Mechanism of fatigue during maximal cycling exercise

Numerous research models have been designed to investigate potential mechanisms leading to fatigue during short-term maximal exercise. However, the neuromuscular mechanisms responsible for fatigue are still a matter of debate and interest, particularly in a human exercising model. Two likely mechanisms include excitation/relaxation and force-velocity kinetics. In this study short cycle cranks (120 mm) were used to accentuate fatigue associated with muscle excitation/relaxation and long cranks (220 mm) were used to emphasize contractile (force-velocity) origins of fatigue. Fatigue index (peak power - min power / peak power) was used to quantify fatigue. Ten competitive cyclists (7 male, 3 female) cycled maximally for 30 seconds on crank lengths of 120 mm at 136 rpm and 220 mm at 110 rpm using an isokinetic cycling protocol. Power data (averaged over a complete revolution of the cranks) were recorded at 10 Hz with a power meter. Peak power did not differ between cranks (901 ± 309 W for 120 mm, and 898 ± 3 1 1 W for 220 mm,/? = 0.873). Fatigue index differed significantly between cranks (57.5 ± 8.4% for 120 and 51.1 ± 11.3% for 220, p < 0.01). Work performed also differed significantly between cranks (18.0 ± 5.5 kJ for 120 and, 19.2 ± 5.9 kJ for 220 p < 0.01). These results suggest that fatigue during a maximal short-term exercise stems mainly from kinetics of excitation and relaxation of the sarcomere. Improving fatigue resistance during maximal exercise may require improvements in the processes of excitation and relaxation.

EXERCISE Aleksandar Tomas die in partial fulfillment of the requirements for the degree of Master of Science MECHANISM OF FATIGUE DURING MAXIMAL CYCLING EXERCISE by A thesis submitted to the faculty of The University of Utah Department of Exercise and Sport Science The University of Utah December 2007 Copyright© Aleksandar Tomas 2007 All Rights Reserved SCHOOL satisfactory. THE UNIVERSITY OF UTAH GRADUATE SCHOOL SUPERVISORY COMMITTEE APPROVAL of a thesis submitted by Aleksandar Tomas This thesis has been read by each member of the following supervisory committee and by majority vote has been found to be satisfactory. 7r /a .3I/ O 7 1 £ Chair: James C. Martin '" - r r , v w ·nc- 2: V - . 7' Bradley T. Hay s THE UNIVERSITY OF UTAH GRADUATE SCHOOL final manuscript is satisfactory to the supervisory committee and is ready for submission to The Graduate School. D)aaxree / JJame s C. Martin Chair: Supervisory Committee airy B. Shultz Chair if- Approved for the Graduate Council \ SCHOOL FINAL READING APPROVAL To the Graduate Council of the University of Utah: I have read the thesis of Aleksandar Tomas in its final form and have found that (1) its format, citations, and bibliographic style are consistent and acceptable; (2) its illustrative materials including figures, tables, and charts are in place; and (3) the D e 7 James c. Mirtin Committee Approved by the Major Department 1- -- {)3a;;' B. Shultz 0"'" , David S. Chapman r Dean of The Graduate School mechanisms leading to fatigue during short-term maximal exercise. However, the neuromuscular mechanisms responsible for fatigue are still a matter of debate and interest, particularly in a human exercising model. Two likely mechanisms include excitation/relaxation and force-velocity kinetics. In this study short cycle cranks (120 mm) were used to accentuate fatigue associated with muscle excitation/relaxation and long cranks (220 mm) were used to emphasize contractile (force-velocity) origins of fatigue. Fatigue index (peak power - min power / peak power) was used to quantify fatigue. Ten competitive cyclists (7 male, 3 female) cycled maximally for 30 seconds on crank lengths of 120 mm at 136 rpm and 220 mm at 110 rpm using an isokinetic cycling protocol. Power data (averaged over a complete revolution of the cranks) were recorded at 10 Hz with a power meter. Peak power did not differ between cranks (901 ± 309 W for 120 mm, and 898 ± 3 1 1 W for 220 mm,/? = 0.873). Fatigue index differed significantly between cranks (57.5 ± 8.4% for 120 and 51.1 ± 11.3% for 220, p < 0.01). Work performed also differed significantly between cranks (18.0 ± 5.5 kJ for 120 and, 19.2 ± 5.9 kJ for 220 p < 0.01). These results suggest that fatigue during a maximal short-term exercise stems mainly from kinetics of excitation and relaxation of the sarcomere. Improving fatigue resistance during maximal exercise may require improvements in the processes of excitation and relaxation. ABSTRACT Numerous research models have been designed to investigate potential quantify 10Hz ± 311 mm, p = significantly perfonned ± ± sterns Problem Statement 4 Research Questions 4 Hypotheses 5 Assumptions 5 Equipment .23 AND RECOMMENDATIONS 30 Summary 30 31 31 TABLE OF CONTENTS ABSTRACT .......... . ......................... .. .... ..... ... . .... .. .. . .. .. .. .. .. .. . ... . .. ......... .. iv Chapter Page I. INTRODUCTION . . ..... . ... ............ .. . .. . ...... ... . ... .. : . ... . .. . ... ........ . ..... . .... 1 Significance of the Study .. .. .... .. ......... .. .. ...... . .. .... . . . ..... .. . .. . .. .. .. ... .. . ... .. 3 Problem Statement. .... .. .. , ..... .... . .... ..... . , ... . ......... " . .... , . ... .. ..... .. .. .. ... ...... 4 Research Questions . ......... . ......................... .. .. ........... ... ... .. .. ...... ...... . 4 Hypotheses ......... . .. .. . . ...... ... .. .. ...... ..... . ..... .. ... . . .. . ... .. ... . ..... . ... ....... . .. 5 Assumptions ......... .... .. . . ...... .... ... ...... ... ... .. ... ... ... . . .. . . .... . . .. ... . .. ... .. .... 5 II. REVIEW OF THE LITERATURE ... .. ....... ... ... . ... . .. .. . .. .. .. ..... .... ............ 7 Defining Fatigue . . ... . .... . .. ..... . . .. .. . ...... .... .. . .. ..... .. ..... .. ..... .. ..... .. .. .. . .. .. 7 Potential Sources of Fatigue .............. ... .. .. .. . ....... .. ..... .. ... ........ .. .. .... .. .. 8 Fatigue During Maximal Voluntary Cyclical Contractions .... . . ..... ..... .. .. .. .... . 13 III. METHODS ........... .... . .... ... .. . .. ... .. .... ..... . . ..... .. . . .. .. .. .... . ... ...... ..... . .. 17 Selection of Participants .. .. . ..... . .. .. . ...... ... .. . . ... .. . .. .... . .. .. . ..... ... . ..... . ... . 17 Equipment. ..... . ........... ... .. ... . .. . , ... .. ... .. .... . ... . ... . ..... .. . .. .. ... . . ... . , .. . .... 17 Protocol ... . ... . .. ... ... .. ...... ... . .. . .. . . ....... .. .... .. ..... . .. . .. . .... ... . .. . . ... . , ....... 18 Statistical Methods and Data Analysis .. ... ... .. ....... .. . ... ... .. ......... .. ........ .. 19 IV. RESULTS AND DISCUSSION .. .. .. ...... .... .... ........ .. .... ...... .... ...... ..... .. . 21 Results .. ... .. ........ .. .. .. ..... .... ... . . .. .. . .. ...... .. .... .. . ... .... ....... .. ... ... .. .... .. 21 Discussion .. .. ....... .. . ... ........ . ....... .. .. .. . ...... .. . ..... . .... .. .. ... . .... .... ........ 23 V. SUMMARY, FINDINGS, IMPLICATIONS, AND RECOMMENDA nONS . .. .. ............. .. .... .. ... .. . .. , .... .. , .... .... .. . .. ... ...... . 30 Sulnmary ... ... ... . . ... .. .. .... ..... . ..... . .... .. ... . .. .. .. .... .. .. ... . ..... .. .... ... ... .. . .. 30 Findings .... ... . .. .... ' .... ..... .. .... .. ........... . .. .. . . .. .. .. .... ... . .. .... . ........ .... .. .31 Implications of the Study ... .......... . .. ....... .. ...... ... .. ......... .......... .. . . ..... . .31 33 VI Future Research Recommendations ..................... ....... ............. ...... .... ... 32 REFERENCES ............................ .................................................. CHAPTER 1 INTRODUCTION order for a muscle to produce power in a cyclical manner (i.e., cycling, locomotion, etc.) there must be a neural input from the central nervous system via alpha motor neurons. The neural impulse must also cross the neuromuscular junction and enter the skeletal muscle cell. Calcium ions must be released from the sarcoplasmic reticulum (SR) in order formed Ca2 + ) & & & during Power produced during maximal cycling exercise is limited by numerous mechanisms at various locations along the neuromuscular and contractile pathways. In thc to initiate activation (excitation). Actin/myosin cross-bridges must be fonned quickly and force produced. Finally, calcium (ion, Ca2+) must be re-sequestered into the SR to relax the muscle and allow lengthening before the next contraction can occur. Furthermore, these processes must occur with adequate speed in order for the muscle, and therefore the entire organism, to maintain maximum power output (McArdle, Katch, Katch, 2001). Several studies (Martin, Brown, Anderson, Spirduso, 2000; Van Soest Casius, 2000) demonstrated that the maximal power produced dUling cycling is influenced both by excitation/relaxation kinetics as well as force/velocity characteristics. Martin and Spirduso (2001) have used cranks of different lengths to emphasize either excitation/relaxation or force/velocity mechanisms. ("Standard" crank lengths are 170 mm - 175 mm. Cranks used in this study varied from 120 mm to 220 mm.) When exercising with a longer crank, maximum power is produced with greater pedal speed 2 (muscle shortening velocity) and less cycle frequency (excitation/relaxation). Conversely, when exercising with a shorter crank, maximum power is produced with greater cycle frequency (greater reliance on excitation/relaxation kinetics) and less pedal speed. Edman and Matiazzi (1981) have demonstrated that during a maximal short-term exercise there is both a decline in velocity-dependent force production, as well as prolongation of the excitation/relaxation period with respect to time. However, the relative contributions of excitation/relaxation and force/velocity kinetics have not been investigated during a fatiguing bout in human exercising models. Thus, the purpose of this study was to investigate the effects of crank length on muscle fatigue mechanisms during a maximal bout of sprint cycling. Syme and Tonks (2004) fatigued a rat soleus muscle using a work-loop technique, from frequency tenn excitation/relaxation and force/velocity kinetics have not been investigated during a fatiguing bout in human exercising models. Thus, the purpose of this study was to investigate the effects of crank length on muscle fatigue mechanisms during a maximal bout of sprint cycling. teclmique, in which a servomotor shortened and lengthened a muscle and the muscle was stimulated to produce force during shortening. During fatigue, the positive work declined by 30%. However, the negative work increased by 500% indicating that the muscle was unable to relax at a sufficient rate. In other words, the muscle was working against the motor during lengthening. Two groups of researchers have investigated the effect of different pedaling rates on the maximal power production and consequent fatigue. Using a maximal human cycling model McCartney, Heigenhauser, and Jones (1983) varied pedaling rate from 60 to 160 rpm. The authors of this study reported that work accomplished during 30 second maximal sprint efforts at 60, 100, and 140 rpm did not differ. This finding was due to the combined effects of peak power and fatigue. Specifically, initial peak power increased with increasing pedaling rate, whereas the rate of fatigue also increased with increased 3 pedaling rate. Beelan and Sargeant (1991) induced fatigue V02max versus a control condition of cycling for the same duration, but at 30% V 0 2 m a x - Both conditions were immediately followed by an all-out 30-second sprint at 60, 75, 90, 105, or 120 rpm. They made 60 rpm and 120 rpm their primary comparison. The peak power did not differ between the control and fatigued condition at 60 rpm. Fatigue index was the same as well. However, at 120 rpm the initial peak power was lower by about 500 watts (W) in the fatigued condition. This finding indicated that during fatigue, muscles have more difficulty generating power at faster pedaling cadences than at slower ones. In each of these studies, the researchers detected a greater decline in power at faster pedaling cadences. Therefore, because the same crank length was used for each pedaling cadence, the cyclists had concurrently increased pedal speed and pedal frequency. In physiological terms, they had concurrently increased muscle shortening velocity and excitation/relaxation frequency. Consequently, the extent to which each of these mechanisms contributed to fatigue could not be separated. In this study, my goal was to exploit the way pedal speed and pedaling frequency interact to limit power so as to determine whether pedal speed (muscle shortening velocity) or cycle frequency (excitation/relaxation kinetics) is the dominant mechanism leading to fatigue during maximal cycling. Data obtained during fatiguing bouts of maximal intensity cycling using two cycle crank lengths allowed us to determine whether excitation/relaxation or force/velocity kinetics contribute more to fatigue. of the fatigue mechanisms during a short-term maximal cycling exercise and add to the body of by 6 min of exercise at 90% V02max versus a control condition of cycling for the same duration, but at 30% V02max. Both conditions were immediately followed by an all-out 30-second sprint at 60, 75, 90, 105, or 120 rpm. They made 60 rpm and 120 rpm their primary comparison. The peak power did not differ between the control and fatigued condition at 60 rpm. Fatigue index was the same as well. However, at 120 rpm the initial peak power was lower by about 500 watts (W) in the fatigued condition. This finding indicated t11at during fatigue, muscles have more difficulty generating power at faster pedaling cadences than at slower ones. In each of these studies, the researchers detected a greater decline in power at faster pedaling cadences. Therefore, because the same crank length was used for each pedaling cadence, the cyclists had concurrently increased pedal speed and pedal frequency. In physiological terms, they had concurrently increased muscle shortening velocity and excitation/relaxation frequency. Consequently, the extent to which each of these mechanisms contributed to fatigue could not be separated. frequency detennine sh0l1ening Significance ofthe Study First, in this study I have attempted to investigate the basic science question of the amyotrophic fatigue plays a central role in patients' level of physical activity and exercise capacity (Gandevia, Enoka, McComas, Stuart, & Thomas, 1995). Although the results obtained in this study may not directly provide diagnostic or curative advice, these results give a more complete picture of fatigue that may relate to a disordered condition. Third, the results obtained in this study could have practical implications for testing of maximal cycling performance as well as sprint cycling competitions. Proper crank length and offer performance. significant cycling on any specific crank length (Martin et al., 2000) it has been impossible to differentiate between the two using a traditional cycling model. By extension, it is also difficult to determine which factor has a greater limiting influence in a fatiguing muscle. 4 knowledge in this area. Second, in several disease populations such as amyotrophic lateral sclerosis, chronic fatigue syndrome, myotonic dystrophy, and McArdle's disease, perfomlance pedaling rate are debated within the cycling community; therefore, this study might offer practical advice on crank length and sprint cycling performance. Problem Statement Excitation/relaxation and force/velocity characteristics are both significant contributing factors to overall neuromuscular performance during maximal exertion. These two processes are both potential limiting factors during a fatiguing exercise bout. However, because excitation/relaxation and force/velocity are linearly related during a1., detenlline Research Questions In this study I have tried to answer the following research questions: 1. What is the fatigue index over the 30-second maximal iso-kinetic cycling trial? 2. Is there a difference in the rate of fatigue with regard to crank length? 5 preferential? & fatigue preferentially affects excitation/relaxation kinetics (resequestering Ca2 + ) . This finding is Assumptions 3. During a fatiguing bout, are excitation/relaxation and force/velocity equally contributing factors or is one preferential? Hypotheses The following hypotheses were tested in this study: 1. There will be no difference in maximal power output (first 3-4 seconds) between crank lengths (Martin Spirduso, 2001). 2. Longer cranks (220 mm vs. 120 mm) with a lower frequency and higher pedal speed, will have a lower fatigue index during the 30 seconds implying that the fatigue Ca2+). consistent with the findings of Syme and Tonks (2004). 3. More work will be accomplished with the longer cranks. (Because work is directly related to power, this hypothesis follows directly from hypothesis 2.) The following assumptions were made for this study: 1. The athletes recruited are trained cyclists rested and motivated to participate in the study. 2. The participants exerted themselves maximally during both trials. 3. Two components of cyclic velocity, pedaling rate and pedal speed, represented intramuscular processes, excitation/relaxation and muscle shortening velocity, respectively. This relationship did not differ between peak and fatigued segment of the sprint bout. 6 4. The equipment used accurately measured power output from the muscles to the pedals and pedaling rate. LITERATURE of this study. Next, I will cover several potential sites of fatigue. I will then describe the use of the human cycling model in studying physiological phenomena. Finally, I will describe our model and compare it with of different lengths (with an underlying attempt for maximal performance) have multiple combinations of metabolites and mechanisms that present an obstacle for continued work at a desired intensity. Fatigue is also defined differently depending on the field of study. Fatigue could be referred to as a decline in physical or mental work output or a psychological phenomenon. Brooks and co-workers (1999) defined fatigue as an "inability to maintain a given exercise intensity" (p. 701). McArdle et al. (2001) defined anaerobic fatigue as "the percentage decline in power output during the test" (p. 227), referring to the Wingate anaerobic test. However, the same group of authors (later in their widely used exercise physiology textbooks) stated that neuromuscular fatigue "represents the decline in muscle tension (force) capacity with repeated stimulation" (p. 400). CHAPTER 2 REVIEW OF THE LITERATURE In this chapter, I will review pertinent literature regarding maximal exercise fatigue. First, I will discuss the various definitions of fatigue commonly used by authors and define fatigue within the context previous studies on maximal sprint fatigue. Defining Fatigue Fatigue during physical activity is task-specific. Fatigue is also time specific; endeavors perfonnance) a1. defined widely used exercise physiology textbooks) stated that neuromuscular fatigue "represents contraction of skinned animal muscle as opposed to a cyclical contraction. Edwards (1981) stated that muscle fatigue is a complex phenomenon that can be demonstrated through the inability to sustain further exercise at a required power. Other discussions seem to reach a consensus on the definition: fatigue is usually defined at the beginning of a review as an inability to sustain some arbitrary level and measure of performance (Kurihara & Brooks, 1975; Lambert, St. Clair Gibson, & Noakes, 2005). In the current study I adopted a definition more closely aligned with that of McArdle et al. (2001), in which fatigue is viewed as the reduction of performance and power output as the key measure of performance during maximal cycling. performance al. concentration followed excitation/relaxation. 8 This last statement is probably a more accurate representation of the isometric demonstrated performance a1. perfonnance Potential Sources of Fatigue There is no single cause of fatigue. Rather, a deviation from a maximal or desired level of perfonnance to a lesser level of performance occurs due to changes in several neuromuscular systems. Lambert et a1. (2005) proposed a model in which peripheral limiting steps and concentrabon of metabolites served as "sensors" that lead to an afferent feedback to the brain. The brain then accordingly adjusted metabolic and motor activity in a feed-forward fashion. On the list of potential limiting steps, in the order of steps needed for a muscle to contract, central nervous system (CNS) is the first, followed by neuromuscular junction (NMJ), contractile (actin-myosin) coupling, and from brain and/or descending motor pathways prior to the NMJ. In a study by Asmussen (1979) individuals performed maximal contractions on a finger ergo graph with their eyes closed. The performance gradually declined, and was restored almost completely (though not permanently) once the individuals were allowed to open their eyes. There have also been attempts to directly stimulate the motor cortex using transcranial magnetic stimulation (Taylor et al., 1996). The researchers found that such stimulation attenuated decline during maximal voluntary contraction of elbow flexors. Both of these studies demonstrate the important role of central drive in maximal neuromuscular function. of Ca2 + & & Kwanbunbumpen, C a 2 Ca Ca Ca Ca2 + al., C a 2 + ACh vesicles released (Jones & Kwanbunbumpen, 1970). The two main postsynaptic sites for the NMJ fatigue are cholinergic receptors and reduction in sarcolemmal 9 Central Nervous System Fatigue Some of the limitation in the power output during maximal exertion might come finger ergograph aI., function. Fatigue at the Neuromuscular Junction Possible mechanisms of fatigue, including limitations at both pre and post­synaptic cleft, could occur at the NMJ. For the neurotransmitter acetylcholine (ACh) to be released from a terminal membrane of the motor neuron, there has to be an adequate influx ofCa2 + into the nerve terminal (Castillo Katz, 1954; Jones Kwanbunbumpen, 1970; In this case the Ca2 + discussed is at the terminal end of the motoneuron, rather than ci+ that is moved into the myoplasm and back into the SR). A decrease in Ca2 + influx or sensitivity to Ca2+ could be a limiting factor in repeated muscular contractions (Sieck & Prakash, 1995). Influx of ci+ is usually related to a decrease in the amount of ACh per vesicle released (Gandevia et a1., 1995). Sensitivity to Ca2 + is related to the number of postsynaptic sarcolemmal fatigue favorable Na+-K+ gradient along the sarcolemma (McArdle et al., 2001). It follows that the disruption of this gradient could reduce the transmission of action potential and thereby cause fatigue. Because the gradient must be restored quickly enough (with the time associated with one contraction cycle), this type of fatigue has been referred to as high-frequency fatigue (Fitts, 1994). Clausen and Nielsen (1994) have found that Na+-K+ pump enzymes' activity is diminished during fatigue. Thus, the gradient is not restored quickly enough and there could be no rapid propagation of the action potential. With respect to the repeatedly contracting muscle, this type of fatigue would also reduce excitation (but not relaxation). The model of our laboratory could potentially be adapted to study the CNS and K+ actin-coupling and excitation/relaxation kinetics. binding sites. Hydrolysis of one ATP molecule per myosin cycle allows for actin and formation (during which the force is produced) varies depending on the type of isoform, and velocity of shortening (Macintosh, Gardiner, & McComas, 2006). It has been 10 excitability (Sieck & Prakash, 1995). Therefore, it is reasonable to speculate that fatigue at the NMJ could reduce excitation of the muscle. Na+-K+ Gradient In order to spread an action potential throughout the muscle cell, there must be a refened Na + -K+ maybe the NMJ and Na+-K' fatigue; however, the focus of my study was on actin-myosin Actin-Myosin Coupling Active muscle force is produced by the coupling of myosin heads with actin myosin binding and fonnation of cross-bridges. The duration of the cross-bridge cycle isofonn, MacIntosh, reduced in a fatigued state. Edman and Matiazzi (1981) stimulated a frog fiber for a duration of 1 second with a 15 second interval between contractions. After 25-30 contractions the force declined to 75% of the starting force (where it remained unchanged). The same research group (Curtin & Edman, 1994; Edman & Lou, 1992) has observed that shortening velocity is reduced along with the reduction in force. Interestingly, the reduction in shortening velocity was observed to occur with a slight delay after the reduction in force. These results suggest that reductions in force and velocity could contribute to reductions in power during shortening contractions. & C a 2 + Ca2 + play a H + C a 2 + & Ca observations Macintosh technique to fatigue a rat soleus muscle and reported dramatic changes in relaxation kinetics. Once the muscle fatigued, the positive work was reduced by about 30%). 11 documented that both maximal force production and muscle shortening velocity are Excitation/Relaxation Fatigue There is evidence that fatigue preferentially affects excitation/relaxation kinetics (Syme Tonks, 2004). For the purposes of the current study, excitation was considered the release of ci+ from the SR into the myoplasm, and relaxation as pumping the Ca2+ back into the SR. Several agents could affect excitation and therefore playa role in fatigue. A low pH - a high concentration of H+ - directly affects the release of Ca2 + into the myoplasm (Meissner, 1994; Rousseau Pinkos, 1990). However, Lamb and Stephenson (1994) reported that in skinned fibers a variation of pH from 6.1 to 8.0 had no effect on Ca 2+ release. Fitts (1994) argued that excitation/contraction coupling (resulting in Ca2+ release) is not a limiting factor in vivo. The decrease in rate of muscle relaxation has been one of the main observations of a fatigued muscle (MacIntosh et al., 2006). Syme and Tonks (2004) used a work-loop 30%. 500% suggesting that relaxation of the muscle ceased to be performed by the muscular processes and was driven by the servomotor against the muscle. Lee, Westerblad, and Allen (1991) have found that the slow relaxation could be due to inadequate re-sequestering of Ca back into SR (after the dissociation of Ca -troponin complex). Cady, Elshove, Jones, and Mole (1989) have found that the main cause for slowing in Ca2 + re-sequestering could be H+ . It is unclear if H + could affect slow removal of Ca2 + from myoplasm is due to parvalbumin (Ca2 + shuttle) saturation with Ca2 + (Macintosh et al., 2006). Slow removal may indeed be directly related to the mechanisms of energy delivery. The enzyme C a 2 + ATPase (which is responsible for active C a 2 + pumping) has diminished activity during fatigued conditions (Green, 1997). This could decrease the ability of the SR to sequester the + . Green (1997) further noted, however, that in order to identify a structural deficiency of the SR as a cause in fatigue, a decrease in production of power output must also be observed. Pi) Pj , cross-bridges interferes Ca 12 However, the work required to lengthen the muscle (negative work) was increased by re­sequestering Ca2+ Ca2+ Ca2+ H+. H+ Ca2+ Ca2+ Ca2+ MacIntosh Ca2 + Ca2+ diminished activity during fatigued conditions (Green, 1997). This could decrease the Ca2 +. As a result of creatine phosphate breakdown during maximal activity, inorganic phosphate (PD is abundant in a fatigued condition. Westerblad, Allen, and Lannergren (2002) have argued that Pi may affect both the force production as well as calcium handling. At the level of velocity dependent force production, Pi can reduce tropomyosin's sensitivity to Ca 21 -, which could obviously reduce the number of cross­bridges forming in any given voluntary contraction. Inorganic phosphate also interferes with Ca2+ handling, both during re-sequestering as well as storing it in the SR. 13 Contractions Most of the above cited studies were performed using in vitro animal muscle preparations. Such studies have many advantages compared to human exercising models. However, one obvious limitation is direct translation to a human exercising voluntarily. Although ideally, one would hope that a voluntarily exercising human model could mirror an animal model in which the data have been collected and analyzed with greater resolution, with respect to cellular mechanisms. One such relationship exists between a work-loop technique (Caiozzo & Baldwin, 1997) and a human cycling model (Martin et al., 2000), specifically pertaining to the cyclical power production of skeletal muscle. In a work-loop technique, researchers have been able to vary the muscle shortening velocity and cycle frequency of the muscle contraction as well muscle length change (excursions). Similarly, while cycling on an ergometer, a researcher can vary the same parameters by Martin and co-workers (2000) reported that the impulse and power versus cyclic velocity (i.e., product of muscle shortening velocity and cycle frequency, CV = Vs x Cf) single curve. work-loop (120 mm, 145 mm, 170 mm, 195 mm, and 220 mm), any given value of cyclic velocity represents a different combination of shortening velocity and cycle frequency. For example, for 120 mm cranks, maximum power occurred at pedaling rate of 136 rpm and pedal speed of 1.71 m/s, whereas for 220 mm cranks, maximum power occurred at Fatigue During Maximal Voluntary Cyclical Contractions perfonned frequency changing pedal speed, pedaling frequency and crank length, respectively. Martin and co-workers (2000) reported that the impulse and power versus cyclic velocity (i.e., product of muscle shortening velocity and cycle frequency, CV Vs x Cf) curves from cycle crank lengths of 120 to 220 mm converge onto a The work-loop data of power versus cyclic velocity in study by Swoap, Caiozzo, and Baldwin (1997) similarly converges onto a single curve, implying a strong relationship with work­loop technique and human cycling model. For the five crank lengths in the Martin model frequency. mis, m/s. relationships for these crank lengths may give us insight into the relationship of reduced actin/myosin binding (and thus force/velocity characteristics) and prolonged activation/relaxation kinetics in a fatigued state. If fatigue preferentially effects force/velocity characteristics or activation/relaxation kinetics, the power-cyclic velocity relationships for different crank lengths will diverge in the fatigued state. Specifically, if force-velocity characteristics are more affected, power during fatigue will be lower with longer cranks. If activation/relaxation kinetics are more affected, power during fatigue will be lower with shorter cranks. performance Yoshihuku Martin frequencies McCartney 14 pedaling rate of 110 rpm and pedal speed of 2.53 mls. Thus, the power - cyclic velocity effects Cranks of different lengths have also been used to investigate any performance improvements or detriments. Most recently, Martin and Spirduso (2001) reported a 4% difference in peak power output with regard to crank length. Specifically, power produced with 145 mm and 170 mm crank length was about 4% greater than power produced with 120 mm and 220 mm. Y oshihuku and Herzog (1996) have reported larger differences, between 8-10% in favor of the shorter (less than 170 mm) cranks. However, these findings have been criticized because relaxation kinetics were not taken into account with respect to developing their model for optimal crank length (Mariin & Spirduso, 2001). Researchers have also used a single crank length, but different cycle frequencies (and therefore pedal speeds) to investigate the resulting effects on fatigue. McCaJiney and co-workers (1983) used 60 rpm and 140 rpm for a 30-second maximal bout. The work accomplished was the same, however, the maximal power for the 140 rpm was about 300 watts greater than at 60 rpm. In a somewhat similar study, Beelen and Sargeant rpm) and compared power output in controlled and fatigued conditions. They found that the peak power with higher pedaling frequencies (120 rpm) declined by about 25%, whereas peak power at lower pedaling frequencies (60 rpm) did not change. However, at the start of the sprint bout, peak power for 120 rpm was greater than at 60 rpm, so even though the power declined, the total amount of work accomplished was greater for 120 rpm versus 60 rpm. The researchers speculated that fiber-type accounted for these results. Specifically, type II fiber type (faster, more powerful, but more fatigueable muscle fiber) generated greater power in a condition (faster pedaling frequencies) that favors their characteristics, but fatigued more quickly. The results of these two studies were extremely valuable in providing the rationale for my hypotheses and determining the methods needed to investigate them. Specifically, in both of these studies the peak power reached was greater at higher pedaling rates. Based on the work by Martin and Spirduso (2001), there is a way to optimize the peak power production and therefore control for the peak power produced. Once the peak power was controlled, one could investigate the power produced in a fatigued condition. In both studies, the power produced in a fatigued condition was greatly influenced by the magnitude of the peak power. Furthermore, performed using a single crank length, the effects of frequency and shortening velocity could not be differentiated. The previous investigations have also focused on fiber-type and fatigue 15 (1991) used a single crank length, but different pedaling frequencies (60, 75, 90, and 120 frequencies though the power declined, the total amount of work accomplished was greater for 120 rpm versus 60 rpm. The researchers speculated that fiber-type accounted for these results. Specifically, type II fiber type (faster, more powerful, but more fatigueable muscle fiber) generated greater power in a condition (faster pedaling frequencies) that favors their characteristics, but fatigued more quickly. The results of these two studies were extremely valuable in providing the rationale for my hypotheses and determining the methods needed to investigate them. Specifically, in both of these studies the peak power reached was greater at higher pedaling rates. Based on the work by Martin and Spirduso (2001), there is a way to optimize the peak power production and therefore control for the peak power produced. Once the peak power was controlled, one could investigate the power produced in a fatigued condition. In both studies, the power produced in a fatigued condition was greatly influenced by the magnitude of the peak power. To conclude the literature review, fatigue has been shown to be greater when cycling at greater pedaling rates. These data have been confounded because initial power was greater and therefore more work was accomplished in the early part of the trials at higher pedaling rates. Furthennore, because previous investigations were performed fiber-fatigue al., contributions to fatigue, regardless of the fiber-type recruitment. Of course, it would be difficult to directly implicate a specific intracellular mechanism based on a study that does not directly investigate these processes; rather this study depends on the validity of a model (Martin et al., 2000). However, I have attempted to contribute to the body of literature by investigating a valid cycling model that is relevant to the study of human movement. Furthermore, my study offers an alternative approach to studying fatigue and could lead to a greater understanding of the concept. 16 (Beelen & Sargeant, 1991; McCartney et ai., 1983), whereas our study identified two intracellular mechanisms (force/velocity, excitation/relaxation) and their relative fiber-ai., Seven male (182.3 ± 7.41 cm, 73.1 3.31 kg) and three female (172.0 ± 5.29 cm, 57.5 ± 12.32 kg) trained competitive cyclists participated in the study. Five males were road racers, one was a triathlete, and one a mountain biker. Two females were triathletes and one was a road racer. Trained cyclists are known to be capable of producing stable and reliable values for maximum power (Martin, Diedrich, & Coyle, 2000). The participants cycled easily the day before the data collection, but otherwise followed their regular training programs. It is therefore assumed that their training and racing schedules did not affect the results of this study. ergometer CDP3605, regenerative CHAPTER 3 METHODS This chapter will cover the methodology used in this study. I will describe the athletes who participated in the study, the equipment used, protocol under which the study was conducted, and methods of statistical analyses. Selection of Participants em, ± em, 57.5 12.32 kg) trained competitive cyclists participated in the study. Five males were road racers, one was a triathlete, and one a mountain biker. Two females were triathletes and one was a road racer. Trained cyclists are known to be capable of producing stable & Equipment A Monark (Vansbro, Sweden) cycle crgometer frame and flywheel were used to construct an isokinetic ergometer. The flywheel was driven by a 3750 watt direct current motor (Baldor Electric Company model CDP360S, Fort Smith, AR, USA) via pulleys and a belt. The motor was controlled by a speed controller equipped with regenerative applied power to the ergometer, the motor acted as a generator and the generated current was dissipated by a resistor and heat sink built into the speed controller. The controller could, therefore, maintain a specified pedaling rate while resisting power outputs of up to 3750 watts. There was a small compliance to the system with respect to pedaling rate: at the begimiing of the sprint bout, cadence was 1-2 rpm above target and towards the end 1-2 rpm below target. These small variations likely did not affect the results in a meaningful way. Power was measured by a Shoberer Rad Masstechnik power meter (SRM); the company claims that the four-strain version accuracy has a 2.5% accuracy (http://www.snn.de/usa/prod_snnts_str_amat.html). Both Gardner et al. (2004) and Martin, Milliken, Cobb, McFadden, and Coggan (1998) established that when used according to manufacturer's instructions the SRM gave users an accurate and valid measure of power. Data were collected at 10 Hz and averaged over one pedal revolution via the following mathematical model: P = T a> = [(FO|o adcd - FOz e r ooffset) f 2 n I Fc a i 60], where P is power, T is torque, a) is angular velocity, FOio ad«i is frequency output when a known load is applied, F O z e r o 0ffs et is frequency output when no load is applied, f is pedaling frequency, and F c a i is a calibration factor or slope of the power meter (www.snn.de/Software/SRMManual.pdf). All participants wore cleated cycling shoes that locked the feet to the pedal. participating participants 18 braking capability (Minarik model RG5500U, Glendale, CA, USA). When a cyclist i11to beginning splint ± (http://www.snn.de/usalprod_snnts_str_amat.html). Both Gardner et al. (2004) and Mmiin, Milliken, Cobb, McFadden, and Coggan (1998) established that when used according to manufacturer's instructions the SRM gave users an accurate and valid 10Hz revol ution via the following mathematlcal model: P = T ()) = [(FOlo3d,'c FOzcrooffsct) f2 FCill 60J, Ul FOloadt'd FOlClo offset cal SRMManuaLpdf). Protocol All procedures used in this study were reviewed by the University of Utah Institutional Review Board. Prior to data collection, we explained all procedures to those who were interested in pariicipating and the pariicipants provided informed consent. The 45-consisted of 20-minute practice on the novel cranks. Data were collected on the second and fourth visit. Cranks were presented in a counterbalanced order. Half of the participants were first introduced to the 120 mm cranks, and the other half were first introduced to the 220 mm cranks. Trials were separated between 5 and 6 days. Pedaling rate was optimized for maximal power production (Martin & Spirduso, 2001). For 120 mm cranks, the maximal sprint bouts were performed at 136 rpm (pedal speed of 1.71 m/s; pedal speed = crank length (m) x pedal frequency (rpm) x 2 n I 60), and for 220 mm cranks at 110 rpm (2.53 m/s). On test day, participants warmed up for 12 minutes. The experimental trial consisted of a maximal 30-second effort. Standardized verbal encouragement was given for the entire duration of the trial. Statistical Methods and Data Analysis Peak power was considered to be the maximal power reading registered on the SRM power meter. Minimum power was the lowest reading registered on the SRM. Fatigue index (FI) was calculated as follows: FI (peak power - min power)/ peak power. Work was calculated as a product of power and change in time and summed for the entire trial. fatigue performed differences adjusted 0.05/= I error. not 19 participants came to the lab for a total of four 4S-minute sessions. The first and third visit Sand 1.71 pedal speed crank length (m) x pedal frequency (rpm) x 2 n: 60), and for 220 mm cranks at 110 rpm (2.S3 m/s). On test day, participants warmed up for 12 minutes. The = Three paired student's t-tests were performed to discern differences in peak power output, Lltigue index, and total work perf(mned during the trial. Significant differences were hypothesized for the later two variables and the level of significance value adjusted by one third (O.OS/3 = 0.0167), to avoid making a type 1 emJr. For peak power, it was predicted that the null hypothesis would 110t be rejected. Statistical Package for Social program Sciences (SPSS-14.0) pro!:,rram was used to perform the actual calculations of statistical significance. 20 CHAPTER 4 RESULTS AND DISCUSSION second sprint bout. I will first present the results of the data analysis and subsequently discuss these results with respect to hypotheses and relevant previous studies. Results second bout within ± 3 rpm. Most cyclists started the sprint trial at a cadence that was 1-2 rpm greater than the target cadence and finished sprinting at cadence that was 1 -3 less than the target cadence. These deviations were less than 3% of the target frequency of pedaling. 1). ± ±W for the 220 mm cranks (t ^,p 0.87). [± DISCUSSION In this study I have investigated the effect of crank length on maximal cycling performance, including peak power, fatigue index and work accomplished during a 30- All cyclists reached peak power within 3 seconds of the start of the experimental trial at the target cadence (110 rpm for 220 mm cranks and 136 rpm for 120 mm cranks). Following the peak, power declined for the remainder of the bout in all cyclists (see Figure 1). Target cadence was maintained by the isokinetic ergometer throughout the 30- :::1= 1-1-3 less 3 % Peak power reached at the beginning of the trial did not differ between the cranks (Figure 1 ). Average peak power for the 120 mm cranks was 901 309 W, and 898 ± 311 (9), P = Fatigue Index differed significantly (p < 0.01) between cranks in support of my hypothesis. Fatigue Index was greater for the 120 mm cranks (57.5 8.4%) than the 220 22 Time (sec) 1. 850 750 ~ (/] t ro ~ 650 '-" I-< Il) ~ p0. . 550 450 350 5 10 15 -.-120mm 1-e-220mm 20 25 30 Figure Power during the maximal 30-second bout of cycling exercise using 120 mm and 220 mm cranks. At the beginning the bout the power output is the same for both cranks. At the onset of fatigue power generated with the longer cranks is greater. ± in the FI category for 120 mm cranks. One was 73.1% and the other 40.3%. Both numbers were kept in data set (see Discussion). Work accomplished during the entire trial was greater for the 220 mm cranks than the 120 mm cranks (p < 0.01), 19.2 ± 5.9 kJ vs. 18.0 ± 5.5 kJ. Because power (and therefore work) accomplished during the first several seconds was similar for the two cranks, it follows that the difference of 1.2 kJ occurred during the period of power decline (fatigue, see Table 1). ± Beelan following 23 mm cranks (51.1 11.3%). There were two potential outliers in the entire data set, both 73.1 % ± k1. Figure 2 shows a relationship of power and accumulated number of revolutions for both cranks. Looking at fatigue in this way, it appears that the decline in power is linked to the number of revolutions, because the two curves converge. The line for the short cranks is longer, because more revolutions were completed in 30 seconds at 136 rpm (120 mm cranks) than at 110 rpm (220 mm cranks). Discussion In support of my hypothesis, the power decline due to fatigue was greater with the shorter, 120 mm cranks, pedaled at 136 2 rpm. The finding that more rapid maximal cycling induces greater fatigue is not completely novel or surprising. Two groups of authors (Beelen & Sargeant, 1991; McCartney et al., 1983) have found similar results using one (standard, 170 mm) crank length and widely varying cadence. Both Beclan and Sargeant (1991) and McCartney et al. (1983) have found that more rapid pedaling cadences induce greater fatigue. However, these two studies have prompted the following comments: (a) although the fatigue was lower with less rapid pedaling, the peak power produced was also lower at the beginning of the bout, that is, methods were not optimized for maximal power production during the entire duration of the bout, and (b) increased 2244 1000 900 800 700 -*-120 mm ~ 600 -0- 220 mm b 500 ~ c ~ 400 300 200 100 0 10 20 30 40 50 60 70 Pedal Revolutions Figure 2. Relationship of power and accumulated pedal revolutions. Cranks Fatigue Index 120 Fatigue Index 220 Work 120 Work 220 (%) (%) 39,5 8 179 9 269 51,5 44,8 14 108 15 718 3 60,1 54,3 21 745 22 448 1176 56 23 170 25 463 % 47,7 17 344 17 829 57,7 20 454 21 784 27,3 9 666 9 876 73,1 64,3 20 653 22 025 58,9 22263 24 878 63,3 60,8 22 379 23 170 901,0 51,1 17 996 19 246 5 504 5 888 ( 3,52 5,15 0,01 0,001 p 0,878 0,995 eta2 0,572 0,747 Table 1 Peak Power, Work, and Fatigue of 120 mm Cranks versus 220 mm Cranks Peak Power 120 Peak Power 220 Cyclists (Watts) (Watts) (%) (%) (J) (J) 1 402 408 54,7 9269 2 621 672 51 ,5 .".)) 1070 1024 22448 4 1084 11 76 59,5 25463 5 995 889 ", 58 17344 17829 6 956 932 54,7 20454 7 402 388 40,3 9666 9876 8 1099 1085 73 ,1 20653 22025 9 1155 1245 59,3 24878 10 1226 1157 22379 M 901 ,0 897,6 57,5 17996 19246 SD 309,1 310,6 8,4 11,4 5504 5888 t (a) 0,17 P 0,87 1 - ~ 0,053 eta2 0,003 frequency, leaving the unanswered question: which of the two muscular mechanisms is more responsible for the decline in power, the force and velocity of actin and myosin binding (pedal speed) or excitation/relaxation kinetics (pedal frequency)? Because the two mechanisms are linearly related when using the same crank length, it is impossible to study the relative contribution of each mechanism to the overall fatigue and decline in power output. The methods of this study have allowed for distinguishing between the two mechanisms and the results show that excitation-relaxation could be the limiting intramuscular mechanism for power production in a fatigued state. of the on the same line (Figure 2). The line for the short cranks is longer because the rate of pedaling is more rapid, thus greater number of pedal revolutions are accumulated over the 30-second test period. The finding that fatigue for both cranks followed a similar pattern modifies the theory of excitation/relaxation kinetics as the limiting factor during a maximal cyclical effort and suggests that each maximal cycle, regardless of rate, exerts a specific increment of fatigue. Bundle, Ernst, Matthew, Wright, and Weyand (2006) 26 pedaling rates using the same cranks increased both pedal speed as well as pedal myosin binding (pedal speed) or excitation/relaxation kinetics (pedal frequency)? Because the two mechanisms are linearly related when using the same crank length, it is impossible to study the relative contribution of each mechanism to the overall fatigue and decline in power output. The methods of this study have allowed for distinguishing between the two mechanisms and the results show that excitation-relaxation could be the limiting intramuscular mechanism for power production in a fatigued state. Work accomplished with longer, 220 mm cranks was greater than shorter ones and is likely related to the differences during the fatigued condition, because work during the initial stage ofthe bout is the same for both cranks. In the study by McCartney et al. (1983) work accomplished between high and low frequencies was the same, because the power produced at both the beginning and at the end of the bout was different, but in opposite directions. There was a finding of an unexpected relationship of power decline and accumulated pedal revolutions. For both cranks the curves for power decline converged on the same line (Figure 2). The line for the short cranks is longer because the rate of pedaling is more rapid, thus greater number of pedal revolutions are accumulated over the 30-second test period. The finding that fatigue for both cranks followed a similar pattern modifies the theory of excitation/relaxation kinetics as the limiting factor during a maximal cyclical effort and suggests that each maximal cycle, regardless of rate, exerts a specific increment of fatigue. Bundle, Ernst, Matthew, Wright, and Weyand (2006) reported that EMG during submaximal efforts of various durations increased for the entire duration and reached maximum at the end of the bout. Fatigue likely occurred one contraction, one motor unit at a time and more recruitment was needed to maintain a given power output, hence the increase in EMG. Alternatively, once maximal EMG is exerted, the next revolution is less powerful. The last statement could be one possible explanation for the pattern of neuromuscular fatigue in my investigation. Although the EMG data was not collected to support this theory, it is reasonable to speculate that once the cyclists reached peak power (and theoretically the maximal EMG reading), the following contractions were less powerful. As stated above, the power generated at the beginning of the bout (non-fatigue condition) did not differ between cranks that differed 10 cm in length. These results were hypothesized and replicate earlier work of Martin and Spirduso (2001). Furthermore, the methods of obtaining these results were slightly different. Martin and Spirduso (2001) used inertial derive fatigue muscle fatigue 27 exerted, the next revolution is less powerful. The last statement could be one possible explanation for the pattern of neuromuscular fatigue in my investigation. Although the EMG data was not collected to support this theory, it is reasonable to speculate that once the cyclists reached peak power (and theoretically the maximal EMG reading), the following contractions were less powerful. (non-em uscd the incliial load method (Martin, Wagner, & Coyle, 1997) to deri ve maximal cycling power, whereas the current study used isokinetic method and measured power delivered to the crank via SRM power meter. We used the pedaling rates that were predicted to be optimal. All of our cyclists' data showed the same tendencies (Figure 1) regardless of the magnitude of the fatigue index. This finding may offer insight into patterns of fatigue among different fiber types. However, musclc biopsies were not performed in my study, so the following explanation is only speculation. It is known that type II fibers fatigue faster than type I (Brooks et al., 1999). Thus, individuals with greater distribution of type II are likely to have a greater fatigue index than individuals with type I dominance. The of fiber-type distribution. Two outliers in the data occurred in the data set for fatigue index using 120 mm cranks: a high of 73.1% and a low of 40.3%. Both cyclists recorded the highest and the lowest marks for both cranks (64.3% and 27.3%, respectively, for 220 mm cranks), staying consistent with their place in the data set. The lowest fatigue index was recorded by a female Olympic cross-country skier, suggesting a type I fiber dominance accompanied by superior fatigue resistance. The highest fatigue index value was recorded by a male cyclist who specialized in sprinting during cycling races, and thus was likely type II fiber dominant. fatigable & finish fatigue resistance are equally important. Longer crank length will likely delay fatigue in a sprint to the finish line. However, because of the importance of generating peak power at 28 wide range of fatigue indexes (27-73%) suggests that our group likely had a wide range fatigue nun of73.1 % was recorded by a female Olympic cross-country skier, suggesting a type I fiber dominance accompanied by superior fatigue resistance. The highest fatigue index value was recorded by a male cyclist who specialized in sprinting during cycling races, and thus was likely type II fiber dominant. Another, less microscopic theory could also explain our results. Power delivered to the cranks is produced at the ankle, knee, and hip joints. The relative contribution of each of these joints to total crank power is not currently known. Consequently, the rate at which power at those joints decreases during a fatiguing bout is also not known. It is possible that the muscles that span one joint are less fatigable than the muscles spanning the other joint. If pedaling longer cranks caused our participants to rely on a less fatigable joint then the net power delivered to the cranks would be greater during fatigue. A biomechanical analysis of this theory is being currently conducted at our lab. The main limitation of my study is that peak power produced for cranks of 120 mm and 220 mm is 96% of that produced with more conventional cranks (Martin Spirduso, 2001). Thus, practical application of our findings is limited as well. In a typical sprint to the tIn ish at the end of the race, both the initial jump (i.e., peak power) as well as sprint, likely produce the same peak power and might even help delay fatigue in a long sprint to the finish. Alternatively, our results argue for the use of longer gear ratios or lower pedaling rates during long sprints. Elite track sprint cyclists are known to perform 200 m time trial at an average of 130 rpm (Dorel et al., 2005), which is about 10 rpm greater than the optimal pedaling rate (Martin & Spirduso, 2001). Using a longer gear ratio may not only enhance power production throughout the trial, but may also help delay fatigue at the very end of the race, resulting in a better athletic performance. 29 the beginning of the splint, a cyclist would be well advised to choose a more conventional crank length (i.e., 170-175 mm). Finally, a crank length of 177.5 mm will CHAPTER 5 SUMMARY, FINDINGS, IMPLICATIONS, RECOMMENDATIONS of this length on muscle fatigue during a maximal bout of sprint cycling. I was also indirectly investigating the underlying biomechanical and cellular mechanisms emphasized by cranks of different lengths. Specifically, I was interested in relationships of velocity dependent force production and excitation/relaxation kinetics. The participants were trained competitive cyclists, 7 males and 3 females. The sample included professional and elite level cyclists, mountain bikers, and triathletes. The participants were familiarized with one practice day before performing an actual test. The participants sprinted maximally for 30 seconds. I hypothesized that the shorter cranks would have a greater fatigue index due to greater reliance on excitation/relaxation kinetics, which I hypothesized would be a more contributing factor in anaerobic fatigue. CHAPTERS AND RECOMMENDATIONS In this chapter I will summarize the findings ofthis study, draw conclusions on the study's implications, and offer recommendations for continued research. Summary My purpose for conducting this study was to investigate the effects of crank 1 professional pmiicipants 31 Findings As hypothesized, fatigue (decline in muscle power output) proceeded rapidly after the first 3-4 seconds of the bout for both crank lengths. support of my hypothesis, the short crank length showed more fatigue during the bout, implicating greater reliance on rapid excitation/relaxation. Additionally, a post hoc analysis revealed an interesting relationship of power and accumulated pedal revolutions. The data for both cranks converged on a single line, implying a strong relationship of fatigue and number of maximal concentric muscle contractions. Implications of the Study vitro testing has suggested that rapid excitation/relaxation as the dominant limiting factor of fatigue during maximal cyclical muscle contraction. To my knowledge, this is the first human study that implicated excitation/relaxation processes as a limiting source during an exercise activity. Of course, this is not a definitive explanation for my results. The explanation should be viewed as a continuation of studies on short-term fatigue. These findings should inspire future studies on this topic using the human cycling model. Also, this study gives some practical insights into crank lengths and bicycle racing. We used a 10 cm difference in crank length to obtain a 6% difference in fatigue index. These extreme length changes may not be reasonable for bicycles because of constraints such as ground clearance. Nonetheless, longer cranks, even at smaller increments allow maximum power at lower pedaling rates and this should reduce fatigue. Finally, the effect of the number of accumulated muscle contraction warrants further investigations. A well-designed investigation could possibly reveal a "governing In In all em diffcrence fatigue Finally, the etTect of the number of accumulated muscle contraction warrants further investigations. A well-designed investigation could possibly reveal a "governing 32 relationship" (Martin et al., 2000) of muscle contractions during maximal cyclical Future Research Recommendations This study offered slightly more than a pilot inquiry. A larger inquiry could benefit from recruiting more cyclists and repeating the protocols with five crank lengths: 120 mm, 145 mm, 170 mm, 195 mm, and 220 mm. A possible hypothesis would be that the remaining three crank lengths (145 mm, 170 mm, 195 mm) would reach the same peak power, and have different degrees of fatigue. Because the difference in fatigue index was only 6% in the current study, one would likely need more participants to detect smaller differences in fatigue index between cranks of smaller differences in length (and frequency mm), accumulated this thesis and would help further illuminate the concepts of fatigue. aI., contractions and fatigue conditions. Recommendations therefore lesser perturbations in pedal frequency and pedal speed). Similarly, we could also hypothesize that irrespective of the five crank lengths (120 mm - 220 111m), power - accu111lllated pedal revolutions relationship would also converge on the single curve. Finally, an extension to the present study could examine the improvement of fatigue resistance, specifically whether sprint cyclists trained to sustain faster pedaling rates with shorter cranks would also improve their performances in long sprint bouts. 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