Heat limits athletic performance. The way heat causes fatigue may be through an elevated brain temperature.
Our bodies do not perform as well in hot conditions. Hyperthermia is when the body gets overheated resulting in a decrease in maximal power output. Most of us have experienced the fatigue that occurs with heat while exercising or during labor. Personal experience tells us that heat creates fatigue, but what is the physiologically basis of this heat-induced fatigue?
Before looking at how heat affects performance it is important to understand fatigue. There is much debate among today's exercise physiologists about what actually limits performance during maximal-effort exercise. It is a muscles versus brain dissension. Do the muscles tire, signaling fatigue to the brain or does the brain, in an effort to avoid injuring muscle tissue, signal fatigue to the muscles? The idea that the brain is actually responsible for limiting performance was first introduced in the late 19th century, but has not yet been proven.
A hot environment makes it harder for the body to regulate its body temperature during exercise for several reasons. Blood cools off muscle tissue by moving into the body's core and out to the skin. A hot environment means that the skin is unable to dissipate heat easily due to a reduced temperature gradient. The elevated temperature of the skin also lowers the temperature gradient between the body's core and skin. During exercise in a hot environment, blood is simultaneously needed to deliver oxygen to the muscles and to thermoregulate by going to the skin. To make matters worse, blood pressure is reduced because water is being lost as sweat. This strain on available blood is why dehydration is so detrimental to athletic performance in hot environments.
One study found that regardless of the temperature of the exterior environment fatigue always sets in at the same core body temperature [Walters, et al. (2000). Exercise in the heat is limited by a critical internal temperature.]. The authors reasoned that a warm environment simply means that the "critical" core body temperature is reached sooner. However, this critical core body temperature theory has been challenged recently by studies showing ways of altering the critical core body temperature. Dopamine and caffeine were both shown to increase the core body temperature that fatigue sets in. Dehydration, on the other hand, lowered the core body temperature at which fatigue set in. Therefore, not only does being dehydrated mean that your body has a harder time regulating its body temperature, but the body temperature at which fatigue comes on is lower.
The brain's ability to regulate its temperature is stressed during exercise. Cerebral metabolism increases during exercise. Yet, the brain must deal with reduced cerebral blood flow because blood is being diverted to active muscles and thermoregulating skin. It is hard to determine if the core body temperature or brain temperature is responsible for fatigue. Because the brain gets arterial blood from the body core their temperatures are closely linked. Thus, a hot body core results in a hot brain. The brain is typically a fifth of a degree Celsius above the core body temperature. One recent study used experimental techniques to selectively heat the brain during exercise [Nybo, Lars (2012). Brain temperature and exercise performance]. The results suggest that the brain's temperature has a significant impact on performance. However, other studies have concluded that the skin's temperature sensors are responsible for hyperthermia fatigue [Sawka et al. (2012). High skin temperature and hypohydration impair aerobic performance].
In conclusion, it appears that hyperthermia causes fatigue by elevating the brain's temperature. Much debate still remains regarding the source of fatigue and the role that hyperthermia plays on fatigue. Understanding the way that heat decreases performance will provide avenues for increasing athletic capability in warm environments.
Muscle protein synthesis is activated through exercise and nutrition. This myosin molecule (right) is one of many muscle proteins that are generated during muscle protein synthesis following exercise or an amino acid rich meal.
For a competitive athlete, one of the primary goals of working out is to stimulate muscle protein synthesis. Muscle protein synthesis drives muscle hypertrophy, an increase in muscle mass. There are two ways to drive muscle protein synthesis: nutrition and exercise. Foods with essential amino acids stimulate muscle protein synthesis. Muscle protein synthesis is especially important after resistance training like lifting weights, but is also at play following endurance activities such as swimming or cycling.
If essential amino acid intake stimulates muscle growth why can't someone build muscle mass by eating lots of protein? The reason is the "muscle full" response. According to a 2012 review by PJ Atherton and K Smith entitled Muscle Protein synthesis in response to nutrition and exercise (Issue 590 of The Journal of Physiology) the "muscle full" response halts amino acid uptake. Muscles will take up amino acids for about 90 minutes before the muscle full point is reached. Following resistance training, the muscle will take up amino acids for an extended period of time. Interestingly, this exercise-induced extension of the muscle full response occurs up to 24 hours post-exercise bout.
Following exercise the body uses the amino acid equivalent of 20 grams of protein. In addition, the way in which the body stores amino acids for muscle protein synthesis suggests that a greater frequency of small protein meals trumps one large meal. While amino acids trigger muscle protein synthesis, insulin decreases muscle protein breakdown. Insulin controls sugar levels in the blood by lowering blood sugar levels following a meal. However, insulin also rises following a meal that is carbohydrate free in order to halt catabolic muscle protein breakdown.
A trained athlete will have a specific muscle protein synthesis response. Due to increased efficiency, the trained athlete will spend less time doing muscle protein synthesis following exercise. This specificity means that an endurance athlete will build mitochondrial protein (mitochondria power aerobic work), but not myofibrillar protein. Resistance trained athletes will have post-exercise myofibrillar synthesis, but not mitochondrial protein synthesis. An elegant study demonstrated this by having athletes exercise one leg on a cycle bike and another leg on a resistance machine (Wilkinson et al 2008). A person who rarely exercises will have a less specific and efficient muscle protein synthesis response following a workout.
In conclusion, nutrition and exercise have an overlapping role in regulating muscle protein synthesis. Determining the optimal conditions of muscle protein synthesis would aid athletes interested in bettering their performance.
Fat literally accrues in the brain of mice consuming a diet high in fat. Exercise was unable to reverse the fat accumulation. The consequences of hypothalamic lipid accumulation may include neural dysfunction and problems with brain regulation.
Adipocytes are cells whose specific function is to take up fat. However, fat can also be stored in other cells, a process called lipotoxicity. Excessive fat accumulation in non-adipose tissue can lead to cellular dysfunction and in extreme cases, cell death or apoptosis.
The central nervous system can be affected by lipotoxicity. In a study published this month in the Journal of Physiology, fat content in the hypothalamus region of the brain was observed in mice fed a high-fat diet (Consumption of a high-fat diet, but not regular endurance exercise training, regulates hypothalamic lipid accumulation in mice, 2012, Melissa L Borg, et al.). Fats generally are not a source of fuel for the brain (glucose is the brain's primary fuel and fat-derived ketone bodies substitute when the body is starved of carbohydrates). Yet, fatty acids can cross the blood-brain barrier and reach the hypothalamus for regulatory purposes. The hypothalamus is the body's hunger and body weight regulator. In addition to neuronal signals, the hypothalamus receives input from the levels of fatty acids in the cerebral spinal fluid. The hypothalamus has a limited means of oxidizing fatty acids; therefore, high levels of fatty acids result in fat being stored in the hypothalamus.
The study found that a high fat diet resulted in an increased amount of lipotoxicity in the hypothalamus. Surprisingly, exercise did not reduce the amount of lipids in the high fat diet mice. The mice were fed a high fat diet (59% of calories from fat) or low fat diet (5% of calories from fat) for twelve weeks. Half of the high fat diet mice were exercised six weeks into the study. As the graph below shows, exercise in the high fat diet mice was able to drop most of the added body weight.
The high fat diet increased a variety of fats in the hypothalamus. Phospholipids, glycerol lipids, saturated fatty acids and monounsaturated fatty acids were all increased in the hypothalamus as a result of a high fat diet. In addition, high fat feeding increased hypothalamic lipid species known to cause insulin resistance. Yet, exercise was unable to reverse the increase in hypothalamus lipids.
The figure above demonstrates that a substantial, 6-week exercise program was not able to substantially reduce the hypothalamus lipid content in mice fed a high fat diet. This suggests that the only way to control fat accumulation in the brain is through diet. Since exercise is not a viable means of reversing fat accumulation in the hypothalamus, other means of reducing lipid accumulation, and the harm it may cause to brain regulation, must be sought.
In conclusion, excess lipid accumulation in non-adipose tissue causes cellular dysfunction leading to diseases such as diabetes. Therefore, lipid accumulation in the hypothalamus due to a high fat diet probably harms regulatory processes in the brain. In the study discussed, exercise was found not to reverse hypothalamus lipid accumulation. The fat content of one's diet should be monitored even in people with a healthy body weight.
Chocolate milk is shown by one study to perform as well, if not better than, leading sports recovery drinks.
US gymnast Aly Raisman stunned Olympic viewers by winning two gold medals and one bronze medal at the London 2012 Olympics. Many fans were surprised to learn that Raisman drinks chocolate milk after every workout. However, given the scientific research behind chocolate milk as a recovery drink, such a habit is not surprising. Perhaps most exercise enthusiasts are surprised to learn that chocolate milk is one the most efficient post-workout drinks because chocolate milk is not marketed as an athletic recovery drink. Gatorade, which is simply sugar, salts and water, has a sports-specific marketing campaign behind it as well as paid endorsements by many top athletes. The purpose of a recovery drink is to replace depleted glycogen stores. Chocolate milk, with a high concentration of carbohydrates, fats and protein, is well qualified at restoring glycogen stores.
One study supporting chocolate milk's workout recovery ability compared the recovery efficiency of chocolate milk with a carbohydrate replacement drink and a fluid replacement drink (Chocolate Milk as a Post-Exercise Recovery Aid; 2006; Jason R. Karp, et al.). A carbohydrate replacement drink, such as Endurox, focuses primarily on replacing carbohydrates lost during exercise. A fluid recovery drink, such as Gatorade, focuses primarily on rehydration and replacing lost electrolytes. Chocolate milk is closer to a carbohydrate replacement drink because both have a similar composition of carbohydrate and protein.
In the aforementioned study, nine healthy, highly-trained cyclists from Indiana University took part in a maximum effort interval workout designed to deplete glycogen stores. The subjects then had a four hour recovery period in the lab. During the recovery period the subjects received either Kroger low-fat chocolate milk, Gatorade fluid replacement drink, or Endurox carbohydrate replacement drink. Each drink was administered in an isocaloric amount. Following the four hour recovery period each subject did a maximum effort endurance test at 70% of VO2max. As Figure 1 (below) shows, both chocolate milk aided recovery and the fluid replacement drink (Gatorade) aided recovery saw significant increases in total work and time to exhaustion in the post-recovery workout compared to carbohydrate replacement drink (Endurox) aided recovery.
To understand the physiological differences resulting from each recovery drink, heart rate, blood lactate and water mass measurements were taken. As Figure 2 (below) presents, trials with chocolate milk aided recovery had a lower heart rate. In addition, blood lactate levels were lower at the end of the four hour recovery period in the chocolate milk aided recovery trial.
The authors suggest that because the endurance test was at 70% of VO2max, chocolate milk's fatty acids may have played a role. This is because at 70% of VO2max the body is primarily aerobic where it is using both glycogen and fatty acids in the blood. In addition, because the recovery time was only four hours the muscles were able to take up the simple monosaccharides and disaccharides found in chocolate milk, but possibly not more complex carbohydrates found in Endurox. As a footnote, the authors used many precautions to prevent scientific bias, but they did receive money from the Dairy and Nutrition Council.
In conclusion, chocolate milk appears to perform as well as, if not better than, commercially marketed sports recovery drinks.