What has Soren Mavrogenis been doing lately?
If you're an athlete, that question has not exactly been rolling off your lips, especially since Soren's latest published paper - 'Pyeloureteral Junction Stenosis and Ureteral Valve Causing Hydronephrosis' (Scandinavian Journal of Urology and Nephrology, Vol. 35(3), pp. 245-247, June 2001) - has nothing at all to do with athletics.
But give the fellow a chance! In addition to his pyeloureteral pursuits, the Dane is currently carrying out extremely interesting research on the treatment of athletic injuries, and his findings may one day help you bounce back from an injury more quickly than expected - and as a result set a new personal record or win an important competition.
A physiotherapist with Denmark's Olympic Committee, Mavrogenis has effectively treated several hundred cases of recurrent inflammatory injuries with a novel new treatment (Reuters Health, April 27, 2001). Tested for the first time in 1996 on a group of rowers from Denmark's National Rowing Team, Soren's nostrum appears to have remarkable anti-inflammatory properties (research on the healing properties of the treatment will be published in a peer-reviewed journal shortly).
Of course, most routine athletic injuries are treated with icing, rest, physiotherapy, and the use of non-steroidal anti-inflammatory drugs (NSAIDS), and Soren is not against either rest or ice. However, the innovative Dane leaves the NSAIDS on the shelf, instead relying on a combination of essential fatty acids, vitamins, and minerals to soothe inflammation and restore injured body parts. He has reportedly found success with a variety of ailments, including both 'tennis elbow' and 'golf elbow'.
The Mavrogenis mixture
'Don't golfers already eat enough fat?' you may be wondering, but the problem is of course that they usually eat the wrong fats (ie, the ones which seem to be pro-inflammatory). Soren's nutritional supplement contains a rich lode of inflammation-fighting omega-3 fatty acids (from fish oil), some omega-6 fats (from borage oil), four vitamins (A, B6, C, and E), and also the minerals selenium and zinc. According to Mavrogenis, most patients respond positively to the treatment in just two to three weeks, although very serious cases may require several months. He says: 'The results of this research confirm our clinical observations and leave us with the clear impression that inflam-matory injuries can be treated without the use of NSAIDS. I see this as a breakthrough in modern physio-therapy. For the first time, we are able to offer our patients a safe and reliable treatment for stress injuries with chronic inflammatory response. In fact, it is our experience that with this new treatment, as opposed to conventional treatment, athletes are able to train actively while receiving treatment.'
'The bad cases require the use of intensive ultrasound and certain massage techniques in addition to the antioxidants and essential fatty acids, but in the milder cases the use of nutrients alone is adequate.'
Norwegian sports authorities have been carefully watching Soren's work (Norwegians do not want the Danes to leave them behind). Since inflam-matory injuries to shoulders, elbows, knees, and Achilles tendons account for 25% of all job-related absences in Norway, Soren's anti-inflammatory regimen is now being tested by NIMI (the Norsk Idrettsmedisinsk Institut), one of Scandinavia's foremost treatment facilities for sports injuries. We'll report on NIMI's findings in a future issue of SIB.
But isn't this all a little far-fetched? How can a few fatty acids - plus several vitamins and minerals - foster fast healing in an elbow nearly wrecked by overuse on the tennis courts - or in a knee shattered by thousands of miles of endurance running? The story just sounds too good to be true.
But it may not be. Bear in mind that scientific research has actually been fairly kind to the idea that omega-3 fatty acids and anti-oxidants can help to control inflammatory injuries. To understand why this is so, remember that exercise generates increased quantities of 'oxygen free radicals' and increases lipid peroxidation (the oxidative attack on key fats found in cell membranes, including muscle-fibre membranes). Strenuous exercise can induce oxidative damage in muscles and result in serious muscle injury.
The human body is well aware of this disastrous possibility, of course, and as a defence it produces a potent anti-oxidant called superoxide dismutase; superoxide-dismutase production speeds up when individuals embark on regular and at least moderately strenuous training programmes. Evidence suggests, however, that the superoxide-dismutase system is prone to being overwhelmed. Prolonged submaximal exercise has been shown to result in elevated amounts of skeletal-muscle lipid-peroxidation byproducts, indicating significant damage to the muscles (Free Radicals and Tissue Damage Produced by Exercise, Biochem Biophys Res Commun, Vol. 107, pp. 1198-1205, 1982).
Before we continue, let's recap. Exercise can greatly increase the production of cell-damaging free radicals. The magnified rates of lipid peroxidation resulting from this oxygen-radical production may cause skeletal damage. The human body has its own anti-radical defence system, but it doesn't always work effectively. In addition, the damage produced in the muscles as a result of exercise can snowball over relatively short periods of time. For example, in one study researchers found more muscle damage three days after a strenuous workout than they had found one hour after exercise ceased ('Adaptive response in human skeletal muscle subjected to prolonged eccentric training', Int J Sports Med, Volume 4, pp. 177-183, 1983). This was a bit surprising, since researchers believed significant muscle repair would have occurred during the three-day interim.
Delayed-onset muscle soreness
In another investigation, exercise scientists found that intense exercise produced immediate muscle damage, but the damage actually became much worse 24 and 48 hours after the workout was over, even though no follow-up exercise had taken place ('Ultrastructural changes after concentric and eccentric contractions of human muscle', J Neurol Sci Vol. 61, pp. 109-122, 1983). In other words, in a muscle traumatised by exertion, there is a post-exercise period lasting for up to three days or more in which muscle damage is actually accelerated, rather than minimised, even when no further exercise occurs.
If this seems a bit strange, think about your own exercise experiences. If you are a tennis player, for example, and you have played three sets on a particular day instead of your usual two, you may notice just a little background throbbiness and heat in your shoulder for the rest of the day, but nothing more. When you wake up the following morning, the story has changed, and your shoulder is stiff and painful. Time is a great healer, you think, but by the end of the day your shoulder has become an enraged, inflamed mass, and the following dawn brings even more pain, instead of relief. You reach for the NSAIDS and ice and begin thinking about calling your doctor. You have just uncovered a bizarre and surprising bit of information about your muscles: once they are insulted and hurt by exercise, they actually get steadily worse, sometimes for two to three days after exertion, before they grudgingly begin to get better. This phenomenon is of course the source of something almost all athletes know about - delayed-onset muscle soreness (DOMS).
The importance of vitamin E
Enter Soren's panaceal ingredients, which seem to have the ability to partially arrest this post-exercise cell suicide and thus spur recovery. Remember that three of Mavrogenis' key ingredients are omega-3 fatty acids, vitamin C, and vitamin E. The anti-inflammatory properties of omega-3 fats have been well documented, and research has indicated that supplementation with vitamin C and (especially) vitamin E can help to decrease the extent of the exercise-induced spike in the rate of lipid peroxidation and thus the extent of post-exercise muscle breakdown.
Vitamin E is found in virtually all cell membranes (one of its functions is to protect the membranes from peroxidation), but the major store of membrane-bound vitamin E is in the inner mitochondrial membrane, the site of the electron transport system, aerobic respiration, and potential free-radical damage during strenuous or prolonged exercise (during challenging exertions, free-radical generation may be so great that routine levels of superoxide dismutase and vitamin E may fail to provide adequate protection against peroxidation). Research indicates that vitamin-E supplementation can dramatically increase the vitamin-E content of mitochondrial membranes ('Muscle Uptake of Vitamin E and Its Association with Muscle Fiber Type', J Nutr Biochem, Vol. 8, pp. 74-78, 1997) and thus - in theory - keep the membranes sound, even in the face of rugged exertion.
Interestingly enough, scientists have found an inverse relation between plasma vitamin-E concentration and the percentage of type-I (slow-twitch) muscle fibres in individuals who do not supplement their diets with vitamin E. This inverse relationship may indicate that to minimise oxidative stress, physically active people with a high percentage of type-I fibres may have a greater need for vitamin E than those with more type-II, glycolytic (fast-twitch) fibres. It is interesting to note that in rats a deficiency of vitamin E increases susceptibility to free-radical damage during exercise and produces a 40% decline in endurance capacity, perhaps because mitochondrial membranes are not well maintained and thus aerobic energy production declines ('Vitamin E, Vitamin C, and Exercise', American Journal of Clinical Nutrition, Vol. 72(2), pp. 647S-652S, August 2000; the author's e-mail address is firstname.lastname@example.org).
Not in athletes?
Recently, researchers examined the protective effect of vitamin E on exercise-induced oxidative damage in young and older men and also in women. In all three groups studied, the researchers showed that 48 days of vitamin-E supplementation (800 IU per day) lowered the exercise-induced increase in oxidative injury, as indicated by a sparing of muscle fatty acids and the decreased excretion of various metabolic products. However, the study suggested that the anti-oxidant protection provided by vitamin E may reduce the amount of membrane damage following exercise in untrained subjects - but not necessarily in high-performance athletes ('Protective effect of vitamin E on exercise-induced oxidative damage in young and older adults', Am J Physiol, Vol. 264, pp. R992-8, 1993). Why is this so? It's likely that high-end athletes' muscles were less challenged by the experimental workout, compared to sedentary individuals (as muscles become functionally stronger, they are less likely to be hurt by exertion); no doubt the top-quality athletes had superior intrinsic anti-oxidant systems in place, too.
In addition to controlling peroxidation, vitamin E seems to play a role in controlling the activities of special white-blood cells called neutrophils and monocytes. For example, within hours after an injury or strenuous bout of exercise, neutrophils migrate to the site of muscle injury, where they pick up tissue debris and also release free radicals which increase protein breakdown ('Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release', Am J Physiol, Vol. 259, pp. R1214-1219, 1990). Vitamin E may help control the extent to which these released free radicals produce damage to the surrounding tissues.
Vitamin E also works together with vitamin C to influence monocytes and also protein synthesis in muscles. The story goes this way: monocytes also work their way to the 'scene of the accident' (ie, a site of muscle damage), joining arms with the neutrophils which are already there. Substantial monocyte accumulation in skeletal muscle was found after the completion of a marathon by runners aged 20 to 50 years who ranged from elite (including the world record-holder) to those who took longer than three hours to finish ('Skeletal muscle injury and repair in marathon runners after competition', Am J Pathol, Vol. 118, pp. 331-339, 1985), and monocytes have been found in muscles after many other forms of strenuous exercise as well. As it turns out, monocytes secrete chemicals called cytokines, including a very important cytokine called IL-1. IL-1 and its sibling cytokines mediate a wide range of metabolic events. During infection,
IL-1 produces an elevated core temperature in humans ('Endogenous pyrogen activity in human plasma after exercise', Science, Vol. 220, pp. 617-619, 1983). In laboratory animals, IL-1 liberates amino acids, probably boosting protein synthesis ('Administration of endotoxin, tumor necrosis factor, or interleukin 1 to rats activates skeletal muscle branched-chain alpha-keto acid dehydrogenase', J Clin Invest, Vol. 85, pp. 256-63, 1990).
Vitamins E and C together
Here's the punch-line. Recently, investigators supplemented their subjects' diets with 400 mg of vitamin E per day, one gram (1000 mg) of vitamin C daily, or the combination of both vitamins and found that the E-C combination had a greater effect on stimulating IL-1 production, compared to using either one of the vitamins by itself ('Supplementation with vitamins C and E enhances cytokine production by peripheral blood mononuclear cells in healthy adults', Am J Clin Nutr, Vol. 64, pp. 960-965, 1996). This suggests that after muscle-damaging exercise, a combined course of vitamins E and C creates a bigger boost in circulating and muscle cytokines and, as a result, an improved adaptive response.
As important as vitamin E is to aerobic respiration, recovery, and muscle integrity, you might think that it could be a potent ergogenic aid. However, to date only one study has linked vitamin-E supplementation with higher performance: cyclists training at high altitudes have been shown to have higher lactate thresholds when they are vitamin-E supplemented ('Influence of vitamin E on physical performance', Int J Vitam Nutr Res, Vol. 58, pp. 49-54, 1988).
If you doubt that free-radical damage underlies a significant part of the loss in integrity and strength which occurs in a muscle after it has been damaged, consider an investigation in which researchers checked the extensor digitorum longus muscles in young, adult, and old mice after a challenging bout of eccentric contractions (eccentric contractions refer to situations in which muscles generate force and attempt to shorten while they are actually being forced to elongate; eccentric actions are notorious for producing injury). Actual muscle injury was assessed by measuring maximum isometric force in the muscle, as well as by looking at morphologic damage ('Free radical injury to skeletal muscles of young, adult, and old mice', Am J Physiol, Vol. 258, pp. C429-435, 1990).
Three days after the injury-producing exercise, maximal isometric force in the old mice was 15% lower, compared with the young and adult mice. However, when the mice were treated with a free-radical scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD), they exhibited much less delayed injury and were also much stronger during the days after the exercise bout. Amazingly enough, they found that PEG-SOD afforded some protection from damage just 10 minutes after exercise in the older animals.
What does this all mean?
Free radicals, as well as sheer mechanical forces, contribute to exercise-associated muscle damage. However, the extent to which the free radicals produce mayhem can be checked by the use of anti-oxidants like PEG-SOD (and Soren's formula?). Finally, old muscles seem to be more susceptible to oxidative damage, compared to younger sinews.
Other research sounds the same theme - that older muscles are more prone to peroxidation and may need more anti-oxidant help. For example, one study found significantly more ultrastructural muscle damage in older men performing 45 minutes of high-intensity eccentric exercise, compared with young men performing eccentric exercise at a similar intensity ('Plasma creatine kinase activity and exercise-induced muscle damage in older men', Med Sci Sports Exerc, Vol. 23, pp. 1028-1034, 1991).
Bear in mind that older men are typically less active and fit than younger men, and lower levels of physical activity may increase the degree of eccentric-exercise-induced muscle damage. However, it is also possible that skeletal muscle in older individuals may simply be prone to more intrinsic damage as a result of exercise, perhaps because the anti-oxidant system declines with age. Some experts also believe that older individuals have higher populations of muscle cells which are susceptible to injury during exercise, and rates of skeletal muscle lipid peroxidation have been shown to increase in older people ('Alteration of antioxidant enzymes with aging in rat skeletal muscle and liver', Am J Physiol, Vol. 258, pp. R918-R923, 1990). Older individuals display a greater accumulation of oxidised proteins in their muscles, compared to young people, which suggests that with ageing the increase in the rate of lipid peroxidation is greater than the increase in the activities of natural anti-oxidant enzymes. It appears that older athletes need to be particularly careful about taking in adequate levels of anti-oxidants, especially if they exercise strenuously; naturally, older athletes might benefit more than younger ones when given something akin to Soren's formula.
So, what's the bottom line? Although it is not an ergogenic aid, vitamin E appears to limit muscle-damaging peroxidation processes and enhance the adaptive response to exercise, especially in older athletes and individuals of medium to low fitness. There may also be a synergism between vitamins C and E which boosts recovery following severe workouts. Finally, Soren Mavrogenis' anti-inflammatory formula looks really promising; it may well control inflammation and speed recovery in damaged muscles and connective tissues (we'll keep you posted as more information becomes available). His supplements are good for your overall health - and may be just the right pacifier for your angry Achilles tendon, too.