High-intensity interval training has been shown in recent studies to boost endurance performance and health. High-intensity interval training offers benefits seen in continuous endurance training with less time commitment.
The time commitment required for exercise on a daily basis is often cited as the reason people don't exercise. High-intensity interval training may be a time-saving tool for both the recreational exerciser trying to stay healthy and the elite endurance athlete trying to out-train the competition.
Studies on the physiological effects of high-intensity training have been produced since the 1990's. A study was published in 1997 on the effect of high intensity interval training on cyclists. Cyclists who replaced 2% of their weekly endurance training mileage with short (6-9 minutes) high-intensity (80% max) intervals were found to show significant improvements in a 40km time trial. In 1999, a study looked at the affects of varying the high-intensity time interval (Effects of different interval-training programs on cycling time trial performance, 1999, NK Stepto, et al.). The results can be seen in the figure below.
For elite athletes, the success garnered with intensity polarization cannot be limited to cyclists. In 2009, a study found that rowers who dedicated just 5% of their training to more intense intervals had a higher chance of going on to compete on an international stage. The study looked at rowers over a three-year time frame (Training methods and intensity distribution of young world-class rowers, 2009, A Guellich, S Seller, E Emrich).
Most people, however, are not interested in exercise as a means of improving peak performance. For many, exercise is a prescription for staying healthy. A study published in 2012 found that through high-intensity interval training patients could achieve the same physiological benefits of continuous endurance training in a third of the time (Physiological adaptations to low volume, high intensity interval training in health and disease, 2012, Martin J. Gibala, et al.). The study found that participants who did 10 one-minute bouts at 90% maximal heart rate with a minute of recovery (10 minutes of work, 20 minutes total) showed similar skeletal muscle metabolic adaptations and cardiovascular adaptations to a control group doing 60 minutes of continuous exercise. This suggests that this high-intensity interval training may alleviate diseases just like endurance training. However, no research has been done yet to set up a link between disease risk and high-intensity interval training.
In summary, performance and health can both be boosted by high-intensity interval training. The benefits include a more enjoyable workout (most people prefer interval training to continuous endurance training) in less time and improvement in functional performance.
Regular exercise causes long-lasting elevations in the brains basal glycogen levels though the buildup of repeated supercompensation.
Exercise supercharges your brain. According to the latest findings from a Japanese study, exercise results in sustained elevated glycogen levels (Brain glycogen super compensation following exhaustive exercise, 2012, Takashi Matsui, et al.). Glycogen levels have been shown to be elevated in skeletal muscle following exercise, but this is the first study to report of the phenomenon in the brain.
Exercise's effect on glycogen levels in the skeletal muscle have been known for some time. During exercise, glycogen stores are depleted, but the body returns to an elevated level of glycogen in a process called supercompensation. Supercompensation was first reported in the skeletal muscle in the 1960s. In the 1980s researchers found that skeletal muscle responds to exercise training by maintaining higher basal levels of glycogen. This adaptation to exercise training lengthens the amount of time the muscle can work before exhaustion.
To study the effects of exercise on glycogen levels in the brain, researchers trained mice for 60 minutes a day, 5 days a week for 3 weeks. At the end of the study glycogen levels were observed in the liver, skeletal muscle and brain. During exhaustive exercise, glycogen levels in the brain dropped 50-60%. Glycogen levels in the liver and skeletal muscle dropped 80-90%. The brain was the first to recover from exercise-induced glycogen depletion by peaking at 6 hours after exercise. This supports the "Selfish Brain Theory": the brain wins during competition for energy resources within the body. Following supercompensation, the brain returned to pre-exercise glycogen levels about 48 hours after exercise. The skeletal muscle took 48 hours to return to pre-exercise glycogen levels following exercise. A supercompensation peak 24 hours after exercise was recorded in the skeletal muscle. The liver did not show supercompensation and took 48 hours to recover pre-exercsise glycogen levels. These results can be seen in the figure below.
More insight was achieved by comparing glycogen levels in the brain between exercise-trained mice and a sedentary control. Glycogen levels in the brain were found to be significantly higher in the exercise-trained mice. The exercise-trained mice were killed 72 hours following the last bout of exercise and their brain tissue was evaluated. The cortex and hippocampus, but not the hypothalamus, brainstem or cerebellum, were found to have significantly higher levels of glycogen than the control. This suggests that supercompensation in the brain results in a long-lasting increase in glycogen levels. The differences in brain glycogen levels between exercise-trained and sedentary control mice can be seen in the figure below.
An interesting correlation was found between exercise-induced glycogen depression and the supercompensation that followed. The glycogen depression and supercompensation that followed were positively correlated; that is, a greater glycogen depression results in a stronger glycogen supercompensation in the brain.
Exercising daily causes the brain to have elevated levels of basal glycogen after just three weeks. What are some potential benefits? There are obvious benefits to endurance athletes. Low sugar levels in the brain are a major source of fatigue. Therefore, elevated glycogen levels would help alleviate onset of fatigue during endurance competition. In addition, increases in glycogen levels have been linked to an increase in cognitive. It has been reported on exercismed.org that students who exercise demonstrate better academic performance (See Lifestyle Impact on Academic Performance). Could the glycogen that supercharges their brain be the biological mechanism?
Exercise is the supercharger of brains.
Belly cramps are caused by a variety of gastrointestinal tract issues. However, they can be prevented by staying hydrated, eating a diet high in fiber, avoiding potential allergens and clearing the colon before intense physical activity.
Every athlete has suffered through belly cramps. Often they appear out of the blue. However, they can be fought with the right diet, hydration and empty colon. The intense abdominal pain is caused by disturbances in the gastrointestinal tract. The symptoms can range from a minor disturbance during or following exercise to nausea, vomiting, diarrhea and severe abdominal pain.
A recent study looked at 12 endurance athletes, ranging from recreational to elite, for causes of gastrointestinal symptoms. All 12 athletes were found to suffer from gastrointestinal ischaemia during periods of maximal exercise (Abdominal symptoms during physical exercise and the role of gastrointestinal ischaemia: a study in 12 symptomatic athletes; 2011; Steege, et al.). Gastrointestinal ischaemia is the depletion of blood flowing to the colon. When not enough blood reaches the colon it hurts due to the lack of oxygen. In hot or humid environments, gastrointestinal ischaemia is especially acute because more blood is diverted to the skin for thermoregulation. Two other causes of gastrointestinal complaints during exercise are gastric emptying delay and food-dependent exercise-induced anaphylaxis (FDEIA). Gastric emptying delay is when food remains in the stomach for an extended amount of pain. FDEIA is any allergen reaction in the gut. Exercise facilitates allergen absorption in the gastrointestinal tract.
How are these gastrointestinal complaints prevented? A Brazilian review on the subject provides some answers (Food-dependent, exercise-induced gastrointestinal distress; 2011, EP Oliveiera and RC Burini). FDEIA is caused by consuming allergen-specific foods within a few hours preceding exercise. Foods found to be associated with FDEIA include cereals, seafood, peanuts, tree nuts, eggs, milk and vegetables. Gastric emptying delay can be fought by staying hydrated and avoiding replacement fluid with high levels of glucose and hypertonic solutions in general. A fructose-glucose mix has been shown to replenish muscle energy with increased gastrointestinal carbohydrate oxidation. Staying hydrated, but not overly so, is the best way to fight gastrointestinal complaints with the added benefit that it assists with thermoregulation.
The best way to fight gastrointestinal ischemia is by clearing the colon. Exercise induces powerful contractions in the intestines that drive food forward along the gastrointestinal tract. This increases the amount of blood desired by the colon. Fiber holds moisture in the colon. Foods high in fiber keep stool soft allowing it to clear out easier. To ensure your diet is high in fiber, eat a diet with lots of fruits and vegetables. Avoid white-flour foods which are low in fiber and bulky. Passing stool at the same time time on a daily basis can condition the processes driving stool out of the colon.
In summary, in order to prevent abdominal cramping: stay hydrated, eat fiber, avoid potential allergens and clear your colon before an intense workout or race.
Genetic differences have been found to explain the hypoxia (oxygen starvation) physiological adaptations in Tibetans and Andeans necessary for surviving at high altitude.
For proof of how we adapt to our environment one can look at the Tibetans and the altitude adaptations they have developed. The Tibetan Plateau has an average elevation over 5000 meters (16,400 ft.) and covers an area almost half the size of the continental United States. Tibetans have been estimated to been residing at these extreme altitudes for at least 5000 years and possibly as long as 21,000 years. Tibetans exhibit a suite of physiological adaptations at altitude: decreased arterial oxygen content, increased resting ventilation, lack of hypoxic pulmonary vasoconstriction and reduced hemoglobin concentration.
Interestingly, these physiological traits are not all exhibited in the Andeans of South America who live at similar high altitude conditions. A study by Cynthia M. Beall compared the physiological mechanisms Tibetan and Andean natives have developed to deal with the hypoxia (oxygen starvation) experienced at high-altitude (Two routes to functional adaptation: Tibetan and Andean high-altitude natives, 2007, Cynthia M. Beall).
There are several points on the path from atmospheric air to venous blood (called the oxygen transport cascade) to make up for differences in oxygen concentration seen at high-altitude and sea level. The figure below shows these points.
Tibetans show ventilation rates similar to sea-level populations in response to hypoxic conditions. Andeans have a decreased hypoxic ventilation response. Despite the higher levels of ventilation seen by Tibetans, the oxygen concentration in the blood at high elevations is lower in Tibetans than Andeans. This is because hemoglobin (the protein that transports oxygen in the blood) concentration is higher in the Andeans. However, high hemoglobin concentrations are not necessarily advantageous because it alters the viscosity of the blood and may cause chronic mountain sickness. Tibetans have also been found to have higher blood flow to the brain during exercise.
Tibetans have higher blood flow to compensate of their low levels of oxygen in the blood. In addition, Tibetans have a higher rate of oxygen diffusion as their capillarity density is much higher than Andeans at similar elevation. Mitochondrial density decreases at altitude for normal populations (the reason is unknown). Tibetans have decreased mitochondrial density at sea-level as well as at elevation suggesting a purely genetic trigger for mitochondrial density in Tibetans. The differences in mitochondrial and capillarity density is shown in the figure below.
To explain the physiological adaptations Tatum Simonson, PhD led a team to Tibet to look at the genetics of native Tibetans (Genetic Evidence for High Altitude Adaptation in Tibet, 2010. Tatum S. Simonson, et al.). The research team identified SNPs (single nucleotide polymorphisms) unique to Tibetans. A SNP is a single nucleotide difference in the DNA code that is unique to, or more frequent in, certain populations. Generally, SNPs occur in noncoding sections of the DNA gene so that the associated protein's function is not affected. SNPs propagate and reach a peak at about 10,000 years in a population before disappearing due to random mutation.
Tatum and her team found 10 genes that were both unique to Tibetans as identified with SNPs and labeled as associated with hypoxia resistance. Several of these genes, PPARA and EGLN1, are associated with the regulation of hemoglobin concentration.
In summary, Tibetans and Andeans have developed physiological adaptations to the hypoxia conditions associated with living at high altitude. A genomics analysis of Tibetans has found several genes of interest related to hypoxia and hemoglobin concentration. This research is important because understanding the genetics behind hypoxia adaptation may help develop a cure to alleviate chronic mountain sickness.