Abstract
troduction: In supramaximal exercises such as repeated sprinting (RSA), neuromuscular fatigue can lead to reduced power output even though the task may be sustained. It is known that fatigue can be related to central (neural) or peripheral (muscle) alterations depending upon the task. However, fatigue may appear prematurely in hostile environments such as hypoxia or under restricted blood flow (BFR) (Amann et al., 2006). The induced ischemia during BFR creates a local hypoxic environment, which affects intramuscular function and motor unit recruitment thus exacerbating fatigue (Scott et al., 2014). To the best of our knowledge, no previous research has investigated the effect of BFR and hypoxia on neuromuscular fatigue during repeated sprints, which was therefore the aim of the current study. Methods: Eleven athletes (6 men; 5 women) (26.7±4.2 yrs; 68.0±14.0 kg; 172±12 cm) participated in the study including one familiarization session followed by nine experimental trials (0%, 45%, 60%BFR; and 400m, 2000m, 3800m simulated altitude, respectively). Subjects were familiarized with neuromuscular stimulation and maximal voluntary contraction (MVC). Each test session included RSA until exhaustion with the assessment of MVC, central activation (twitch interpolation technique), as well as electrical evoked force at rest (twitch) and doublet at frequencies of 10Hz (P10) and 100Hz (P100) pre- and post-RSA. Power output was obtained during RSA. Two way repeated measures ANOVA were performed to assess differences pre- to post- (condition x time) and between conditions (hypoxia x occlusion) with Bonferroni post-hoc test (p<0.05). Results: Voluntary activation level (VAL) decreased pre- to post- at 60%BFR independent of altitude (by 15.6, 17.2, and 16.2 % at 400m, 2000m, and 3800m, respectively, P<0.001). Additionally, a 7.1% decrease (P<0.05) was observed in 45%BFR-3800m. The normalization of RMS by the M-wave also decreased (P<0.001) at post in 60%BFR independent of altitude (by 36.2%, 43.4%, and 41.5%). The P10, P100, P10/P100, and twitch decreased pre- to post- (P<0.001) across all conditions. Specifically, there was a difference with increased hypoxia for P10 (P<0.05), P100 (P<0.01) and twitch (P<0.05). In addition, the difference with increased occlusion was demonstrated for P100 (P<0.01) and twitch (P<0.05). Power output decreased throughout all
in 60%BFR independent of altitude (by 36.2%, 43.4%, and 41.5%). The P10, P100, P10/P100, and twitch decreased pre- to post- (P<0.001) across all conditions. Specifically, there was a difference with increased hypoxia for P10 (P<0.05), P100 (P<0.01) and twitch (P<0.05). In addition, the difference with increased occlusion was demonstrated for P100 (P<0.01) and twitch (P<0.05). Power output decreased throughout all conditions with an effect of hypoxia and occlusion (P<0.001). Discussion: Indeed, the RSA-induced central and peripheral fatigue parameters were different across conditions. Previous research has suggested that peripheral fatigue is closely controlled during exercise, meaning that central motor drive and thus performance (power output) may be self- regulated to prevent muscle fatigue from rising above a tolerated level (Gandevia, 2001). Accordingly, in the current study, the peripheral factors (P10, P100, and twitch) were affected in all conditions, while the central factors (VAL and RMS/M) were affected solely by 60%BFR conditions independent of altitude. Thus, central drive seems to be more affected by higher levels of occlusion than hypoxia, even when peripheral fatigue occurs.
4 Table of contents 1. INTRODUCTION .............................................................................................................. 7 1.1 The neuromuscular fatigue ................................................................................................. 7 1.2 Fatigue in repeated sprints ................................................................................................ 10 1.3 Fatigue in hypoxia ............................................................................................................. 12 1.4 Fatigue under blood flow restriction ................................................................................. 14 2. MATERIALS AND METHODS .......................................................................................... 16 2.1 Participants ....................................................................................................................... 16 2.2 Experimental design .......................................................................................................... 16 2.3 Repeated Sprint Test ......................................................................................................... 18 2.4 Neuromuscular fatigue assessment and analysis ............................................................. 19 2.4.1 Materials ........................................................................................................... 19 2.4.2 Sequence of stimulation .................................................................................... 20 2.5 Statistical analysis ............................................................................................................. 21 3.RESULTS ........................................................................................................................ 22 3.1 Performance and global fatigue ........................................................................................ 22 3.2 Central fatigue .................................................................................................................. 25 3.3 Peripheral fatigue .............................................................................................................. 28 4. DISCUSSION ................................................................................................................. 33
5 4.1 Performance and global fatigue ........................................................................................ 33 4.1.1 Effect of hypoxia and BFR on total work ........................................................... 33 4.1.2 Effect of BFR and hypoxia on MVC .................................................................... 37 4.2 Central fatigue .................................................................................................................. 40 4.1.1 Effect of BFR and hypoxia on central fatigue .................................................... 40 4.2.2 Arc reflexes ........................................................................................................ 42 4.3 Peripheral fatigue .............................................................................................................. 49 4.3.1 Muscle excitability ............................................................................................. 49 4.3.2 Evoked forces and performance of the contractile apparatus .......................... 49 4.3.3 Effect of BFR and hypoxia on peripheral fatigue ............................................... 51 5. PRACTICAL RECOMMENDATIONS ................................................................................. 53 6. STRENGTHS AND LIMITATIONS .................................................................................... 54 7. CONCLUSION ............................................................................................................... 55 8. REFERENCES ................................................................................................................. 56 9. APPENDIX .................................................................................................................... 66
6 Index of abbreviations AOP: Arterial occlusion pressure ATP: Adenosine triphosphate BFR: Blood flow restriction Ca2+: Calcium CNS: Central nervous system CO: Cardiac output EMG: Electromyography EPR: Exercise pressor reflex FI: Fatigue index FiO2: Fraction inspired of oxygen H+: Hydrogen ion HFF: High frequency fatigue LFF: Low frequency fatigue MAP: Mean arterial pressure MVC: Maximal voluntary contraction N2: Nitrogen P10: 10Hz stimulation P100: 100Hz frequency stimulation PCr: Phosphocreatine RF: Rectus femoris RMS: Root mean square RSA: Repeated sprint ability RSH: Repeated sprint in hypoxia TIT: Twitch interpolation technique VAL: Voluntary activation level VL: Vastus lateralis VM: Vastus medialis VO2max: maximal oxygen uptake
7 1. INTRODUCTION 1.1 The neuromuscular fatigue Muscle fatigue is a multifactorial, complex, and reversible phenomenon that can be defined as an exercise-induced decrease in maximal force production or an inability to sustain further exercise at a required force (Gandevia, 2001). Regarding this definition, one may interpret that fatigue is delayed and appears only after a protracted period of exercise. However, modifications occur as soon as the effort begins, even if the physiological mechanisms underlying fatigue may not always be detected at the onset of exercise (Bigland-Ritchie and Woods, 1984). Apparition of fatigue is common in all types of exercise and thus occurs in both low intensity as well as high intensity exercise. Likewise, different origins of fatigue may occur according to these modalities, which are also dependent on the duration of exercise (Millet and Lepers, 2004). Many models have been proposed (physiological, biochemical, psychological, biomechanical, and neurological) in order to explain fatigue, whereas some others have characterized fatigue as an interaction of central and peripheral processes (Allen et al., 2008; Gandevia, 2001). Hence, fatigue does not only occur within the muscles. Degradation of performance may be attributed to the failure of both muscle and neural components and therefore to the neuromuscular system. The latter, as represented in Figure 1 below, shows the different sites where alterations can occur that can affect fatigue. Figure 1. The neuromuscular system (Bigland-Ritchie, 1985)
8 The neuromuscular system distinguishes central and peripheral mechanisms underlying fatigue with the neuromuscular junction as the communication site (synapse) between the nerve (motor neuron) and the muscle. Peripheral fatigue is defined as fatigue produced by changes at or distal to the neuromuscular junction, whereas central fatigue is a progressive reduction in voluntary activation of muscle during exercise (Gandevia, 2001) due to failure of the central nervous system (CNS) to excite or drive motoneurons adequately (Goodall et al., 2012). Despite the complexity of this system, the determination of the origin of fatigue (central versus peripheral) is possible. Moreover, spinal or supraspinal origination of central fatigue may be distinguished depending on the technique of investigation used. Specifically, the assessment of the peripheral component is usually distinguished by stimulating the motor nerve (neurostimulation) in a relaxed muscle state (Millet et al., 2011), although muscle stimulation (myostimulation) and magnetic stimulation are also widely used techniques. Comparisons pre- and post-exercise in parameters such as peak twitch (mechanical response to a stimulation), M-wave (electrical response to the stimulation) and force evoked at different frequencies (usually 10 Hz and 100 Hz) can reflect perturbations downstream of the neuromuscular junction. On the other side, central fatigue can be examined by assessing two parameters: the voluntary activation level (VAL) and ratio RMS/M (root mean square (RMS) of the amplitude of muscle activation/M-wave (M)), in order to provide information about neural alterations upstream to the neuromuscular junction. The gold standard to assess VAL is the twitch interpolation technique (TIT) from Merton (Merton, 1954) that consists in superimposing a twitch or high frequency stimulation (generally 80-100 Hz) during a maximal voluntary (isometric) contraction (MVC), and comparing the superimposed response to the same potentiated response evoked on the relaxed muscle (Allen et al., 1995). The use of high frequency potentiated stimulations is now usually recommended (Duchateau, 2009; Place et al., 2007), although the level of discomfort and pain is greater with this type of stimulation (Bampouras et al., 2012). Furthermore, the ratio RMS/M corresponds to the root mean square of the maximal response in the amplitude of muscle activation via electromyography
et al., 1995). The use of high frequency potentiated stimulations is now usually recommended (Duchateau, 2009; Place et al., 2007), although the level of discomfort and pain is greater with this type of stimulation (Bampouras et al., 2012). Furthermore, the ratio RMS/M corresponds to the root mean square of the maximal response in the amplitude of muscle activation via electromyography (EMG) during a MVC and normalized by the amplitude of the M-wave. Although larger variations of measurement have been found for this ratio (Place et al., 2007), its use allows individual assessment of muscles or muscle groups, in opposite of TIT. However, these two central parameters do not allow insight to determine if the distinction of fatigue is from a spinal or supraspinal origin. Figure 2 displays the different anatomical locations linked with the potential mechanisms of fatigue and their assessment techniques.
9 The apparition and degree of fatigue are closely related to the task (Enoka, 1995) and alterations of the neuromuscular system are thus specific to exercise and its modalities. In team and intermittent sports (i.e, tennis, soccer, hockey, etc.), athletes are required to produce repeated short bouts of exercise (<30sec) at high intensities interspersed with brief recovery periods (<60sec) over an extended period of time (1-4 hours) (Bangsbo et al., 1991; Bishop et al., 2001; Manrique & González-Badillo, 2003; Faude et al., 2007; Girard, 2011; Girard & Millet, 2008; Glaister, 2005; Spencer et al., 2005). Although sprinting activity represents a relatively short duration of a total game (1-3% of effective playing time) (Spencer et al., 2005; Spencer et al., 2004), it is estimated that intense periods of sprinting activity may determine the outcome of a game, and thus influence the ability to win possession of the ball or to concede goals (Trapattoni, 1999). Furthermore, reductions in sprinting speed and high speed running actions, which can potentially affect the game, have been observed during elite soccer matches in men and women (Krustrup et al., 2005; Mohr et al., 2003). The improvement of repeated sprint ability (RSA) may therefore be effective to improve performance during a game. Figure 2. Potential mechanisms of fatigue linked to their anatomical location and their assessment techniques (adapted from Girard & Millet, 2008)
10 1.2 Fatigue in repeated sprints In repeated sprints, fatigue manifests as a decline in the maximal sprinting speed (running) or a reduction in peak power (cycling) or total work over sprint repetitions (Bishop, 2012). Fatigue can be evaluated through the comparison of “Pre and Post exercise” status, during the task with the collection of the EMG muscle activation as well as via fatigue index (FI) or percentage decrement score (Sdec). This indicates the ability to resist fatigue during repeated sprints (Girard et al., 2011). Finally, other indices such as mechanical work and sprint time can be useful in combination with the previous indices to assess RSA performance and fatigue. Muscle excitability, limitation of energy supply as well as metabolites accumulation have been listed as limiting muscular factors in RSA (Girard et al., 2011). With regard to muscle excitability, ionic disturbances have been observed following intense dynamic contractions and linked to decreases in sodium (Na+)/potassium (K+)-adenosine triphosphatase (ATPase) activity (Clausen et al., 1998). Indeed Juel et al. (2000) showed that during one leg knee extensor exercise, concentration of potassium (K+) outside of muscle cells was exacerbated (at least doubled), potentially due to a failure of the sodium/potassium pump (Na+/K+ pump). These modifications, including an accumulation of extracellular K+, impair cell membrane excitability and diminish the force development. It is, however, necessary to add that most of the studies investigated muscle excitability in in vitro conditions and it is therefore still unclear if RSA is affected by ionic disturbances. Additionally, alterations of muscle excitability in RSA, which can be evaluated by changes in amplitude of the M-wave, have led to contradictory results. Some researchers (Racinais et al., 2007) have shown an increase of the M-wave, whereas some others have reported a steady level (Billaut et al., 2013; Girard et al., 2013; Hureau et al., 2015) or a decrease (Perrey et al., 2010) after RSA. Further, performance decrement in RSA has been associated with a metabolic accumulation, which presents as a muscular acidosis and an accumulation of inorganic phosphate (Pi) in the muscle tissue. The decrease in blood and muscle pH (Ratel
Description
The thesis explores neuromuscular fatigue in cycling sprints under varying conditions.