Stroke-Specific Swimming Critical Speed Testing: Balancing Feasibility and Scientific Rigour.

This study aimed to assess the reliability of a two-distance critical speed protocol in the specialist strokes of national-level swimmers and understand the practical feasibility of extending the protocol to increase its validity. Thirty-two national-level swimmers (butterfly n = 7; backstroke n = 8; breaststroke n = 7; front crawl n = 10) swum three 200-m and three 400-m performance trials over a three-week period. Critical speed and supra-critical speed distance capacity were computed from the linear modelling of the distance-time relationship. Swimmers were subsequently asked whether they felt they could or would want to complete an 800-m trial as part of a three-distance critical speed protocol to enhance validity. Both 200-m and 400-m performances (coefficient of variation of < 2%) and derived critical speed (typical error of ≤ 0.04 m·s-1; coefficient of variation of < 4%) were reliable for all strokes, while supra-critical speed distance capacity (typical error from 4 to 9 m; coefficient of variation from 13 to 45%) was not reliable. Response rates to the follow-up questions were 100%. Few butterfly swimmers said they felt they could complete an 800-m performance trial (39%), with more positive responses for breaststroke (71%), backstroke (100%), and front crawl swimmers (100%). Butterfly swimmers were significantly less likely to say they could or would want to complete an 800-m trial than backstroke and front crawl swimmers (p < 0.05). Including a third distance 800-m trial to increase critical speed validity would not be acceptable to butterfly swimmers, would be challenging to breaststroke swimmers, but would be acceptable to front crawl and backstroke swimmers.

Is airway damage during physical exercise related to airway dehydration? Inputs from a computational model.

In healthy subjects, at low minute ventilation (V̇e) during physical exercise, the water content and temperature of the airways are well regulated. However, with the increase in V̇e, the bronchial mucosa becomes dehydrated and epithelial damage occurs. Our goal was to demonstrate the correspondence between the ventilatory threshold inducing epithelial damage, measured experimentally, and the dehydration threshold, estimated numerically. In 16 healthy adults, we assessed epithelial damage before and following a 30-min continuous cycling exercise at 70% of maximal work rate, by measuring the variation pre- to postexercise of serum club cell protein (cc16/cr). Blood samples were collected at rest, just at the end of the standardized 10-min warm-up, and immediately, 30 min and 60 min postexercise. Mean V̇e during exercise was kept for analysis. Airway water and heat losses were estimated using a computational model adapted to the experimental conditions and were compared with a literature-based threshold of bronchial dehydration. Eleven participants exceeded the threshold for bronchial dehydration during exercise (group A) and five did not (group B). Compared with post warm-up, the increase in cc16/cr postexercise was significant (mean increase ± SE: 0.48 ± 0.08 ng·L-1 only in group A but not in group B (mean difference ± SE: 0.10 ± 0.04 ng·L-1). This corresponds to an increase of 101 ± 32% [range: 16%-367%] in group A (mean ± SE). Our findings suggest that the use of a computational model may be helpful to estimate an individual dehydration threshold of the airways that is associated with epithelial damage during physical exercise.NEW & NOTEWORTHY Using a computational model for heat and water transfers in the bronchi, we identified a threshold in ventilation during exercise above which airway dehydration is thought to occur. When this threshold was exceeded, epithelial damage was found. This threshold might therefore represent the ventilation upper limit during exercise in susceptible individuals. Our results might help to prevent maladaptation to chronic exercise such as exercise-induced bronchoconstriction or asthma.

Effect of the subjective intensity of fatigue and interoception on perceptual regulation and performance during sustained physical activity.

BACKGROUND: The subjective experience of fatigue impairs an individual's ability to sustain physical endurance performance. However, precise understanding of the specific role perceived fatigue plays in the central regulation of performance remains unclear. Here, we examined whether the subjective intensity of a perceived state of fatigue, pre-induced through prior upper body activity, differentially impacted performance and altered perceived effort and affect experienced during a sustained, isometric contraction in lower body. We also explored whether (cardiac) interoception predicted the intensity of experienced perceptual and affective responses and moderated the relationships between constructs during physical activity. METHODS: Using a repeated-measures study design, thirty male participants completed three experimental conditions, with the intensity of a pre-induced state of fatigue manipulated to evoke moderate (MOD), severe (SEV) and minimal (control; CON) intensity of perceptions prior to performance of the sustained contraction. RESULTS: Performance of the sustained contraction was significantly impaired under a perceived state of fatigue, with reductions of 10% and 14% observed in the MOD and SEV conditions, respectively. Performance impairment was accompanied by greater perceived effort and more negative affective valence reported during the contraction. However, effects were limited to comparisons to CON, with no difference evident between the two experimental trials (i.e. MOD vs. SEV). Individuals' awareness of their accuracy in judging resting heartbeats was shown to predict the subjective intensity of fatigue experienced during the endurance task. However, interoception did not moderate the relationships evident between fatigue and both perceived effort and affective valence. CONCLUSIONS: A perceived state of fatigue limits endurance performance, influencing both how effortful activity is perceived to be and the affective experience of activity. Though awareness of interoceptive representations of bodily states may be important to the subjective experience of fatigue, interoception does not modulate the relationships between perceived fatigue and other perceptual (i.e. effort) and affective constructs.

Sodium Bicarbonate Supplementation Delays Neuromuscular Fatigue Without Changes in Performance Outcomes During a Basketball Match Simulation Protocol.

Ansdell, P and Dekerle, J. Sodium bicarbonate supplementation delays neuromuscular fatigue without changes in performance outcomes during a basketball match simulation protocol. J Strength Cond Res 34(5): 1369-1375, 2020-To investigate the development of neuromuscular fatigue during a basketball game simulation and to ascertain whether sodium bicarbonate (NaHCO3) supplementation attenuates any neuromuscular fatigue that persists. Ten participants ingested 0.2 g·kg of NaHCO3 (or an equimolar placebo dosage of sodium chloride [NaCl]) 90 and 60 minutes before commencing a basketball game simulation (ALK-T vs. PLA-T). Maximal voluntary isometric contractions (MVICs) of the knee extensors and potentiated high- (100 Hz) and low- (10 Hz) frequency doublet twitches were recorded before and after each match quarter for both trials. In addition, 15-m sprint times and layup completion (%) were recorded during each quarter. Maximal voluntary isometric contraction, 100- and 10-Hz twitch forces declined progressively in both trials (p ≤ 0.05) with a less pronounced decrease in MVIC during ALK-T (p < 0.01). Both 100- and 10-Hz twitch forces were also significantly greater in ALK-T (p ≤ 0.05). Fifteen-meter sprint time increased over the course of both trials (∼2%, p < 0.01); however, no significant condition or time effect was found for layup completion (p > 0.05). A basketball simulation protocol induces a substantial amount of neuromuscular (reduction in knee extensor MVICs) and peripheral fatigue with a concomitant increase in 15-m sprint time over the protocol. NaHCO3 supplementation attenuated the rate of fatigue development by protecting contractile elements of the muscle fibers. This study provides coaches with information about the magnitude of fatigue induced by a simulated basketball game and provides evidence of the efficacy of NaHCO3 in attenuating fatigue.

Creatine supplementation improves performance above critical power but does not influence the magnitude of neuromuscular fatigue at task failure.

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 with four to five 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- (PS10) frequency 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%). No significant difference was found between ISO and either PLA or 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.

Improving the measurement of TMS-assessed voluntary activation in the knee extensors.

PURPOSE: To test the accuracy, validity, reliability and sensitivity of an alternative method for the measure of TMS-assessed voluntary activation (VATMS) in the knee extensors. METHODS: Ten healthy males (24 ± 5 years) completed a neuromuscular assessment protocol before and after a fatiguing isometric exercise: two sets of five contractions (50%, 62.5%, 75%, 87.5%, 100% Maximal Voluntary Contraction; MVC) with superimposed TMS-evoked twitches for calculation of VATMS using either the first 5 stimulations (1x5C) or all 10 (2x5C). This was performed on two separate occasions (between-day reliability). Accuracy and validity were compared with a routinely used protocol [i.e. 50%, 75%, and 100% of MVC (1x3C) performed three times (3x3C)]. RESULTS: 95% confidence interval for estimated resting twitch, a key determinant of VATMS, was similar between 1x5C, 2x5C, and 3x3C but improved by six-fold when compared to 1x3C (P<0.05). In a fresh state, potentiated twitch force was unchanged following 1x5C but decreased following 2x5C (P<0.05). A recovery was found post-exercise but was smaller for 1x5C compared to 2x5C (P<0.05), with no difference between the latter two (P>0.05). Absolute reliability was strong enough for both 1x5C and 2x5C to depict a true detectable change in the sample's VATMS following the fatiguing exercise (TEM < 3% at rest, <9% post-exercise) but 2x5C was marginally more sensitive to individual's changes from baseline. CONCLUSION: Both 1x5C and 2x5C provide reliable measures of VATMS. However, 1x5C may hold stronger internal validity. Both protocols allow detection of 'true' changes in sample's means but not individual scores following a fatiguing isometric exercise.

Methodological issues with the assessment of voluntary activation using transcranial magnetic stimulation in the knee extensors.

PURPOSE: The assessment of voluntary activation of the knee extensors using transcranial magnetic stimulation (VATMS) is routinely performed to assess the supraspinal function. Yet methodological scrutiny of the technique is scarce. The aim of the present study was to examine face validity and reliability of VATMS and its two main determinants (superimposed twitch during a maximal voluntary contraction [SIT100%] and estimated resting twitch [ERT]). METHODS: SIT100%, ERT, and VATMS were measured on ten healthy males (age 24 ± 5 years) before and following intermittent isometric fatiguing exercise on two separate occasions. RESULTS: The findings indicated issues regarding the accuracy of ERT and suggested a three-point relationship should not be used to determine ERT. Reliabilities for VATMS, SIT100%, and ERT were acceptable pre- but much weaker post-exercise (especially for SIT100%). Despite statistically significant changes in main neuromuscular variables following the intermittent isometric fatiguing exercise (P < 0.05), when post-exercise reliability was considered, the exercise effect on VATMS was smaller than the smallest detectable change in 18 of the 20 individual tests performed, and for the whole sample for one of two visits. Finally, maximal voluntary contraction was reduced significantly following the neuromuscular assessment (NMA) pre-exercise but recovered during the NMA post-exercise. CONCLUSION: This is the first study to demonstrate a lack of sensitivity of key neuromuscular measurements to exercise and to evidence both presence of neuromuscular fatigue following the NMA in itself, and recovery of the neuromuscular function during the NMA post-exercise. These results challenge the face validity of this routinely used protocol.

Continuous exercise induces airway epithelium damage while a matched-intensity and volume intermittent exercise does not.

BACKGROUND: While continuous exercise (CE) induces greater ventilation ([Formula: see text]E) when compared to intermittent exercise (IE), little is known of the consequences on airway damage. Our aim was to investigate markers of epithelial cell damage - i.e. serum levels of CC16 and of the CC16/SP-D ratio - during and following a bout of CE and IE of matched work. METHODS: Sixteen healthy young adults performed a 30-min continuous (CE) and a 60-min intermittent exercise (IE; 1-min work: 1-min rest) on separate occasions in a random order. Intensity was set at 70% of their maximum work rate (WRmax). Heart rate (HR) and [Formula: see text]E were measured throughout both tests. Blood samples were taken at rest, after the 10th min of the warm-up, at the end of both exercises, half way through IE (matched time but 50% work done for IE) as well as 30- and 60-min post-exercise. Lactate and CC16 and SP-D were determined. RESULTS: Mean [Formula: see text]E was higher for CE compared to IE (85 ± 17 l.min- 1 vs 50 ± 8 l.min- 1, respectively; P < 0.001). Serum-based markers of epithelial cell damage remained unchanged during IE. Interaction of test × time was observed for SP-D (P = 0.02), CC16 (µg.l- 1) (P = 0.006) and CC16/SP-D ratio (P = 0.03). Maximum delta CC16/SP-D was significantly correlated with mean [Formula: see text]E sustained (r = 0.83, P < 0.001) during CE but not during IE. CONCLUSION: The 30-min CE performed at 70% WRmax induced mild airway damage, while a time- or work-matched IE did not. The extent of the damage during CE was associated with the higher ventilation rate.

The magnitude of neuromuscular fatigue is not intensity dependent when cycling above critical power but relates to aerobic and anaerobic capacities.

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 after two bouts of supra-CP cycling (3 versus 12 min) when controlling for W' depletion but is larger for individuals of greater anaerobic capacity after the shorter bout and smaller for individuals of greater aerobic capacity after the longer exercise bout. 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 peak oxygen consumption, critical power (CP) and W', followed by two randomly assigned constant-load supra-CP trials set to deplete W' fully in 3 (P-3) and 12 min (P-12). Pre- to postexercise changes in maximal voluntary contraction, potentiated quadriceps twitch force evoked by single (Qpot ) and paired high- (PS100) and low-frequency (PS10) stimulations and voluntary activation were determined. Cycling above CP reduced maximal voluntary contraction (P-3, -20 ± 10% versus P-12, -15 ± 7%), measures associated with peripheral fatigue (Qpot , -35 ± 13 versus -31 ± 14%; PS10, -38 ± 13 versus -37 ± 17%; PS100, -18 ± 9 versus -13 ± 8% for P-3 and P-12, respectively) and voluntary activation (P-3, -12 ± 3% versus P-12, -13 ± 3%; P < 0.05), with no significant difference between trials (P > 0.05). Changes in maximal voluntary contraction and evoked twitch forces were inversely correlated with CP and peak oxygen consumption after P-12, whereas W' was significantly correlated with changes in Qpot and PS10 after 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; nonetheless, exploration of inter-individual variations suggests that mechanisms underpinning exercise tolerance within this domain differ between short- and long-duration exercise.

Once- and twice-daily heat acclimation confer similar heat adaptations, inflammatory responses and exercise tolerance improvements.

This experiment aimed to investigate the efficacy of twice-daily, nonconsecutive heat acclimation (TDHA) in comparison to once-daily heat acclimation (ODHA) and work matched once- or twice-daily temperate exercise (ODTEMP, TDTEMP) for inducing heat adaptations, improved exercise tolerance, and cytokine (immune) responses. Forty males, matched biophysically and for aerobic capacity, were assigned to ODHA, TDHA, ODTEMP, or TDTEMP. Participants completed a cycling-graded exercise test, heat acclimation state test, and a time to task failure (TTTF) at 80% peak power output in temperate (TTTFTEMP : 22°C/40% RH) and hot conditions (TTTFHOT : 38°C/20% RH), before and after 10-sessions (60 min of cycling at ~2 W·kg-1 ) in 45°C/20% RH (ODHA and TDHA) or 22°C/40% RH (ODTEMP or TDTEMP). Plasma IL-6, TNF-α, and cortisol were measured pre- and postsessions 1, 5, and 10. ODHA and TDHA induced equivalent heat adaptations (P < 0.05) (resting rectal temperature [-0.28 ± 0.22, -0.28 ± 0.19°C], heart rate [-10 ± 3, -10 ± 4 b·min-1 ], and plasma volume expansion [+10.1 ± 5.6, +8.5 ± 3.1%]) and improved heat acclimation state (sweat set point [-0.22 ± 0.18, -0.22 ± 0.14°C] and gain [+0.14 ± 0.10, +0.15 ± 0.07 g·sec-1 ·°C-1 ]). TTTFHOT increased (P < 0.001) following ODHA (+25 ± 4%) and TDHA (+24 ± 10%), but not ODTEMP (+5 ± 14%) or TDTEMP (+5 ± 17%). TTTFTEMP did not improve (P > 0.05) following ODHA (+14 ± 4%), TDHA (14 ± 8%), ODTEMP (9 ± 10%) or TDTEMP (8 ± 13%). Acute (P < 0.05) but no chronic (P > 0.05) increases were observed in IL-6, TNF-α, or cortisol during ODHA and TDHA, or ODTEMP and TDTEMP. Once- and twice-daily heat acclimation conferred similar magnitudes of heat adaptation and exercise tolerance improvements, without differentially altering immune function, thus nonconsecutive TDHA provides an effective, logistically flexible method of HA, benefitting individuals preparing for exercise-heat stress.

Physiological comparison of intensity-controlled, isocaloric intermittent and continuous exercise.

VO2 fluctuations are argued to be an important mechanism underpinning chronic adaptations following interval training. We compared the effect of exercise modality, continuous vs. intermittent realized at a same intensity, on electrical muscular activity, muscular oxygenation and on whole body oxygen uptake. Twelve participants (24 ± 5 years; VO2peak: 43 ± 6 mL·â€…min-1·kg-1) performed (i) an incremental test to exhaustion to determine peak work rate (WRpeak); two randomized isocaloric exercises at 70%WRpeak; (ii) 1 bout of 30 min; (iii) 30 bouts of 1 min work intercepted with 1 min passive recovery. For electromyography, only the CON exercise showed change for the vastus lateralis root-mean-square (+6.4 ± 5.1%, P < .01, 95%CI 3.2, 8.3) and mean power frequency (-5.2 ± 4.8, P < .01, 95%CI -8.2, -3.5). Metabolic fluctuations (i.e. Oxygen Fluctuation Index and HHb Fluctuation Index) were higher in the intermittent modality, while post-exercise blood lactate concentrations (4.80 ± 1.50 vs. 2.32 ± 1.21 mM, respectively, for the CON and INT, P < .01, 95%CI 1.72, 3.12) and the time spent over 90% of VO2 target (1644 ± 152 vs. 356 ± 301 sec, respectively, for the CON and INT, P < .01, 95%CI 1130, 1446) were higher in the continuous modality. In conclusion, despite a similar energy expenditure and intensity, intermittent and continuous exercises showed two very different physiological responses. The intermittent modality would lead to a larger recruitment of fast twitch fibres that are less mitochondria-equipped and therefore may be more likely respondent to mitochondrial adaptations. In addition, this modality induces greater metabolic variations, a stimulus who could lead to mitochondrial development.

Exercise-induced Fatigue in Severe Hypoxia after an Intermittent Hypoxic Protocol.

PURPOSE: Exercise-induced central fatigue is alleviated after acclimatization to high altitude. The adaptations underpinning this effect may also be induced with brief, repeated exposures to severe hypoxia. The purpose of this study was to determine whether (i) exercise tolerance in severe hypoxia would be improved after an intermittent hypoxic (IH) protocol and (ii) exercise-induced central fatigue would be alleviated after an IH protocol. METHODS: Nineteen recreationally active men were randomized into two groups who completed ten 2-h exposures in severe hypoxia (IH: partial pressure of inspired O2 82 mm Hg; n = 11) or normoxia (control; n = 8). Seven sessions involved cycling for 30 min at 25% peak power (W˙peak) in IH and at a matched heart rate in normoxia. Participants performed baseline constant-power cycling to task failure in severe hypoxia (TTF-Pre). After the intervention, the cycling trial was repeated (TTF-Post). Before and after exercise, responses to transcranial magnetic stimulation and supramaximal femoral nerve stimulation were obtained to assess central and peripheral contributions to neuromuscular fatigue. RESULTS: From pre- to postexercise in TTF-Pre, maximal voluntary contraction (MVC), cortical voluntary activation (VATMS), and potentiated twitch force (Qtw,pot) decreased in both groups (all P < 0.05). After IH, TTF-Post was improved (535 ± 213 s vs 713 ± 271 s, P < 0.05) and an additional isotime trial was performed. After the IH intervention only, the reduction in MVC and VATMS was attenuated at isotime (P < 0.05). No differences were observed in the control group. CONCLUSIONS: Whole-body exercise tolerance in severe hypoxia was prolonged after a protocol of IH. This may be related to an alleviation of the central contribution to neuromuscular fatigue.

Effect of work:rest cycle duration on [Formula: see text] fluctuations during intermittent exercise.

The succession of on-transient phases that induce a repetition of metabolic changes is a possible mechanism responsible for the greater response to intermittent training (IT). The objective of this study was to quantify [Formula: see text] fluctuations during intermittent exercise characterised by the same work:rest ratio, but different durations and identify which duration leads to the greatest fluctuations. Ten participants (24 ± 5 years; [Formula: see text]: 42 ± 7 mL·min-1·kg-1) performed (1) an incremental test to exhaustion to determine peak work rate (WRpeak) and oxygen uptake ([Formula: see text]), (2), and three 1 h intermittent exercises alternating work period at 70% WRpeak with passive recovery period of different 1:1 work:recovery duty cycles (30 s:30 s, 60 s:60 s, 120 s:120 s). [Formula: see text] response analysis revealed differences in the fluctuations across the intermittent conditions despite an identical total energy expenditure. The sum of the cycle's nadir-to-peak [Formula: see text] differences (ΣΔ[Formula: see text]) and the oxygen fluctuation index (OFI) were both greater in the 60 s:60 s condition (ΣΔ[Formula: see text]: +38% ± 13% and +19% ± 18% vs. 120 s:120 s and 30 s:30 s, P < 0.05; OFI: +41% ± 29% and +67% ± 62% vs. 120 s:120 s and 30:30 s, P < 0.05). [Formula: see text] fluctuation analysis was successful in identifying the intermittent condition associated with the greatest disturbances: the 60 s:60 s duty cycle induces more [Formula: see text] fluctuations. The present findings also demonstrate that the selection of the duty cycle duration for submaximal intermittent exercise (70% of WRpeak) prescription is of interest to produce high [Formula: see text] fluctuations.

Rate of utilization of a given fraction of W' (the curvature constant of the power-duration relationship) does not affect fatigue during severe-intensity exercise.

NEW FINDINGS: What is the central question of this study? Does the rate of utilization of W' (the curvature constant of the power-duration relationship) affect fatigue during severe-intensity exercise? What is the main finding and its importance? The magnitude of fatigue after two severe-intensity exercises designed to deplete the same fraction of W' (70%) at two different rates of utilization (fast versus slow) was similar after both exercises. Moreover, the magnitude of fatigue was related to critical power (CP), supporting the contention that CP is a key determinant in fatigue development during high-intensity exercise. Thus, the CP model is a suitable approach to investigate fatigue mechanisms during high-intensity exercise. The depletion of W' (the curvature constant of the power-duration relationship) seems to contribute to fatigue during severe-intensity exercise. Therefore, the aim of this study was to determine the effect of a fast versus a slow rate of utilization of W' on the occurrence of fatigue within the severe-intensity domain. Fifteen healthy male subjects performed tests to determine the critical power, W' and peak torque in the control condition (TCON ) and immediately after two fatiguing work rates (THREE and TEN) set to deplete 70% W' in either 3 (TTHREE ) or 10 min (TTEN ). The TTHREE and TTEN were significantly reduced (F = 19.68, P = 0.01) in comparison to TCON . However, the magnitude of reduction in peak torque (TTHREE  = -19.8 ± 10.1% versus TTEN  = -16.8 ± 13.3%) was the same in the two fatiguing exercises (t = -0.76, P = 0.46). There was a significant inverse relationship between the critical power and the reduction in peak torque during both THREE (r = -0.49, P = 0.03) and TEN (r = -0.62, P = 0.02). In contrast, the W' was not significantly correlated with the reduction in peak torque during both THREE (r = -0.14, P = 0.33) and TEN (r = -0.30, P = 0.10). Thus, fatigue following severe-intensity exercises performed at different rates of utilization of W' was similar when the same work was done above the critical power (i.e. same amount of W' used).

Muscle Fatigue When Swimming Intermittently Above and Below Critical Speed.

PURPOSE: To examine muscle fatigue of the shoulder internal rotators alongside swimming biomechanics during long-duration submaximal swimming sets performed in 2 different speed domains. METHODS: Eight trained swimmers (mean ± SD 20.5 ± 0.9 y, 173 ± 10 cm, 71.3 ± 10.0 kg) raced over 3 distances (200-, 400-, 800-m races) for determination of critical speed (CS; slope of the distance-time relationship). After a familiarization with muscle isokinetic testing, they subsequently randomly performed 2 constant-speed efforts (6 × 5-min blocks, 2.5-min recovery) 5% above (T105) and 5% below CS (T95) with maximal voluntary contractions recorded between swimming blocks. RESULTS: Capillary blood lactate concentration ([La]), rating of perceived exertion (RPE), peak torque, stroke length, and stroke rate were maintained throughout T95 (P < .05). [La], RPE, and stroke rate increased alongside concomitant decreases in maximal torque and stroke length during T105 (P < .05) with incapacity of the swimmers to maintain the pace for longer than ~20 min. For T105, changes in maximal torque (35.0 ± 14.9 to 25.8 ± 12.1 Nm) and stroke length (2.66 ± 0.36 to 2.23 ± 0.24 m/cycle) were significantly correlated (r = .47, P < .05). CONCLUSION: While both muscle fatigue (shoulder internal rotators) and task failure occur when swimming at a pace greater than CS, the 2.5-min recovery period during the sub-CS set possibly alleviated the development of muscle fatigue for the pace to be sustainable for 6 × 5 min at 95% of CS. A causal relationship between reduction in stroke length and loss of muscle strength should be considered very cautiously in swimming.

Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.

During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of V˙O2peak. Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (~2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (~2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (~4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated.

Exercise Tolerance Can Be Enhanced through a Change in Work Rate within the Severe Intensity Domain: Work above Critical Power Is Not Constant.

INTRODUCTION: The characterization of the hyperbolic power-time (P-tlim) relationship using a two-parameter model implies that exercise tolerance above the asymptote (Critical Power; CP), i.e. within the severe intensity domain, is determined by the curvature (W') of the relationship. PURPOSES: The purposes of this study were (1) to test whether the amount of work above CP (W>CP) remains constant for varied work rate experiments of high volatility change and (2) to ascertain whether W' determines exercise tolerance within the severe intensity domain. METHODS: Following estimation of CP (208 ± 19 W) and W' (21.4 ± 4.2 kJ), 14 male participants (age: 26 ± 3; peak VO2: 3708 ± 389 ml.min(-1)) performed two experimental trials where the work rate was initially set to exhaust 70% of W' in 3 ('THREE') or 10 minutes ('TEN') before being subsequently dropped to CP plus 10 W. RESULTS: W>CP for TEN (104 ± 22% W') and W' were not significantly different (P>0.05) but lower than W>CP for THREE (119 ± 17% W', P<0.05). For both THREE (r = 0.71, P<0.01) and TEN (r = 0.64, P<0.01), a significant bivariate correlation was found between W' and tlim. CONCLUSION: W>CP and tlim can be greater than predicted by the P-tlim relationship when a decrement in the work rate of high-volatility is applied. Exercise tolerance can be enhanced through a change in work rate within the severe intensity domain. W>CP is not constant.

The critical power concept in all-out isokinetic exercise.

UNLABELLED: The critical power concept has been applied to constant-load exhaustive exercise and recently validated for 3-min all-out exercise. OBJECTIVES: To test the application of critical power to a 3-min all-out isokinetic cycling exercise. DESIGN: Single-group, experimental, comparative design. METHOD: Nine participants performed a 3-min all-out isokinetic test and 4-5 constant-load exhaustive trials, at 60 and 100 rpm, on an electrically-braked cycle. The linear P-t-1 relationship was modelled using a 2-parameter model (slope: critical power; intercept: Anaerobic Work Capacity). End power and accumulated work done above EP were calculated from the 3-min tests. RESULTS: No significant difference and a significant correlation was found between end power and critical power (60 rpm: 259 ± 40 W vs. 245 ± 38 W, P > 0.05; r = 0.85, P<0.01; 100 rpm: 227 ± 57 W vs. 212 ± 44 W, P > 0.05; r = 0.86, P<0.01). The Bias ± 95% limits of agreement were 14 ± 42 W at 60 rpm and 15 ± 57 W at 100 rpm. Work done above EP (60 rpm: 14.7 ± 3.0 kJ; 100 rpm: 17.3 ± 3.1 kJ) was not significantly different to the anaerobic work capacity (60 rpm: 16.2 ± 3.2 kJ; 100 rpm: 20.6 ± 6.4 kJ; P>0.05) but with only a significant correlation at 60 rpm (r = -0.71, P<0.05). CONCLUSIONS: The 2-parameter model underpinning the critical power construct can be applied to a 3-min all-out isokinetic test. End power does not differ and correlates with critical power. However, a further insight into levels of agreement leads to some scepticism concerning the use of the two variables interchangeably. The great intra-subject differences between work done above EP and the intercept of the P-t-1 relationship should also be considered.

Test-retest reliability of a 3-min isokinetic all-out test using two different cadences.

OBJECTIVES: To investigate the test-retest reliability of mechanical parameters derived from a 3-min isokinetic all-out test, performed at 60 and 100 rpm. Reliability and validity of the peak oxygen uptake derived from 3-min isokinetic all-out test were also tested. DESIGN: 14 healthy male subjects completed an incremental ramp testing and four randomized 3-min isokinetic all-out test (two at 60 rpm and two at 100 rpm). METHODS: The absolute and relative reliability of the following parameters were analyzed: peak power, mean power, end power, fatigue index, work performed above end power and peak oxygen uptake. RESULTS: No difference was found between each two sets of data, although there were between-cadence differences for peak power, mean power, end power, and fatigue index. Higher intra-class correlation (ICC) and lower coefficient of variation (CV) were found for end power (ICC = 0.91 and 0.95; CV = 5.6 and 5.7%) and mean power (ICC = 0.97 and 0.98; CV = 2.4 and 3.1%), than for peak power (ICC = 0.81 and 0.84; CV = 8.7 and 10%) and work performed above end power (ICC = 0.79 and 0.84; CV = 7.9 and 10.6%; values reported for 60 rpm and 100 rpm, respectively). High reliability scores were also observed for peak oxygen uptake at both cadences (60 rpm, CV = 3.2%; 100 rpm, CV = 2.3%,) with no difference with the incremental ramp testing peak oxygen uptake. CONCLUSIONS: The power profile and peak oxygen uptake of a 3-min isokinetic all-out test are both highly reliable, whether the test is performed at 60 or 100 rpm. Besides, peak oxygen uptake and work performed above end power were not affected by the change in cadence while peak power, mean power, end power, and fatigue index were.