The long run is a staple for marathon runner (such as former marathon World Record holder Haile Gebrelassie, right) training. An experiment on the subject shows that the long run does not negatively effect running economy in the days following despite causing muscle soreness.
The long distance run is a staple of marathon training. Sometimes referred to as the long-duration training run (LTR) or long slow distance (LSD), the goal of the long distance run is to train the aerobic system. The long run is generally performed at 15% to 25% of weekly mileage at aerobic threshold, typically around 60% of VO2 Max. The intensity is not high, but by the end of the run the runner will feel expended due to the extended duration. The long run was popularized in the 1960s by Arthur Lydiard, the legendary New Zealand distance coach considered to be the father of modern distance training. The long run takes a toll on athletes, so it is important when planning a training sequence to understand the physiological effects of the long run. A team at the University of New Hampshire, Durham Kinesiology Department evaluated the effects of the long run on 15 male runners from New England running clubs (The impact of a long training run on muscle damage and running economy in runners training for a marathon, 2012. Quinn TJ and Manley MJ).
The study found that despite causing muscle damage, the long run did not cause a decrease in running economy. Running economy is basically a measure of efficiency; oxygen uptake is measured at a given velocity to determine the running economy. The participants, who were training for their first marathon, performed a 16 mile (26 km) run over a course with rolling hills. Every 5 km they were monitored for adequate hydration and and heart rate was measured. Following the run, creatine kinase levels and running economy was measured every 24 hours for the following three days.
Creatine kinase levels, a measure of muscle damage, were elevated for the following three days. Creatine kinase can be used to measure measure muscle damage because micro tears in the muscle allow creatine kinase in the muscle to leak into the plasma. This muscle damage is what causes muscle soreness or DOMS, delayed onset muscle soreness. Perceived muscle soreness was also determined and correlated with creatine kinase levels. A figure with creatine kinase levels following the long run can be seen below. The baseline measurement was taken during a prior visit to the kinesiology lab.
Although the participants displayed physiological signs of muscle soreness, running economy was not effected in these participants by the long run. The runners' running economy was not statistically different from baseline at 24 hours, 48 hours or 72 hours post-long run. The subjects' running economy was tested at velocity corresponding to their sub-maximal aerobic capacity. This result suggests that aerobic demand is not hindered by a long run. Other papers have shown that a full-fledged marathon negatively affects running economy. These contradictory results may mean that anaerobic work performed in the marathon, as the racer goes above aerobic threshold, are responsible for the decrease in running economy. Type I fiber (slow twitch, responsible for aerobic performance) damage may not be as detrimental to running economy as Type II fiber (fast twitch, responsible for anaerobic performance) damage.
For the runner training for the marathon, the weekly long run should not negatively impact the running economy of subsequent aerobic training runs despite muscle soreness. However, factors other than running economy play a role at determining running pace. It is likely one's aerobic threshold velocity differs between the day before the long run and the day after the long run.
Mitochondria are synthesized in the brain in response to training, but this process is hindered by cigarette smoking.
There are numerous studies that discuss the beneficial effects exercise has on the brain. Many of them are featured in this blog and include preventing parkinson's disease, fighting Alzheimer's, and stroke recovery. Many researchers believe that one of the exercise-related factors contributing to these improvements in brain health is exercise's antioxidant effects. Exercise leads to mitochondrial biogenesis (production of new mitochondria) in cerebral neurons. Mitochondria yield an antioxidant effect because their job is oxidative metabolism, which reduces oxygen thereby preventing free radical oxygen formation. On the other hand, smoking is well-known to have a negative effect on one's health. With regards to smoking's interaction with exercise, smoking has been shown to generate muscle degradation. In addition, here we'll discuss a study that demonstrated smoking inhibits the production of new mitochondria in the brain in response to exercise (Cigarette Smoke Inhibits Brain Mitochondrial Adaptations of Exercised Mice, 2011 Speck AE, et al.).
The study found that exercise increased mitochondria density in the brain, but smoking prior to exercise training dampened the mitochondria biogenesis response. To conduct the experiment, mice were divided into four groups: trained and untrained smokers and trained and untrained nonsmokers. Smoking mice were exposed to high dosages of cigarette smoke for eight weeks. Following the eight weeks of cigarette smoke exposure, the trained mice exercised in a swimming pool for 8 weeks while the untrained mice rested in an empty swimming pool. After, the mice were exercise tested and mitochondrial complex activity measured.
The complexes that make up the electron transport chain were measured using an enzymatic activity assay. The mitochondrial complex activity was significantly elevated in both the hippocampus and frontal cortex in response to exercise. No effect was observed in the smoking exercise-trained mice. In addition, in the untrained controls no smoking effect was observed. Therefore, exercise alone increases mitochondrial synthesis, but this is negated with the addition of cigarette smoking in the 8 weeks prior to the exercise training. It should be noted that these results do not necessarily signify new mitochondria per se, but at least improved capacity of the mitochondria. The results can be seen in the figure below.
Although mitochondrial biogenesis did not significantly change the mitochondrial count of untrained mice, other studies have shown that an acute bout of smoke inhalation actually protects mitochondrial function in the central nervous system (Nicotine protects rat brain mitochondria against experimental injuries, 2003. Cormier A, et al.). The effect is apparently mediated through nicotine. How long the smoking affect lasts on mitochondria biogenesis is not known, but from the results of the Speck paper it must be at least eight weeks.
In summary, smoking's antioxidant effects are controversial. Studies show that smoking alone may both protect and harm mitochondrial function in the brain. However, it is shown conclusively in the Speck paper that smoking harms mitochondrial brain function.
Isoforms of the transcriptional coactivator PGC-1a determine the response to resistance training and endurance training. The PGC-1a4 isoform causes hypertrophy (an increase in muscle mass) in response to resistance training. In response to endurance training, the PGC-1a1 isoform causes mitochondrial biogenesis and increases fatty acid oxidation. Transcriptional activators influence gene expression (image to the right) by recruiting RNA polymerase and transcriptional factors.
Resistance training and endurance training cause visibly different effects on muscle tissue. Lifting weights, a typical example of resistance training, results in enlargement of the muscles, called hypertrophy. On the other hand cycling, an endurance activity, increases mitochondrial density in muscle, but does not generally enlarge the muscle. Endurance training relies on improvement in the cardiovascular system for a good portion of its effected increase in VO2 Max. The answer to why endurance training and resistance training lead to such different effects in muscle fibers can be found in an exciting study recently published in Cell (A PGC-1alpha Isoform Induced by Resistance training Regulates Skeletal Muscle Hypertrophy, 2012. Ruas JL, et al.).
According to this paper, the answer is centered around the molecule PGC-1alpha. Over the past several years PGC-1alpha has generated excitement in the biomedical community for its influence across a wide variety of avenues, several of which have been discussed on this blog: PGc-1alpha reduces muscle wasting in ALS mice models, correlates with the reduction in muscle mass in cigarette smoking mice models, mediates fiber-type switching to type I fibers and is responsible for triggering brown fat production. PGC-1alpha is thought to be responsible for many of the adaptive changes in the muscle to endurance training. The transcriptional coactivator causes mitochondrial biogenesis (increase in mitochondria density results in an increase in aerobic energy production), angiogenesis (increase in blood capillaries within the muscle) and fatty acid oxidation (using fat for energy prolongs complete depletion of vital glycogen stores in the muscle). However, none of these aforementioned effects would increase anaerobic performance.
The authors found PGC-1alpha has four different isozymes through an alternate promoter (a gene promoter is where mRNA transcription machinery binds to the DNA) and alternate splicing (cutting up and piecing together the mRNA stand produced from the gene). They are named PGC-1alpha1, PGC-1alpha2, PGC-1alpha3 and PGC-1alpha4. PGC-1alpha1 is the isoform first discovered and was formerly known as simply PGC-1alpha. Of interest to the researchers was PGC-1alpha4 because it was found to increase Insulin Growth Factor-1 (IGF-1). IGF-1 has been found to induce hypertrophy. Because it increases muscle mass, IGF-1 has gained notoriety as a performance enhancing drug. In addition to increasing IGF-1 expression, PGC-1alpha4 was also found to decrease expression of myostatin, a potent negative regulator of muscle size. PGC-1alpha4 apparently accomplishes this by altering the chromatin structure of the IGF-1 and myostatin genes to respectively increase and decrease gene expression. A model of the PGC-1alpha isomers' exercise-mediated effects on the muscle is shown below.
The researchers measured the levels of PGC-alpha1 and PGC-alpha4 in humans. Muscle biopsies were taken out of humans before and after an endurance training protocol, resistance training protocol and both resistance training and endurance training protocol. It was found that the combination of endurance and resistance training led to the greatest increase in PGC-1alpha1 and PGC-1alpha4. All training protocols increased PGC-alpha1. Although the endurance training protocol did not increase PGC-1alpha4 in the human muscle biopsies, resistance training alone and both resistance and endurance training did increase PGC-alpha4 1.5 fold and 3 fold, respectively.
In mice, PGC-1alpha4 was found to cause hypertrophy relative to a GFP control. The increase in muscle mass was accompanied by increased force production in the muscle. In addition, muscle wasting was decreased in PGC-1alpha4 expressing mice during muscle disuse caused by hindlimb suspension. In addition, cachexia (severe muscle weakening) brought about by tumors introduced in muscle tissue was significantly curtailed in PGC-1alpha4 transgenic mice. The figure below demonstrates the PGC-1alpha4 induced muscle hypertrophy in mice gastrocnemius muscle cross sections.
PGC-1alpha4 has the potential to be a centerpiece of muscle therapy. Because PGC-1alpha4 modulates both IGF-1 and myostatin, it could in theory be used in place of IGF-1 and myostatin regulatory drugs currently in the pharmaceutical pipeline. Furthermore, PGC-1alpha4's potent effects on muscle hypertrophy and muscle force make it a practical marker of the effectiveness of a resistance training program. A resistance training program optimized for increasing muscle mass and force would generate a maximal rise in PGC-1alpha4 expression.
A future direction with this research is to determine the molecules that lead to transcription at the alternate PGC-1alpha gene promoter and cause alternate splicing to generate the four PGC-1alpha isoforms.
A study using a room calorimeter (picture, right) finds that exercising before breakfast increases fat oxidation during and in the 24 hours following the exercise bout.
Excessive post-exercise consumption, or EPOC, refers to an increased oxygen uptake in the minutes and hours following intense anaerobic or aerobic exercise. EPOC encompasses the term "oxygen debt", which is often used by athletes, but not exercise physiologists. EPOC refers to a variety of physiological functions that body performs following exercise. Immediately following a bout of exercise oxygen consumption remains noticeably elevated due to thermoregulation, an elevated heart rate, lactate oxidation and hormone. Oxygen consumption continues to be raised for up to 24 hours after the exercise bout as the body begins repairing structurally damaged muscle and replenishing lost glycogen.
The body prefers carbohydrate sources during intense exercise because they are more oxygen efficient. In other words, carbohydrates require less oxygen consumption per unit of energy than fats or protein energy sources. The body's carbohydrate sources are primarily located in the liver and muscle as glycogen. However, fat represents a far more abundant source of energy. When glycogen stores are depleted the body begins oxidizing fat for energy. Interestingly, elite endurance athletes begin fat oxidation much sooner during a bout of exercise. This is believed to be an attempt by the body to stave off complete depletion of carbohydrates.
The body's energy sources can be calculated by measuring inspired and expired gas composition. The ratio of CO2 expired to O2 consumed is called the respiratory quotient. The respiratory quotient is about 1.0 for carbohydrates, 0.8 for protein and 0.7 for fats. Protein breakdown results in nitrogen waste, which can be measured with the respiratory quotient to determine substrate mixture used for energy. Furthermore, total energy utilization can be measured used a room calorimeter (shown in the picture above). A recent used these techniques to look at subjects energy expenditure and energy sources following exercise (Effects of post-absorptive and postprandial exercise on 24 h fat oxidation, 2013. Shimada K, et al.).
The aforementioned study found that fat oxidation increases when exercise is performed in the post-absorptive state, or after no more glucose is available. This occurs after a fast, such as in the morning before breakfast. Participants were put in a room calorimeter were energy expenditure, and energy utilization was measured. Participants cycled on an ergometer for an hour at 50% of VO2 max. In one trial the participants exercised before breakfast and in the other they exercised after breakfast. As expected, carbohydrates were primarily used in participants who exercised after breakfast while fats were used by those who exercised before breakfast. Those who exercised before breakfast had a negative carbohydrate balance. The figure below demonstrates this relationship.
This finding suggests that exercising before breakfast leads to more fat oxidation, which may help with weight loss. In addition, the increase in fat oxidation is the result of enzymatic changes that can have long lasting effects. Increases in fat oxidizing and fat transporting proteins have been observed in carbohydrate depleted subjects following exercise (Effect of training in the fasted state on metabolic responses during exercise with carbohydrate intake, 2008. Bock KD, et al.). This increase in energy utilization following exercise stems from the EPOC effects mentioned above: muscle repair and glycogen replenishment.
In terms of training, these results may suggest that training with low glycogen stores may be beneficial. Elite endurance athletes have an ability to quickly tap into their fat stores, saving precious carbohydrates during intense exercise. This prolongs or eliminates "hitting the wall". However, the jury is still out on whether or not this approach is beneficial to competitive fitness (Does training fasted make you fast? 2009. McConnell G).
In conclusion, exercising on a fast increases fat oxidation. This increase in fat oxidation is not compensated for in the 24 hours post exercise session. This suggests that superior weight loss can be achieved by exercising on a fasted body. Now that is some motivation for getting up early to get a work out in!
Cardiovascular drift occurs during prolonged exercise and is the result of an increasing heart rate and decreasing stroke volume. Cardiovascular drift results from a decrease in blood volume and sympathetic nervous system triggered increase in heart rate. Studies show ways to reduce cardiovascular drift are staying hydrated and biking at a lower pedal cadence.
Cardiovascular drift is the term that describes the physiological changes in heart function during prolonged exercise. During prolonged exercise, stroke volume steadily drops as the heart rate increases. Stroke volume is the amount of blood the heart pumps with every beat. Cardiac output is a function of stroke volume times heart rate. Therefore, cardiac output may remain constant during prolonged exercise despite the increase in heart rate due to compensation from a drop in stroke volume. Often the decrease in stroke volume actually drops cardiac output despite the increasing heart rate. When exercise physiologists encountered cardiovascular drift in the late 70's, a clear explanation of the cause of this phenomenon was lacking. However, three and a half decades of research on the subject has increased our understanding of cardiovascular drift.
In 1994 a study found that athletes who were well hydrated before an exercise bout displayed less cardiovascular drift (Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise, 1992, Mountain SJ and Coyle EF). In this study, athletes were monitored on cycle ergometers at moderate intensity for two hours in a high temperature (91°F) and high humidity (50% humidity) environment. Participants were divided into the following groups based hydration before the exercise bout: no fluid, small fluid, moderate fluid and large fluid intake 24 hours prior to exercise bout. Although all four groups saw their body temperature rise over the course of the exercise bout, the groups with a lower level of hydration had a significantly higher core body temperature in the second hour of the cycling protocol. The figure below demonstrates the increase in core body temperature over the exercise bout.
Not only did the dehydrated groups have trouble controlling core body temperature, cardiovascular function was affected as well. All four groups saw a decrease in stoke volume and increase in heart rate over the course of the exercise bout. However, these changes had a graded response corresponding to hydration level. In the fully hydrated group, the increased heart rate was able to compensate for the decreased stroke volume and cardiac output was not affected. Cardiac output decreased over the course of the exercise bout in the other three less hydrated groups. The figure below shows cardiovascular data from this study.
Two hypotheses emerged to explain why dehydration and hyperthermia (increase in core body temperature) bring on cardiovascular drift. One hypothesis said that cutaneous blood flow (blood flow in vessels in the skin) resulted in the drop in stroke volume. The idea is that as blood pools in veins in the skin less blood is available to return to the heart. An alternate hypothesis is that an increase in heart rate is responsible for the reduction in stroke volume. An increase in heart rate means there is less filling time for the ventricles; thus, stroke volume is reduced. The second hypothesis is supported by several studies (Cardiovascular Drift During Prolonged Exercise: New Perspectives, 2001, Coyle EF and Alonso JG).
First, blood flow in the skin does not change after 30 minutes of steady exercise. Thus, cutaneous blood flow can't explain the changes in blood flow. Second, a study that blocked sympathetic activation of the heart (via beta adrenergic receptor blockers) in humans cycling showed no cardiovascular drift. The sympathetic system accelerates heart rate, a chronotropic effect. Stroke volume and heart rate did not change after reaching a steady state in the participants with blocked sympathetic innervation of the heart. This supports the idea that an increasing heart rate is responsible for the decrease in stroke volume. In addition, hypovolemia (reduced blood volume) is thought to play a role. Hypovolemia may occur when blood plasma is lost as sweat. A decrease in blood volume triggers a further increase in cardiac output because the body must maintain its blood pressure or mean arterial pressure (MAP). The body resists a drop in MAP by increasing cardiac output through increased sympathetic activity to the heart raising heart rate. An increase in core body temperature also triggers the sympathetic nervous system to increase cardiac output (via heart rate) for thermoregulation purposes. The figure below demonstrates the interplay between cardiovascular factors.
Hydration is a double edged sword against cardiovascular drift. It fights the increase in core body temperature and it maintains blood volume. For this reason, studies have found hydrating during exercise also reduces cardiovascular drift. Hydrating replaces lost blood plasma to sweat, maintaining arterial pressure. The increase in body water helps resist changes to the core temperature.
Why is cardiovascular drift important? Cardiac output decreases as stroke volume decreases. In addition to pumping less blood with every beat, the heart is able to generate maximal force when fully stretched (this property is called the Frank-Starling law of the heart). Blood oxygenation decreases as cardiac output decreases. This decreases cerebral blood oxygenation, likely a major input in fatigue. Of interest to cyclers, a recent study found that an increase in pedal cadence, but not external workload, increased cardiovascular drift and an exercise-induced decrease in cerebral oxygen saturation (Cardiovascular drift and cerebral and muscle tissue oxygenation during prolonged cycling at different pedaling cadences, 2012, Kounalakis SN and Geladas ND).
This suggests that maintaining a lower pedal cadence is beneficial to cyclers in competition. The reason for this may be because muscle capillaries in active muscle are occluded during contraction (due to increased pressure of the surrounding contracting muscle fibers). At a higher pedal cadence the muscle capillaries would have less opportunity to fill between contractions. This study also demonstrates that maintaining cardiac output is essential for maintaining cerebral oxygen saturation, a key component of central fatigue.
In conclusion, the best way to alleviate cardiovascular drift is by staying hydrated and, if you're on a bike, biking at a lower pedal cadence.