This article discusses the ongoing research debate of the exact causes of exercise fatigue. Two distinct theories of fatigue are discussed with respect to different types of exercise, in addition to understanding fatigue from a different perspective which allows greater application for coaches, trainers, and athletes to better prepare for and determine the causes of fatigue.
- Discuss the traditional view of fatigue: The peripheral catastrophe model.
- Discuss the power of the brain in regulating fatigue: The central nervous system control
- Redefine fatigue as an emotional sensation of subconscious CNS calculations.
Fatigue during exercise is a multifaceted phenomenon. The feelings of fatigue experienced after sprinting 100 meters are much different than those experienced after a marathon. Fatigue during exercise can occur due to various reasons, and there is no single locus or mechanism that explains fatigue under all conditions (Hargreaves, 2008). In this article, two distinct theories on the cause of fatigue will be discussed. The traditional view is that fatigue is primarily due to peripheral conditions of the muscles themselves and the metabolic environment that causes a decrease in performance. Another view is that fatigue is centrally controlled by the nervous system and it governs the overall work capacity of the muscles themselves. In addition, this article will describe a new way of considering the complexity of fatigue and its effects on the body during exercise.
Traditional View of Exercise Fatigue
Fatigue is best defined as a decrease in performance or the inability to maintain a work output at a given intensity. What differentiates fatigue from muscular weakness or injury is that the effects of fatigue are often reversed with rest (Kenney, Wilmore, & Costill, 2012). There is a difference however in the fatigue experienced by a marathon runner, and the fatigue experienced by a person bench pressing three-repetitions to failure. One of the most common explanations for the cause of fatigue during all types of exercise usually involves factors within the working muscles; also referred to as peripheral fatigue.
The overall theory of peripheral fatigue resides in the changing metabolic environment of the working muscles as the primary cause of fatigue. Since energy consumption can increase 100-fold when transitioning from rest to high intensity exercise, adenosine triphosphate (ATP) demands must be met through anaerobic metabolism (Westerblad, Allen, & Lännergren, 2002). Since it is hard to maintain maximal intensity exercise for a prolonged period, it seems logical that fatigue occurs as a result of the use of anaerobic metabolism, which creates changes in the metabolic environment of the working muscles. The ability of muscles to maintain a given work output can be affected in several ways: through the excitation-contraction coupling, contractile mechanisms themselves, and metabolic energy supply to the muscles (Hargreaves, 2008).
Lactic acid has long been considered to be the main culprit in causing muscular fatigue during anaerobic glycolysis. Most exercise physiology textbooks describe lactic acid as a byproduct of anaerobic glycolysis, along with hydrogen ions (H+) and inorganic phosphate (Pi), which undergoes constant turnover during exercise. Any activity heavily depending on anaerobic glycolysis, such as sprints or high-intensity exercise lasting less than approximately 90 seconds, will cause an accumulation of lactic acid. Once the build-up of lactic acid reaches a greater level than can be consumed, it will dissociate, and convert to lactate which therefore causes an accumulation of H+. The increase in H+ results in a decrease in the pH level of the blood. This pH drop is then thought to cause intracellular acidosis. Although there are buffers in the body to prevent extreme drops in pH levels (because too low of pH can be lethal) the drop in pH is thought to be enough to disrupt muscle contractions (Kenney, Wilmore, & Costill, 2012). It has been proposed that lactate accumulation within muscles is the root cause for intracellular acidosis, because it is a strong acid anion, which alters the behavior of water (Lindinger, Kowalchuk, & Heigenhauser, 2005; Böning & Maassen, 2008). However, there are conflicting views among researchers with this cause-effect relationship between lactic acid, acidosis, and exercise fatigue and the overall impact lactic acid has on the intracellular environment.
The Lactate Debate
The classical explanation for the cause of muscular acidosis for the past 80 years has been due to the buildup of lactic acid. This interpretation led to the belief that lactate production therefore causes fatigue during high intensity exercise (Robergs, Ghiasvand, & Parker, 2004). Lactate has long been proven to accumulate in the working muscles during high intensity exercise, but lactate can also be used as a fuel source during prolonged exercise. In fact, the production of lactate actually retards acidosis; with plenty of research providing evidence acidosis is caused by other reactions (Robergs, Ghiasvand, & Parker, 2004). Lactate along with H+ might actually improve aerobic endurance exercise because lactate can be shuttled back to the muscle cells for fuel and is also proficient in reducing the deformability of red blood cells; helping to maintain optimal oxygen supply to the muscles (Messonnier, Denis, Féasson, & Lacour, 2006). Lactate production is however a good indirect marker for cellular metabolic conditions. In a study which proves this theory, two groups of students both performed eight-30-meter sprints, whereas one group had 20 seconds of rest between sprints (R20) and the second group had 120 seconds of rest (R120). Both groups had very similar blood lactate increases after completing the sprints. If blood lactate was solely responsible for acidosis and a subsequent decrease in performance, both groups should have noticed a decrease in performance. The R20 group sprint velocity did decrease over the course of the eight sprints, however the R120 group sprint velocities were consistent for all eight sprints. This evidence rejects the cause and effect relationship between lactate production and muscular fatigue and does not explain the observed fatigue in the R20 group. It was concluded that the decrease in performance was due to less phosphocreatine replenishment in the R20 group as compared to the R120 group. If there was acidosis, it is likely due to the increased hydrolysis of ATP in this type of high intensity exercise and not from lactate production (Vaz Macedo, Lazarim, da Silva, Tessuti, & Hohl, 2009). Increased ATP usage from the phosphagen energy system during intense exercise increases proton release, which contributes to muscular acidosis (Robergs, Ghiasvand, & Parker, 2004). However lactate may be essential for metabolic acidosis, for when individuals who suffer from McArdle’s disease (a metabolic disorder in which muscle cells are unable to break down glycogen into glucose) exercise at high intensities, their muscle pH actually increases instead of decreasing (Böning, Strobel, Beneke, & Maassen, 2005). The increased use of the phosphagen system involves the hydrolysis of creatine phosphate (CrP), yielding creatine and Pi. Downplaying acidosis as such an important factor, it may be the buildup of H+ and Pi are the most important contributors of fatigue during high intensity exercise, because in vitro studies have shown muscle acidification has little effect on the velocity of cross-bridge functioning (Westerblad, Allen, & Lännergren, 2002). The acidification of muscles has also been thought to inhibit energy metabolism, however a recent human study failed to detect any reductions in the rate of glycogenolysis or glycolysis in acidified muscles, and the inhibition of key enzymes in vitro seem to be counteracted by other factors in vivo (Westerblad, Allen, & Lännergren, 2002). Regardless, there is evidence of more complicated explanations for muscular fatigue and to blame fatigue solely on lactic acid is a drastic oversimplification for the decrease in performance.
The Catastrophe Model
The traditional, peripheral explanation for fatigue during high intensity exercise has been described as a catastrophe model whereas theoretically exercise would terminate when physiological and biomechanical limits of the body are exceeded, thus causing a disturbance in intracellular homeostasis (Noakes, & St Clair Gibson, 2004). This indicates that fatigue is a peripherally-based, metabolite-induced impairment on skeletal muscle restricting the capacity of force production (Swart, Lamberts, Lambert, St. Clair Gibson, Lambert, Skowno, & Noakes, 2009). It is a simple, linear explanation suggesting that system failure will occur when some metabolite concentration reaches absolute maximal capacity. However no single metabolite has been discovered to directly cause this relationship, and no example of this type of absolute system failure, such as skeletal muscle rigor, has ever been reported (Noakes, Gibson, & Lambert, 2004). The catastrophe model does not take into account most forms of exercise fatigue, or possible regulation of the central nervous system (CNS) which can decrease muscle activation by reducing efferent output from the motor cortex (Noakes, & St Clair Gibson, 2004). It suggests that fatigue is regulated exclusively by the changes in the exercising muscles; whereas if fatigue develops, exercise is then terminated.
The central fatigue model has also been proposed to describe the fatigue phenomenon in that the CNS receives somatosensory feedback from the working muscles in relation to how hard they are working, what the environment is like, and how much additional work is necessary. The brain then regulates exercise through a negative feedback system, very much the same way a home thermostat operates. The information gets processed and therefore future amounts of neuromuscular recruitment are influenced with the overall intent of maintaining homeostasis (Amann, 2008). It has been proven that the CNS alters its central motor drive during conditions of hypoglycemia, hypoxia, and hyperthermia, and exercise is no different (Hargreaves, 2008). During high velocity knee extensions, it was determined the co-activation of the hamstrings and quadriceps even when fatigued was regulated by the CNS in attempt to help support the ligament structures of the knee (Weir, Keefe, Eaton, Augustine, & Tobin, 1998). This view describes fatigue as more of a behavior, whereas behaviors are regulated by the brain in order to protect the body, and thus the complexity of which cannot be understood by any single factor (Noakes, 2008).
Central Nervous System Control
Fatigue can occur from the CNS regulation of different factors such as: the excitatory input to the motor cortex, motor-neuron excitability, neuromuscular transmission, and sarcolemma excitability (Hargreaves, 2008). During any type of voluntary exercise, the amount of motor unit recruitment allowed by the CNS will never reach maximal (Weir, Beck, Cramer, & Housh, 2006), and the CNS regulates motor unit recruitment by always keeping some motor units on “reserve” in attempt to avoid a disturbance in metabolic homeostasis or catastrophe such as an injury (Noakes, Gibson, & Lambert, 2004; Swart et al., 2009). Therefore other factors must contribute to the phenomenon of fatigue.
The CNS regulates fatigue due to prolonged endurance exercise. In elite cyclists exercising to exhaustion, subjects who received a dose of pharmacological amphetamines were able to cycle 32% longer compared to a placebo. The enhanced performance was not due to any reduction in metabolic or cardiorespiratory stress; in fact, the subjects who received the amphetamines experienced significantly greater VO2 output, heart rates, ventilatory rates, and lactate accumulations even though both groups recorded the same rate of perceived exertion (RPE). This demonstrates that amphetamines do not enhance performance by preventing peripheral fatigue factors; rather they are capable of inhibiting the CNS’s regulatory access over a natural ‘metabolic reserve’ to ensure homeostasis is preserved because the placebo group terminated their trial with metabolic and cardiorespiratory reserves not accessible without the use of the amphetamines (Swart et al., 2009).
Just as endurance exercise is regulated, so may be the case when attempting a 1-repetition maximum (1RM). An individual will obviously attempt to recruit maximal motor units during the lift, but the peripheral fatigue model does not explain the cessation in performance. The muscles are fully stored with ATP, and creatine phosphate stores do not get depleted, yet if enough motor units were activated to complete one lift, why could they not be activated again to complete a second? For starters, ATP concentrations in muscles are regulated with precise accuracy during exercise just as they are at rest. It has also been suggested that neither ATP usage nor lactic acid buildup are the most important factors for influencing muscle contraction, whereas calcium concentrations in the sarcoplasmic reticulum may be of greater importance because of its responsibility for initiating muscle contraction (Noakes, Gibson, & Lambert, 2004). Fatigue during maximal lifts is most likely due to the neurological pathways regulated by the CNS; one in which golgi-tendon organs detect the amount of stress, and therefore inhibit motor neuron excitability as a protective mechanism to maintaining homeostasis and avoid injury. This is an area for future research to better understand the body’s ability to self-regulate output at a subconscious level.
Fatigue is a very complex, non-linear, dynamic system in which power output is subconsciously regulated and modified by the CNS. These calculations take into account the peripheral environment (substrate and metabolite concentrations), prior familiarity of similar exercise bouts, the current metabolic rate; and the pre-determined end point of the current exercise bout, among other variables. This information is continuously calculated to adjust power output possibly through a feed-forward system of efferent CNS command. This is an entirely new way of appreciating fatigue in which it is not purely a physiological or neurological event as much as it is an emotional sensation of these subconscious CNS calculations. Additionally, an individual’s incentive to continue exercising also contributes to the sensation of fatigue. The distinct feeling of fatigue is more of an emotion, rather than a physical state, because it is not a direct result from a peripheral muscular end point, but rather from an interpretation of the current capacity to maintain a given level of activity along with immediate or future measures that potentially threaten homeostasis. In maintaining homeostasis, the journey is just as important as the end when it comes to fatigue (Noakes, Gibson, & Lambert, 2004).
Clearly the mechanisms that cause fatigue are quite complex, and it is a drastic oversimplification to view fatigue as an either/or situation in regards to peripheral or central control (Ameredes, 2008). Fatigue should not be viewed as the end result of a single mechanism, but rather the combination of a variety of mechanisms depending on the type of exercise performed (Weir, Beck, Cramer, & Housh, 2006). Fatigue is a combination of the peripheral and central theories with the addition of motivational factors because in the real world any of these scenarios could occur; the peripheral muscles can become functionally impaired in maintaining muscle contractions, the CNS can decrease the activation of muscle cells, or an athlete may not care to push themselves on a given day (Jaquinandi, 2008).
For coaches and trainers of athletes, understanding that the CNS naturally holds back a metabolic ‘reserve’ should help athletes confidently know there is always more in the tank when they begin to notice the sensation of fatigue. Focusing on pushing through those emotions during practice will improve the body’s ability to call upon that reserve when it really counts in competition; as the best athletes in any sport consistently practice with the same mental focus and intensity they use in competition. Caffeine is also a known CNS stimulant, and as of 2004 has been removed from the World Anti-Doping Association’s (WADA) prohibited list, therefore making it acceptable for use in all sports. Caffeine essentially has the same effects of improving exercise in the way amphetamines unlock the metabolic reserve capacity and reduce the RPE, in addition to increasing motor unit recruitment. This explains why athletes ranging from power-lifters to endurance cyclists will notice performance gains. The dosages used in most studies typically range anywhere from 3-9mg/kg, and caffeine has been shown to improve a wide variety of exercise performance including: sprint performance, intermittent interval performance, exercise endurance to exhaustion, maximal voluntary contractions, all while decreasing respiratory-exchange ratios, and increasing serum free-fatty acids, beta-endorphins, and cortisol (Bazzucchi, Felici, Montini, Figura, & Sacchetti, 2011; Laurent, Schneider, Prusaczyk, Franklin, Vogel, Krssak, & Shulman, 2000; Mohr, Nielsen, & Bangsbo, 2011; Bruce, Anderson, Fraser, Stepto, Klein, Hopkins, & Hawley, 2000). Since caffeine sensitivity is different for each individual, athletes should experiment with different dosages during practice to know how much is tolerable. Sports that require more refined motor skills may not chose to use caffeine because it could negatively affect performance due to jitters or increased heart rates.
For sprint-type athletes, or team sports in which there is a high demand on the phosphagen energy system, muscle function may become the main contributor to overall fatigue. The CNS may want to push as hard as possible, and motivation may be extremely high, but the rate and intensity of muscle contractions may cause a metabolic environment that potentially disturbs peripheral homeostasis. By paying close attention to dietary intake of creatine and calcium either by supplement or through meat/dairy consumption may prove beneficial because the rapid depletion of CrP and calcium may be the biggest contributors to impaired muscle contractions in this situation.
There may be other conditions for athletes where central fatigue plays a larger role and muscle function contributes less to the sensation of fatigue. For example when exercising at a low intensity but with a high environmental heat stress, the CNS may fatigue faster than the muscles, and therefore inhibit neural drive to the muscles to avoid dehydration.
When reflecting on past performances, successful or not, these are all factors coaches and athletes should consider when judging what impacted the performance. The goal is to match motivation with preparation (nutrition and training) and a competition game plan to achieve optimal level of performances.
The complexity of fatigue and the different causes that decrease exercise performance is not fully understood. There are many different forms of fatigue, with no one mechanism causing fatigue for all situations. Fatigue can vary depending on multiple factors such as exercise type, duration, intensity, familiarity, motivation, and environmental stresses. It is established that fatigue can occur in the working muscles, and those muscles can also be inhibited by the CNS to maintain homeostasis. Most likely fatigue is a constant blend of peripheral and central mechanisms constantly sending signals to the brain for interpretation. In this view, the complexity of fatigue and its effects on the body during exercise should be thought of as more of an emotion, rather than a physical event.
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