Peak Performance looks the relationship between increased training intensity/load and the impact on sleep quality, and explains how athletes can optimise sleep quality regardless of training loads MORE
Carbohydrate protection against muscle damage
Eating in a way that keeps your body primed for peak fitness can also reduce your risk of injury. Firstly, eating foods that will help to fend off fatigue will minimise injuries arising from tiredness and weakness. Secondly, some of the metabolic processes which can lead to muscle soreness and damage can be counteracted to a degree by dietary factors.
It’ s old news that keeping your muscles stacked with glycogen can help your endurance capacity. But did you know that a respectable glycogen credit will also make injury less likely? There’s evidence linking muscle glycogen depletion with both fatigue and injury. The connection is simple – muscles that are fatigued lose their strength, and thus their ability to protect joints. For example, take that favourite injury, the shin splint. While you’re running, you rely on one particular muscle to take proportionately more strain – a strip of sinew that runs down the shin to the inside edge of the foot and pulls the foot inward and upward. During running, this muscle works at least twice as hard as other local muscles, and is therefore most likely to fatigue first. As it gets tired, the risk of shin splints and stress fractures is likely to rise, as does the risk of knee injuries.
Sports scientists argue that apart from the risk of direct damage to an overworked muscle, fatigue may result in the athlete employing different movement patterns, thereby exposing untrained muscles to an unexpected demand, and making joint injury more likely. For example, researchers found that repetitive overhand throwing fatigues the stabilising muscles surrounding the shoulder, making dislocation more of a risk.
The two causes of muscle fatigue
Fatigue itself is a broad concept, including a number of different components – from mental through the nervous system to the muscle itself. Your diet can help to offset fatigue at the muscular level.
There are two distinct metabolic components of fatigue that develop in the muscles: 1) accumulation of certain metabolites and 2) depletion of other metabolites. The accumulation component includes an increase in the amount of hydrogen ions (eg, as a result of lactate buildup). Depletion includes decreasing amounts of fuels found inside the muscle cells – ie, ATP, phosphocreatine and glycogen.
Fatigue may not be the sole cause of injury, but one of a number of contributing factors. Researchers Worrell and Perrin reviewed the literature on the causes of hamstring strains, and concluded that fatigue was one of several factors that can contribute to this type of injury (J Orthop Sport Phys Ther v0116, ppl2-18).
The fatigue-injury link
Common sense would suggest that exercising with muscles which are fatigued is likely to damage those muscles. This has been borne out when samples of athletes’ muscle fibres have been extracted and inspected under the microscope. Various groups of researchers have examined skeletal muscle tissue taken by biopsy from athletes after endurance exercise. They found deterioration and degeneration in the structures inside the muscle cells, together with significant inflammation in the muscle tissue. Oedema, increase in connective tissue and degeneration of muscle fibre has also been observed after distance running.
This type of muscle damage is not always accompanied by a perception of soreness, unlike damage which occurs after eccentric exercise. ‘Eccentric’ activity is where your muscles are contracting while simultaneously being stretched. An example of this is running downhill – your thigh muscles are being stretched by the force of gravity at the same time as they are contracting as part of the mechanics of running.
Prolonged exercise and eccentric exercise represent two distinct mechanisms of muscle damage, both of which end up with the same result. Muscle damage due to eccentric exercise appears to have mechanical causes. High tension developed in single muscle fibres during muscle lengthening may bring about the damage. Glycogen depletion is probably not important in injuries sustained as a result of eccentric exercise. But some experts believe that restocking glycogen after this type of exercise may speed up repair.
In comparison, prolonged exercise is associated with a depletion in muscle glycogen stores, which in turn results in a decrease in energy production. The stress of trying to sustain a level of work output which cannot be met by sufficient fuel is thought to contribute to muscle damage. Glycogen, when broken down into its constituent units of glucose, can be used to make ATP.
Who is affected by glycogen-deficient fatigue?
Fatigue experienced in sports performed at low intensities (less than 50% V02 max) is not due to running out of fuel, because at this pace, fat can be used to provide a steady supply of ATP. ATP is the ultimate fuel used by muscles for energy, and can be made at a slow steady pace from fat (glycogen can be used to supply ATP at a faster rate). Most of us carry enough fat to fuel many hours of low- intensity exercise. Fatigue in this scenario is usually a result of a central nervous system component.
In contrast, fatigue in trained athletes exercising at moderate to heavy intensity (SO-75% V02 max), is related to depletion of the glycogen needed to fuel a faster pace. Stores of glycogen stashed away in the muscles and liver will be running low after about 90 minutes of this level of exercise. Blood glucose will start to drop, and to compound this, muscles will be less able to take up what glucose is circulating in the blood, as glucose needs to be conserved for use by the brain. Eventually, there will be a shortfall between the muscle cells’ demand for glucose and the amount available. Fatigue and discomfort will set in – and this is when injury is most likely to strike.
At this pace, an unfit individual is less likely to experience fatigue due to depletion of glycogen, and more likely to experience the accumulation component. Lactic acid will start to build up, and force a reduction in pace. As exercise intensity increases to 75-90% V02 max, trained athletes may experience fatigue from a combination of the depletion and accumulation factors – ie, both glycogen depletion and lactic acid buildup. Untrained people will be unable to keep up such a pace for very long because of high levels of lactic acid.
Very short supramaximal bursts of activity (greater than 100% V02 max – eg, in sprinting) are limited by availability of creatine phosphate. This is stored in the muscle cell in limited amounts and is the only substance that can be used to regenerate ATP.
Intermittent exercise, too
Similar to continuous exercise, intermittent exercise results in glycogen depletion. Thus, a footballer alternately sprinting and walking during a match will end up low on glycogen, as will a tennis player at the end of a match.
So, athletes most vulnerable to glycogen depletion-related injury will be those in regular training, who are exercising at moderate intensities for over an hour. Several studies have supported this, finding that prolonged moderate and intermittent exercise coincide with muscle glycogen depletion and are related to injury (‘Carbohydrate strategies for injury prevention’, Journal of Athletic Training Vol 29, pp244-254).
For example, a study which investigated injuries in downhill skiers used examination of muscle biopsies. There was a large decline in muscle glycogen content after an entire day of downhill skiing. The investigators concluded that depleted glycogen stores were the reason that more injuries occur toward the end of the day, (‘Physiological demand in downhill skiing’, Phys Sportsmed Vol 5, pp28-37).
Another team of researchers examined the association of exercise-induced muscle glycogen depletion and repletion with structural changes in muscle cells. Forty runners completed a marathon and needle muscle biopsies were performed immediately, one week, and one month after the race. They found that the glycogen depletion and repletion pattern immediately after the race and during recovery correlated with the pattern of muscle fibre damage and repair. The researchers concluded that the damage resulted from metabolic stress – ie, the continued demand on the muscle to produce work despite depleted glycogen stores (Am J Pathol, vol 1 1 8, pp33 1 -339).
Although studies tend to focus on specific events, keeping your glycogen level topped up is just as essential in training. It’s all too easy to gradually drain your glycogen stores if you’re training without eating a diet high enough in carbohydrates.
So how much carbo do you need?
There’ s consensus that 8- lOg of carbohydrate per kg of body weight will maintain appropriate glycogen levels during heavy training. For competition itself, carbohydrate loading is a protocol which is only likely to be of benefit for athletes whose event involves continuous moderate exercise for longer than 60 minutes, or whose event requires repeated bouts of high-intensity exercise. A recommended regime is to begin seven days before D-day, gradually tapering your activity while stepping up the proportion of carbohydrate that you eat. For the last three days, your carbo consumption should be around 500-600g/day.
Before exercising, it may be beneficial for endurance competitors to consume a liquid carbohydrate meal one hour beforehand. Most importantly, if you are competing for longer than an hour, if you can take in carbohydrate while exercising, you will delay the onset of fatigue. Glucose polymers (such as maltodextrin) are a good way of taking in carbohydrate while on the move. Ideally, you should aim for a 6-8% solution containing 15-20g of carbohydrate per 7OZ of water, and try to drink some every 15 minutes.
Free, radical and harmful
In addition to making sure that your diet minimises muscle fatigue, it may be possible to minimise a different type of direct muscle damage by using particular nutrients.
The process of using oxygen to generate energy has a potentially harmful side-effect. This is the production of free radicals – highly charged chemicals which can play havoc with cell contents. Cell membranes of red blood cells and muscle cells are particularly vulnerable to attack. Muscle cells can become leaky, or most extremely, completely torn open. If this happens, enzymes can be let loose from inside the cell and significantly disrupt the ability of skeletal muscles to contract. In addition, the products of membrane damage attract neutrophils (a type of white blood cell), encouraging them to create local inflammation. Athletes are more prone to free radical damage because they are processing more oxygen to provide energy.
There is something you can do, however. As we’ve pointed out before in PP, antioxidants are substances which can protect against, or minimise, free-radical damage. A key player is Vitamin E, which lies in wait in cell membranes, capable of disarming any free rads that come flying by. It becomes deactivated in the process, however, so if there is a high load of free radicals to deal with, Vitamin E can get used up. Vitamin C plays a role in helping to regenerate the active form of vitamin E.
Animal studies have found that vitamin E deficiency leads to muscle damage, and impaired endurance capacity. However, studies where supplements of vitamins E and C have been given to athletes have not come up with very impressive results in terms of improved performance. But it’s still possible that they can reduce the risk of muscle damage. For example, in one short-term study, giving vitamin E supplements decreased measures of cellular damage after endurance exercise (Int J Biochem, Vol 21, pp835-838). There isn’t agreement over what the optimal levels of antioxidants are – however, megadoses of vitamin E are not recommended as they seem to be without effect.
Good and bad fat
Another nutritional factor which has a bearing on free radical damage is the type of fat in your diet. Cell membranes in your body are made up of specially adapted fats and proteins. It’s been discovered that membranes which are rich in polyunsaturated fats are far more vulnerable to free radical attack. Luckily, this is something that can be influenced by diet. Eating more monounsaturated fat in place of polyunsaturates will reduce the polyunsaturate levels in cell membranes, meaning that muscle and red blood cells will be more resistant to damage. One of the commonest sources of polyunsaturated fat in most people’s diets is vegetable cooking oil (eg sunflower, corn oil) and , vegetable margarines. Monounsaturated alternatives are olive oil for cooking, and spreads based on olive oil.