, M. (1991). Effects of massage on alpha motoneuron excitability. Physical therapy. 71; 555-560.
Weinberg, R., Jackson, A., and Kodny, K. (1988). The relationship of massage and exercise to mood enhancement. Sport Psychologist 2:202-211.
Wilmore, J., Costill, D. (1994). Physiology of sport and exercise. Champaign: Human Kinetics.
Wolfe, J.H.N. (1984). Treatment of lymphedema. In: Rutherford R.B, ed. Vascular Surgery. 2nd ed. Philadelphia: WB Saunders, 1463-1465.
Zelikovski, A., Kaye, C., Fink, G. (1993). The effects of the modified intermittent sequential pneumatic device (MISPD) on exercise performance following an exhaustive exercise bout. British Journal of Sports Medicine, 27:255-259.