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# Power Output Manipulation from Below to Above the Gas Exchange Threshold Results in Exacerbated Performance Fatigability

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## Abstract

Introduction: Performance fatigability is substantially greater when exercising in the severe versus heavy intensity domain. However, the relevance of the boundary between moderate and heavy intensity exercise, the gas exchange threshold (GET), to performance fatigability is unclear. This study compared alterations in neuromuscular function during work-matched exercise above and below the GET. Methods: Seventeen male participants completed work-matched cycling for 90, 110 and 140 min at 110, 90 and 70% of the GET, respectively. Knee extensor isometric maximal voluntary contraction (MVC), high-frequency doublets (Db100) low- to high-frequency doublet ratio (Db10:100) and voluntary activation (VA) were measured at baseline, 25, 50, 75 and 100% of task-completion. During the initial, baseline visit, and following each constant work rate bout, ramp-incremental exercise was performed, and peak power output and oxygen uptake (V̇O2peak) were determined. Results: Following the 70% and 90% GET trials, similar reductions in MVC (-14 ± 6% and - 14 ± 8%, respectively, p = 0.175) and Db100 (-7 ± 9% and - 6 ± 9%, respectively, p = 0.431) were observed. However, for a given amount of work completed, reductions in MVC (-25 ± 15%, p = 0.008) and Db100 (-12 ± 8%, p = 0.029) were up to 2.6-fold greater during the 110% than 90% GET trial. Peak power output and V̇O2peak during ramp-incremental exercise were reduced by 7.0 ± 11.3% and 6.5 ± 9.3%, respectively, following the 110% GET trial relative to the baseline ramp (p ≤ 0.015), with no changes following the moderate intensity trials (p ≥ 0.078). Conclusions: The lack of difference in fatigability between the trials at 70% and 90% GET, coupled with the greater fatigability at 110% relative to 90% GET, shows that exceeding the moderate-heavy intensity boundary has implications for performance fatigability, whilst also impairing maximal exercise performance capacity.

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We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.
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Introduction Running and cycling represent two of the most common forms of endurance exercise. However, a direct comparison of the neuromuscular consequences of these two modalities after prolonged exercise has never been made. The aim of this study was to compare the alterations in neuromuscular function induced by matched intensity and duration cycling and running exercises. Methods During separate visits, 17 endurance-trained male participants performed 3 h of cycling and running at 105% of the gas exchange threshold. Neuromuscular assessments were taken are pre-, mid- and post-exercise, including knee extensor maximal voluntary contractions (MVC), voluntary activation (VA), high- and low-frequency doublets (Db100 and Db10, respectively), potentiated twitches (Qtw,pot), motor evoked potentials (MEP) and thoracic motor evoked potentials (TMEPs). Results Following exercise, MVC was similarly reduced by ~25% following both running and cycling. However, reductions in VA were greater following running (−16 ± 10%) than cycling (−10 ± 5%; p < 0.05). Similarly, reductions in TMEP were greater following running (−78 ± 24%) than cycling (15 ± 60%; p = 0.01). In contrast, reductions in Db100 (running: −6 ± 21% vs. cycling: −13 ± 6%) and Db10:100 (running: −6 ± 16% vs. cycling: −19 ± 13%) were greater for cycling than running (p ≤ 0.04). Conclusions Despite similar decrements in the knee extensor MVC following running and cycling, the mechanisms responsible for force loss differed. Running-based endurance exercise is associated with greater impairments in nervous system function, particularly at the spinal level, while cycling-based exercise elicits greater impairments in contractile function. Differences in the mechanical and metabolic demands imposed on the quadriceps could explain the disparate mechanisms of neuromuscular impairment following these two exercise modalities.
Article
Aim If the development of the oxygen uptake slow component (V̇O2SC) and muscle fatigue are related, these variables should remain coupled in a time- and intensity-dependent manner. Methods Sixteen participants (7 females) visited the laboratory on seven separate occasions: 1) three 6-min moderate-intensity cycling exercise bouts proceeded by a ramp incremental test; 2-3) 30-min constant power output (PO) exercise bout to determine the maximal lactate steady state (MLSS); 4-7) constant-PO exercise bouts to task failure (TTF), pseudorandomized order, at (i) 15% below the PO at MLSS; (ii) 10 W below MLSS; (iii) MLSS; and (iv) 10 W above MLSS (first intensity and randomized order thereafter). Neuromuscular fatigue was characterized by isometric maximal voluntary contractions and femoral nerve electrical stimulation of knee extensors to measure peripheral fatigue at baseline, at min 5, 10, 20, 30, and TTF. Pulmonary oxygen uptake (V̇O2) was continuously recorded during the constant-PO bouts and V̇O2SC was characterized based on each individual V̇O2 kinetics during moderate transitions. Results The development of V̇O2SC and peripheral fatigue were correlated across time (r²adj range of 0.64-0.80) and amongst each exercise intensity (r²adj range of 0.26-0.30) (all p < 0.001). Also, TTF was correlated with V̇O2SC and neuromuscular fatigue parameters (r²adj range of 0.52-0.82, all p < 0.001). Conclusion The V̇O2SC and peripheral fatigue development are correlated throughout the exercise in a time- and intensity-dependent manner, suggesting that the V̇O2SC may depend on muscle fatigue even if the mechanisms of reduced contractile function are different amongst intensities.
Article
Purpose: This study aimed to compare the concordance between CP and MLSS estimated by various models and criteria and their agreement with MMSS. Methods: After a ramp test, 10 recreationally active males performed four to five severe-intensity constant-power output (PO) trials to estimate CP and three to four constant-PO trials to determine MLSS and identify MMSS. CP was computed using the three-parameter hyperbolic (CP3-hyp), two-parameter hyperbolic (CP2-hyp), linear (CPlin), and inverse of time (CP1/Tlim) models. In addition, the model with the lowest combined parameter error identified the "best-fit" CP (CPbest-fit). MLSS was determined as an increase in blood lactate concentration ≤1 mM during constant-PO cycling from the 5th (MLSS5-30), 10th (MLSS10-30), 15th (MLSS15-30), 20th (MLSS20-30), or 25th (MLSS25-30) to 30th minute. MMSS was identified as the greatest PO associated with the highest submaximal steady-state V˙O2 (MV˙O2ss). Results: Concordance between the various CP and MLSS estimates was greatest when MLSS was identified as MLSS15-30, MLSS20-30, and MLSS25-30. The PO at MV˙O2ss was 243 ± 43 W. Of the various CP models and MLSS criteria, CP2-hyp (244 ± 46 W) and CPlin (248 ± 46 W) and MLSS15-30 and MLSS20-30 (both 245 ± 46 W), respectively, displayed, on average, the greatest agreement with MV˙O2ss. Nevertheless, all CP models and MLSS criteria demonstrated some degree of inaccuracies with respect to MV˙O2ss. Conclusions: Differences between CP and MLSS can be reconciled with optimal methods of determination. When estimating MMSS, from CP the error margin of the model estimate should be considered. For MLSS, MLSS15-30 and MLSS20-30 demonstrated the highest degree of accuracy.
Article
We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a "critical threshold" of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 "slow component" and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits.
Article
Neuromuscular fatigue (NMF) and exercise performance are affected by exercise intensity and sex differences. However, whether slight changes in power output (PO) below and above the maximal lactate steady-state (MLSS) impact NMF and subsequent performance (time to exhaustion, TTE) is unknown. Purpose: This study compared NMF and TTE in females and males in response to exercise performed at MLSS, 10 W below (MLSS-10) and above (MLSS+10). Methods: Twenty participants (9 females) performed three 30-min constant-PO exercise bouts followed (1 min delay) by a TTE at 80% of the peak-PO. NMF was characterized by isometric maximal voluntary contractions (IMVC) and femoral nerve electrical stimulation of knee extensors [e.g. peak torque of potentiated high-frequency (Db100) and single twitch (TwPt)] before and immediately after the constant-PO and TTE bouts. Results: IMVC declined less after MLSS-10 (-18±10%) compared to MLSS (-26±14%) and MLSS+10 (-31±11%) (all p<0.05), and the Db100 decline was greater after MLSS+10 (-24±14%) compared to the other intensities (MLSS-10: -15±9%; MLSS: -18±11%) (all p<0.05). Females showed smaller reductions in IMVC and TwPt compared to males after constant-PO bouts (all p<0.05), this difference being not dependant on intensity. TTE was negatively impacted by increasing the PO in the constant-PO (p<0.001), with no differences in end-exercise NMF (p>0.05). Conclusion: Slight changes in PO around MLSS elicited great changes in the reduction of maximal voluntary force and impairments in contractile function. Although NMF was lower in females compared to males, the changes in PO around the MLSS impacted both sexes similarly.
Article
Prior constant-load exercise performed for 30-min at or above maximal lactate steady state (MLSS p ) significantly impairs subsequent time-to-task failure (TTF) compared with TTF performed without prior exercise. We tested the hypothesis that TTF would decrease in relation to the intensity and the duration of prior exercise compared with a baseline TTF trial. Eleven individuals (6 males, 5 females, aged 28 ± 8 yrs) completed the following tests on a cycle ergometer (randomly assigned after MLSS p was determined): (i) a ramp-incremental test; (ii) a baseline TTF trial performed at 80% of peak power (TTF b ); (iii) five 30-min constant-PO rides at 5% below lactate threshold (LT −5% ), halfway between LT and MLSS p (Delta 50 ), 5% below MLSS p (MLSS −5% ), MLSS p , and 5% above MLSS p (MLSS +5% ); and (iv) 15- and 45-min rides at MLSS p (MLSS 15 and MLSS 45 , respectively). Each condition was immediately followed by a TTF trial at 80% of peak power. Compared with TTF b (330 ± 52 s), there was 8.0 ± 24.1, 23.6 ± 20.2, 41.0 ± 14.8, 52.2 ± 18.9, and 75.4 ± 7.4% reduction in TTF following LT −5% , Delta 50 , MLSS −5% , MLSS p , and MLSS +5% , respectively. Following MLSS 15 and MLSS 45 there were 29.0 ± 20.1 and 69.4 ± 19.6% reductions in TTF, respectively (P < 0.05). It is concluded that TTF is reduced following prior exercise of varying duration at MLSS p and at submaximal intensities below MLSS. Novelty: Prior constant-PO exercise, performed at intensities below MLSS p , reduces subsequent TTF performance. Subsequent TTF performance is reduced in a linear fashion following an increase in the duration of constant-PO exercise at MLSS p.
Article
During exhaustive ramp-incremental cycling tests, the incidence of O 2 uptake (V̇O 2 ) plateaus is low. To verify the attainment of maximum V̇O 2 (V̇O 2max ), it is recommended that a trial at a power output (PO) corresponding to 110% of the ramp-derived peak (PO peak ) is performed. It remains unclear whether verification trials set at this PO can be tolerated for long enough to allow attainment of V̇O 2max . Eleven recreationally-trained individuals performed five ramp tests of varying slope (5, 10, 15, 25, 30 W·min ⁻¹ ), each followed, in series, by two verification trials: the 1 st at 110%PO peak of the 25 W·min ⁻¹ ramp and the 2 nd at 110% PO peak attained in the preceding ramp test. Exercise duration of the 1 st verification trial was on average 81±15 s (CV=9±3%) versus 162±32, 121±24, 103±15, and 73±10 s for the 2 nd verification trials at 110% of PO peak of the 5, 10, 15, and 30 W·min ⁻¹ ramp tests, respectively (P<0.05). Compared to the highest V̇O 2 recorded during ramp tests, V̇O 2 from the subsequent verification trials were not different for the 5, 10, and 15 W·min ⁻¹ ramp tests (P>0.05), but lower for the 25 and 30 W·min ⁻¹ ramp tests (P<0.05). Verification trials at 110%PO peak of rapidly-incrementing ramp tests (i.e., 25 W·min ⁻¹ ) were not sustained for long enough to allow the attainment of V̇O 2max . With commonly used rapidly-incrementing ramp tests engendering exhaustion within 8-12 min, verification trials <PO peak should be preferred as they can be sustained sufficiently long to allow the attainment of V̇O 2max .
Article
PurposeThe consequences of the assumption that the additional ATP usage, underlying the slow component of oxygen consumption ($$\dot{\text{V}}\text{O}_{2}$$) and metabolite on-kinetics, starts when cytosolic inorganic phosphate (Pi) exceeds a certain “critical” Pi concentration, and muscle work terminates because of fatigue when Pi exceeds a certain, higher, “peak” Pi concentration are investigated.MethodsA previously developed computer model of the myocyte bioenergetic system is used.ResultsSimulated time courses of muscle $$\dot{\text{V}}\text{O}_{2}$$, cytosolic ADP, pH, PCr and Pi at various ATP usage activities agreed well with experimental data. Computer simulations resulted in a hyperbolic power–duration relationship, with critical power (CP) as an asymptote. CP was increased, and phase II $$\dot{\text{V}}\text{O}_{2}$$ on-kinetics was accelerated, by progressive increase in oxygen tension (hyperoxia).Conclusions Pi is a major factor responsible for the slow component of the $$\dot{\text{V}}\text{O}_{2}$$ and metabolite on-kinetics, fatigue-related muscle work termination and hyperbolic power–duration relationship. The successful generation of experimental system properties suggests that the additional ATP usage, underlying the slow component, indeed starts when cytosolic Pi exceeds a “critical” Pi concentration, and muscle work terminates when Pi exceeds a “peak” Pi concentration. The contribution of other factors, such as cytosolic acidification, or glycogen depletion and central fatigue should not be excluded. Thus, a detailed quantitative unifying mechanism underlying various phenomena related to skeletal muscle fatigue and exercise tolerance is offered that was absent in the literature. This mechanism is driven by reciprocal stimulation of Pi increase and additional ATP usage when “critical” Pi is exceeded.
Article
We tested the hypotheses that the parameters of the power-duration relationship, estimated as the end-test power (EP) and work done above EP (WEP) during a 3-min all out exercise test (3MT), would be reduced progressively following 40 min, 80 min and 2 h of heavy-intensity cycling, and that carbohydrate (CHO) ingestion would attenuate the reduction in EP and WEP. Sixteen participants completed a 3MT without prior exercise (control), immediately after 40 min, 80 min and 2-h of heavy-intensity exercise while consuming a placebo beverage, and also after 2-h of heavy-intensity exercise while consuming a CHO supplement (60 g/h CHO). There was no difference in EP measured without prior exercise (260 ± 37 W) compared to EP following 40 min (268 ± 39 W) or 80 min (260 ± 40 W) of heavy-intensity exercise; however, after 2-h, EP was 9% lower compared to control (236 ± 47 W; P<0.05). There was no difference in WEP measured without prior exercise (17.9 ± 3.3 kJ) compared to after 40 min of heavy-intensity exercise (16.1 ± 3.3 kJ), but WEP was lower ( P<0.05) than control after 80 min (14.7 ± 2.9 kJ) and 2-h (13.8 ± 2.7 kJ). Compared to placebo, CHO ingestion negated the reduction of EP following 2-h of heavy-intensity exercise (254 ± 49 W) but had no effect on WEP (13.5 ± 3.4 kJ). These results reveal a different time course for the deterioration of EP and WEP during prolonged endurance exercise and indicate that EP is sensitive to CHO availability.
Article
HIGHLIGHTS: 1) The reliance on anaerobic metabolism causes fatigue during high-intensity exercise. 2) Metabolic pathways maintain ATP at levels that do not impair contractile function. 3) Intracellular homeostasis is disrupted by metabolite accumulation, namely H+ and Pi. 4) Multifaceted and synergistic effects of H+ and Pi markedly impair muscle contraction. 5) Fatigue has a bioenergetic basis determined by the rate and extent of metabolite accumulation. ABSTRACT: Energetic demand from high-intensity exercise can easily exceed ATP synthesis rates of mitochondria leading to a reliance on anaerobic metabolism. The reliance on anaerobic metabolism results in the accumulation of intracellular metabolites, namely inorganic phosphate (Pi) and hydrogen (H+), that are closely associated with exercise-induced reductions in power. Cellular and molecular studies have revealed several steps where these metabolites impair contractile function demonstrating a causal role in fatigue. Elevated Pi or H+ directly inhibits force and power of the cross-bridge and decreases myofibrillar Ca2+ sensitivity, whereas Pi also inhibits Ca2+ release from the sarcoplasmic reticulum (SR). When both metabolites are elevated, they act synergistically to cause marked reductions in power, indicating that fatigue during high-intensity exercise has a bioenergetic basis.
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Article
During ramp-incremental exercise, the mean response time (MRT) of oxygen uptake (V˙O2) represents the time delay for changes in muscle V˙O2 to be reflected at the level of the mouth and is generally calculated by linear (MRTLIN) and monoexponential (τ') fitting of V˙O2 data. However, these methods yield MRT values that are highly variable from test-to-test. Purpose: Therefore, we examined the validity and the reproducibility of a novel method to calculate the MRT. Methods: On two occasions, 12 healthy men (age, 30 ± 10 yr; V˙O2max: 4.14 ± 0.47 L·min, 53.5 ± 7.3 mL·kg·min) performed a ramp-incremental cycling test (30 W·min) that was preceded by a step transition to 100 W. The ramp power output corresponding to the steady-state V˙O2 at 100 W was determined and the difference between that power output and 100 W was converted to time to quantify the MRT (MRTSS). Results: The values of MRTLIN, τ', and MRTSS were 28 ± 16 s, 27 ± 12 s, and 26 ± 11 s, respectively, which were not different (P > 0.05) from each other. However, compared to the MRT parameters derived from the fitting-based methods, MRTSS had a higher correlation coefficient (R = 0.87) and a smaller coefficient of variation (15% ± 9%) from test-to-test. Conclusions: In conclusion, the novel method proposed in the current study was found to be valid and highly reproducible in a test-retest design. Therefore, we advocate the use of this approach when a precise and accurate determination of the MRT is needed to properly align the V˙O2 data with power output during ramp-incremental exercise.
Article
During fatiguing voluntary contractions, the excitability of motoneurons innervating arm muscles decreases. However, the behavior of motoneurons innervating quadriceps muscles is unclear. Findings may be inconsistent because descending cortical input influences motoneuron excitability and confounds measures during exercise. To overcome this limitation, we examined effects of fatigue on quadriceps motoneuron excitability tested during brief pauses in descending cortical drive after transcranial magnetic stimulation (TMS). Participants (n=14) performed brief (~5 s) isometric knee extension contractions before and after a 10-min sustained contraction at ~25% maximal EMG of vastus medialis (VM) on one (n=5) or two days (n=9). Electrical stimulation over thoracic spine elicited thoracic motor evoked potentials (TMEP) in quadriceps muscles during ongoing voluntary drive and 100ms into the silent period following TMS (TMS-TMEP). Femoral nerve stimulation elicited maximal M-waves (Mmax). On the two days, either large (~50% Mmax) or small (~15% Mmax) TMS-TMEPs were elicited. During the 10-min contraction, VM EMG was maintained (P=0.39) whereas force decreased by 52% (SD 13%) (P<0.001). TMEP area remained unchanged (P=0.9), whereas large TMS-TMEPs decreased by 49% (SD 28%) (P=0.001) and small TMS-TMEPs by 71% (SD 22%) (P<0.001). This decline was greater for small TMS-TMEPs (P=0.019; n=9). Therefore, without the influence of descending drive, quadriceps TMS-TMEPs decreased during fatigue. The greater reduction for smaller responses, which tested motoneurons that were most active during the contraction suggests a mechanism related to repetitive activity contributes to reduced quadriceps motoneuron excitability during fatigue. By contrast, the unchanged TMEP suggests that ongoing drive compensates for altered motoneuron excitability.
Article
Purpose: When assessing neuromuscular fatigue (NMF) from dynamic exercise using large muscle mass (e.g. cycling), most studies have delayed measurement for 1-3 min after task failure. This study aimed to determine the reliability of an innovative cycling ergometer permitting the start of fatigue measurement within 1 s after cycling. Methods: Twelve subjects participated in two experimental sessions. Knee-extensor NMF was assessed by electrical nerve and transcranial magnetic stimulation with both a traditional chair set-up (PRE and POST-Chair, 2 min post-exercise) and the new cycling ergometer (PRE, every 3 min during incremental exercise and POST-Bike, at task failure). Results: The reduction in maximal voluntary contraction (MVC) force POST-Bike (63 +/- 12% PRE; P < 0.001) was not different between sessions and there was excellent reliability at PRE (ICC = 0.97; CV = 3.2%) and POST-Bike. Twitch (Tw) and high-frequency paired-pulse (Db100) forces decreased to 53 +/- 14 and 62 +/- 9% PRE, respectively (P < 0.001). Both were reliable at PRE (Tw: ICC = 0.97, CV = 5.2%; Db100: ICC = 0.90, CV = 7.3%) and POST-Bike (Tw: ICC = 0.88, CV = 11.9%; Db100: ICC = 0.62, CV = 9.0%). Voluntary activation did not change during the cycling protocol (P > 0.05). Vastus lateralis and rectus femoris M-wave and motor-evoked potential areas showed fair to excellent reliability (ICC = 0.45 to 0.88). The reduction in MVC and Db100 was greater on the cycling ergometer than the isometric chair. Conclusion: The innovative cycling ergometer is a reliable tool to assess NMF during and immediately post-exercise. This will allow fatigue etiology during dynamic exercise with large muscle mass to be revisited in various populations and environmental conditions. (C) 2017 American College of Sports Medicine
Article
Lactate or gas exchange threshold (GET) and critical power (CP) are closely associated with human exercise performance. We tested the hypothesis that the limit of tolerance (Tlim) during cycle exercise performed within the exercise intensity domains demarcated by GET and CP is linked to discrete muscle metabolic and neuromuscular responses. Eleven men performed a ramp incremental exercise test, 4–5 severe-intensity (SEV; >CP) constant-work-rate (CWR) tests until Tlim, a heavy-intensity (HVY; GET) CWR test until Tlim, and a moderate-intensity (MOD; <GET) CWR test until Tlim. Muscle biopsies revealed that a similar (P > 0.05) muscle metabolic milieu (i.e., low pH and [PCr] and high [lactate]) was attained at Tlim (approximately 2–14 min) for all SEV exercise bouts. The muscle metabolic perturbation was greater at Tlim following SEV compared with HVY, and also following SEV and HVY compared with MOD (all P < 0.05). The normalized M-wave amplitude for the vastus lateralis (VL) muscle decreased to a similar extent following SEV (−38 ± 15%), HVY (−68 ± 24%), and MOD (−53 ± 29%), (P > 0.05). Neural drive to the VL increased during SEV (4 ± 4%; P < 0.05) but did not change during HVY or MOD (P > 0.05). During SEV and HVY, but not MOD, the rates of change in M-wave amplitude and neural drive were correlated with changes in muscle metabolic ([PCr], [lactate]) and blood ionic/acid-base status ([lactate], [K⁺]) (P < 0.05). The results of this study indicate that the metabolic and neuromuscular determinants of fatigue development differ according to the intensity domain in which the exercise is performed. NEW & NOTEWORTHY The gas exchange threshold and the critical power demarcate discrete exercise intensity domains. For the first time, we show that the limit of tolerance during whole-body exercise within these domains is characterized by distinct metabolic and neuromuscular responses. Fatigue development during exercise greater than critical power is associated with the attainment of consistent “limiting” values of muscle metabolites, whereas substrate availability and limitations to muscle activation may constrain performance at lower intensities.
Article
Muscle fatigue can result from either the accumulation of metabolic by-products (e.g. Pi and H+) or a decrease in myoplasmic Ca++, however individually neither change can quantitatively explain the decrease in force capacity. Therefore, the emerging view is that, by decreasing the sensitivity of myofilaments to calcium, Pi and H+ act synergistically with decreased Ca++ levels to contribute to fatigue. SUMMARY: Skeletal muscle fatigue resulting from intense contractile activity is caused, in large part, by the synergistic action of increased metabolic by-products and reduced myoplasmic calcium.
Article
During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O2 uptake (V̇O2p) features a developing slow component (V̇O2pSC). This progressive increase in O2 cost of exercise is suggested to be related to the effects of muscle fatigue development. We hypothesized that peripheral muscle fatigue, as assessed by contractile impairment, would be associated with the V̇O2pSC Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ~∆60 (very heavy, VH) where ∆ is 60% of the difference between LT and peak V̇O2p The VH exercise was completed for each of 3, 8, 13, and 18min (i.e., VH3, VH8, VH13, VH18) with each preceded by 3min of 20W. Peripheral muscle fatigue was assessed via pre- vs post-exercise measurements of quadriceps torque in response to brief trains of electrical stimulation delivered at low (10Hz) and high (50Hz) frequencies. During exercise, breath-by-breath V̇O2p was measured by mass spectrometry and volume turbine. The magnitude of the V̇O2pSC increased (p<0.05) from 244±81mL·min(-1) at VH3 to 520±119mL·min(-1), 625±134mL·min(-1), and 678±156mL·min(-1) at VH8, VH13, and VH18, respectively. The ratio of the low-to-high frequency (10/50Hz) response was reduced (p<0.05) at VH3 (-12±9%) and further reduced (p<0.05) at VH8 (-25±11%), VH13 (-42±19%) and VH18 (-46±16%); mirroring the temporal pattern of V̇O2pSC development. The reduction in 10/50 Hz ratio was correlated (p<0.001, r=-0.65) with V̇O2pSC amplitude.The temporal and quantitative association of decrements in muscle torque production and the V̇O2pSC suggest a common physiological mechanism between skeletal muscle fatigue and the loss of muscle efficiency.
Article
A computer model of skeletal muscle bioenergetic system is used to study the background of the slow component of the V'O2 on-kinetics in skeletal muscle. Two possible mechanisms are analyzed: inhibition of ATP production by anaerobic glycolysis by progressive cytosol acidification (together with a slow decrease in ATP supply by creatine kinase) and gradual increase of ATP usage during exercise of constant power output. It is demonstrated that the former novel mechanism is potent to generate the slow component. The latter mechanism further increases the size of the slow component. It also moderately decreases metabolite stability and has small impact on muscle pH. An increase in anaerobic glycolysis intensity increases the slow component, elevates cytosol acidification during exercise and decreases PCr and Pi stability, although slightly increases ADP stability. A decrease in the P/O ratio during exercise cannot be also excluded as a relevant mechanism, although this issue requires further study. It is postulated that both the progressive inhibition of anaerobic glycolysis by accumulating protons (together with a slow decrease of the net creatine kinase reaction rate) and gradual increase of ATP usage during exercise, and perhaps decrease in P/O, contribute to the generation of the slow component of the V'O2 on-kinetics in skeletal muscle. Copyright © 2015, Journal of Applied Physiology.
Article
During high-intensity submaximal exercise muscle fatigue and decreased efficiency are closely intertwined, and each contributes to exercise intolerance. Fatigue and muscle inefficiency share common mechanisms, e.g. decreased "metabolic stability", muscle metabolite accumulation, decreased free energy of ATP breakdown, limited O2 or substrate availability, increased glycolysis, pH disturbance, increased muscle temperature, ROS production, and altered motor unit recruitment patterns.SUMMARYDuring high-intensity submaximal exercise muscle fatigue and a decreased efficiency of contractions are strictly intertwined, and share several common mechanisms.
Article
Exercise represents a major challenge to whole-body homeostasis provoking widespread perturbations in numerous cells, tissues, and organs that are caused by or are a response to the increased metabolic activity of contracting skeletal muscles. To meet this challenge, multiple integrated and often redundant responses operate to blunt the homeostatic threats generated by exercise-induced increases in muscle energy and oxygen demand. The application of molecular techniques to exercise biology has provided greater understanding of the multiplicity and complexity of cellular networks involved in exercise responses, and recent discoveries offer perspectives on the mechanisms by which muscle "communicates" with other organs and mediates the beneficial effects of exercise on health and performance.
Article
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.
Article
During fatigue caused by a sustained maximal voluntary contraction (MVC), motoneurones become markedly less responsive when tested during the silent period following transcranial magnetic stimulation (TMS). To determine whether this reduction depends on the repetitive activation of the motoneurones, responses to TMS (motor evoked potentials, MEPs) and to cervicomedullary stimulation (cervicomedullary motor evoked potentials, CMEPs) were tested during a sustained submaximal contraction at a constant level of electromyographic activity (EMG). In such a contraction, some motoneurones are repetitively activated whereas others are not active. On four visits, eight subjects performed a 10 min maintained-EMG elbow flexor contraction of 25% maximum. Test stimuli were delivered with and without conditioning by TMS given 100 ms prior. Test responses were MEPs or CMEPs (two visits each, small responses evoked by weak stimuli on one visit and large responses on the other). During the sustained contraction, unconditioned CMEPs decreased ∼20% whereas conditioned CMEPs decreased ∼75 and 30% with weak and strong stimuli, respectively. Conditioned MEPs were reduced to the same extent as CMEPs of the same size. The data reveal a novel decrease in motoneurone excitability during a submaximal contraction if EMG is maintained. Further, the much greater reduction of conditioned than unconditioned CMEPs shows the critical influence of voluntary drive on motoneurone responsiveness. Strong test stimuli attenuate the reduction of conditioned CMEPs which indicates that low-threshold motoneurones active in the contraction are most affected. The equivalent reduction of conditioned MEPs and CMEPs suggests that, similar to findings with a sustained MVC, impaired motoneurone responsiveness rather than intracortical inhibition is responsible for the fatigue-related impairment of the MEP during a sustained submaximal contraction.
Article
During constant work rate (CWR) exercise above the lactate threshold (LT), the exponential kinetics of oxygen uptake ((V) over dot(O2)) are supplemented by a (V) over dot(O2) slow component ((V) over dot(O2)) which reduces work efficiency. This has been hypothesised to result from 'fatigue and recruitment', where muscle fatigue during supra-LT exercise elicits recruitment of additional, but poorly efficient, fibres to maintain power production. To test this hypothesis we characterised changes in the power-velocity relationship during sub- and supra-LT cycle ergometry in concert with (V) over dot(O2) kinetics. Eight healthy participants completed a randomized series of 18 experiments consisting of: (1) a CWR phase of 3 or 8 min followed immediately by; (2) a 5 s maximal isokinetic effort to characterize peak power at 60, 90 and 120 rpm. CWR bouts were: 20 W (Con); 80% LT (Mod); 20% Delta (H); 60% Delta (VH); where Delta is the difference between the work rate at LT and (V) over dot(O2) (max). The (V) over dot(O2sc) was 238 +/- 128 and 686 +/- 194 ml min(-1) during H and VH, with no discernible (V) over dot(O2sc) during Mod. Peak power in Con was 1025 +/- 400, 1219 +/- 167 and 1298 +/- 233 W, at 60, 90 and 120 rpm, respectively, and was not different after Mod (P > 0.05). Velocity-specific peak power was significantly reduced (P < 0.05) by 3 min of H (-103 +/- 46 W) and VH (-216 +/- 60 W), with no further change by 8 min. The (V) over dot(O2sc) was correlated with the reduction in peak power (R-2 = 0.49; P < 0.05). These results suggest that muscle fatigue is requisite for the (V) over dot(O2). However, the maintenance of velocity-specific peak power between 3 and 8 min suggests that progressive muscle recruitment is not obligatory. Rather, a reduction in mechanical efficiency in fatigued fibres is implicated.
Article
It is well known that physiological variables such as maximal oxygen uptake (VO2max), exercise economy, the lactate threshold, and critical power are highly correlated with endurance exercise performance. In this review, we explore the basis for these relationships by explaining the influence of these ‘‘traditional’’ variables on the dynamic profiles of the VO2 response to exercise of different intensities, and how these differences in VO2 dynamics are related to exercise tolerance and fatigue. The existence of a ‘‘slow component’’ of VO2 during exercise above the lactate threshold reduces exercise efficiency and mandates a greater consumption of endogenous fuel stores (chiefly muscle glycogen) for muscle respiration. For higher exercise intensities (above critical power), steady states in blood acid-base status and pulmonary gas exchange are not attainable and VO2 will increase with time until VO2max is reached. Here, we show that it is the interaction of the VO2 slowcomponent, VO2max, and the ‘‘anaerobic capacity’’ that determines the exercise tolerance. Essentially, we take the view that an appreciation of the various exercise intensity ‘‘domains’’ and their characteristic effects on VO2 dynamics can be helpful in improving our understanding of the determinants of exercise tolerance and the limitations to endurance sports performance. The reciprocal effects of interventions such as training, prior exercise, and manipulations of muscle oxygen availability on aspects of VO2 kinetics and exercise tolerance are consistent with this view.
Article
Excess CO2 is generated when lactate is increased during exercise because its [H+] is buffered primarily by HCO-3 (22 ml for each meq of lactic acid). We developed a method to detect the anaerobic threshold (AT), using computerized regression analysis of the slopes of the CO2 uptake (VCO2) vs. O2 uptake (VO2) plot, which detects the beginning of the excess CO2 output generated from the buffering of [H+], termed the V-slope method. From incremental exercise tests on 10 subjects, the point of excess CO2 output (AT) predicted closely the lactate and HCO-3 thresholds. The mean gas exchange AT was found to correspond to a small increment of lactate above the mathematically defined lactate threshold [0.50 +/- 0.34 (SD) meq/l] and not to differ significantly from the estimated HCO-3 threshold. The mean VO2 at AT computed by the V-slope analysis did not differ significantly from the mean value determined by a panel of six experienced reviewers using traditional visual methods, but the AT could be more reliably determined by the V-slope method. The respiratory compensation point, detected separately by examining the minute ventilation vs. VCO2 plot, was consistently higher than the AT (2.51 +/- 0.42 vs. 1.83 +/- 0.30 l/min of VO2). This method for determining the AT has significant advantages over others that depend on regular breathing pattern and respiratory chemosensitivity.
Article
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.
Article
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.
Article
The on- and off-transient (i.e. phase II) responses of pulmonary oxygen uptake (V(O(2))) to moderate-intensity exercise (i.e. below the lactate threshold, theta;(L)) in humans has been shown to conform to both mono-exponentiality and 'on-off' symmetry, consistent with a system manifesting linear control dynamics. However above theta;(L) the V(O(2)) kinetics have been shown to be more complex: during high-intensity exercise neither mono-exponentiality nor 'on-off' symmetry have been shown to appropriately characterise the V(O(2)) response. Muscle [phosphocreatine] ([PCr]) responses to exercise, however, have been proposed to be dynamically linear with respect to work rate, and to demonstrate 'on-off' symmetry at all work intenisties. We were therefore interested in examining the kinetic characteristics of the V(O(2)) and [PCr] responses to moderate- and high-intensity knee-extensor exercise in order to improve our understanding of the factors involved in the putative phosphate-linked control of muscle oxygen consumption. We estimated the dynamics of intramuscular [PCr] simultaneously with those of V(O(2)) in nine healthy males who performed repeated bouts of both moderate- and high-intensity square-wave, knee-extension exercise for 6 min, inside a whole-body magnetic resonance spectroscopy (MRS) system. A transmit-receive surface coil placed under the right quadriceps muscle allowed estimation of intramuscular [PCr]; V(O(2)) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. For moderate exercise, the kinetics were well described by a simple mono-exponential function (following a short cardiodynamic phase for V(O(2))), with time constants (tau) averaging: tauV(O(2))(,on) 35 +/- 14 s (+/- S.D.), tau[PCr](on) 33 +/- 12 s, tauV(O(2))(,off) 50 +/- 13 s and tau[PCr](off) 51 +/- 13 s. The kinetics for both V(O(2)) and [PCr] were more complex for high-intensity exercise. The fundamental phase expressing average tau values of tauV(O(2))(,on) 39 +/- 4 s, tau[PCr](on) 38 +/- 11 s, tauV(O(2))(,off) 51 +/- 6 s and tau[PCr](off) 47 +/- 11 s. An associated slow component was expressed in the on-transient only for both V(O(2)) and [PCr], and averaged 15.3 +/- 5.4 and 13.9 +/- 9.1 % of the fundamental amplitudes for V(O(2)) and [PCr], respectively. In conclusion, the tau values of the fundamental component of [PCr] and V(O(2)) dynamics cohere to within 10 %, during both the on- and off-transients to a constant-load work rate of both moderate- and high-intensity exercise. On average, approximately 90 % of the magnitude of the V(O(2)) slow component during high-intensity exercise is reflected within the exercising muscle by its [PCr] response.