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Fueling for Exercise and Recovery How to Optimize Carbohydrate Intake by Justin Robinson, MA, RD, CSSD, FAFS, CSCS

The Case for Carbohydrate: An Overview

 

You’ve seen the images on TV: a struggling athlete sweating and in pain, trying to cross the finish line of a race, or another, in agony, being helped off the racecourse. These are highly trained athletes who are competing at the highest level. Others, famously called “weekend warriors,” also are looking to improve performance so they are fit enough to participate in individual or team sports. How does carbohydrate fit in with these images?

 

Athletes continually seek new strategies to improve performance, whether these strategies are beneficial or potentially dangerous. Nourishing the body with adequate nutrients, especially carbohydrates, before, during and after an athletic event can improve performance in a number of sports or activities.

 

Carbohydrate ingestion is important before, during and after exercise. Adequate endogenous carbohydrate stores (muscle and liver glycogen and blood glucose) are critical for optimum athletic performance during intermittent high-intensity work and prolonged endurance exercise. Consuming carbohydrate-rich foods and fluids before exercise restores liver glycogen, especially for morning exercise when liver glycogen is depleted following an overnight fast. Timing is important, however, so athletes should adjust the amount of carbohydrates ingested before exercise to allow sufficient time for digestion and absorption and to avoid gastrointestinal upset.

 

Consuming carbohydrates during exercise can improve performance by maintaining blood glucose levels and carbohydrate oxidation. Also, consuming adequate carbohydrates after glycogen-depleting exercise facilitates rapid glycogen restoration, especially among athletes engaged in daily intense training or tournament activity.¹

 

In addition to fueling with carbohydrates according to intensity and endurance levels required by the activity, using multiple carbohydrate sources compared to a single source allows for greater performance in events lasting more than three hours. Multiple transportable carbohydrate consumption also allows for rapid resynthesis of muscle glycogen after exercise, which is especially important for athletes who train intensely every day or for those who compete in multiple events over a short period of time.²

 

Nutritional strategies that enhance and improve carbohydrate availability before, during and after exercise are recommended to enhance endurance performance.¹

 

Substrate Utilization

 

Carbohydrate and fat. Carbohydrates and fats are the primary fuel sources used during endurance exercise (protein provides a minimal contribution). The relative amount of fat and carbohydrate oxidized depends on the intensity of exercise. At low intensities, fat provides the majority of energy to the system; but as intensity increases, a greater percentage of carbohydrate is oxidized to provide energy. As a result, exercise performance in endurance events is dependent upon carbohydrate ingestion and use, and it may even be directly correlated to carbohydrate intake.^2-4

 

As a high-energy substrate (more than twice that of protein and carbohydrate), fat has the potential to provide hours of fuel to the exercising body. Research on the application of fat ingestion during exercise, with limited carbohydrate intake, may have its application; however, research is still emerging. Likewise, metabolic efficiency, or other fat-adaptation practices may be appropriate for some endurance athletes; however, the current position stances of the American College of Sports Medicine and the Academy of Nutrition and Dietetics (formerly the ADA) support the included guidelines and recommendations.⁵

 

Protein and fiber. Both protein and fiber are essential nutrients for overall health and play an important role in the overall diets of athletes. Protein with meals typically slows gastric emptying and therefore may be beneficial only in small amounts before exercise, or farther from the beginning of exercise (>2 hours). Likewise, fiber (albeit having numerous general health benefits) also slows gastric emptying, which may contribute to gastric upset, or increased transit time, during exercise.

 

Energy Stores in Humans6
Tissue Fuel	Reserve (g)	Provides Fuel For
		Starvation	Walking	Marathon
Blood Glucose*	20	40 minutes	15 minutes	4 minutes
Liver Glycogen*	80	3.5 hours	70 minutes	18 minutes
Muscle Glycogen*	350	14 hours	5 hours	70 minutes
Fat	9,000 to 15,000	34 days	11 days	3 days
Body Protein	6,000	15 days	5 days	1.3 days
*Endogenous carbohydrate stores

 

 

Effectiveness of a Pre-Exercise Meal

 

Consuming carbohydrate-rich foods and fluids two to four hours before exercise contributes to a number of positive effects in the body. This practice may:⁷

• Restore liver glycogen, especially for morning exercise when liver glycogen is depleted
• Increase muscle glycogen stores, if they are not fully restored from the previous exercise session
• Ensure hydration
• Diminish hunger, which may impair performance
• Provide a psychological boost

Research suggests that the pre-exercise meal contain 1 g to 4 g of carbohydrates per kilogram of body weight (1g/kg to 4 g/kg) and be consumed one to four hours before exercising.¹ To avoid potential gastrointestinal distress, when blood is diverted from the gut to the exercising muscles, the carbohydrate and calorie content of the meal should be reduced the closer to exercise it is consumed. For example, a carbohydrate feeding of 1 g/kg is appropriate one hour before exercise, 2 g/kg of carbohydrates two hours prior, 3 g/kg of carbohydrates three hours prior, and 4 g/kg of carbohydrates four hours before exercise. To further decrease the chances of gastrointestinal distress, all pre-competition rituals, including food and fluid consumption, should be practiced regularly to account for individual reactions.

 

Outside of the laboratory, carbohydrate intake is strongly associated with race day performance among marathon runners and triathletes.^2,3 A study of the 2009 London Marathon determined that competitors who consumed greater than 7 g/kg body weight of carbohydrate the day prior to the race had significantly faster race speed and maintained that pace longer than those who consumed less than 7 g/kg.³ Similarly, analysis of an Ironman triathlon revealed that carbohydrate intake during the event inversely correlated to finishing time, resulting in a better performance.²

 

Studies That Defined Carbohydrate Use for Athletes

 

Based on the results of a study from the late 1970s, athletes were cautioned to abstain from eating carbohydrates in the hour before exercise. This study concluded that consuming glucose 30 minutes prior to high-intensity cycling caused an initial, rapid drop in blood glucose, which reduced exercise time.⁷ The authors attributed the impaired endurance to accelerated muscle glycogen depletion, although muscle glycogen was not measured. High blood insulin levels induced by the pre-exercise carbohydrate feeding were determined to be the cause for this chain of events.⁷

 

Subsequent studies have contradicted these results.⁷ Pre-exercise carbohydrates either improve performance by 7% to 20% or have no detrimental effect. In most cases, the decline in blood glucose (likely resulting from post-prandial insulin rebound) observed during the first 20 minutes of exercise is self-correcting with no apparent effects on the athlete.⁷ The exercise-induced rise in epinephrine, norepinephrine and growth hormone inhibits the release of insulin and counters insulin’s effect in lowering blood glucose.

 

Glycemic index. A 1991 study that manipulated the glycemic response to pre-exercise meals first sparked interest in the use of the glycemic index (GI) in the sports setting. The GI is a measure of the effect of carbohydrates on blood sugar levels. Carbohydrates that break down quickly during digestion and release glucose rapidly into the bloodstream have a high GI; carbohydrates that break down more slowly, releasing glucose more gradually into the bloodstream, have a low GI.⁷

 

In theory, low-GI food choices may provide a more sustained source of fuel when consumed before exercise. Low-GI foods (beans, milk and pasta) provide a slow and sustained release of glucose to the blood, without an accompanying insulin surge. Lentils (low GI) were consumed one hour prior to moderate-intensity cycling and increased endurance compared with the same amount of carbohydrates from potatoes (high GI). The lentils promoted lower postprandial blood glucose and insulin responses, as well as more stable blood glucose levels during exercise than the potatoes.⁷

 

Some athletes react negatively to carbohydrate feedings in the hour before exercise and experience symptoms of hypoglycemia and a rapid onset of fatigue. The precise reason for this extreme reaction is not known, further emphasizing the importance of practicing fueling strategies. Preventive strategies for these individuals include consuming low-GI carbohydrates before exercise, eating carbohydrates only a few minutes before exercise, and waiting until exercising to consume carbohydrates.⁷ It is important to consider the overall importance of the pre-exercise meal for maintaining carbohydrate availability, since endurance athletes also consume carbohydrate-rich foods and fluids during prolonged exercise. Research has evaluated the effects of the GI of pre-exercise meals on metabolism and performance when carbohydrates were also consumed during prolonged cycling. There were no differences in carbohydrate oxidation or time to fatigue among the low-GI meal (pasta), high-GI meal (potatoes) and controls.⁸ Thus, the beneficial effects of the pre-exercise meal are diminished when adequate carbohydrates are consumed during exercise.

 

In recent years, though, the practice of basing carbohydrate intake recommendations on GI has faded. The measurement of GI is highly variable, and most athletes (and non-athletes) consume meals with multiple food items rather than a single serving of carbohydrate. Moreover, most studies have failed to show performance benefits from consuming low-GI meals before exercise.^7-10

 

Endurance Exercise

 

Consuming carbohydrates during exercise that lasts one hour or longer can delay the onset of fatigue and improve endurance capacity by maintaining blood glucose levels and carbohydrate oxidation in the latter stages of exercise.¹¹ Carbohydrates eaten while exercising supplement the body’s limited endogenous stores of carbohydrates. It has been found that consuming carbohydrates during cycling at 70% of VO₂max can delay fatigue by 30 to 60 minutes.^4,11 Carbohydrates have also been shown to improve performance during running. The simple truth is that athletes can exercise longer and/or sprint harder at the end of exercise when carbohydrates are available.

 

Blood glucose becomes an increasingly important source of carbohydrates as muscle glycogen stores decline. Consuming carbohydrates during endurance exercise maintains blood glucose levels at a time when muscle glycogen stores are diminished. During prolonged exercise, ingested carbohydrates can account for up to 30% of the total carbohydrates oxidized. Carbohydrate use — and therefore ATP production — can continue at a high rate, enhancing endurance.¹¹ The performance benefits of consuming carbohydrates during exercise may be additive to those of a pre-exercise meal. Cyclists who received carbohydrates both three hours before and during exercise were able to exercise longer than when receiving carbohydrates either before exercise or during exercise. Combining carbohydrate feedings improved performance more than either fueling alone; however, the improvement in performance with pre-exercise carbohydrates was less than when smaller quantities of carbohydrates were consumed during exercise.¹¹ Thus, to obtain a continuous supply of glucose, the endurance athlete should consume carbohydrates during exercise.

 

Central Nervous System Benefits of Carbohydrate Consumption

 

Beyond physiological benefits, recent evidence suggests that carbohydrates may improve performance during high-intensity exercise lasting 45 to 75 minutes (i.e. 15-kilometer run or 25-mile bicycle time-trial) by exerting a positive influence on the central nervous system. Further, studies have demonstrated that a carbohydrate mouth rinse improves performance, possibly by activating areas of the brain associated with motivation and reward. Beneficial effects are typically seen when an athlete has not eaten for a while, such as after an overnight fast or several hours after a meal.^4,12

 

Stop-and-Go Sports

 

Carbohydrates may also improve performance in stop-and-go sports such as basketball, soccer, football and tennis, which require repeated bouts of high-intensity, short-duration effort lasting an hour or longer.¹³ At the least, carbohydrate ingestion does not seem to impede performance.⁴ Carbohydrates may improve performance in stop-and-go sports by:^2,4,13

• Selectively sparing glycogen in type II (fast-twitch) muscle fibers
• Increasing glycogen resynthesis in type II muscle fibers during rest or low-intensity periods
• A combination of both
• Increasing blood glucose
• Stimulating the central nervous system

Appropriate Food Choices for Optimum Fueling

 

High-carbohydrate foods for pre-exercise meals include fruit, cereal, bread products, low-fat or nonfat dairy products, dairy substitutes, vegetables and legumes. One-hundred percent fruit juices and nonfat milk are quality high-carbohydrate beverages. Athletes may also use liquid meals or high-carbohydrate liquid supplements.

 

Foods that are low in fat, low to moderate in protein, and low in fiber are less likely to cause gastrointestinal upset.¹ The high fat content of popular breakfast foods (bacon, sausage, cheese and biscuits) slows gastric emptying and can contribute to feeling sluggish. Carbohydrates are the most efficient source of energy and are rapidly digested. Liquid meal supplements or smoothies may be easier for some athletes to digest and can therefore be consumed if an athlete is unable to tolerate solid foods before competition.⁷

 

Athletes should choose palatable, familiar and well-tolerated foods. The timing, amount and type of carbohydrate foods and drinks should be chosen to suit the needs of the event and individual preferences/experiences. Choices high in fat, protein and fiber may need to be avoided to reduce risk of gastrointestinal discomfort during the event (as these foods have a slower gastric emptying rate than carbohydrates).

 

Limiting fiber intake, for example, in the pre-exercise meal close to the beginning of exercise may prevent a bathroom stop during exercise (while merely inconvenient during training, it can be disastrous during competition). Gas-forming foods such as beans, broccoli, cauliflower and onions should also be avoided. However, eating higher amounts of fiber four hours before exercise or a competition should not cause any distress.

 

Liquid meals. Liquid-meal products, such as homemade smoothies or shakes, can easily fulfill the requirements for pre-exercise fueling, as many are high in carbohydrates, palatable and provide energy and fluid. Liquid meals can often be consumed closer to competition than solid foods because of their shorter gastric emptying time; this may help to avoid pre-competition nausea for athletes, as tension may cause an associated delay in gastric emptying resulting in discomfort.

 

Liquid meals also produce a low stool residue, thereby minimizing immediate weight gain following the meal. This may be especially advantageous for athletes who need to “make weight.” Liquid meals are also convenient fuel for athletes competing in daylong competitions, tournaments or meets, and they can be used for nutritional supplementation during heavy training when calorie requirements are extremely elevated. Benefits of liquid meals include:

• Shorter gastric emptying time (minimizes nausea)
• Low stool residue (minimizes weight gain)
• Convenience
• Nutritional supplementation without feeling “full”
• Potential for high energy-dense meal or meal replacement

 

Many athletes and nutritionists choose to make custom smoothies, which may include milk, protein powder and fruit in a blender (athletes with lactose intolerance can use soy, almond, coconut or lactose-free milk). For variety, yogurt and natural flavoring (vanilla or cinnamon) can be added, and fruit juice or honey can provide sweetness and more carbohydrates. Currently, other popular “boosts” to smoothies include chia gel, flax seeds, coconut oil, unsweetened cocoa powder and raw greens.

 

Liquid vs. solid carbohydrates. Liquid and solid carbohydrates are equally effective in increasing blood glucose and improving performance, although each has certain advantages.^5,14

 

Sports drinks and other fluids containing carbohydrates encourage the consumption of water needed to maintain normal hydration during exercise. Carbohydrate ingestion and fluid replacement independently improve performance and their beneficial effects are additive.¹¹ The electrolytes, especially sodium, in sports drinks help replace sweat sodium losses and stimulates thirst.⁵ Sports drinks are a practical way to obtain water, carbohydrates and sodium during most sports and offer the benefit of simplifying the athlete’s nutrition plan for competition.

 

Carbohydrate-rich foods, energy bars and gels are compact, can be easily carried, provide variety (different flavors and textures) to prevent a boredom-related decline in food intake and help relieve hunger.^14,15

 

Athletes should drink plenty of water when they eat solid food, especially a sports bar or energy gel; otherwise, the athlete may feel “a rock in the gut.” In addition to aiding digestion, drinking water while eating solid foods encourages the athlete to hydrate adequately. Essentially, water with gels or solid food is equal to a sports drink, if comparable calories are consumed.

 

When the athlete’s gut blood flow is low (e.g., during intense cycling or running), the athlete should emphasize carbohydrate-rich fluids (sports drinks, liquid meals, high-carbohydrate liquid supplements, fruit juices and carbohydrate gels) to promote rapid gastric emptying and intestinal absorption. When the athlete’s gut blood flow is moderate (e.g., during moderate-paced cycling or slow running), the athlete may be able to consume easily digested carbohydrate-rich foods, such as sports bars, fruit and grain products (fig bars, bagels or graham crackers) in addition to liquid foods and fluids.¹⁶

 

Athletes can, therefore, generally consume more calories per hour cycling than running and may consume as much as three times the energy on the bike than the run during a race.^2,16 Ironman triathlon competitors often decrease their calorie intake toward the end of the bike segment to start the run with a fairly empty gut to lower the risk of developing gastrointestinal distress. During the run segment of a triathlon, athletes usually consume only sports drinks, gels and water to further reduce the risk of distress.

 

An athlete’s foods and fluids should be familiar (tested in training), easily digested and enjoyable (to encourage eating and drinking). New food and fluids should never be tested during competition, as the result may be severe indigestion and/or impaired performance. It may also be advantageous to eat or drink before feeling hungry or tired, usually within 30 to 60 minutes after beginning exercise. Adopting a strategy of consuming small amounts of foods and fluids at frequent intervals helps to keep the athlete hydrated while minimizing gastrointestinal discomfort.¹⁶

 

Carbohydrate Content of Selected Foods*
Food	Portion	Carbohydrate
Gatorade	1 quart (~1 liter)	60 g
PowerBar	1 bar	45 g
GU Energy Gels	2 gels	50 g
Sport Beans	28 beans	50 g
Clif Shot Blok	6	50 g
Graham crackers	3 large	66 g
Fig bars	4 bars	42 g
Banana	1	30 g
* Information sourced from product labels.

 

Multiple transportable carbohydrates. The maximum amount of carbohydrates that can be oxidized during exercise from a single carbohydrate source such as glucose is approximately 1 g/min (60 g/hr) because the transporter responsible for carbohydrate absorption in the intestine becomes saturated.⁷ Consuming more than 1 g/min from one source does not raise the rate of carbohydrate oxidation and increases the risk of gastrointestinal distress.¹⁷

 

By consuming multiple forms of carbohydrates (e.g., glucose and fructose) that use different intestinal transporters (SGLT1 for glucose and GLUT5 for fructose), the total amount of carbohydrates that can be absorbed and oxidized is increased. Research has shown that when glucose and fructose are ingested together in a 2:1 ratio during exercise at a rate of 2.4 g/min (144 g/hr), the rate of exogenous carbohydrate oxidation can reach 1.7 g/min or about 105 g/hr.¹⁷

 

Drinks containing multiple transportable carbohydrates are also less likely to cause gastrointestinal distress.¹⁷ In theory, consuming multiple transportable carbohydrates should enhance endurance performance by increasing exogenous carbohydrate oxidation and reducing the reliance on endogenous carbohydrate stores. Compared with an isocaloric amount of glucose, the ingestion of glucose and fructose (1.5 g/min) increased peak exogenous carbohydrate oxidation, reduced ratings of perceived exertion and increased self-selected pedaling rate in the latter stages of five hours of cycling at 50% of maximal work rate. While these findings suggested a reduction in fatigue with the ingestion of glucose and fructose compared with glucose alone, direct measures of performance were not obtained.¹⁷

 

In another study, ingesting glucose and fructose (1.8 g/min) improved cycling time trial performance by 8% compared with an isocaloric amount of glucose following two hours of cycling at 55% of maximal work rate. The glucose and fructose may have promoted better ATP resynthesis compared with glucose, thus allowing the maintenance of a higher power output. This was the first study to provide evidence that increased exogenous carbohydrate oxidation improves endurance performance.¹⁷

 

The series of studies conducted by researchers at the University of Birmingham in the United Kingdom demonstrates that consuming between 1.8 to 2.4 g/min of carbohydrates (108 to 144 g/hr) from a mixture of carbohydrates increases oxidation up to 75 to 104 g/hr of carbohydrates.¹⁷ Further research from this group also determined that the athlete’s gut is “trainable” and that adopting a high-carbohydrate diet and consuming multiple transportable carbohydrates during exercise can, over time, improve the absorptive capacity of the intestine, thereby diminishing gastric upset.¹⁸

 

As stated, protein has a number of benefits in the overall diet of athletes and potentially as part of the pre-and post-exercise feedings. The addition of protein to sports drinks, though, does not improve performance when carbohydrate intake is adequate.¹⁹

 

High concentrations of pure fructose should be avoided due to the risk of gastrointestinal upset. Fructose is absorbed relatively slowly and must be converted to glucose by the liver before oxidized in the muscle. Since the maximum rate of oxidation of ingested fructose is less than for glucose, sucrose or glucose polymers, ingesting fructose alone does not improve performance. However, in combination with other carbohydrate sources, fructose is well tolerated and increases exogenous carbohydrate oxidation and improves performance.^1,5

 

Sports drinks that include several different carbohydrate sources (glucose and fructose) may also enhance water absorption, compared with solutions containing only one carbohydrate source. The addition of a second carbohydrate activates additional mechanisms for intestinal transport and involves transport by separate, non-competitive pathways.¹⁷

 

Carbohydrate Dose and Timing of Intake

 

Updated recommendations for carbohydrate intake during exercise are absolute (g/hr), rather than based on body weight.^1,17 Athletes should consume 30 g/hr to 60 g/hr of carbohydrates from carbohydrate-rich fluids or foods during endurance and intermittent, high-intensity exercise lasting 1 to 2.5 hours.¹ As the duration of the event increases, so does the amount of carbohydrates required to enhance performance. During endurance and ultra-endurance exercise lasting 2.5 to 3 hours and longer, athletes should consume up to 80 to 90 g/hr of carbohydrates. Products providing multiple transportable carbohydrates are necessary to achieve these high rates of carbohydrate oxidation.¹

 

Athletes should decide on a refueling plan that meets their nutritional goals (including hydration) and minimizes gastrointestinal distress.¹

 

Carbohydrate Intake Guidelines2
Duration of Exercise	Amount of CHO Needed	Recommended Type of CHO	Additional Recommendations
30 to 75 minutes	Small amounts or mouth rinse	Single or multiple transportable CHO	Nutritional training recommended
1 to 2 hours	30 g/hr	Single or multiple transportable CHO	Nutritional training recommended
2 to 3 hours	60 g/hr	Single or multiple transportable CHO	Nutritional training highly recommended
>2.5 hours	90 g/hr	Only multiple transportable CHO	Nutritional training ESSENTIAL

 

Eating for Recovery

 

The restoration of muscle and liver glycogen stores is important for recovery following strenuous training. It is common for an athlete to engage in prolonged, high-intensity workouts once or twice a day, with a limited amount of time (six to 24 hours) to recover before the next exercise session. Using effective refueling strategies helps to optimize recovery and promote the desired adaptations to training. During competition, especially multi-day events such as bicycle stage races, there may be less control over the exercise-to-recovery ratio. In this case, the goal is to recover as much as possible for the next day’s event. Several factors limiting recovery include:²⁰

• Fatigue interfering with ability to obtain or eat food
• Decrease in appetite following high-intensity exercise
• Limited access to suitable foods at exercise location
• Other commitments (e.g. coach meetings, equipment maintenance)
• Celebration with excessive alcohol intake or “cheat” meals (high sugar, high fat) after competition

 

When there are fewer than eight hours between workouts or competitions, the athlete should start consuming carbohydrates immediately after the first exercise session to maximize the effective recovery time between sessions.¹ The athlete should consume 1 to 1.2 g/kg/hr of carbohydrates for the first four hours after glycogen-depleting exercise. Consuming small amounts of carbohydrates frequently further enhances muscle glycogen resynthesis (every 15 to 30 minutes).¹ Recovery meals/snacks contribute to the athlete’s daily carbohydrate and energy requirements.²⁰

 

During longer periods of recovery (24 hours), it does not matter how carbohydrate intake is spaced throughout the day as long as the athlete consumes adequate carbohydrates and energy (6 to 10 g/kg). The type, pattern and timing of carbohydrate intake can be chosen according to what is practical and enjoyable.^1,7

 

Carbohydrate-rich foods should be emphasized in recovery meals and snacks to supply a readily available source of carbohydrates for muscle glycogen synthesis.^1,20 There is no difference in glycogen synthesis when liquid or solid forms of carbohydrates are consumed; however, liquid forms may be appealing when athletes have decreased appetites due to fatigue and/or dehydration.²⁰

 

Glycogen repletion. There are several reasons why glycogen repletion occurs faster after exercise:

• Blood flow to the muscles is much greater immediately after exercise
• Active muscle cells are more likely to take up glucose
• Muscle cells are more sensitive to the effects of insulin during this time period, which promotes glycogen synthesis
• Phosphorylases and other enzymes are more active immediately following exercise

 

Glucose and sucrose are more effective than fructose in restoring muscle glycogen after exercise, as fructose must first travel through the liver. The type of carbohydrate (simple vs. complex) does not seem to influence glycogen repletion, although like pre-exercise fueling, high-fat, -protein and -fiber foods may slow digestion.²⁰

 

The foods consumed during recovery meals/snacks should contribute to the athlete’s overall nutrient and energy intake. Nutrient-rich carbohydrate foods and lean protein and dairy also contain vitamins and minerals that are essential for health and performance. These micronutrients may be important for post-exercise recovery processes.²⁰ Endurance athletes should avoid consuming large amounts of foods high in fat and/or protein when total energy requirements or gastrointestinal distress limit food intake during recovery. These foods can displace carbohydrate-rich foods and reduce muscle glycogen storage.^1,20

 

Unaccustomed exercise that results in muscle damage and delayed-onset muscle soreness may impair muscle glycogen synthesis. Such muscle damage appears to decrease both the rate of muscle glycogen synthesis and the total muscle glycogen content. While a diet providing 10 g/kg of carbohydrates daily will usually replace muscle glycogen stores within 24 hours, the damaging effects of unaccustomed exercise result in significant delays to muscle glycogen repletion. Even the normalization of muscle glycogen stores does not guarantee normal muscle function after unaccustomed exercise.²⁰

 

Protein. Consuming protein with the recovery meal or snack helps to increase net muscle protein balance, promote muscle tissue repair and enhance adaptations involving synthesis of new proteins.²¹ Adding protein to the recovery feeding, though, does not enhance muscle glycogen storage when the amount of carbohydrates is at or above the threshold for maximum glycogen synthesis (1 to 1.2 g/kg/hr).^1,20 Adding a small amount of protein (0.2 to 0.4 g/kg/hour) to a suboptimal carbohydrate intake (less than 1 g/kg/hour), however, can accelerate muscle glycogen restoration.^4,21

 

Recommendations for carbohydrate and protein intake following exercise include:¹

• When there are fewer than eight hours between exercise sessions, start consuming carbohydrates immediately after exercise to maximize recovery time
• Consume 1 to 1.2 g/kg/hr of carbohydrates for the first four hours after glycogen-depleting exercise
• Early refueling may be enhanced by consuming small amounts of carbohydrates more frequently (e.g. every 15 to 30 minutes)
• Add a small amount of protein to first feeding to stimulate muscle protein synthesis/repair: 15 to 25 grams or 0.2 to 0.4 g/kg

 

The beneficial 15 to 25 g of high-quality protein in addition to carbohydrates can be provided by 16 oz of skim milk (16 g), two to three large eggs (14 to 21 g) or 2 to 3 oz of lean red meat (14 to 21 g).^1,22

 

Putting it All Together

 

Giving competitive athletes or “weekend warriors” good advice on how to optimally fuel for exercise helps them improve their performance. The take-away messages that you can share with your clients, family and friends include:

• Carbohydrate-rich foods are typically the easiest to digest, tolerate and utilize before, during and after exercise
• Carbohydrate intake for exercise performance is well-supported in the research, whereas low-carb, high-fat and high-protein regimens are not yet well-documented (despite the fact that they may be appropriate for some individuals)
• Various forms of carbohydrate (liquid, solid, gel) are equally effective; base the recommendations on an athlete’s tastes, likes, dislikes, trained status and intensity of exercise
• The Glycemic Index (GI) is less useful than previously determined
• Multiple sources of carbohydrates (glucose, fructose, starches and glucose polymers) are important for increased oxidation
• With the use of multiple transportable carbohydrates, the body can oxidize more than 60 g/hr of carbohydrate during exercise
• Provide absolute carbohydrate intake recommendations during exercise (30-90 g/hour)
• Provide relative carbohydrate intake recommendations (based on body weight) before exercise and during recovery
• Carbohydrate intake is also effective in exercise sessions lasting 30 to 60 minutes
• A dose response for carbohydrate intake and race day performance may exist
• Any sports nutrition protocol needs to be specific to the needs of the athlete and familiar to the athlete.

 

Research Reveals the Benefits of Meditation by Susan Taylor, PhD

The practitioner looked at her patient and said, “Your physical symptoms are being caused by stress. One of the many ways to reduce stress and think more clearly is to meditate.”

 

What does “meditation” mean? It can mean many things to many people. But no matter what the meditation style or technique, during meditation people sit quietly, witnessing internal thoughts and external stimuli without getting caught up in them. Some of the practice forms are ancient, and they come from numerous sources.

 

Modern science has developed sophisticated tools to explore meditative practice for clues about how it affects our body and brain. The findings shed new light on the power of meditation to make a measurable difference in our experience of the world. A variety of studies examining different approaches to meditation show that we can exercise some degree of control over things we didn’t think we could change. These scientific studies show that new options for self-healing may be possible through meditation.

 

Concentration practices found in Transcendental Meditation and mindfulness meditation are perhaps the best-known meditation techniques. TM is a technique, derived from Hindu traditions, that promotes deep relaxation through the use of a mantra. A mantra is a sacred word or sound used to focus attention or concentration. Mindfulness meditation uses a process of intentionally paying attention to what is happening in the present moment, both internally and externally, without being distracted by what has already happened or what might happen. Mindfulness meditation trains the participant to be an observer without passing judgment.

 

The relaxation response described by Herbert Benson, MD — the author of the 1970s’ best seller “The Relaxation Response” and a pioneer in studying the effects of relaxation and meditation techniques — cites four basic elements common to eliciting such a response: a quiet environment, a mental device (such as a word), a passive attitude and a comfortable posture.^1,2 Benson’s framework has been established as the “relaxation response” that produces the opposite of the fight-or-flight response.³ The response includes decreases in oxygen consumption, carbon dioxide elimination, respiratory rate and volume, heart rate, muscle tension, and blood pressure, especially in hypertensive people. This relaxation response, or relaxation response meditation, has been used in a variety of healthcare settings by healthcare professionals of various disciplines to treat hypertension and anxiety.^4,5 Because of its physiological benefits, relaxation response meditation is used in most stress-reduction programs.

 

While other relaxation methods, such as prayer, visualization, guided imagery and hypnosis, help people work through stressful issues, they are not categorized as meditation. That is because they keep the client focused on the body, mind and senses. Meditation, in contrast, allows the client to quiet the mind to ultimately go beyond it. This can only be achieved without engaging the senses — sight, hearing, touch, smell and taste — and thoughts.

 

About 13% of U.S. adults use deep-breathing exercises, and 9.4% use meditation as complementary to their healthcare, according to a National Institutes of Health survey. These numbers are higher than for yoga and massage therapy, 6% and 8% respectively.⁶

 

Relaxation and meditation have been shown to be beneficial in the treatment of many diseases because they improve psychological and physical health. As complementary modalities, including meditation, gain more acceptance, healthcare providers as a team need to be informed about their uses and application to clinical practice.

 

Ancient Origins

 

Today’s meditation techniques have their origins in ancient spiritual and healing practices, mostly from Asian religions, particularly those of India, China and Japan. But similar techniques can be found in many other cultures around the world and throughout history. These cultures viewed the mind and body as inseparable, and meditation was the way to access the mind-body-spiritual matrix, allowing for greater awareness.¹ Meditation has been traditional in the East, but became more accessible to the West in the 1960s within the context of science. Researchers began recording changes in physical functions — such as the production of stress hormones and changes in blood pressure, heart rate and respiratory function — that occur with meditation.

 

Although Benson’s description of a relaxation response was convenient as an initial explanation for what happens in the meditative state, later work showed that what was happening physiologically was much more complex than just a reduction in heart and respiratory rate. By the 1990s, meditation was becoming accepted as part of Western medicine, especially through the stress-reduction programs in healthcare facilities. One well-known example is the mindfulness programs organized by Jon Kabat-Zinn, PhD, author, professor and stress-reduction expert at the Stress Reduction Clinic at the University of Massachusetts Medical Center.

 

Inside the Brain

 

Using brain research, medical science has found concrete evidence for meditation’s effect on the body and mind. Research has found that mental discipline and meditative practice can change the workings of the brain and allow people to achieve different levels of awareness, including changes in states of consciousness and learning.⁷ Studies on the meditating brain are becoming more sophisticated with advances in brain imaging and other techniques. Imaging advances have led neuroscientists to reject the view that the brain is fixed early in life and does not change in adulthood, replacing it with a belief that the brain can adapt and change, a concept called neuroplasticity.

 

Some of the first research studies mapping the brain during meditation used electroencephalography. This technique records the electrical activity of the brain during meditation using an EEG monitor. Probes are placed on the scalp, and the changes in electrical activity occur as brain waves. Different regions of the brain are recorded and compared. Such studies on meditation usually report increased alpha waves, the waves that are extensive in anterior channels in the central and frontal regions of the brain and are associated with relaxation of the entire nervous system.^7,8 Theta waves have also been recorded during meditation. Theta waves are dominant in the frontal region, indicating a deeper state of mental silence and pleasant experiences.^9,10 Because these waves occur mostly in the part of the brain occupied by the limbic system — the home of emotional response — they are believed to activate our emotions. During deep meditation, experienced subjects sometimes enter into delta waves, associated with dreamless sleep.⁷

 

Through EEG monitoring during meditation, scientists have discovered increased correlated activity between the two hemispheres with respect to the distribution of alpha activity between the four anatomically distinct regions of the brain — left, right, anterior and posterior — or what is termed brain synchronicity. The research outcome linked hemispheric coherence (the correlated activity) to clear and pure thinking and to creativity.^11,12 This provides evidence that meditation can train the mind to influence and change the structure and connectivity of the brain.^{13 (Level B)}

 

In past two decades, neuroimaging techniques — such as positron emission tomography, single photon emission tomography and functional magnetic resonance imaging — have been used to explore meditation’s effects on the brain. These techniques all measure cerebral blood flow and, therefore, record the metabolic activity in the brain. Because of their expense, these techniques have not been used as extensively as EEG monitoring. The first published study using neuroimaging to examine the meditative state recorded the metabolic state using glucose as the marker.¹⁴ Later, a study measuring oxygen metabolism among meditators proved to be more sensitive in detecting the increased frontal lobe activity.^{15 (Level B)}

 

Recent studies involving functional magnetic resonance imaging (fMRI) and meditation are advancing the understanding of mind-body mechanisms.¹⁶ With fMRI, it is possible to get a reading on brain activity in just seconds. The research involving fMRI suggests that various parts of the brain known to be involved in attention and in the control of the autonomic nervous system are activated, providing a neurochemical and anatomical basis for the effects of meditation on various physiological activities. Studies have shown signal increases during meditation in the areas that govern concentration, mood and memory, which include the dorsolateral prefrontal and parietal cortices, hippocampus/parahippocampus, temporal lobe, pregenual anterior cingulate cortex, striatum, and precentral and postcentral gyri.¹⁶

 

Data have shown that people who meditated 40 minutes a day had a thicker cerebral cortex (the area playing a critical role in decision-making) than people who did not meditate.¹⁷ This research suggests that daily meditation can alter the physical structure of the brain, and it may have positive applications related to aging, such as enhanced memory. Meditation has been shown to produce significant increases in left-sided anterior brain activity, which is associated with positive emotional states. Neuronal firings in the amygdala have been associated with positive emotions and have led researchers to discover and measure the connection between the brain’s lighted activity centers and mood.^{18 (Level B)} Not only did this map brain activity, but it also took the concept of neuroplasticity a step further by showing that meditation may change the mapping of brain circuitry. In a recent review, researchers say that meditation may be of benefit to adults with cognitive impairment, such as Alzheimer disease, but more research is needed.¹⁹ 

 

Mind Over Matter

 

Many studies have shown the health benefits of meditation on various disorders and diseases.

 

Affective disorders. Studies have examined the effects of meditation-based practices on the treatment of depression and anxiety. In one study, patients diagnosed with generalized anxiety disorder with or without agoraphobia showed a reduction in symptoms after a stress-reduction program based on mindfulness meditation.^{20 (Level B)} Patients who participated in a three-year follow-up study using mindfulness meditation techniques — which included body scanning (a practice of turning one’s attention to various areas of the body to de-stress), sitting meditation and mindful hatha yoga — showed a significant improvement in the number of occurrences and severity of anxiety symptoms.²¹ Others studies have shown a significant reduction in anxiety and depressive symptoms among subjects with a mean age of 49.^{22 (Level B)} In a recent meta-analysis of randomized controlled trials, researchers found significant benefits for using mindfulness-based interventions for current episodes of depression, but not for anxiety.^{23 (Level B)}

 

Sleep disturbances related to cancer. A common problem for patients with cancer, sleep disturbance has remained largely unaddressed in the clinical intervention literature. In a study examining the effects of an eight-week program of mindfulness-based stress reduction on a sample of 63 outpatients with cancer, clinical benefits included improved sleep and mood and reduced stress and fatigue. The study findings suggest that programs based on meditation may improve quality of life in patients with cancer.^{24 (Level B)}

 

Chronic pain. Strong evidence exists that relaxation practices are useful for pain. Mindfulness meditation was the basis for an effective behavioral program in self-regulation for chronic-pain patients experiencing low-back, neck and shoulder pain and headache. The 10-week study showed an improvement in patients while traditional medicine had not.²⁵ Another examination of mindfulness meditation in a 10-week study of 90 patients with chronic pain showed positive results in measures of pain, negative body image, symptoms, mood disturbance, anxiety and depression as compared to patients who were given traditional treatment protocols.^{26 (Level B)} A study looking at mindfulness meditation for the treatment of chronic low-back pain in adults with a mean age of 75 showed that an eight-week program may lead to improvement in pain acceptance as well as physical function.^{27 (Level A)}

 

Fibromyalgia. The chronic illness fibromyalgia is characterized by widespread pain, fatigue, sleep disturbance and resistance to treatment. Seventy-seven patients meeting the 1990 criteria of the American College of Rheumatology for fibromyalgia took part in a 10-week group outpatient program to evaluate the effectiveness of a meditation-based stress-reduction program on their illness. The program proved effective, with patients experiencing increased pain relief, global well-being and reduced fatigue.²⁸

 

Immunity. A study compared 10 male runners who practiced meditation for a mean of 12 years to a control group of runners who did not practice meditation. Blood samples were taken before, immediately after and two hours after a race. The study found that runners practicing meditation had lower lymphocyte counts at rest before the race. Just after the race, both groups had more than doubled their white blood cell counts. The study suggests that the long-term practice of meditation may influence absolute lymphocyte counts at rest.²⁹

 

Recent studies involving psychosocial factors and immunologic functioning prove positive. A study based on participation in a mindfulness-based stress reduction program for eight weeks showed not only reductions in anxiety and distress, but those experiencing psychosocial improvements also had reductions in C-reactive protein and an increase in natural killer cell cytolytic activity.^{30 (Level B)}

 

Quality of life. Mindfulness-based cognitive therapy has been shown to enhance quality of life in patients with cancer in different areas and stages. The study involved eight weekly two-hour sessions; participants showed improvement in depression, anxiety, stress and quality of life.³¹

 

Stress. Scientists now understand that under stress, the nervous system activates the fight-or-flight response. The activity of the sympathetic portion of the nervous system increases, causing an increased heart rate, increased respiratory rate, elevated blood pressure and increased oxygen consumption. This fight-or-flight response has an important survival function: It helps an organism to run quickly and escape an attack or to fight off an attacker. But if the fight-or-flight response is activated repeatedly, as often happens in modern societies, the effects are harmful. Many researchers believe that the epidemic of hypertension and heart disease in the Western world is a direct result of this stress. Through meditation, the body gains a state of deep relaxation that diminishes accumulated stress and fatigue.²

 

Other studies have shown that an eight-week meditation program may be effective in reducing perceived stress and improving sleep, mood and memory.^{13 (Level B)}

 

Disordered eating and weight loss. Obesity is an epidemic. A new movement, “mindful eating” brings awareness to an individual about their relationship to food and how that shapes our actions, thoughts and feelings. In a systematic review of the literature, mindful meditation was effective at decreasing binge eating and emotional eating, but had mixed results for weight loss.³²

 

The Contemplative Connection

 

Healthcare practitioners of various disciplines and patients use meditation in a variety of settings. A healthcare provider’s relationship with patients can influence the outcome of clinical problems as well as the satisfaction of provider and patient. A healthcare provider’s physical, emotional and mental health can influence the provider-patient relationship. A study showed that healthcare providers practicing hospice care benefited from meditation practice and that patients in general benefited when their healthcare providers practiced meditation.³³ Meditation training has proved an excellent adjunct therapy for many conditions and should be discussed as an option among healthcare providers.³⁴ And meditation and relaxation techniques are part of a program to help patients reverse heart disease.³⁵

 

Meditation is being incorporated into many clinical practices by teams of healthcare providers. By reducing stress and developing concentration, meditation can not only increase concentration but also may help prevent job burnout.^{36 (Level C)} The result is a better relationship with patients and perhaps a method for self-healing.

 

Meditation is contraindicated in certain conditions and situations. A rule of thumb is that meditation should be used with caution if concerns exist about a patient’s reality testing, ego boundaries, lack of empathy or rigid overcontrol. For example, when treating a patient with schizophrenia with active psychotic symptoms, it may be inadvisable to include meditation as part of treatment because reality testing may be impaired.³⁷

 

Similarly, meditation may be inadvisable in treating some personality disorders that involve a lack of empathy. In such cases, meditation could reinforce the preoccupation with the self that characterizes the disorders.³⁸

 

Meditation is becoming more accessible. The National Center for Complementary and Alternative Medicine, which is part of the National Institutes of Health, considers meditation a “mind-body method,” a category of complementary and alternative medicine that includes interventions that use a variety of techniques to boost the mind’s capacity to affect bodily function and symptoms. Research on meditation and mind-body interventions continues through the National Institutes of Health. With the growing concern about stress-related illness, there may be room for meditation programs as a component of protocols.

 

 

Regulation of Body Weight

At any given time, up to 40 million Americans are on a diet, and probably as many more think they should be on a diet. Interestingly, weight itself often has nothing to do with people’s feelings about dieting — many people just think they are too fat, when in reality their weight is perfectly acceptable and well within health parameters.

 

While the quest for thinness is a national preoccupation, at the same time, obesity is the No. 1 nutritional disease in the U.S. More than two-thirds of adults are overweight; the prevalence of overweight Americans (body mass index [BMI] of 25 kg/m² or more) is 69% in adults older than 20. The percentage of overweight people increased from 47% in 1980, to 56% in 1994, to 68.5% in 2012.¹ The obesity rate for adults jumped from 15% in 1970, to 32% in 2004, and to 35% in 2012 (this indicates there was no significant change among obesity rates for adults and children from 2003–2004 to 2011–2012, according to the National Health and Nutrition Examination Survey [NHANES] data, which is good news).^{1,2 (Level B)} Although obesity crosses ethnic and socioeconomic boundaries, it is more prevalent in African Americans and Hispanics than in Caucasians or Asian-Americans.³

 

Weight Loss and Weight Control

 

From the 1970s, when the obesity epidemic was beginning, to today, the estimated caloric change is approximately 400 kcal/day. What is debated is if the change is from increased calories, decreased physical activity, or a combination of the two.⁴ Clearly, overweight, obesity, and associated diseases and conditions are major problems that most people try to solve by dieting.

 

Unfortunately, 80% of all diets fail. Of the 20% of dieters who do manage to lose weight, an estimated 95% regain what they took off, and many gain back even more weight than they originally lost. Only 5% of dieters who lose weight maintain the weight loss.

 

The quest for thinness can have lifelong health risks. Many diets are not nutritionally balanced. They have too few calories and nutrients, which puts stress on the body. Because improper nutrient intake is a risk factor for many diseases, some diets may put the dieter at increased risk for disease. Accordingly, health professionals across disciplines are examining many long-held beliefs about weight control in light of revolutionary findings concerning regulation of energy metabolism and which types of diets are effective. Hormone-like proteins, produced by genes in fat cells, are involved in the regulation of energy metabolism, energy expenditure and, ultimately, a person’s weight. Many diet strategies (such as low carbohydrate) appear to be an effective way to lose weight, although the long-term consequences are unknown.

 

These findings have sparked a re-examination of basic assumptions concerning weight and weight control, such as:

• What weight is healthy?
• What weight contributes to disease?
• How do adipose tissue, proteins, hormones and gut microbes regulate weight?

 

To answer the first question, it is important to understand how a healthy weight is determined, and the role of body composition in energy balance.

 

BMI

 

BMI is the recommended method to determine weight status and health risk. In metric measurements, BMI equals kg/m², or weight (in kilograms) divided by height (in meters squared). Using imperial measurements, BMI equals weight (in pounds) divided by height (in inches squared), and then multiplied by 703.

 

BMI = kg/m² OR lbs/in² x 703

 

According to the National Institutes of Health, this is an easy and useful guide for determining normal weight, overweight and obesity. BMI correlates to direct measures of body fat. The BMI ranges below are based on the relationship between body weight and disease and death.^5,6 Software and apps to calculate BMI are readily available.

 

BMI Classification of Overweight and Obesity7 (Level ML)
	BMI (kg/m2)	Obesity Class
Underweight	<18.5	—
Normal	18.5 to 24.9	—
Overweight	25 to 29.9	—
Obese	30 to 34.9	I
	35 to 39.9	II
Extreme Obesity	40+	III

 

A person with a BMI of 25 or greater is at increased risk for developing a number of health conditions, including diabetes, heart disease, stroke, hypertension, gallbladder disease and some cancers.

 

Body Composition

 

While useful, BMI does not take body composition into consideration. The body is made up of lean body mass (muscle), fat and bone. Fat-free mass is used to define “everything in the body except fat.” In some circumstances, a person may be classified as overweight based on BMI despite having a very low percentage of body fat and high percentage of lean body mass. Highly muscular athletes often fit into this category.

 

Another person may not be statistically overweight, but if his or her percentage of body fat is high, he or she may be at increased risk of developing one of the conditions associated with obesity. The average body fat percentage for an American woman is about 25% to 31%, while the average American man has approximately 18% to 24% body fat. The recommended amount of body fat for women is between 21% and 24% and between 14% and 17% for men. A man with more than 25% body fat is considered obese; a women with more than 32% body fat is considered obese.⁸

 

Distribution of body fat. Both the amount and the location of fat are important health considerations. Upper-body obesity (also known as android or central obesity) is associated with greater metabolic disturbances, such as glucose intolerance, elevated blood pressure and serum lipids, than lower-body obesity (also known as gynoid obesity). Those with more fat around the waist are at greater risk for increased morbidity and mortality, compared with those with more fat around the hips.

 

Upper-body obesity includes both visceral and subcutaneous abdominal fat deposits. Visceral fat refers to fat storage within the abdominal cavity, surrounding the organs. It is comprised of mesenteric and omental fat cells. Visceral fat is approximately 20% of total fat storage of adult males, and approximately 6% of total fat storage in adult females. Subcutaneous abdominal fat deposits are just below the skin in the abdominal area. Visceral fat is related to increased disease risk, not subcutaneous abdominal fat. In gynoid obesity, all fat storage sites are subcutaneous.^{9 (Level B)}

 

Unfortunately for many, genetics plays a more significant role in determining body fat distribution than any other factor. Environmental factors, such as diet and exercise, are more important in determining total body fat.¹⁰

 

Waist circumference. Both BMI and waist circumference should be considered in diagnosis and evaluation of obesity. Measuring waist circumference is a tool to help determine if a person carries excess fat around the abdomen. Experts recommend measuring waist circumference at least annually in the overweight and obese.⁷

 

To measure waist circumference, locate the upper hip bone and top of right iliac crest. Place a measuring tape in a horizontal plane around the abdomen at level of iliac crest. Before reading tape measure, ensure that tape is snug but does not compress skin, and is parallel to the floor. The measurement is made at the end of an exhalation. A waist circumference greater than 40 inches (102 cm) in men and greater than 35 inches (88 cm) in women is associated with increased disease risk, especially if the person falls into the overweight or obese category.⁶

 

What Is a “Healthy” Weight?

 

Being overweight or obese has health risks, but at what level of “fatness” does a person increase his or her risk of chronic disease? This is an important question for the healthcare team because so many people are overweight, and so few successfully lose weight and keep it off.

 

Losing weight can help reduce blood pressure, serum lipids and elevated blood glucose levels, all of which are risk factors for cardiovascular disease. Many people with type 2 diabetes can stop taking oral medications or avoid having to take insulin shots when they lose weight. High blood pressure is treated more easily as weight decreases. Moderate weight loss in those with hypertension can eliminate the need for medication in up to 50% of cases. Clearly, being overweight or obese has health risks that can be minimized by losing weight.^{10 (Level B), 11}

 

Furthermore, adults who maintain a healthy BMI seem to have an improved quality of life as they age.¹² Only 24.3% of women and 36.5% of men with a BMI more than 30 reported being in good or excellent health, compared with 46.8% of women and 53.8% of men who were at a healthy weight.^{12 (Level B)}

 

Yet the question remains: What is a healthy weight? The answers are not easy to come by. Many studies have investigated the relationship of BMI to morbidity and mortality, and come to different conclusions. Some studies have found that being overweight does not increase mortality, but being underweight does.¹³ Others have found an increase in morbidity and mortality in being overweight or having class I obesity, while other studies have not.¹⁴ It may also be a question of fitness: Those who are fit and overweight may be healthier than those of normal weight who are physically inactive.¹⁵

 

The 2010 Dietary Guidelines for Americans recommend a BMI of 18.5 kg/m² to 24.9 kg/m² to maintain a healthy weight. Weight loss of 3% to 5% of body weight is associated with clinically significant health improvements, with larger losses leading to even greater health improvements.^{7 (Level ML)}

 

Regulation of Food Intake

 

The body is able to regulate food intake and energy balance to maintain constant weight and fat stores through a complex network that includes many systems of the body: sensory perceptions, organs, nervous system, hormones, peptides, neurotransmitters, metabolism and metabolites.¹⁶

 

The brain monitors neural and chemical signals from the GI tract, liver, adipose (fat) tissue, nervous system and bloodstream. Once the signal is received and processed, the brain sends a message to turn eating cues on or off. The signaling travels two ways, as messages from the body are sent to the brain, and the brain sends signals back, via chemicals and the nervous system.

 

The process begins when the brain determines that blood glucose levels are too low. The vagus nerve and sympathetic nervous system send messages to begin to eat. Once food is ingested, chemical and neural feedback signals are sent continually to the brain so it can monitor levels of nutrients, and determine when to inhibit eating. Gastric distention occurs when the stomach is full, sending a message to stop eating; however, not everyone heeds this message.

 

Once food reaches the stomach and digestion begins, certain enzymes, hormones and peptides such as cholecystokinin, insulin, bombesin and somatostatin are produced and travel to the brain via the bloodstream. Based on the levels in the bloodstream, the brain turns eating cues on or off.

 

During and after a meal, serum insulin levels rise to clear glucose from the bloodstream. The insulin binds to receptors in the brain; when a certain level is reached, brain signals inhibit eating. Three to five hours after a meal, serum insulin levels fall, indicating low amounts of glucose in the bloodstream. This signals a need for more food, so the brain stimulates eating. As weight increases, the body becomes more resistant to insulin; more insulin is needed to get glucose into the cells. The resulting hyperinsulinemia very possibly increases hunger, so the person eats more food, contributing to obesity.

 

The vagus nerve provides feedback on the amount of nutrients ingested and when to alter food intake. It also stimulates the production of enzymes and hormones necessary for digestion and absorption. Neurotransmitters, produced in the peripheral or central nervous system, signal the brain about the need either to continue or to stop eating. Serotonin, a neurotransmitter, has a calming effect on the body and is understood to affect what some people call a “carbohydrate craving.” Serotonin is converted from tryptophan, which is an amino acid that crosses the blood-brain barrier. Tryptophan competes with five other large, neutral amino acids (tyrosine, leucine, phenylalanine, isoleucine and valine) for absorption. In protein foods, the ratio of tryptophan to other amino acids is low, so there is competition for access to the carrier molecule to cross the blood–brain barrier. Less tryptophan gets across, so less serotonin is produced. In carbohydrates, there is a higher ratio of tryptophan to the other amino acids, so more tryptophan can cross the blood–brain barrier, increasing serotonin production. Thus, carbohydrates can produce a biologically based calming effect.

 

In a classic study, when subjects were given a drug that increased serotonin production, their voluntary intake of carbohydrates decreased significantly, indicating that serotonin production has some effect on cravings for carbohydrates.¹⁷ Serotonin plays an important role in energy balance; not only is the amount of serotonin important, but having an adequate amount of serotonin transporter proteins is critical as well. It appears that epigenetic changes (hypermethylation) of the serotonin transporter gene could be associated with obesity by reducing the number of proteins and the amount of serotonin in the brain.¹⁸

 

Regulators are also responsible for increasing intake when needed. Hormones and neurotransmitters are sent from the blood and nervous system to indicate that energy is needed. These signals are translated into the motor actions necessary to obtain food and eat it.

 

Genes, Adipocyte Hormones and Proteins

 

The understanding of food intake and weight regulation has been revolutionized with the identification of the genes in adipocytes (fat cells) that are responsible for obesity. These genes have the ability to encode hormone-like proteins, and integrate feedback mechanisms from various parts of the body to control food intake, energy metabolism, body weight, and patterns of body fat distribution. These hormone-like proteins are known as adipokines.¹⁹

 

Leptin. The most-studied obesity gene, the human obese (ob) gene, encodes leptin, which is a protein. It is secreted from fat cells in proportion to body fat levels, and travels to the hypothalamus where it does its work.²⁰ The apparent role of leptin is to inhibit the production and release of neuropeptide Y (NPY), agouti-related protein (AgRP) and melanin-concentrating hormones (MCH). NPY stimulates food intake, reduces energy expenditure and promotes the activation of enzymes in fat cells, leading to weight gain.²⁰ The more NPY present, the greater the amount of food consumed, which results in increased body weight. Increased levels of leptin decrease NPY and prevent overconsumption of food and increased body weight.

 

Leptin is released in proportion to body fat levels, as shown by studies demonstrating a correlation of leptin levels with BMI. Most obese and severely obese humans produce high levels of leptin in direct proportion to their BMI.²¹ “Leptin resistance,” which is the inability to respond to high levels of leptin, appears to contribute to obesity and is caused by a number of pathophysiological factors.²¹

 

The size of fat cells makes a difference in leptin production. Large fat cells produce more leptin than normal or small ones. To prevent too much weight gain, the body will increase leptin levels in tandem with increasing fat mass and food intake. As leptin increases, NPY decreases, signaling the body to turn off appetite to prevent weight gain.

 

 

Leptin and Weight Regulation20
Food intake increases	Food intake decreases
↓	↓
Leptin increases	Leptin decreases
↓	↓
NPY, AgRP and MCH decreases	NPY, AgRP and MCH increases
↓	↓
Food intake decreases	Food intake increases
↓	↓
Weight decreases	Weight increases

 

 

The opposite would occur with a decrease in food intake. When a person goes on a diet, the fat cells shrink and less leptin is produced, allowing an increase in the production of NPY. The increased NPY stimulates the appetite to make up for the energy deficit. This may explain why diets fail, and why so many people gain back the weight they lose. Once weight is lost, the body, due to the decrease in leptin, tries to gain that fat mass back. In essence, human genetic makeup is biased in favor of weight gain as a means of survival. However, if there is leptin resistance, the body would not get the signal that intake had increased, and would not decrease production of NPY or other signals to decrease intake.

 

Ghrelin. This peptide was discovered in 1999. It is involved in meal initiation in the gut. Produced in the small intestine, stomach, pituitary and ghrelin neurons in the hypothalamus, it works by altering levels of peptides in the hypothalamus that control eating.^16,22 Data indicate that ghrelin is a potent stimulator of food intake; however, increases in ghrelin after weight loss have not been associated with regaining weight.²³

 

Adiponectin and resistin. Secreted by fat cells, these proteins affect storage and breakdown of fat, and the regulation of appetite via communication with the central nervous system and GI tract.¹⁹

 

Cholecystokinin (CCK). This peptide stimulates bile production in the liver and the release of enzymes from the pancreas, and decreases the rate of gastric emptying. CCK also stimulates the vagus nerve, affecting neurotransmitters in the brain that provide a message of satiety. CCK may also stimulate short-term satiety by influencing the release of leptin.²⁴

 

Peptide YY (PYY). Similarly to CCK, PYY increases the release of neurotransmitters in the brain to increase satiety. PYY also delays gastric emptying and inhibits gastric acid secretion.²⁵

 

Glucagon-like peptide-1 (GLP-1). GLP-1 is a peptide hormone that stimulates the release of insulin from the pancreatic beta cells in response to a meal. GLP-1 also suppresses glucagon secretion from alpha cells of the pancreas, delaying gastric emptying and suppressing appetite.^{26 (Level B), 27}

 

Select Genes, Adipocyte Hormones and Proteins and Their Role in Obesity19,20,23-27
	Origin	Role in Obesity
Leptin	Protein secreted from fat cells	Inhibits production and release of NPY in hypothalamus to prevent overeating/weight gain May correlate with BMI and adipose tissue
Neuropeptide Y (NPY)	Peptide released from the hypothalamus	Stimulates food intake, reduces energy expenditure Promotes activation of enzymes in fat cells, leading to weight gain
Ghrelin	Gut peptide produced in small intestine, stomach, pituitary and hypothalamus	Alters levels of peptides in hypothalamus that control eating Stimulates food intake
Adiponectin and Resistin	Proteins secreted by fat cells	Role in storage and breakdown of fat and regulation of appetite via communication with central nervous system and GI tract Adiponectin may lower glucose by increasing sensitivity to insulin Healthy eating may improve adiponectin levels
Cholecystokinin (CCK)	GI tract, produced in the duodenum of small intestine by cells on the mucosal epithelium	Stimulates bile production in the liver Stimulates release of enzymes from the pancreas Decreases the rate of gastric emptying Stimulates the vagus nerve, affecting neurotransmitters in the brain that provide a message of satiety
Peptide Y (PYY)	GI tract, mainly by cells in the ileum and colon	Increases release of neurotransmitters in the brain to increase satiety Delays gastric emptying Inhibits gastric secretion
Glucagon-like Peptide-1 (GLP-1)	GI tract, mainly by cells in the ileum and colon	Stimulates release of insulin from the pancreatic beta cells in response to a meal Suppresses glucagon secretion from alpha cells of the pancreas Delays gastric emptying and suppresses appetite

 

 

Genetics and Weight Regulation

 

Considerable research confirms that genetics play a major role in the human response to food and in energy balance; estimates are that 35% to 60% of obesity is attributed to hereditary factors. Some factors include the basic neurophysiological systems of the brain that regulate food intake, body composition, metabolic rates that affect ability to lose and regain weight, and eating behavior traits.¹⁰

 

Research has identified hundreds of genes associated with body weight, energy balance and food intake regulation. Mutations in one particular gene, melanocortin-4 receptor (MC4R), have been related to uncontrolled overeating, binge-eating behaviors, hyperinsulinemia, leptin resistance, increased fat mass and body size.^{28 (Level B)} Researchers found strong evidence that mutations in the MC4R gene contributed to obesity in Hispanic children by altering the regulation of physical activity, energy expenditure and fasting serum ghrelin.²⁸

 

A study of 12 pairs of identical twins supports the theory that some have a genetic tendency to gain more weight than others, even when energy intakes are comparable. When identical twins ate an extra 1,000 kcal/day for 100 days, some of the pairs gained 9 pounds each; while others gained up to 29 pounds each. Although the weight gained varied from twin set to twin set, it was found that each pair of twins gained similar amounts of weight; percentage and distribution of body fat was also similar.²⁹

 

Although research suggests that a significant percentage of obesity is linked genetically, the contribution of genetic factors to obesity is highly variable. It is possible that one person’s weight may be 90% genetically influenced, while another’s is only 10% influenced by genetics.³⁰

 

A recent large-scale review looking at 12 studies including 8,179 monozygotic and 9,977 dizygotic twin pairs in addition to individual participant data for 629 monozygotic and 594 dizygotic pairs suggests that the heritability of BMI over all age categories from preadolescence through late adulthood ranges from 61% to 80% for men and women combined.³¹ Much work remains to be done to determine the interaction of obesity genes, their mutations and the predisposition to gain weight.

 

Adipose Tissue and Energy Balance

 

The discovery that adipose tissue secretes many peptides and hormones has altered our understanding radically of its role in weight regulation, metabolism and chronic disease. Now considered an endocrine organ, adipose tissue regulates the storage and breakdown of fat, communicates with the central nervous system and GI tract, and constitutes an important factor in energy balance, inflammation, glucose regulation, insulin sensitivity and chronic diseases.¹⁹

 

Researchers have found that as the amount of adipose tissue changes, so does the quantity of the peptides and proteins secreted. For instance, adiponectin is a protein involved in lowering serum glucose by increasing sensitivity to insulin. It is also anti-atherogenic, anti-inflammatory and antihypertensive, and having low concentrations of adiponectin has been linked to occurrences of some types of malignancies.³² As fat cell mass increases, adiponectin levels decrease, and the pro-inflammatory cytokines tumor necrosis factor-alpha and interleukin-6 increase. This causes a corresponding decrease in the sensitivity of muscles to insulin and increases inflammation in the tissues.^{33 (Level B)} Adiponectin levels are influenced by genetics, nutrition, exercise, and abdominal adiposity, and are probably inversely associated with visceral fat. The obese who have metabolic syndrome, diabetes and heart disease have lower adiponectin levels than healthy or non-obese people with type 2 diabetes. When someone goes on a diet and loses weight, adiponectin levels increase, as does insulin sensitivity.³²

 

The obese produce less adiponectin, and more resistin and pro-inflammatory cytokines, leading to a systemic inflammatory state. Obesity is now seen as a low-grade inflammatory state, characterized by increased C-reactive protein (CRP) levels and other inflammatory mediators.³² Chronic inflammation may be at the root of metabolic syndrome.¹⁹

 

As weight is lost and fat mass decreases, there is improvement in glucose regulation, insulin sensitivity, immune function, blood pressure regulation and atherosclerosis as adiponectin increases and pro-inflammatory cytokines decrease. This may explain how obesity causes metabolic syndrome, diabetes, heart disease and other chronic diseases.³⁴

 

Healthy eating may also improve adiponectin levels. The Nurses Health Study found that the nurses with the healthiest diet had a 24% higher median total adiponectin, 32% greater high molecular weight adiponectin, 41% lower CRP, and 16% lower resistin.³⁵

 

Energy balance is complex.

 

What’s Involved in Energy Balance?
Organs	Chemicals	Genetics	Diet	Behaviors
Brain	Peptides	DNA	Hunger	Physical activity
Nervous system	Neurotransmitters	Epigenetics	Nutrient composition	Psychological eating
GI tract/ gut microbes	Hormones	Body composition	Total intake	Food habits
Stomach	Cytokines	—	Metabolism	Environment
Pancreas	Adipokines	—	Gut microbes	—
Fat cells	—	—	—	—
Liver	—	—	—	—

 

 

Intestinal Microbiota

 

Variations in the types and amounts of bacteria naturally occurring in the human GI tract have also been linked to obesity. The human GI tract is host to trillions of bacteria that have metabolic interactions with each other and the human host, influencing human nutrition and metabolism.³⁶ Gut microbiota synthesize essential B vitamins and vitamin K, and harvest energy from the diet that is used to produce short-chain fatty acids. These fatty acids provide an energy source for cells in the colon and liver. Through their interactions with receptors on the epithelial cells, they release various cellular factors that influence human metabolism that may play a role in the development of metabolic syndrome, diabetes and nonalcoholic fatty liver disease.³⁶

 

The role of gut microbiota on body-weight regulation originated from studies using mice models in which transplantation of intestinal microbiota from obese mice to lean mice led to 60% increase in body fat content and development of insulin resistance despite reduced food intake.³⁷ Additional studies using animal models have indicated that obesity is associated with characteristic changes in the composition of gut microbiota.

 

Bacteria within the intestine play an important role in energy absorption (particularly of complex carbohydrates), and in sugar and short-chain fatty acid metabolism. Studies in obese mice lacking the leptin gene suggest that these mice absorb more energy (calories) from dietary carbohydrate than conventional (non-obese) mice, which may be contributing to obesity. While there is less data in humans, association studies indicate there are alterations in the gut microbiota in the obese compared with lean people, with the obese having reduced microbial diversity and alterations in the genes involved in metabolic pathways.³⁸

 

Roux-en-Y gastric bypass (RYGB) surgery in obese humans has been shown to result in changes in the gut microbiota, suggesting that weight reduction may influence gut microbiota composition.³⁸ While there are several possible mechanisms that may explain the link between weight and gut microbiota in humans, increased efficiency of energy absorption from food in obese compared with lean people is one possible factor.³⁶

 

Conclusion

 

While new discoveries point to a genetic and molecular basis for obesity, they are not the entire story. Genetics and environment combine to play a role in people who are overweight or obese — and who can successfully lose weight and keep it off. Other factors such as metabolism, thermic effect of food, body composition, hormones, activity of the sympathetic nervous system, gut microbiota, epigenetics and nutrient composition of the diet all interact to determine how weight is regulated.