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Creatine supplementation attenuates the rate of fatigue development during intermittent isometric exercise performed above end‐test torque
Experimental Physiology
Abstract
New findings:
What is the central question of this study? Does creatine supplementation augment the total torque impulse accumulated above end-test torque (IET) during severe-intensity knee-extensor exercise by attenuating the rate of decrease in peak potentiated twitch torque (PT)? What is the main finding and its importance? Creatine augmented the IET and attenuated the rate of decrease in both voluntary activation and PT during severe-intensity exercise. The IET was related to the rate of decrease in PT. These findings reveal an important role for the rates of neuromuscular fatigue development as key determinants of exercise tolerance within the severe domain.
Abstract:
This study investigated the effect of creatine supplementation on exercise tolerance, total torque impulse accumulated above end-test torque (total IET) and neuromuscular fatigue development of the knee extensors during severe-intensity intermittent isometric exercise. Sixteen men were randomly allocated into Creatine (n = 8, 20 g day-1 for 5 days) or Placebo (n = 8) groups and performed knee-extensor maximal voluntary contraction (MVC) testing, all-out testing to determine end-test torque (ET) and the finite torque impulse accumulated above end-test torque (IET'), and three submaximal tests at ET + 10%: (i) time to task failure without supplementation (Baseline); (ii) time to task failure after creatine or placebo supplementation; and (iii) time matched to Baseline after creatine (Creatine-Isotime) or placebo (Placebo-Isotime) supplementation. Creatine supplementation significantly increased the time to task failure (Baseline = 572 ± 144 s versus Creatine = 833 ± 221 s) and total IET (Baseline = 5761 ± 1710 N m s versus Creatine = 7878 ± 1903 N m s), but there were no significant differences within the Placebo group. The percentage change pre- to postexercise in MVC, voluntary activation, peak potentiated twitch torque and integrated EMG during MVC were not significantly different between Baseline and Creatine but were all significantly attenuated in Creatine-Isotime compared with Baseline. There were no significant differences in these variables within the placebo group. The total IET was significantly correlated with the rates of change in potentiated twitch torque peak (r = 0.83-0.87) and rate of torque development (r = -0.83 to -0.87) for the submaximal tests to task failure. These findings reveal an important role for the rates of neuromuscular fatigue development as key determinants of exercise tolerance during severe-intensity intermittent isometric exercise.
... We recently demonstrated that creatine supplementation augmented the total impulse performed above end-test torque (total IET ′ ) during intermittent isometric exercise of constant load in severe domain (Abdalla et al., 2020), which is consistent with previous findings for cycling exercise (Eckerson et al., 2004;Miura et al., 1999;Smith et al., 1998). Interestingly, this increase in total IET ′ was not concomitant with an increase in peripheral fatigue development (Abdalla et al., 2020). ...
... We recently demonstrated that creatine supplementation augmented the total impulse performed above end-test torque (total IET ′ ) during intermittent isometric exercise of constant load in severe domain (Abdalla et al., 2020), which is consistent with previous findings for cycling exercise (Eckerson et al., 2004;Miura et al., 1999;Smith et al., 1998). Interestingly, this increase in total IET ′ was not concomitant with an increase in peripheral fatigue development (Abdalla et al., 2020). It has been suggested that creatine supplementation attenuates the development of neuromuscular fatigue, mainly peripheral, due to its buffering capacity of protons within the muscle (Abdalla et al., 2020;Yquel et al., 2002). ...
... Interestingly, this increase in total IET ′ was not concomitant with an increase in peripheral fatigue development (Abdalla et al., 2020). It has been suggested that creatine supplementation attenuates the development of neuromuscular fatigue, mainly peripheral, due to its buffering capacity of protons within the muscle (Abdalla et al., 2020;Yquel et al., 2002). Given that the improvement in muscle performance after creatine loading appears to be more prominent during intermittent exercise (Abdalla et al., 2020;Bird, 2003;Branch, 2003), it also has been suggested that creatine supplementation may exert its ergogenic action via facilitated muscle phosphocreatine resynthesis during recovery periods between vigorous contractions (Bogdanis, Nevill, Boobis, Lakomy, & Nevill, 1995). ...
We previously reported that creatine supplementation improved intermittent isometric exercise performance by augmenting the total impulse performed above end‐test torque (total IET′). However, our previous analyses did not enable mechanistic assessments. The objective of this study was to determine if creatine supplementation affected the IET′ speed of recovery. To achieve this objective, we retrospectively analyzed our data using the IET′ balance model to determine the time constant for the recovery of IET′ ( τ IET′). Sixteen men were randomly allocated into creatine ( N = 8) or placebo ( N = 8) groups. Prior to supplementation, participants performed quadriceps all‐out exercise to determine end‐test torque (ET) and IETʹ. Participants then performed quadriceps exercise at ET + 10% until task‐failure before supplementation (Baseline), until task‐failure after supplementation (Creatine or Placebo), and until the Baseline time after supplementation (Creatine‐ or Placebo‐Isotime). τ IET′ was faster than Baseline for Creatine (669 ± 98 vs 470 ± 66 s), but not Placebo (792 ± 166 vs 786 ± 161 s). The creatine‐induced change in τ IET′ was inversely correlated with the creatine‐induced changes in both the rate of peripheral fatigue development and time to task‐failure. τ IET′ was inversely correlated with total IET′ and ET in all conditions, but creatine supplementation shifted this relationship such that τ IET′ was faster for a given ET. Creatine supplementation, therefore, sped the recovery of IET′ during intermittent isometric exercise, which was inversely related to the improvement in exercise performance. These findings support that the improvement in exercise performance after creatine supplementation was, at least in part, specific to effects on the physiological mechanisms that determine the IET′ speed of recovery.
... Although the role of creatine for reducing muscular fatigue development is well documented during short-duration, high-intensity activities, its role in mitigating central fatigue during exertional-heat stress has received considerably less attention [148]. Hadjicharalambous and colleagues [149] determined the association between brain 5-HT and DA responses and perception of effort during prolonged exercise in the heat following creatine supplementation (20 g·day −1 for 7 days; Table 2). ...
Global warming is attributed to an increased frequency of high ambient temperatures and humidity, elevating the prevalence of high-temperature-related illness and death. Evidence over recent decades highlights that tailored nutritional strategies are essential to improve performance and optimise health during acute and chronic exertional-heat exposure. Therefore, the purpose of this review is to discuss the efficacy of various nutritional strategies and ergogenic aids on responses during and following acute and chronic exertional-heat exposure. An outline is provided surrounding the application of various nutritional practices (e.g., carbohydrate loading, fluid replacement strategies) and ergogenic aids (e.g., caffeine, creatine, nitrate, tyrosine) to improve physiological, cognitive, and recovery responses to acute exertional-heat exposure. Additionally, this review will evaluate if the magnitude and time course of chronic heat adaptations can be modified with tailored supplementation practices. This review highlights that there is robust evidence for the use of certain ergogenic aids and nutritional strategies to improve performance and health outcomes during exertional-heat exposure. However, equivocal findings across studies appear dependent on factors such as exercise testing modality, duration, and intensity; outcome measures in relation to the ergogenic aid’s proposed mechanism of action; and sex-specific responses. Collectively, this review provides evidence-based recommendations and highlights areas for future research that have the potential to assist with prescribing specific nutritional strategies and ergogenic aids in populations frequently exercising in the heat. Future research is required to establish dose-, sex-, and exercise-modality-specific responses to various nutritional practices and ergogenic aid use for acute and chronic exertional-heat exposure.
Introdução: A prática de exercícios físicos é essencial para a saúde e o bem-estar, promovendo benefícios como a prevenção de doenças crônicas e a melhora da qualidade de vida. Nesse contexto, a busca por estratégias que otimizem o desempenho esportivo, como a suplementação nutricional, é crescente. Entre os suplementos mais estudados está a creatina, devido ao seu potencial ergogênico em atividades de alta intensidade e curta duração. Este estudo tem como objetivo revisar as evidências científicas sobre os efeitos da suplementação com creatina no desempenho esportivo, abordando seus mecanismos de ação e aplicações práticas. Metodologia: O estudo consistiu em uma revisão integrativa da literatura realizada nas bases PubMed e BVS. Foram selecionados artigos publicados entre 2020 e 2025, em inglês ou português, que abordassem o uso da creatina em atividades físicas. Após triagem inicial de 1.697 estudos, uma amostra final de 10 artigos foi analisada. Resultados e discussão: Os resultados indicaram que a suplementação com creatina aumenta as reservas musculares de fosfocreatina, melhorando a ressíntese de ATP e a capacidade de realizar esforços intensos e repetitivos. Além disso, promove a recuperação muscular, aumenta a força e a massa muscular magra e reduz a fadiga. A creatina também apresenta efeitos antioxidantes e neuroprotetores, beneficiando a saúde geral e o desempenho cognitivo. Além disso, destaca-se o papel da creatina como um suplemento ergogênico seguro e eficaz, com benefícios amplamente reconhecidos no contexto esportivo. Contudo, a eficácia pode variar conforme as características individuais e o tipo de atividade física praticada. Considerações finais: Conclui-se que a suplementação com creatina é uma estratégia eficaz para otimizar o desempenho esportivo e promover adaptações musculares, sendo amplamente recomendada para atletas e praticantes de atividades físicas intensas, desde que utilizada de forma individualizada e com orientação profissional.
The objective of this study was to test the hypothesis that neuromuscular fatigue influences the rate of torque development (RTD) in a similar manner to isometric torque. Nine men participated in this study and performed 5-min all-out isometric tests for knee extensors (KE) and plantar flexors (PF) muscles, to determine the end-test torque (ET) and the critical rate of torque development (critical RTD). Additionally, participants performed submaximal constant-torque tests to task failure for KE and PF muscles. Both maximal voluntary contraction and RTD exhibited hyperbolic behavior and reached an asymptote at the end of the 5-min all out isometric test with similar relative values (KE 29.5 ± 5.6% MVC and PF 50.9 ± 2.9% MVC and KE 25.1 ± 3.6 to 28.5 ± 4.4% RTD and PF 48.4 ± 6.5 to 52.4 ± 5.8% RTD). However, both % MVC and % RTD were statistically different between muscle groups (P < 0.05), even when normalized by muscle volume (P < 0.05). Torque and RTD after the constant-torque test were similar to the values of ET and critical RTD (P > 0.05), respectively. In this study, it was observed that neuromuscular fatigue affects RTD and torque similarly, with the magnitude of this effect varying according to the muscle size.
A creatina é um aminoácido endógeno responsável pela ressíntese de adenosina trifosfato (ATP), quando em sua forma intramuscular de fosfocreatina (PCr), é encontrado em 95% no músculo esquelético e 5% em sua forma livre: creatina. A substância começou a ganhar força a partir dos estudos realizados e em 1990 já possuía grande popularidade com seu uso ergogênico. Hoje, atletas profissionais e praticantes de exercício físico suplementam a creatina com o intuito de aumentar sua reserva intramuscular, a fim de obter mais energia durante os treinos de curta duração e alta intensidade, além de melhorar a performance no exercício e auxiliar no ganho de massa muscular. O presente estudo teve o objetivo de descrever o mecanismo de ação da creatina, relatando as doses de suplementação recomendada, tempo de uso e possíveis efeitos colaterais.
The aim of the present study was to investigate the existence of a critical threshold beyond which peripheral fatigue would not further decrease during knee extensor (KE) exercise in older men, and the consequences of this mechanism on the force-duration relationship. Twelve old men (59 ± 2 years) randomly performed two different sessions, in which they performed 60 maximum voluntary contractions (MVC; 3s contraction, 2s relaxation). One trial was performed in the unfatigued state (CTRL) and one other following fatiguing neuromuscular electrical stimulation of the KE (FNMES). Peripheral and central fatigue were quantified via pre/post-exercise decreases in quadriceps twitch-force (Δ Ptw) and voluntary activation (ΔVA). Critical torque (CT) was determined as the mean force of the last 12 contractions while W′ was calculated as the area above CT. Compared with CTRL, pre-fatigue (Δ Ptw= -10.3 ± 6.2%) resulted in a significant (p < 0.05) reduction in W’ (-18.2 ± 1.6%) in FNMES. However, CT (∼964 N), ΔVA (∼15%) and Δ Ptw (∼25%) post-MVCs were similar between both conditions. In CTRL, W’ was correlated with Δ Ptw (r² = 0.78). Moreover, the difference in W’ between CTRL and FNMES was correlated with the level of pre-fatigue induced in FNMES (r² = 0.76). These findings document that peripheral fatigue is confined to an individual threshold during KE exercise in older men. Furthermore, correlative results suggest that mechanisms regulating peripheral fatigue to a critical threshold also restrict W’, and therefore play a role in exercise capacity in older men.
New findings:
What is the central question of this study? Is the magnitude of neuromuscular fatigue dependent upon exercise intensity above critical power (CP) when W' (the curvature constant of the power-duration relationship) is depleted? What is the main finding and its importance? The magnitude of neuromuscular fatigue is the same following two bouts of supra-CP cycling (3 vs. 12 min) when controlling for W' depletion, but is larger for individuals of greater anaerobic capacity following the shorter, and smaller for individuals of greater aerobic capacity following the longer exercise. These findings provide new insight into the mechanisms underpinning exercise above CP.
Abstract:
The aim of the present study was to test whether the development of neuromuscular fatigue within the severe intensity domain could be linked to the depletion of the curvature constant (W') of the power-duration relationship. Twelve recreationally active men completed tests to determine V̇O2peak , Critical Power (CP) and W', followed by two randomly assigned constant-load supra-CP trials set to fully deplete W' in 3 (P-3) and 12 min (P-12). Pre- to post-exercise changes in maximal voluntary contraction (MVC), potentiated quadriceps twitch force evoked by single (Qpot ) and paired high- (PS100) and low-frequency (PS10) stimulations and voluntary activation (VA) were determined. Cycling above CP reduced MVC (P-3: -20 ± 10% vs. P-12: -15 ± 7%), measures associated with peripheral fatigue (Qpot : -35 ± 13% vs. -31 ± 14%; PS10: -38 ± 13% vs. -37 ± 17%; PS100: -18 ± 9% vs. -13 ± 8% for P-3 and P-12, respectively) and VA (P-3: -12 ± 3% vs. P-12: -13 ± 3%) (P < 0.05), with no significant difference between trials (P > 0.05). Changes in MVC and evoked twitch forces were inversely correlated with CP and V̇O2peak following P-12, while W' was significantly correlated with changes in Qpot and PS10 following P-3 (P < 0.05). Therefore, the magnitude of neuromuscular fatigue does not depend on exercise intensity when W' is fully exhausted during severe intensity exercise, yet exploration of inter-individual variations suggests that mechanisms underpinning exercise tolerance within this domain differ between short- vs. long-duration exercise. This article is protected by copyright. All rights reserved.
The objective of this study was to test the hypotheses that end-test torque (ET) (expressed as % maximal voluntary contraction; MVC) is higher for plantar flexors (PF) than knee extensors (KE) muscles, whereas impulse above ET (IET) is higher for KE than PF. Thus, we expected that exercise tolerance would be longer for KE than PF only during the exercise performed above ET. After the determination of MVC, 40 men performed two 5-min all-out tests to determine ET and IET. Eleven participants performed a further 4 intermittent isometric tests, to exhaustion, at ET + 5% and ET – 5%, and 1 test for KE at the exercise intensity (%MVC) corresponding to ET + 5% of PF. The IET (7243.2 ± 1942.9 vs. 3357.4 ± 1132.3 N·m·s) and ET (84.4 ± 24.8 vs. 73.9 ± 19.5 N·m) were significantly lower in PF compared with KE. The exercise tolerance was significantly longer for PF (300.7 ± 156.7 s) than KE (156.7 ± 104.3 s) at similar %MVC (∼60%), and significantly shorter for PF (300.7 ± 156.7 s) than KE (697.0 ± 243.7 s) at ET + 5% condition. However, no significant difference was observed for ET – 5% condition (KE = 1030.2 ± 495.4 s vs. PF = 1028.3 ± 514.4 s). Thus, the limit of tolerance during submaximal isometric contractions is influenced by absolute MVC only during exercise performed above ET, which seems to be explained by differences on both ET (expressed as %MVC) and IET values.
Although commonly used, the physiological mechanisms underlying all-out exercise performance are still unclear and an in-depth assessment of skeletal muscle bioenergetics is lacking. Therefore, phosphorous magnetic resonance spectroscopy ((31)P-MRS) was utilized to assess skeletal muscle bioenergetics during a 5-min all-out intermittent isometric knee-extensor protocol in 8 healthy men. The metabolic perturbation, adenosine triphosphate (ATP) synthesis rates, ATP cost of contraction, and mitochondrial capacity were determined from intramuscular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), diprotonated phosphate (H2PO4⁻ ), and pH. Peripheral fatigue was determined by exercise-induced alterations in potentiated quadriceps twitch force (Qtw) evoked by supramaximal electrical femoral nerve stimulation. The oxidative ATP synthesis rate (ATPOX) attained and then maintained peak values throughout the protocol, despite a ~63% decrease in quadriceps maximal force production. Thus, the ATPOX normalized to force production (ATPOX gain) significantly increased throughout the exercise (1(st) min: 0.02 ± 0.01: 5(th) min: 0.04 ± 0.01 mM·min(-1)·N(-1)), as did the ATP cost of contraction (1(st) min: 0.048 ± 0.019: 5(th) min: 0.052 ± 0.015 mM·min(-1)·N(-1)). Additionally, the pre- to post-exercise change in Qtw (-52 ± 26 %) was significantly correlated with the exercise-induced change in intramuscular pH (r = 0.75) and [H2PO4⁻ ] (r = 0.77). In conclusion, the all-out exercise protocol utilized in the current study elicited a "slow component-like" increase in the intramuscular ATPOX gain, as well as a progressive increase in the phosphate cost of contraction. Furthermore, the development of peripheral fatigue was closely related to the perturbation of specific fatigue-inducing intramuscular factors (i.e. pH and [H2PO4⁻ ]).
Neuromuscular fatigue compromises exercise performance and is determined by central and peripheral mechanisms. Interactions between the two components of fatigue can occur via neural pathways, including feedback and feedforward processes. This brief review discusses the influence of feedback and feedforward mechanisms on exercise limitation. In terms of feedback mechanisms, particular attention is given to group III/IV sensory neurons which link limb muscle with the central nervous system. Central corollary discharge, a copy of the neural drive from the brain to the working muscles, provides a signal from the motor system to sensory systems and is considered a feedforward mechanism that might influence fatigue and consequently exercise performance. We highlight findings from studies supporting the existence of a 'critical threshold of peripheral fatigue', a previously proposed hypothesis based on the idea that a negative feedback loop operates to protect the exercising limb muscle from severe threats to homeostasis during whole-body exercise. While the threshold theory remains to be disproven within a given task, it is not generalisable across different exercise modalities. The 'sensory tolerance limit', a more theoretical concept, may address this issue and explain exercise tolerance in more global terms and across exercise modalities. The 'sensory tolerance limit' can be viewed as a negative feedback loop which accounts for the sum of all feedback (locomotor muscles, respiratory muscles, organs, and muscles not directly involved in exercise) and feedforward signals processed within the central nervous system with the purpose of regulating the intensity of exercise to ensure that voluntary activity remains tolerable.
Key points:
The purpose of this study was to determine the role of group III/IV muscle afferents in limiting the endurance exercise-induced metabolic perturbation assayed in muscle biopsy samples taken from locomotor muscle. Lumbar intrathecal fentanyl was used to attenuate the central projection of μ-opioid receptor-sensitive locomotor muscle afferents during a 5 km cycling time trial. The findings suggest that the central projection of group III/IV muscle afferent feedback constrains voluntary neural 'drive' to working locomotor muscle and limits the exercise-induced intramuscular metabolic perturbation. Therefore, the CNS might regulate the degree of metabolic perturbation within locomotor muscle and thereby limit peripheral fatigue. It appears that the group III/IV muscle afferents are an important neural link in this regulatory mechanism, which probably serves to protect locomotor muscle from the potentially severe functional impairment as a consequence of severe intramuscular metabolic disturbance.
Abstract:
To investigate the role of metabo- and mechanosensitive group III/IV muscle afferents in limiting the intramuscular metabolic perturbation during whole body endurance exercise, eight subjects performed 5 km cycling time trials under control conditions (CTRL) and with lumbar intrathecal fentanyl impairing lower limb muscle afferent feedback (FENT). Vastus lateralis muscle biopsies were obtained before and immediately after exercise. Motoneuronal output was estimated through vastus lateralis surface electromyography (EMG). Exercise-induced changes in intramuscular metabolites were determined using liquid and gas chromatography-mass spectrometry. Quadriceps fatigue was quantified by pre- to post-exercise changes in potentiated quadriceps twitch torque (ΔQTsingle ) evoked by electrical femoral nerve stimulation. Although motoneuronal output was 21 ± 12% higher during FENT compared to CTRL (P < 0.05), time to complete the time trial was similar (∼8.8 min). Compared to CTRL, power output during FENT was 10 ± 4% higher in the first half of the time trial, but 11 ± 5% lower in the second half (both P < 0.01). The exercise-induced increase in intramuscular inorganic phosphate, H(+) , adenosine diphosphate, lactate and phosphocreatine depletion was 55 ± 30, 62 ± 18, 129 ± 63, 47 ± 14 (P < 0.001) and 27 ± 14% (P < 0.01) greater in FENT than CTRL. ΔQTsingle was greater following FENT than CTRL (-52 ± 2 vs -31 ± 1%, P < 0.001) and this difference was positively correlated with the difference in inorganic phosphate (r(2) = 0.79; P < 0.01) and H(+) (r(2) = 0.92; P < 0.01). In conclusion, during whole body exercise, group III/IV muscle afferents provide feedback to the CNS which, in turn, constrains motoneuronal output to the active skeletal muscle. This regulatory mechanism limits the exercise-induced intramuscular metabolic perturbation, preventing an abnormal homeostatic challenge and excessive peripheral fatigue.
New Findings
What is the central question of this study?
We asked whether exercise performance is regulated during all‐out repeated sprints (involving peak cycling‐specific muscle activation and limited pacing strategy) in order to restrain the total degree of peripheral fatigue development.
What is the main finding and its importance?
Our results showed that power output is adjusted during repeated sprints to limit the development of peripheral fatigue to a critical threshold, independently of the degree of pre‐existing fatigue. These findings emphasize the important role of peripheral fatigue in adjustment of power output during exercise.
We hypothesized that exercise performance is adjusted during repeated sprints in order not to surpass a critical threshold of peripheral fatigue. Twelve men randomly performed three experimental sessions on different days, i.e. one single 10 s all‐out sprint and two trials of 10 × 10 s all‐out sprints with 30 s of passive recovery in between. One trial was performed in the unfatigued state (CTRL) and one following electrically induced quadriceps muscle fatigue (FT NMES ). Peripheral fatigue was quantified by comparing pre‐ with postexercise changes in potentiated quadriceps twitch force (Δ Q tw‐pot ) evoked by supramaximal magnetic stimulation of the femoral nerve. Central fatigue was estimated by comparing pre‐ with postexercise voluntary activation of quadriceps motor units. The root mean square (RMS) of the vastus lateralis and vastus medialis EMG normalized to maximal M‐wave amplitude (RMS. M max ⁻¹ ) was also calculated during sprints. Compared with CTRL condition, pre‐existing quadriceps muscle fatigue in FT NMES (Δ Q tw‐pot = −29 ± 4%) resulted in a significant ( P < 0.05) reduction in power output (−4.0 ± 0.9%) associated with a reduction in RMS. M max ⁻¹ . However, Δ Q tw‐pot postsprints decreased by 51% in both conditions, indicating that the level of peripheral fatigue was identical and independent of the degree of pre‐existing fatigue. Our findings show that power output and cycling EMG are adjusted during exercise in order to limit the development of peripheral fatigue beyond a constant threshold. We hypothesize that the contribution of peripheral fatigue to exercise limitation involves a reduction in central motor drive in addition to the impairment in muscular function.
No non-invasive test exists for forearm exercise that allows identification of power-time relationship parameters (W', critical power) and thereby identification of the heavy-severe exercise intensity boundary and scaling of aerobic metabolic exercise intensity. The aim of this study was to develop a maximal effort handgrip exercise test to estimate forearm critical force (fCF; force analog of power) and establish its repeatability and validity. Ten healthy males (20-43 years) completed two maximal effort rhythmic handgrip exercise tests (repeated maximal voluntary contractions (MVC); 1 s contraction-2 s relaxation for 600 s) on separate days. Exercise intensity was quantified via peak contraction force and contraction impulse. There was no systematic difference between test 1 and 2 for fCFpeak force (p = 0.11) or fCFimpulse (p = 0.76). Typical error was small for both fCFpeak force (15.3 N, 5.5%) and fCFimpulse (15.7 N⋅s, 6.8%), and test re-test correlations were strong (fCFpeak force, r = 0.91, ICC = 0.94, p<0.01; fCFimpulse, r = 0.92, ICC = 0.95, p<0.01). Seven of ten subjects also completed time-to-exhaustion tests (TTE) at target contraction force equal to 10%<fCFpeak force and 10%>fCFpeak force. TTE predicted by W' showed good agreement with actual TTE during the TTE tests (r = 0.97, ICC = 0.97, P<0.01; typical error 0.98 min, 12%; regression fit slope = 0.99 and y intercept not different from 0, p = 0.31). MVC did not predict fCFpeak force (p = 0.37), fCFimpulse (p = 0.49) or W' (p = 0.15). In conclusion, the poor relationship between MVC and fCF or W' illustrates the serious limitation of MVC in identifying metabolism-based exercise intensity zones. The maximal effort handgrip exercise test provides repeatable and valid estimates of fCF and should be used to normalize forearm aerobic metabolic exercise intensity instead of MVC.
This study sought to determine whether afferent feedback associated with peripheral muscle fatigue inhibits central motor drive (CMD) and thereby limits endurance exercise performance. On two separate days, 8 males performed constant-load single-leg knee extensor exercise to exhaustion (85% of peak power) with each leg (Leg1 and Leg2). On another day, the performance test was repeated with one leg (Leg1) and consecutively (within 10-s) with the other/contralateral leg (Leg2-post). Exercise-induced quadriceps fatigue was assessed by reductions in potentiated quadriceps twitch-force from pre- to post-exercise (ΔQtw,pot) in response to supra-maximal magnetic femoral nerve stimulation. The output from spinal motoneurons, estimated from quadriceps electromyography (iEMG), was used to reflect changes in CMD. Rating-of-perceived-exertion (RPE) was recorded during exercise. Time to exhaustion (~9.3min) and exercise-induced ΔQtw,pot (~51%) were similar in Leg1 and Leg2 (P>0.5). In the consecutive leg trial, endurance performance of the first leg was similar to that observed during the initial trial (~9.3min, P=0.8); however, time to exhaustion of the consecutively exercising contralateral leg (Leg2-post) was shorter than the initial Leg2 trial (4.7±0.6min vs 9.2±0.4min, P<0.01). Additionally, ΔQtw,pot following Leg2-post was less than Leg2 (33±3% vs 52±3%, P<0.01). Although the slope of iEMG was similar during Leg2 and Leg2-post, end-exercise iEMG following Leg2-post was 26% lower compared to Leg2 (P<0.05). Despite a similar rate-of-rise, RPE was consistently ~28% higher throughout Leg2-post vs Leg2 (P<0.05). In conclusion, this study provides evidence that peripheral fatigue and associated afferent feedback limits the development of peripheral fatigue and compromises endurance exercise performance by inhibiting CMD.
We tested the hypothesis that muscle high-energy phosphate compounds and metabolites related to the fatigue process would be recovered after exhaustion during recovery exercise performed below but not above critical power (CP) and that these changes would influence the capacity to continue exercise. Eight male subjects completed single-leg knee-extension exercise to exhaustion (for ~ 180 s) on three occasions, followed by a work-rate reduction to either severe-intensity exercise (>CP), heavy-intensity exercise (<CP), or a 10 min passive recovery period, in a random order. The muscle metabolic responses to exercise were assessed using (31)P magnetic resonance spectroscopy. There was a significant difference between the sustainable exercise duration during the recovery from exhaustive exercise between the CP conditions (at least 10 min and 39 ± 31 s, respectively; P<0.05). During passive recovery and <CP recovery exercise, muscle phosphocreatine concentration ([PCr]) increased rapidly after the exhaustion point reaching ~ 96 % and ~ 76 % of baseline values, respectively, after 10 min (P<0.05). Moreover, pH increased abruptly, reaching 7.0 ± 0.0 and 7.0 ± 0.2, respectively, after 10 min recovery (P<0.05). However, during >CP recovery exercise, neither muscle [PCr] nor pH recovered, reaching ~37 % of the initial baseline and 6.6 ± 0.2, respectively. These results indicate that the muscle metabolic dynamics in recovery from exhaustive severe-intensity exercise differ according to whether the recovery exercise is performed below or above the CP. These findings confirm the importance of the CP as an intramuscular metabolic threshold which dictates the accumulation of fatigue-related metabolites and the capacity to tolerate high-intensity exercise.
The extent and characteristics of muscle fatigue of different muscle groups when subjected to a similar fatiguing task may differ. Thirteen healthy young men performed sustained contractions at 50% maximal voluntary contraction (MVC) force until task failure, with four different muscle groups, over two sessions. Per session, one upper limb and one lower limb muscle group were tested (knee extensors and thumb adductor, or plantar and elbow flexors). Changes in voluntary activation level and contractile properties were derived from doublet responses evoked during and after MVCs before and after exercise. Time to task failure differed (p<0.05) between muscle groups (220±64s for plantar flexors, 114±27s for thumb adductor, 77±25s for knee extensors and 72±14s for elbow flexors). MVC force loss immediately after task voluntary failure was similar (-30±11% for plantar flexors, -37±13% for thumb adductor, -34±15% for knee extensors and -40±12% for elbow flexors, p>0.05). Voluntary activation was decreased for plantar flexors only (from 95±5% to 82±9%, p<0.05). Potentiated evoked doublet amplitude was more depressed for upper limb muscles (-59.3±14.7% for elbow flexors and -60.1±24.1% for thumb adductor, p<0.05) than for knee extensors (-28±15%, p<0.05); no reduction was found in plantar flexors (-7±12%, p>0.05). In conclusion, despite different times to task failure when sustaining an isometric contraction at 50% MVC force for as long as possible, diverse muscle groups present similar loss of MVC force after task failure. Thus, the extent of muscle fatigue is not affected by time to task failure, while this latter determines the etiology of fatigue.
The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)
For high-intensity cycling, power (P) can be well described as a hyperbolic function of tolerable work duration (t): P=(W'/t) + PLL W' is a constant and PLL is the lower limit (asymptote) for P which is shown to occur at an O2 uptake ([Vdot]O2) lying above the estimated threshold for sustained blood [lactate] increase (ΘIac) but below the maximum [Vdot]O2 ([Vdot]O2max) obtained during incremental cycling. This relation suggests that, above PLL, only a certain amount of work (W') can be accomplished regardless of its rate of performance, with [Vdot]O2 max being attained at fatigue. Hence, PLL defines a point of discontinuity in the [Vdot]O2-P relation for supra-ΘIac exercise. In order to determine the factors responsible for the continued increase in [Vdot]O2 (to the maximum fatiguing value) at power outputs >PLL, we documented the temporal profiles of metabolic (rectal temperature; blood [lactate], [pyruvate], [norepinephrine], [epinephrine]) and respiratory ([Vdot]E; [Vdot]O2; [Vdot]CO2; blood pH, PCO2, [HCO3 ]) responses to constant-load cycling in eight healthy males at PLL (24 min) and slightly above PLL (to exhaustion, i.e. < 24 min). [Vdot]O2 manifested a delayed steady state at PLL, despite catecholamine levels and core temperature continuing to increase throughout; blood [lactate] and pH plateaued, however. In contrast, [Vdot]O2 continued to increase slowly for the duration of the exercise > PLL and attained [Vdot]O2max. The response patterns at PLL, and > PLL suggest that the slow phase of the [Vdot]O2 response is best correlated with the temporal profile of blood [lactate], and hence the site and route of metabolism of this variable may play a major role in the [Vdot]O2 kinetics for high-intensity exercise.
Currently, considerable research activities are focussing on biochemical, physiological and pathological aspects of the creatine kinase (CK)-phosphorylcreatine (PCr)-creatine (Cr) system (for reviews see [1,2]), but only little effort is directed towards a thorough investigation of Cr metabolism as a whole. However, a detailed knowledge of Cr metabolism is essential for a deeper understanding of bioenergetics in general and, for example, of the effects of muscular dystrophies, atrophies, CK deficiencies (e.g. in transgenic animals) or Cr analogues on the energy metabolism of the tissues involved. Therefore, the present article provides a short overview on the reactions and enzymes involved in Cr biosynthesis and degradation, on the organization and regulation of Cr metabolism within the body, as well as on the metabolic consequences of 3-guanidinopropionate (GPA) feeding which is known to induce a Cr deficiency in muscle. In addition, the phenotype of muscles depleted of Cr and PCr by GPA feeding is put into context with recent investigations on the muscle phenotype of 'gene knockout' mice deficient in the cytosolic muscle-type M-CK.
The validity, reliability, and protocol for the interpolated twitch technique (ITT) were investigated with isometric plantar flexor and leg extension contractions. Estimates of muscle inactivation were attempted by comparing a variety of superimposed with potentiated evoked torques with submaximal and maximal voluntary contraction (MVC) torques or forces. The use of nerve and surface stimulation to elicit ITT was reliable, except for problems in maintaining maximal stimulation with nerve stimulation at 20 degrees plantar flexion and during leg extension. The interpolated twitch ratio-force relationship was best described by a shallow hyperbolic curve resulting in insignificant MVC prediction errors with second-order polynomials (1.1-6.9%). The prediction error under 40% MVC was approximately double that over 60% MVC, contributing to poor estimations of MVC in non-weight-bearing postimmobilized ankle fracture patients. There was no significant difference in the ITT sensitivity when twitches, doublets, or quintuplets were used. The ITT was valid and reliable when high-intensity contractions were analyzed with a second-order polynomial.
The relationship between work rate (W) and time to exhaustion (t) during intense exercise is commonly described by either a hyperbolic function (NLin), t= W'/(W-Wcp), or by its linear equivalent (LinW) Wlim=W' + Wcp(t). The parameter Wcp (critical power) has been described as an inherent characteristic of the aerobic energy system, while W' has been shown to be a ralid estimate of anaerobic work capacity. Recent studies have demonstrated that oral supplementation of creatine monohydrate (CrH2O) increases total muscle creatine stores, and have linked these increases to improved performances in intense intermittent exercise. This study was conducted to determine the effect of CrH2O supplementation on estimates of W' and Wcp derived from the NLin and LinW equations, and to determine the effect of CrH2O on t in exhaustive constant power exercise of different intensities. Fifteen active but untrained university students completed three phases of testing on a cycle ergometer: (1) familiarization, three learning trials, (2) baseline determination of W' and Wcp, four bouts performed at a W selected to elicit fatigue in 90-600 s, and (3) experimental determination of W' and Wcp, four bouts performed at the same W as baseline, but performed after 5 days of ingesting either a placebo (4 x 6 g of glucose/day) or CrH2O (4 x 5 g of CrH2O and 1 g glucose/day). Testing was administered in a double-blind manner. Analyses of covariance revealed a significant effect for CrH2O on both estimates of W' (NLin, P=0.04; LinW, P < 0.01), but not on estimates of Wcp (NLin, P=0.37; LinW; P=0.30). Within groups, t was significantly different for only CrH2O at the two highest Ws (P=0.04). It is concluded that oral ingestion of CrH2O increases estimates of W' due to an improved t at the shorter, more intense exercise bouts.
Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for "central" fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal changes in cortical excitability and inhibitability based on electromyographic (EMG) recordings, and a decline in supraspinal "drive" based on force recordings. Some of the changes in motor cortical behavior can be dissociated from the development of this "supraspinal" fatigue. Central changes also occur at a spinal level due to the altered input from muscle spindle, tendon organ, and group III and IV muscle afferents innervating the fatiguing muscle. Some intrinsic adaptive properties of the motoneurons help to minimize fatigue. A number of other central changes occur during fatigue and affect, for example, proprioception, tremor, and postural control. Human muscle fatigue does not simply reside in the muscle.
To determine the effects of creatine (Cr) supplementation (20 g x d(-1) during 5 d) on maximal strength, muscle power production during repetitive high-power-output exercise bouts (MRPB), repeated running sprints, and endurance in handball players.
Nineteen trained male handball players were randomly assigned in a double-blind fashion to either creatine (N = 9) or placebo (N = 10) group. Before and after supplementation, subjects performed one-repetition maximum half-squat (1RM(HS) and bench press (1RM(BP)), 2 sets of MRPB consisting of one set of 10 continuous repetitions (R10) followed by 1 set until exhaustion (R(max)), with exactly 2-min rest periods between each set, during bench-press and half-squat protocols with a resistance equal to 60 and 70% of the subjects' 1RM, respectively. In addition, a countermovement jumping test (CMJ) interspersed before and after the MRPB half-squat exercise bouts and a repeated sprint running test and a maximal multistage discontinuous incremental running test (MDRT) were performed.
Cr supplementation significantly increased body mass (from 79.4 +/- 8 to 80 +/- 8 kg; P < 0.05), number of repetitions performed to fatigue, and total average power output values in the R(max) set of MRPB during bench press (21% and 17%, respectively) and half-squat (33% and 20%, respectively), the 1RM(HS) (11%), as well as the CMJ values after the MRPB half-squat (5%), and the average running times during the first 5 m of the six repeated 15-m sprints (3%). No changes were observed in the strength, running velocity, or body mass measures in the placebo group during the experimental period.
Short-term Cr supplementation leads to significant improvements in lower-body maximal strength, maximal repetitive upper- and lower-body high-power exercise bouts, and total repetitions performed to fatigue in the R(max) set of MRPB, as well as enhanced repeated sprint performance and attenuated decline in jumping ability after MRPB in highly trained handball players. Cr supplementation did not result in any improvement in upper-body maximal strength and in endurance running performance.
In this study, we examined the effect of creatine ingestion on muscle power output, muscle phosphocreatine resynthesis, inorganic phosphate and pH during repeated brief bouts of maximal exercise. Nine healthy males performed maximal plantar flexion before and after creatine ingestion (20 g x day(-1) for 6 days). The experimental protocol consisted of five 8 s bouts (bouts 1-5) interspersed with 30 s recovery, followed by bouts 6 (8 s) and 7 (16 s) separated by 1 and 2 min, respectively. Muscle phosphocreatine, inorganic phosphate and pH were estimated every 16 s by 31P magnetic resonance spectroscopy. After creatine ingestion, muscle power output increased by approximately 5% (P< 0.05) from bouts 3 to 7 and muscle phosphocreatine resynthesis increased (P< 0.05) during 10 min recovery. The higher phosphocreatine concentration observed after only 30 s of recovery was accompanied by lower inorganic phosphate accumulation and higher pH. Strong correlations were found between exercise power restoration and the corresponding pre-exercise phosphocreatine and inorganic phosphate concentrations and muscle pH after creatine ingestion. The better maintenance of muscle power output observed after creatine ingestion was attributed to a higher rate of phosphocreatine resynthesis, lower accumulation of inorganic phosphate and higher pH.
The purpose of this study was to quantify which dietary supplements augment lean mass and strength gains during resistance training. Peer-reviewed studies between the years 1967 and 2001 were included in the analysis if they met a predetermined set of experimental criteria, among which were at least 3-wk duration and resistance-training 2 or more times a week. Lean mass and strength were normalized for meta-analysis by conversion to percent change per week and by calculating the effect size for each variable. Of the 250 supplements examined, only 6 had more than 2 studies that met the criteria for inclusion in the meta-analysis. Creatine and beta-hydroxy-beta-methylbutyrate (HMB) were found to significantly increase net lean mass gains of 0.36 and 0.28%/wk and strength gains of 1.09 and 1.40%/wk (P < 0.05), respectively. Chromium, dehydroepiandrosterone, androstenedione, and protein did not significantly affect lean gain or strength. In conclusion, two supplements, creatine and HMB, have data supporting their use to augment lean mass and strength gains with resistance training.
The role of group III and IV muscle afferents in controlling the output from human muscles is poorly understood. We investigated the effects of these afferents from homonymous or antagonist muscles on motoneuron pools innervating extensor and flexor muscles of the elbow. In study 1, subjects (n = 8) performed brief maximal voluntary contractions (MVCs) of elbow extensors before and after a 2 min MVC of the extensors. During MVCs, electromyographic responses from triceps were evoked by stimulation of the corticospinal tracts [cervicomedullary motor evoked potentials (CMEPs)]. The same subjects repeated the protocol, but input from fatigue-sensitive afferents was prolonged after the fatiguing contraction by maintained muscle ischemia. In study 2, CMEPs were evoked in triceps during brief extensor MVCs before and after a 2 min sustained flexor MVC (n = 7) or in biceps during brief flexor MVCs before and after a sustained extensor MVC (n = 7). Again, ischemia was maintained after the sustained contractions. During sustained MVCs of the extensors, CMEPs in triceps decreased by approximately 35%. Without muscle ischemia, CMEPs recovered within 15 s, but with maintained ischemia, they remained depressed (by approximately 28%; p < 0.001). CMEPs in triceps were also depressed (by approximately 20%; p < 0.001) after fatiguing flexor contractions, whereas CMEPs in biceps were facilitated (by approximately 25%; p < 0.001) after fatiguing extensor contractions. During fatigue, inputs from group III and IV muscle afferents from homonymous or antagonist muscles depress extensor motoneurons but facilitate flexor motoneurons. The more pronounced inhibitory influence of these afferents on extensors suggests that these muscles may require greater cortical drive to generate force during fatigue.
Much is known about the physiological impairments that can cause muscle fatigue. It is known that fatigue can be caused by many different mechanisms, ranging from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex, and that there is no global mechanism responsible for muscle fatigue. Rather, the mechanisms that cause fatigue are specific to the task being performed. The development of muscle fatigue is typically quantified as a decline in the maximal force or power capacity of muscle, which means that submaximal contractions can be sustained after the onset of muscle fatigue. There is even evidence that the duration of some sustained tasks is not limited by fatigue of the principal muscles. Here we review experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue. Selected comparisons of tasks, groups of individuals and interventions with the task-failure approach can provide insight into the rate-limiting adjustments that constrain muscle function during fatiguing contractions.
We asked whether the central effects of fatiguing locomotor muscle fatigue exert an inhibitory influence on central motor drive to regulate the total degree of peripheral fatigue development. Eight cyclists performed constant-workload prefatigue trials (a) to exhaustion (83% of peak power output (W(peak)), 10 +/- 1 min; PFT(83%)), and (b) for an identical duration but at 67% W(peak) (PFT(67%)). Exercise-induced peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (DeltaQ(tw,pot)) from pre- to post-exercise in response to supra-maximal femoral nerve stimulation (DeltaQ(tw,pot)). On different days, each subject randomly performed three 5 km time trials (TTs). First, subjects repeated PFT(83%) and the TT was started 4 min later with a known level of pre-existing locomotor muscle fatigue (DeltaQ(tw,pot) -36%) (PFT(83%)-TT). Second, subjects repeated PFT(67%) and the TT was started 4 min later with a known level of pre-existing locomotor muscle fatigue (DeltaQ(tw,pot) -20%) (PFT(67%)-TT). Finally, a control TT was performed without any pre-existing level of fatigue. Central neural drive during the three TTs was estimated via quadriceps EMG. Increases in pre-existing locomotor muscle fatigue from control TT to PFT(83%)-TT resulted in significant dose-dependent changes in central motor drive (-23%), power output (-14%), and performance time (+6%) during the TTs. However, the magnitude of locomotor muscle fatigue following various TTs was not different (DeltaQ(tw,pot) of -35 to -37%, P = 0.35). We suggest that feedback from fatiguing muscle plays an important role in the determination of central motor drive and force output, so that the development of peripheral muscle fatigue is confined to a certain level.
Magnetic and electrical stimulation at different levels of the neuraxis show that supraspinal and spinal factors limit force production in maximal isometric efforts ("central fatigue"). In sustained maximal contractions, motoneurons become less responsive to synaptic input and descending drive becomes suboptimal. Exercise-induced activity in group III and IV muscle afferents acts supraspinally to limit motor cortical output but does not alter motor cortical responses to transcranial magnetic stimulation. "Central" and "peripheral" fatigue develop more slowly during submaximal exercise. In sustained submaximal contractions, central fatigue occurs in brief maximal efforts even with a weak ongoing contraction (<15% maximum). The presence of central fatigue when much of the available motor pathway is not engaged suggests that afferent inputs contribute to reduce voluntary activation. Small-diameter muscle afferents are likely to be activated by local activity even in sustained weak contractions. During such contractions, it is difficult to measure central fatigue, which is best demonstrated in maximal efforts. To show central fatigue in submaximal contractions, changes in motor unit firing and force output need to be characterized simultaneously. Increasing central drive recruits new motor units, but the way this occurs is likely to depend on properties of the motoneurons and the inputs they receive in the task. It is unclear whether such factors impair force production for a set level of descending drive and thus represent central fatigue. The best indication that central fatigue is important during submaximal tasks is the disproportionate increase in subjects' perceived effort when maintaining a low target force.
We tested the hypothesis that the asymptote of the hyperbolic relationship between work rate and time to exhaustion during muscular exercise, the "critical power" (CP), represents the highest constant work rate that can be sustained without a progressive loss of homeostasis [as assessed using (31)P magnetic resonance spectroscopy (MRS) measurements of muscle metabolites]. Six healthy male subjects initially completed single-leg knee-extension exercise at three to four different constant work rates to the limit of tolerance (range 3-18 min) for estimation of the CP (mean +/- SD, 20 +/- 2 W). Subsequently, the subjects exercised at work rates 10% below CP (<CP) for 20 min and 10% above CP (>CP) for as long as possible, while the metabolic responses in the contracting quadriceps muscle, i.e., phosphorylcreatine concentration ([PCr]), P(i) concentration ([P(i)]), and pH, were estimated using (31)P-MRS. All subjects completed 20 min of <CP exercise without duress, whereas the limit of tolerance during >CP exercise was 14.7 +/- 7.1 min. During <CP exercise, stable values for [PCr], [P(i)], and pH were attained within 3 min after the onset of exercise, and there were no further significant changes in these variables (end-exercise values = 68 +/- 11% of baseline [PCr], 314 +/- 216% of baseline [P(i)], and pH 7.01 +/- 0.03). During >CP exercise, however, [PCr] continued to fall to the point of exhaustion and [P(i)] and pH changed precipitously to values that are typically observed at the termination of high-intensity exhaustive exercise (end-exercise values = 26 +/- 16% of baseline [PCr], 564 +/- 167% of baseline [P(i)], and pH 6.87 +/- 0.10, all P < 0.05 vs. <CP exercise). These data support the hypothesis that the CP represents the highest constant work rate that can be sustained without a progressive depletion of muscle high-energy phosphates and a rapid accumulation of metabolites (i.e., H(+) concentration and [P(i)]), which have been associated with the fatigue process.
New findings:
What is the central question of this study? Does the magnitude of neuromuscular fatigue depend on the amount of work done (W') at task failure when cycling above critical power (CP)? What is the main finding and its importance? Creatine supplementation increases W' and enhances supra-CP performance, but induces similar magnitudes of neuromuscular fatigue at task failure compared to placebo. Increased W' does not lead to higher levels of neuromuscular fatigue. This supports the notion of a critical level of neuromuscular fatigue at task failure and challenges a direct causative link between W' depletion and neuromuscular fatigue.
Abstract:
The present study examined the effect of creatine supplementation on neuromuscular fatigue and exercise tolerance when cycling above critical power (CP). Eleven males performed an incremental cycling test, 4-5 constant-load trials to task failure (TTF) to obtain asymptote (CP) and curvature constant (W') of the power-duration relationship, followed by three constant-load supra-CP trials: 1) one TTF following placebo supplementation (PLA); 2) one TTF following creatine supplementation (CRE); and 3) one trial of equal duration to PLA following creatine supplementation (ISO). Neuromuscular assessment of the right knee extensors was performed pre- and post-exercise to measure maximal voluntary contraction (MVC), twitch forces evoked by single (Qpot ) and paired high- (PS100) and low-frequency (PS10) stimulations and voluntary activation. Creatine supplementation increased TTF in CRE vs. PLA by ∼11% (P = 0.017) and work done above CP by ∼10% (P = 0.015), with no difference (P > 0.05) in reductions in MVC (-24 ± 8 vs. -20 ± 9%), Qpot (-39 ± 13 vs. -32 ± 14%), PS10 (-42 ± 14 vs. -36 ± 13%), PS100 (-25 ± 10 vs. -18 ± 12%) and voluntary activation (-7 ± 8 vs. -5 ± 7%) in CRE vs. PLA. No significant difference were found between ISO and both PLA and CRE (P > 0.05). These findings suggest similar levels of neuromuscular fatigue can be found following supra-CP cycling despite increases in performance time and amount of work done above CP, supporting the notion of a critical level of neuromuscular fatigue and challenging a direct causative link between W' depletion and neuromuscular fatigue. This article is protected by copyright. All rights reserved.
Background:
Bradykinesia and reduced neuromuscular force exist in Parkinson disease. The interpolated twitch technique has been used to evaluate central versus peripheral manifestations of neuromuscular strength in healthy, aging, and athletic populations, as well as moderate to advanced Parkinson disease, but this method has not been used in mild Parkinson disease. This study aimed to evaluate quadriceps femoris rate of force development and quantify potential central and peripheral activation deficits in individuals with Parkinson disease.
Methods:
Nine persons with mild Parkinson Disease (Hoehn & Yahr≤2, Unified Parkinson Disease Rating Scale total score=mean 19.1 (SD 5.0)) and eight age-matched controls were recruited in a cross-sectional investigation. Quadriceps femoris voluntary and stimulated maximal force and rate of force development were evaluated using the interpolated twitch technique.
Findings:
Thirteen participants satisfactorily completed the protocol. Individuals with early Parkinson disease (n=7) had significantly slower voluntary rate of force development (p=0.008; d=1.97) and rate of force development ratio (p=0.004; d=2.18) than controls (n=6). No significant differences were found between groups for all other variables.
Interpretations:
Persons with mild-to-moderate Parkinson disease display disparities in rate of force development, even without deficits in maximal force. The inability to produce force at a rate comparable to controls is likely a downstream effect of central dysfunction of the motor pathway in Parkinson disease.
The influence of the muscle metabolic milieu on peripheral and central fatigue is currently unclear. Moreover, the relationships between peripheral and central fatigue and the curvature constant (W') have not been investigated. Six men (age: 25 ± 4 years, body mass: 82 ± 10 kg, height: 179 ± 4 cm) completed four constant power handgrip tests to exhaustion under conditions of control exercise (Con), blood flow occlusion exercise (Occ), Con with 5 min post-exercise blood flow occlusion (Con + Occ), and Occ with 5 min post-exercise blood flow occlusion (Occ + Occ). Neuromuscular fatigue measurements and W' were obtained for each subject. Each trial resulted in significant peripheral and central fatigue. Significantly greater peripheral (79.7 ± 5.1% vs. 22.7 ± 6.0%) and central (42.6 ± 3.9% vs. 4.9 ± 2.0%) fatigue occurred for Occ than for Con. In addition, significantly greater peripheral (83.0 ± 4.2% vs. 69.0 ± 6.2%) and central (65.5 ± 14.6% vs. 18.6 ± 4.1%) fatigue occurred for Occ + Occ than for Con + Occ. W' was significantly related to the magnitude of global (r = 0.91) and peripheral (r = 0.83) fatigue. The current findings demonstrate that blood flow occlusion exacerbated the development of both peripheral and central fatigue and that post-exercise blood flow occlusion prevented the recovery of both peripheral and central fatigue. Moreover, the current findings suggest that W' may be determined by the magnitude of fatigue accrued during exercise. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
A new conception of dynamic or static muscular work tests is presented. The authors define the critical power of a muscular work from the notions of maximum work and maximum time of work. The work capacity is then considered in the case of dynamic work, and of continuous or intermittent static work. From the data presented it is possible to define the maximum amount of work that can be performed in a given time as well as the conditions of work performed without fatigue. (French & German summaries) (22 ref.) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Whether the transition in fatigue processes between "low-intensity" and "high-intensity" contractions occurs gradually, as the torque requirements are increased, or whether this transition occurs more suddenly at some identifiable "threshold", is not known. We hypothesized that the critical torque (CT; the asymptote of the torque-duration relationship) would demarcate distinct profiles of central and peripheral fatigue during intermittent isometric quadriceps contractions (3-s contraction, 2-s rest). Nine healthy men performed seven experimental trials to task failure or for up to 60 min, with maximal voluntary contractions (MVCs) performed at the end of each minute. The first five trials were performed to determine CT [~35-55% MVC, denoted severe 1 (S1) to severe 5 (S5) in ascending order], while the remaining two trials were performed 10 and 20% below the CT (denoted CT-10% and CT-20%). Dynamometer torque and the electromyogram of the right vastus lateralis were sampled continuously. Peripheral and central fatigue was determined from the fall in potentiated doublet torque and voluntary activation, respectively. Above CT, contractions progressed to task failure in ~3-18 min, at which point the MVC did not differ from the target torque (S1 target, 88.7 ± 4.3 N·m vs. MVC, 89.3 ± 8.8 N·m, P = 0.94). The potentiated doublet fell significantly in all trials, and voluntary activation was reduced in trials S1-S3, but not trials S4 and S5. Below CT, contractions could be sustained for 60 min on 17 of 18 occasions. Both central and peripheral fatigue developed, but there was a substantial reserve in MVC torque at the end of the task. The rate of global and peripheral fatigue development was four to five times greater during S1 than during CT-10% (change in MVC/change in time S1 vs. CT-10%: -7.2 ± 1.4 vs. -1.5 ± 0.4 N·m·min(-1)). These results demonstrate that CT represents a critical threshold for neuromuscular fatigue development.
The present study was designed to investigate whether central neural mechanisms limit the duration of a sustained low-force isometric contraction and the maximal force-generating capacity of the knee extensors.
Fourteen healthy males (28 ± 7 yr) were asked to sustain, until voluntary exhaustion, an isometric contraction with their right knee extensor muscles at a target force equal to 20% of their maximal voluntary contraction (MVC) force. At task failure, the muscle was immediately electrically stimulated for 1 min aiming the same target force (20% MVC force). Subsequently, subjects were asked to resume the voluntary contraction for as long as possible. Knee extensor neuromuscular function was assessed before and after the entire protocol for comparison.
When electrically stimulated at the point of task failure, all subjects developed the 20% MVC force target, indicating that lack of force-generating capacity from peripheral impairment had not limited the duration of the first task. We observed a reduction in MVC force after the entire protocol (-57% ± 12%), which correlated with a decrease in potentiated peak doublet force (-48% ± 17%, P < 0.001). The level of voluntary activation, as quantified with the interpolated twitch technique, was slightly depressed after the entire protocol (from 93% ± 7% to 87% ± 10%, P < 0.01).
It follows that task failure from a sustained isometric contraction is mainly affected by central/motivational factors, whereas MVC force loss is largely explained by the extent of contractile failure of the muscle.
Severe-intensity constant-work-rate exercise results in the attainment of maximal oxygen uptake, but the muscle metabolic milieu at the limit of tolerance (T(lim)) for such exercise remains to be elucidated. We hypothesized that T(lim) during severe-intensity exercise would be associated with the attainment of consistently low values of intramuscular phosphocreatine ([PCr]) and pH, as determined using (31)P magnetic resonance spectroscopy, irrespective of the work rate and the inspired O(2) fraction. We also hypothesized that hyperoxia would increase the asymptote of the hyperbolic power-duration relationship (the critical power, CP) without altering the curvature constant (W). Seven subjects (mean +/- s.d., age 30 +/- 9 years) completed four constant-work-rate knee-extension exercise bouts to the limit of tolerance (range, 3-10 min) both in normoxia (N) and in hyperoxia (H; 70% O(2)) inside the bore of 1.5 T superconducting magnet. The [PCr] (approximately 5-10% of resting baseline) and pH (approximately 6.65) at the limit of tolerance during each of the four trials was not significantly different either in normoxia or in hyperoxia. At the same fixed work rate, the overall rate at which [PCr] fell with time was attenuated in hyperoxia (mean response time: N, 59 +/- 20 versus H, 116 +/- 46 s; P < 0.05). The CP was higher (N, 16.1 +/- 2.6 versus H, 18.0 +/- 2.3 W; P < 0.05) and the W was lower (N, 1.92 +/- 0.70 versus H, 1.48 +/- 0.31 kJ; P < 0.05) in hyperoxia compared with normoxia. These data indicate that T(lim) during severe-intensity exercise is associated with the attainment of consistently low values of muscle [PCr] and pH. The CP and W parameters of the power-duration relationship were both sensitive to the inspiration of hyperoxic gas.
To determine whether the asymptote of the torque-duration relationship (critical torque) could be estimated from the torque measured at the end of a series of maximal voluntary contractions (MVCs) of the quadriceps, eight healthy men performed eight laboratory tests. Following familiarization, subjects performed two tests in which they were required to perform 60 isometric MVCs over a period of 5 min (3 s contraction, 2 s rest), and five tests involving intermittent isometric contractions at approximately 35-60% MVC, each performed to task failure. Critical torque was determined using linear regression of the torque impulse and contraction time during the submaximal tests, and the end-test torque during the MVCs was calculated from the mean of the last six contractions of the test. During the MVCs voluntary torque declined from 263.9 +/- 44.6 to 77.8 +/- 17.8 N x m. The end-test torque was not different from the critical torque (77.9 +/- 15.9 N x m; 95% paired-sample confidence interval, -6.5 to 6.2 N x m). The root mean squared error of the estimation of critical torque from the end-test torque was 7.1 N x m. Twitch interpolation showed that voluntary activation declined from 90.9 +/- 6.5% to 66.9 +/- 13.1% (P < 0.001), and the potentiated doublet response declined from 97.7 +/- 23.0 to 46.9 +/- 6.7 N.m (P < 0.001) during the MVCs, indicating the development of both central and peripheral fatigue. These data indicate that fatigue during 5 min of intermittent isometric MVCs of the quadriceps leads to an end-test torque that closely approximates the critical torque.
We investigated the role of somatosensory feedback from locomotor muscles on central motor drive (CMD) and the development of peripheral fatigue during high-intensity endurance exercise. In a double-blind, placebo-controlled design, eight cyclists randomly performed three 5 km time trials: control, interspinous ligament injection of saline (5K(Plac), L3-L4) or intrathecal fentanyl (5K(Fent), L3-L4) to impair cortical projection of opioid-mediated muscle afferents. Peripheral quadriceps fatigue was assessed via changes in force output pre- versus postexercise in response to supramaximal magnetic femoral nerve stimulation (DeltaQ(tw)). The CMD during the time trials was estimated via quadriceps electromyogram (iEMG). Fentanyl had no effect on quadriceps strength. Impairment of neural feedback from the locomotor muscles increased iEMG during the first 2.5 km of 5K(Fent) versus 5K(Plac) by 12 +/- 3% (P < 0.05); during the second 2.5 km, iEMG was similar between trials. Power output was also 6 +/- 2% higher during the first and 11 +/- 2% lower during the second 2.5 km of 5K(Fent) versus 5K(Plac) (both P < 0.05). Capillary blood lactate was higher (16.3 +/- 0.5 versus 12.6 +/- 1.0%) and arterial haemoglobin O(2) saturation was lower (89 +/- 1 versus 94 +/- 1%) during 5K(Fent) versus 5K(Plac). Exercise-induced DeltaQ(tw) was greater following 5K(Fent) versus 5K(Plac) (-46 +/- 2 versus -33 +/- 2%, P < 0.001). Our results emphasize the critical role of somatosensory feedback from working muscles on the centrally mediated determination of CMD. Attenuated afferent feedback from exercising locomotor muscles results in an overshoot in CMD and power output normally chosen by the athlete, thereby causing a greater rate of accumulation of muscle metabolites and excessive development of peripheral muscle fatigue.
The technique of twitch interpolation has been used to study the degree of motor unit activation during voluntary effort. In nearly all subjects complete activation of the tibialis anterior was easily achieved during strong dorsiflexion of the ankle; in contrast, it was more difficult to drive plantar-flexor motor units fully. The findings of other studies have been reviewed, and an explanation has been advanced to account for the differences between the tibialis anterior and plantar-flexor muscles.
Biopsy samples were obtained from the vastus lateralis muscle of eight subjects after 0, 20, 60, and 120 s of recovery from intense electrically evoked isometric contraction. Later (10 days), the same procedures were performed using the other leg, but subjects ingested 20 g creatine (Cr)/day for the preceding 5 days. Muscle ATP, phosphocreatine (PCr), free Cr, and lactate concentrations were measured, and total Cr was calculated as the sum of PCr and free Cr concentrations. In five of the eight subjects, Cr ingestion substantially increased muscle total Cr concentration (mean 29 +/- 3 mmol/kg dry matter, 25 +/- 3%; range 19-35 mmol/kg dry matter, 15-32%) and PCr resynthesis during recovery (mean 19 +/- 4 mmol/kg dry matter, 35 +/- 6%; range 11-28 mmol/kg dry matter, 23-53%). In the remaining three subjects, Cr ingestion had little effect on muscle total Cr concentration, producing increases of 8-9 mmol/kg dry matter (5-7%), and did not increase PCr resynthesis. The data suggest that a dietary-induced increase in muscle total Cr concentration can increase PCr resynthesis during the 2nd min of recovery from intense contraction.
Fatigue, defined as the failure to maintain the required or expected power output, is a complex problem, since multiple factors are clearly involved, with the relative importance of each dependent on the fiber type composition of the contracting muscles(s), and the intensity, type, and duration of the contractile activity. The primary sites of fatigue appear to be within the muscle cell itself and for the most part do not involve the central nervous system or the neuromuscular junction. The major hypotheses of fatigue center on disturbances in the surface membrane, E-C coupling, or metabolic events. The cell sites most frequently linked to the etiology of skeletal muscle fatigue are shown in Figure 1. Skeletal muscles are composed of at least four distinct fiber types (3 fast twitch and 1 slow twitch), with the slow type I and fast type IIa fibers containing the highest mitochondrial content and fatigue resistance. Despite fiber type differences in the degree of fatigability, the contractile properties undergo characteristic changes with the development of fatigue that can be observed in whole muscles, single motor units, and single fibers. The Po declines, and the contraction and relaxation times are prolonged. Additionally, there is a decrease in the peak rate of tension development and decline and a reduced Vo. Changes in Vo are more resistant to fatigue than Po and are not observed until Po has declined by at least 10% of its initial prefatigued value. However, the reduced peak power by which fatigue is defined results from both a reduction in Vo and Po. In the absence of muscle fiber damage, the prolonged relaxation time associated with fatigue causes the force-frequency curve to shift to the left, such that peak tensions are obtained at lower frequencies of stimulation. In a mechanism not clearly understood, the central nervous system senses this condition and reduces the alpha-motor nerve activation frequency as fatigue develops. In some cases, selective LFF develops that displaces the force-frequency curve to the right. Although not proven, it appears likely that this condition is associated with and likely caused by muscle injury, such that the SR releases less Ca2+ at low frequencies of activation. Alternatively, LFF could result from a reduced membrane excitability, such that the sarcolemma action potential frequency is considerably less than the stimulation frequency.(ABSTRACT TRUNCATED AT 400 WORDS)
The effect of dietary creatine and supplementation on skeletal muscle creatine accumulation and subsequent degradation and on urinary creatinine excretion was investigated in 31 male subjects who ingested creatine in different quantities over varying time periods. Muscle total creatine concentration increased by approximately 20% after 6 days of creatine supplementation at a rate of 20 g/day. This elevated concentration was maintained when supplementation was continued at a rate of 2 g/day for a further 30 days. In the absence of 2 g/day supplementation, total creatine concentration gradually declined, such that 30 days after the cessation of supplementation the concentration was no different from the presupplementation value. During this period, urinary creatinine excretion was correspondingly increased. A similar, but more gradual, 20% increase in muscle total creatine concentration was observed over a period of 28 days when supplementation was undertaken at a rate of 3 g/day. In conclusion, a rapid way to "creatine load" human skeletal muscle is to ingest 20 g of creatine for 6 days. This elevated tissue concentration can then be maintained by ingestion of 2 g/day thereafter. The ingestion of 3 g creatine/day is in the long term likely to be as effective at raising tissue levels as this higher dose.
The purpose of this study was to test the hypothesis that ingestion of creatine monohydrate increases anaerobic exercise capacity, as reflected by the maximal accumulated oxygen deficit (MAOD). Subjects were assigned, double-blind, to placebo (PL, n = 12) or creatine (CR, n = 14) groups and ingested 5-g doses 4 times daily of artificial sweetener or artificially sweetened creatine monohydrate, respectively, for 5 days. On a separate day subjects exercised to exhaustion at 125% VO2max. After two familiarization trials, MAOD was again determined before treatment, after 5 days of PL or CR treatment, and 7 days later. MAOD increased after CR treatment from 4.04 +/- 0.31 to 4.41 +/- 0.34 L (p < .001) and remained elevated for another 7 days (4.31 +/- 0.33, p < .001). Time to exhaustion also increased in CR from 130 +/- 7 to 141 +/- 7 s (p < .01) and remained increased for another 7 days (139 +/- 8 s, p < .01). These data demonstrate that ingesting creatine monohydrate for 5 days increases the MAOD, and is likely to have an ergogenic effect on supramaximal exercise performance that persists for at least a week after treatment.
To examine some possible sites of fatigue during short-lasting maximally intensive stretch-shortening cycle exercise, drop jumps on an inclined sledge apparatus were analyzed. Twelve healthy volunteers performed jumps until they were unable to maintain jumping height > 90% of their maximum. After the workout, the increases in the blood lactate concentration and serum creatine kinase activation were statistically significant (P < 0.001 and P < 0.05, respectively) but rather small in physiological terms. The major changes after the workout were as follows: the single twitch was characterized by smaller peak torque (P < 0.05) and shorter time to peak (P < 0.05) and half-relaxation time (P < 0.01). The double-twitch torque remained at the same level (P > 0.05), but with a steeper maximal slope of torque rise (P < 0.05); during 20- and 100-Hz stimulation the torque declined (both P < 0.01) and the maximal voluntary torque changed nonsignificantly but with a smaller maximal slope of torque rise (P < 0.01) and a higher activation level (P < 0.05), accompanied by an increased electromyogram amplitude. These findings indicate that the muscle response after the short-lasting consecutive maximum jumps on the sledge apparatus may involve two distinct mechanisms acting in opposite directions: 1) The contractile mechanism seems to be potentiated through a shorter Ca2+ transient and faster cross-bridge cycling, as implied by twitch changes. 2) High-frequency action potential propagation shows an impairment, which is suggested as the possible dominant reason for fatigue in exercise of this type.
The purpose of this study was to use 31P-magnetic resonance spectroscopy to examine the relationships among muscle PCr hydrolysis, intracellular H+ concentration accumulation, and muscle performance during incremental exercise during the inspiration of gas mixtures containing different fractions of inspired O2 (FIO2). We hypothesized that lower FIO2 would result in a greater disruption of intracellular homeostasis at submaximal workloads and thereby initiate an earlier onset of fatigue. Six subjects performed plantar flexion exercise on three separate occasions with the only variable altered for each exercise bout being the FIO2 (either 0.1, 0.21, or 1.00 O2 in balance N2). Work rate was increased (1-W increments starting at 0 W) every 2 min until exhaustion. Time to exhaustion (and thereby workload achieved) was significantly (P < 0.05) greater as FIO2 was increased. Muscle phosphocreatine (PCr) concentration, Pi concentration, and pH at exhaustion were not significantly different among the three FIO2 conditions. However, muscle PCr concentration and pH were significantly reduced at identical submaximal workloads (and thereby equivalent rates of respiration) above 4-5 W during the lowest FIO2 condition compared with the other two FIO2 conditions. These results demonstrate that exhaustion during all FIO2 occurred when a particular intracellular environment was achieved and suggest that during the lowest FIO2 condition, the greater PCr hydrolysis and intracellular acidosis at submaximal workloads may have contributed to the significantly earlier time to exhaustion.
Ten physically active, untrained, college-aged males (26.4 +/- 5. 8 years old) received creatine (CR, 5 g creatine monohydrate + 3 g dextrose) and placebo (PLA, 7 g dextrose) supplementation four times per day for 5 days in a double-blind, randomized, balanced, crossover design. Performance was assessed during maximal and three repeated submaximal bouts of isometric knee extension and handgrip exercise. CR supplementation significantly increased (p <.05) maximal isometric strength during knee extension but not during handgrip exercise. CR supplementation increased time to fatigue during each of the three bouts of submaximal knee extension and handgrip exercise when compared to the PLA trials. These findings suggest that CR supplementation can increase maximal strength and time to fatigue during isometric exercise. However, the improvements in maximal isometric strength following CR supplementation appear to be restricted to movements performed with a large muscle mass.
For high-intensity cycle ergometer exercise, the tolerable duration (t) is well characterized as a hyperbolic function of power output, P : t = W'/(P-thetaF), where thetaF may be termed the "fatigue threshold." The purpose of this study was to determine the effect of oral creatine (Cr) supplementation on the curvature constant parameter (W') of the power-duration curve. A double-blind research method and a cross-over design were employed for creatine/placebo supplementation. Eight healthy male subjects (aged 18 to 22 years) each performed four or five high-intensity square-wave exercise bouts on an electrically braked cycle ergometer after 5 d of Cr monohydrate (CR: 20 g of Cr with artificial sweetener/d) or placebo (PL: 6 g of glucose/d) supplementation. Each subject performed a single high-intensity exercise trial per day for four or five successive days to determination the P-t hyperbolic relation. After 6 weeks (the washout time of Cr from the muscles), each subject performed the other condition (i.e., PL or CR) and repeated the same experimental procedure. There was no significant difference for thetaF between PL and CR conditions (PL: 214.4 +/- 23.6, CR: 207.0 +/- 19.8 W, mean +/- SD). In contrast, W' was significantly increased by the Cr supplementation (PL: 10.9 +/- 2.7, CR: 13.7 +/- 3.0 kJ; p<0.05). The results indicated that Cr and/or PCr content in muscles seems to be one of the important determinants of the curvature constant parameter (W') of the power-duration hyperbolic curve for cycle ergometry.
It has been repeatedly demonstrated that the tolerable duration (t) of high-intensity cycling is well characterized as a hyperbolic function of power (P) with an asymptote that has been termed the "fatigue threshold" and with a curvature constant. This hyperbolic P-t relationship has also been confirmed in running and swimming, when speed (V) is used instead of P; that is, (V - V(F)). t = D', where V(F) is the V at the fatigue threshold, and D' is the curvature constant. Therefore, we theoretically analyzed herein the consequences of an athlete performing the initial part of an endurance event at a V different from the constant rate that would allow the performance time to be determined by the hyperbolic V-t relationship. We considered not only the V-t constraints that limit the athlete's ability to make up the time lost by too slow an early pace but also the consequences of a more rapid early pace. Our analysis demonstrates that both the V(F) and D' parameters of the athlete's V-t curve play an important role in the pace allocation strategy of the athlete. That is, 1) when the running V during any part of the whole running distance is below V(F), the athlete can never attain the goal of achieving the time equivalent to that of running the entire race at constant maximal V (i.e., that determined by one's own best V-t curve); and 2) the "endurance parameter ratio" D'/V(F) is especially important in determining the flexibility of the race pace that the athlete was able to choose intentionally.
For high-intensity cycle ergometer exercise, the relation between power (P) and its tolerable duration (t) has been well characterized by the hyperbolic relationship: (P-thetaF) t = W', or P = W' (1/t)+thetaF, where thetaF may be termed the 'fatigue threshold'. The curvature constant (W') reflects a constant amount of work which is postulated to be equivalent to a finite energy store that relates to the oxygen-deficit: phosphagen pool, anaerobic glycolysis and oxygen stores. Compared to thetaF, the physiological nature of W' has received little consideration. The purpose of this study was therefore to establish the parameters of the power-duration curve (thetaF and W') for subjects in normal glycogen (NG) and glycogen depleted (GD) states. Seven healthy male subjects (aged 22 to 41 years) each performed four high-intensity square-wave exercise bouts on an electrically braked cycle ergometer under two different muscular glycogen content conditions, i.e. NG and GD states. Subjects performed the following exercise on the evening before the trial day to induce the GD state. Initially, they performed a 75-min cycling exercise at 60% of VO2max. After a 5-min rest period, they subsequently repeated a 1-min cycling bout at 115% of VO2max (separated by 1-min rest periods) until the subject could no longer maintain the prescribed pedal rate for the full minute. Subjects then reported to the laboratory after an overnight fast and performed a single high-intensity exercise bout. The GD procedure was repeated four times at 1-week intervals. In the GD state, the respiratory exchange ratio (RER) (VO2/VCO2) value during a recumbent control period prior to the trial was significantly lower than that in the NG state [GD: 0.84+/-0.02, NG: 0.94+/-0.04, mean +/- SD]. There was no significant difference for thetaF between GD and NG state [NG: 197.1+/-31.9 W, GD: 190.6+/-28.2 W]. W' in contrast was significantly reduced by the GD procedure [NG: 12.83+/-2.21 kJ, GD: 10.33+/-2.41 kJ]. The present results indicate that the muscular glycogen store seems to be an important determinant of the curvature constant (W') of the power-duration curve for cycle ergometry.
The purpose of this study was to determine the effects of 2 and 5 days of Cr loading on anaerobic working capacity (AWC) using the critical power (CP) test in women. Ten physically active women randomly received 2 treatments separated by a 5 week washout period: (A) 18 g dextrose as placebo (PL) or (B) 5.0 g Cr + 18 g dextrose taken 4 times per day for 5 days. Following a familiarization trial, each subject completed the CP test at baseline and following 2 and 5 days of supplementation. The PL resulted in no significant changes in AWC following supplementation; however, Cr increased AWC by 22.1% after 5 days of loading (p < 0.05). There was a significant main effect for body weight (BW), however, there was no significant increase in BW due to Cr supplementation. These results suggest that Cr supplementation is effective for increasing AWC in women following 5 days of loading without an associated increase in BW.
The purpose of this study was to determine the effects of 2 and 6 days of creatine phosphate loading on anaerobic working capacity (AWC) and body weight (BW) in men and women. Sixty-one men (n = 31) and women (n = 30) randomly received 1 of 3 treatments (4 x 5 g.d(-1) x 6 days) using a double blind design: (a) 18 g dextrose as placebo (PL); (b) 5.0 g Cr + 20 g dextrose (Cr); or (c) 5.0 g Cr + 18 g dextrose + 4 g of sodium and potassium phosphates (CrP). AWC was determined at baseline and following 2 and 6 days of supplementation using the Critical Power Test. BW increased significantly over time, and the mean value for the men was significantly greater compared to that for women, but there were no interactions (p > 0.05). There were gender-specific responses for AWC expressed in both absolute values (kJ) and relative to BW (kJ. kg(-1)), with the women demonstrating no significant interactions. For the men, CrP loading significantly increased AWC following 2 days (23.8%) and 6 days (49.8%) of supplementation vs. PL (kJ and kJ.kg(-1)). Cr supplementation increased AWC 13-15% in both genders compared to PL (1.1%- 3.0% decline); although this result was not statistically significant, it may have some practical significance.
Changing arterial oxygen content (C(aO(2))) has a highly sensitive influence on the rate of peripheral locomotor muscle fatigue development. We examined the effects of C(aO(2)) on exercise performance and its interaction with peripheral quadriceps fatigue. Eight trained males performed four 5 km cycling time trials (power output voluntarily adjustable) at four levels of C(aO(2)) (17.6-24.4 ml O(2) dl(-1)), induced by variations in inspired O(2) fraction (0.15-1.0). Peripheral quadriceps fatigue was assessed via changes in force output pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation (DeltaQ(tw); 1-100 Hz). Central neural drive during the time trials was estimated via quadriceps electromyogram. Increased C(aO(2)) from hypoxia to hyperoxia resulted in parallel increases in central neural output (43%) and power output (30%) during cycling and improved time trial performance (12%); however, the magnitude of DeltaQ(tw) (-33 to -35%) induced by the exercise was not different among the four time trials (P > 0.2). These effects of C(aO(2)) on time trial performance and DeltaQ(tw) were reproducible (coefficient of variation = 1-6%) over repeated trials at each F(IO(2)) on separate days. In the same subjects, changing C(aO(2)) also affected performance time to exhaustion at a fixed work rate, but similarly there was no effect of Delta C(aO(2)) on peripheral fatigue. Based on these results, we hypothesize that the effect of C(aO(2)) on locomotor muscle power output and exercise performance time is determined to a significant extent by the regulation of central motor output to the working muscle in order that peripheral muscle fatigue does not exceed a critical threshold.