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Power Output Manipulation from Below to Above the Gas Exchange Threshold Results in Exacerbated Performance Fatigability
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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Introduction
Cancer-related fatigue (CRF) is a debilitating symptom that affects around one-third of people for months or years after cancer treatment. In a recent study, we found that people with post-treatment CRF have greater performance fatigability. The aim of this secondary analysis was to examine the aetiology of performance fatigability in people with post-treatment CRF.
Methods
Ninety-six people who had completed cancer treatment were dichotomized into two groups (fatigued and non-fatigued) based on a clinical cut-point for fatigue. Alterations in neuromuscular function (maximal voluntary contraction peak force, MVC; voluntary activation, VA; potentiated twitch force, Qtw,pot; electromyography, EMG) in the knee extensors were assessed across three common stages of an incremental cycling test. Power outputs during the fatigability test were expressed relative to gas exchange thresholds to assess relative exercise intensity.
Results
The fatigued group had a more pronounced reduction in MVC peak force and Qtw,pot throughout the common stages of the incremental cycling test (main effect of group: p < 0.001, ηp2 = 0.18 and p = 0.029, ηp2 = 0.06, respectively). Electromyography was higher during cycling in the fatigued group (main effect of group: p = 0.022, ηp2 = 0.07). Although the relative intensity of cycling was higher in the fatigued group at the final common stage of cycling, this was not the case during the initial two stages, despite the greater impairments in neuromuscular function.
Conclusions
Our results suggest that the rapid impairments in performance fatigability in people with CRF was primarily due to disturbances at the level of the muscle, rather than the central nervous system. This could impact the ability to tolerate daily physical activities.
This study focused on the steady-state phase of exercise to evaluate the relative contribution of metabolic instability (meas-ured with NIRS and haematochemical markers) and muscle activation (measured with EMG) to the oxygen consumption (V O 2) slow component (V O 2sc) in different intensity domains. We hypothesized that (i) after the transient phase, V O 2 , metabolic instability and muscle activation tend to increase differently over time depending on the relative exercise intensity and (ii) the increase in V O 2sc is explained by a combination of metabolic instability and muscle activation. Eight active men performed a constant work rate trial of 9 min in the moderate, heavy and severe intensity domains. V O 2 , root mean square by EMG (RMS), deoxyhaemoglobin by NIRS ([HHb]) and haematic markers of metabolic stability (i.e. [La − ], pH, HCO 3 −) were measured. The physiological responses in different intensity domains were compared by two-way RM-ANOVA. The relationships between the increases of [HHb] and RMS with V O 2 after the third min were compared by simple and multiple linear regressions. We found domain-dependent dynamics over time of V O 2 , [HHb], RMS and the haematic markers of metabolic instability. After the transient phase, the rises in [HHb] and RMS showed medium-high correlations with the rise in V O 2 ([HHb] r = 0.68, p < 0.001; RMS r = 0.59, p = 0.002). Moreover, the multiple linear regression showed that both metabolic instability and muscle activation concurred to the V O 2sc (r = 0.75, [HHb] p = 0.005, RMS p = 0.042) with metabolic instability possibly having about threefold the relative weight compared to recruitment. Seventy-five percent of the dynamics of the V O 2sc was explained by [HHb] and RMS.
Cervicomedullary stimulation provides a means of assessing motoneuron excitability. Previous studies demonstrated that during low-intensity sustained contractions, small cervicomedullary evoked potentials (CMEPs) conditioned using transcranial magnetic stimulation (TMS-CMEPs) are reduced, whilst large TMS-CMEPs are less affected. Since small TMS-CMEPs recruit motoneurons most active during low-intensity contractions while large TMS-CMEPs recruit a high proportion of motoneurons inactive during the task, these results suggest that reductions in motoneuron excitability could be dependent on repetitive activation. To further test this hypothesis, this study assessed changes in small and large TMS-CMEPs across low- and high-intensity contractions. Twelve participants performed a sustained isometric contraction of the elbow flexor for 4.5 min at the electromyography (EMG) level associated with 20% maximal voluntary contraction force (MVC; low-intensity) and 70% MVC (high-intensity). Small and large TMS-CMEPs with amplitudes of ~15 and ~50% M max at baseline, respectively, were delivered every minute throughout the tasks. Recovery measures were taken at 1, 2.5 and 4-min post-exercise. During the low-intensity trial, small TMS-CMEPs were reduced at 2-4 min (p≤0.049) by up to −10% M max , while large TMS-CMEPs remained unchanged (p≥0.16). During the high-intensity trial, small and large TMS-CMEPs were reduced at all time-points (p<0.01) by up to −14% and −33% M max , respectively, and remained below baseline during all recovery measures (p≤0.02). TMS-CMEPs were unchanged relative to baseline during recovery following the low-intensity trial (p≥0.24). These results provide novel insight into motoneuron excitability during and following sustained contractions at different intensities, and suggest that contraction-induced reductions in motoneuron excitability depend on repetitive activation.
Prolonged low‐frequency force depression (PLFFD) induced by fatiguing exercise is characterized by a persistent depression in submaximal contractile force during the recovery period. Muscle glycogen depletion is known to limit physical performance during prolonged low‐ and moderate‐intensity exercise, and accelerating glycogen re‐synthesis with post‐exercise carbohydrate intake can facilitate recovery and improve repeated bout exercise performance. Short‐term, high‐intensity exercise however, can cause PLFFD without any marked decrease in glycogen. Here we studied whether recovery from PLFFD was accelerated by carbohydrate ingestion after 60‐min of moderate‐intensity glycogen‐depleting cycling exercise followed by six 30‐s all‐out cycling sprints. We used a randomized cross‐over study design where nine recreationally‐active males drank a beverage containing either carbohydrate or placebo after exercise. Blood glucose and muscle glycogen concentrations were determined at baseline, immediately post‐exercise, and during the 3‐h recovery period. Transcutaneous electrical stimulation of the quadriceps muscle was performed to determine the extent of PLFFD by eliciting low‐frequency (20Hz) and high‐frequency (100Hz) stimulations. Muscle glycogen was severely depleted after exercise, with a significantly higher rate of muscle glycogen re‐synthesis during the 3‐h recovery period in the carbohydrate than in the placebo trials (13.7 and 5.4 mmol glucosyl units/kg wet weight/h, respectively). Torque at 20Hz was significantly more depressed than 100 Hz torque during the recovery period in both conditions, and the extent of PLFFD (20/100Hz ratio) was not different between the two trials. In conclusion, carbohydrate supplementation enhances glycogen re‐synthesis after glycogen‐depleting exercise but does not improve force recovery when the exercise also involves all‐out cycling sprints.
Purpose
Consequences of combining three ideas proposed previously by other authors: (1) that there exists a critical power (CP), above which no steady state in \(\dot{V}\)O2 (oxygen consumption) and metabolites can be achieved in voluntary constant-power exercise; (2) that muscle fatigue is related to decreased exercise efficiency (increased \(\dot{V}\)O2/power output ratio); and (3) that Pi (inorganic phosphate) is the main fatigue-related metabolite are investigated.
Methods
A previously-developed computer model of the skeletal muscle bioenergetic system is used. It was assumed in computer simulations that skeletal muscle work terminates when cytosolic Pi (inorganic phosphate) exceeds a certain critical level.
Results
Simulated changes in muscle \(\dot{V}\)O2, cytosolic ADP, pH, PCr and Pi as a function of time at various ATP usage activities (corresponding to power outputs) agreed well with experimental data. Computer simulations resulted in a fourth previously-published idea: (4) that the power–duration relationship describing the dependence of power output (PO) on the time to exhaustion of voluntary constant-power exercise at a given PO has a (near-)hyperbolic shape.
Conclusions
Pi is a major factor contributing to muscle fatigue, as such an assumption leads to a (near-)hyperbolic shape of the power–duration relationship, at least for exercise duration of ~ 1–10 min. Thus, a potential mechanism underlying the power–duration relationship shape is offered that was absent in the literature. Other factors/mechanisms, such as cytosol acidification, glycogen stores depletion and central fatigue can contribute to this relationship, especially in longer exercises.
The majority of studies have routinely measured neuromuscular (NM) fatigue with a delay (~1–3 min) after cycling exercises. This is problematic since NM fatigue can massively recover within the first 1-2 minutes after exercise. This study investigated the etiology of knee extensors (KE) NM fatigue and recovery kinetics in response to cycling exercises by assessing NM function as early as 10 s following cycling and up to 8 min of recovery. Ten young males performed different cycling exercises on different days: a Wingate (WING), a 10-min at severe-intensity (SEV), and a 90-min at moderate-intensity (MOD). Electrically evoked and isometric maximal voluntary contractions (IMVC) of KE were assessed before, after, and during recovery. SEV induced the highest decrease in IMVC. Peak twitch (Pt) was more reduced in WING and SEV than in MOD (p < 0.001), whereas voluntary activation (VA) decreased more after MOD than WING (p = 0.043). Regarding Pt and the ratio between low- and high-frequency doublet (i.e. low-frequency fatigue), recovery was faster for WING, whereas IMVC and high-frequency doublet recovered slower during MOD (P < 0.05). Our results confirm that peripheral fatigue is greater after WING and SEV, while central fatigue is greater following MOD. Peripheral fatigue can substantially recover within minutes after a supramaximal exercise while NM function recovered slower after prolonged, moderate-intensity exercise. This study provides an accurate estimation of NM fatigue and recovery kinetics due to dynamic exercise with large muscle mass by significantly shortening the delay for post-exercise measurements.
While fatigue can be defined as an exercise-related decrease in the maximal power or isometric force, most studies have assessed only isometric force. The main purpose of this experiment was to compare dynamic measures of fatigue [maximal torque (Tmax), maximal velocity (Vmax) and maximal power (Pmax)] with measures associated with maximal isometric force [isometric maximal voluntary contraction (IMVC) and maximal rate of force development (MRFD)] 10 s after different fatiguing exercises and during the recovery period (1-8 min after). Ten young men completed 6 experimental sessions (3 fatiguing exercises×2 types of fatigue measurements). The fatiguing exercises were: a 30-s all out (WING), 10-min at severe-intensity (SEV) and 90-min at moderate-intensity (MOD). Relative Pmax decreased more than IMVC after WING (p=0.005) while the opposite was found after SEV (p=0.005) and MOD tasks (p<0.001). There was no difference between the decrease in IMVC and Tmax after the WING, but IMVC decreased more than Tmax immediately following and during the recovery from the SEV (p=0.042) and MOD exercises (p<0.001). Depression of MRFD was greater than Vmax after all the fatiguing exercises and during recovery (all p<0.05). Despite the general definition of fatigue, isometric assessment of fatigue is not interchangeable with dynamic assessment following dynamic exercises with large muscle mass of different intensities, i.e. the results from isometric function cannot be used to estimate dynamic function and vice-versa. This implies different physiological mechanisms for the various measures of fatigue.
PurposeThis investigation examined the development of neuromuscular fatigue during a simulated soccer match incorporating a period of extra time (ET) and the reliability of these responses on repeated test occasions. Methods
Ten male amateur football players completed a 120 min soccer match simulation (SMS). Before, at half time (HT), full time (FT), and following a period of ET, twitch responses to supramaximal femoral nerve and transcranial magnetic stimulation (TMS) were obtained from the knee-extensors to measure neuromuscular fatigue. Within 7 days of the first SMS, a second 120 min SMS was performed by eight of the original ten participants to assess the reliability of the fatigue response. ResultsAt HT, FT, and ET, reductions in maximal voluntary force (MVC; −11, −20 and −27%, respectively, P ≤ 0.01), potentiated twitch force (−15, −23 and −23%, respectively, P < 0.05), voluntary activation (FT, −15 and ET, −18%, P ≤ 0.01), and voluntary activation measured with TMS (−11, −15 and −17%, respectively, P ≤ 0.01) were evident. The fatigue response was robust across both trials; the change in MVC at each time point demonstrated a good level of reliability (CV range 6–11%; ICC2,1 0.83–0.94), whilst the responses identified with motor nerve stimulation showed a moderate level of reliability (CV range 5–18%; ICC2,1 0.63–0.89) and the data obtained with motor cortex stimulation showed an excellent level of reliability (CV range 3–6%; ICC2,1 0.90–0.98). Conclusion
Simulated soccer exercise induces a significant level of fatigue, which is consistent on repeat tests, and involves both central and peripheral mechanisms.
The hyperbolic form of the power-duration relationship is rigorous and highly conserved across species, forms of exercise and individual muscles/muscle groups. For modalities such as cycling, the relationship resolves to two parameters, the asymptote for power (critical power, CP) and the so-called W' (work doable above CP), which together predict the tolerable duration of exercise above CP. Crucially, the CP concept integrates sentinel physiological profiles - respiratory, metabolic and contractile - within a coherent framework that has great scientific and practical utility. Rather than calibrating equivalent exercise intensities relative to metabolically distant parameters such as the lactate threshold or V˙O2 max, setting the exercise intensity relative to CP unifies the profile of systemic and intramuscular responses and, if greater than CP, predicts the tolerable duration of exercise until W' is expended, V˙O2 max is attained, and intolerance is manifested. CP may be regarded as a 'fatigue threshold' in the sense that it separates exercise intensity domains within which the physiological responses to exercise can (<CP) or cannot (>CP) be stabilized. The CP concept therefore enables important insights into 1) the principal loci of fatigue development (central vs. peripheral) at different intensities of exercise, and 2) mechanisms of cardiovascular and metabolic control and their modulation by factors such as O2 delivery. Practically, the CP concept has great potential application in optimizing athletic training programs and performance as well as improving the life quality for individuals enduring chronic disease.
Despite flourishing interest in the topic of fatigue-as indicated by the many presentations on fatigue at the 2015 annual meeting of the American College of Sports Medicine-surprisingly little is known about its impact on human performance. There are two main reasons for this dilemma: (1) the inability of current terminology to accommodate the scope of the conditions ascribed to fatigue, and (2) a paucity of validated experimental models. In contrast to current practice, a case is made for a unified definition of fatigue to facilitate its management in health and disease. Based on the classic two-domain concept of Mosso, fatigue is defined as a disabling symptom in which physical and cognitive function is limited by interactions between performance fatigability and perceived fatigability. As a symptom, fatigue can only be measured by self-report, quantified as either a trait characteristic or a state variable. One consequence of such a definition is that the word fatigue should not be preceded by an adjective (e.g., central, mental, muscle, peripheral, and supraspinal) to suggest the locus of the changes responsible for an observed level of fatigue. Rather, mechanistic studies should be performed with validated experimental models to identify the changes responsible for the reported fatigue. As indicated by three examples (walking endurance in old adults, time trials by endurance athletes, and fatigue in persons with multiple sclerosis) discussed in the review, however, it has proven challenging to develop valid experimental models of fatigue. The proposed framework provides a foundation to address the many gaps in knowledge of how laboratory measures of fatigue and fatigability impact real-world performance.
During constant power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2sc), reflecting reduced work efficiency predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W) To test this hypothesis, we measured intramuscular ATP turnover with 31P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension in healthy participants (n = 14). Unlocalised 31P spectra were collected from the quadriceps throughout using a dual-tuned (1H and 31P) surface coil with a simple pulse and acquire pulse sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD there was no discernable V̇O2sc (mean ± SD: 0.06 ± 0.12 L.min−1) or change in [PCr] (30 ± 8 vs. 32 ± 7 mM) or ATPtot (24 ± 14 vs. 17 ± 14 mM.min−1; each p = n.s.). During HVY the V̇O2sc was 0.37 ± 0.16 L.min−1 (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mM, or 12 ± 15%; p < 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mM.min−1, or 26 ± 30%; p < 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated to the V̇O2sc during HVY (r2 = 0.06; p = n.s.). This lack of relationship between ΔATPtot and the V̇O2sc, together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial (the O2 cost of ATP resynthesis; P/O) sources.This article is protected by copyright. All rights reserved
Purpose:
To examine the reliability and magnitude of change after fatiguing exercise in the countermovement-jump (CMJ) test and determine its suitability for the assessment of fatigue-induced changes in neuromuscular (NM) function. A secondary aim was to examine the usefulness of a set of alternative CMJ variables (CMJ-ALT) related to CMJ mechanics.
Methods:
Eleven male college-level team-sport athletes performed 6 CMJ trials on 6 occasions. A total of 22 variables, 16 typical (CMJ-TYP) and 6 CMJ-ALT, were examined. CMJ reproducibility (coefficient of variation; CV) was examined on participants' first 3 visits. The next 3 visits (at 0, 24, and 72 h postexercise) followed a fatiguing high-intensity intermittent-exercise running protocol. Meaningful differences in CMJ performance were examined through effect sizes (ES) and comparisons to interday CV.
Results:
Most CMJ variables exhibited intraday (n = 20) and interday (n = 21) CVs of <10%. ESs ranging from trivial to moderate were observed in 18 variables at 0 h (immediately postfatigue). Mean power, peak velocity, flight time, force at zero velocity, and area under the force-velocity trace showed changes greater than the CV in most individuals. At 24 h, most variables displayed trends toward a return to baseline. At 72 h, small increases were observed in time-related CMJ variables, with mean changes also greater than the CV.
Conclusions:
The CMJ test appears a suitable athlete-monitoring method for NM-fatigue detection. However, the current approach (ie, CMJ-TYP) may overlook a number of key fatigue-related changes, and so practitioners are advised to also adopt variables that reflect the NM strategy used.
Studies performed already in the beginning of the last century revealed the importance of carbohydrate as a fuel during exercise and the importance of muscle glycogen on performance has subsequently been confirmed in numerous studies. However, the link between glycogen depletion and impaired muscle function during fatigue is not well understood and a direct cause-and-effect relationship between glycogen and muscle function remains to be established. The use of electron microscopy has revealed that glycogen is not homogeneously distributed in skeletal muscle fibres, but rather localized in distinct pools. Further, each glycogen granule has its own metabolic machinery with glycolytic enzymes and regulating proteins. One pool of such glycogenolytic complexes is localized within the myofibrils in close contact with key proteins involved in the excitation-contraction coupling and Ca2+ release from the sarcoplasmic reticulum (SR). We and others have provided experimental evidence in favour of a direct role of decreased glycogen, localized within the myofibrils, for the reduction in SR Ca2+ release during fatigue. This is consistent with compartmentalized energy turnover and distinctly localized glycogen pools being of key importance for SR Ca2+ release and thereby affecting muscle contractility and fatigability.
Muscle fatigue is the decline in performance of muscles observed during periods of intense activity. ATP consumption exceeds production during intense activity and there are multiple changes in intracellular metabolites which may contribute to the changes in crossbridge activity. It is also well-established that a reduction in activation, either through action potential changes or reduction in Ca(2+) release from the sarcoplasmic reticulum (SR), makes an additional contribution to fatigue. In this review we focus on the role of intracellular inorganic phosphate (P(i)) whose concentration can increase rapidly from around 5-30 mM during intense fatigue. Studies from skinned muscle fibers show that these changes substantially impair myofibrillar performance although the effects are strongly temperature dependent. Increased P(i) can also cause reduced Ca(2+) release from the SR and may therefore contribute to the reduced activation. In a recent study, we have measured both P(i) and Ca(2+) release in a blood-perfused mammalian preparation and the results from this preparation allows us to test the extent to which the combined effects of P(i) and Ca(2+) changes may contribute to fatigue.
The use of electrical stimulation (ES) can contribute to our knowledge of how our neuromuscular system can adapt to physical stress or unloading. Although it has been recently challenged, the standard technique used to explore central modifications is the twitch interpolated method which consists in superimposing single twitches or high-frequency doublets on a maximal voluntary contraction (MVC) and to compare the superimposed response to the potentiated response obtained from the relaxed muscle. Alternative methods consist in (1) superimposing a train of stimuli (central activation ratio), (2) comparing the MVC response to the force evoked by a high-frequency tetanus or (3) examining the change in maximal EMG response during voluntary contractions, if this variable is normalized to the maximal M wave, i.e. EMG response to a single stimulus. ES is less used to examine supraspinal factors but it is useful for investigating changes at the spinal level, either by using H reflexes, F waves or cervicomedullary motor-evoked potentials. Peripheral changes can be examined with ES, usually by stimulating the muscle in the relaxed state. Neuromuscular propagation of action potentials on the sarcolemma (M wave, high-frequency fatigue), excitation-contraction coupling (e.g. low-frequency fatigue) and intrinsic force (high-frequency stimulation at supramaximal intensity) can all be used to non-invasively explore muscular function with ES. As for all indirect methods, there are limitations and these are discussed in this review. Finally, (1) ES as a method to measure respiratory muscle function and (2) the comparison between electrical and magnetic stimulation will also be considered.
The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.
Little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. The aim of the present study was to examine the effect of glycogen on sarcoplasmic reticulum (SR) function in the arm and leg muscles of elite cross-country skiers (n = 10, (V) over dot(O2 max) 72 +/- 2 ml kg(-1) min(-1)) before, immediately after, and 4 h and 22 h after a fatiguing 1 h ski race. During the first 4 h recovery, skiers received either water or carbohydrate (CHO) and thereafter all received CHO-enriched food. Immediately after the race, arm glycogen was reduced to 31 +/- 4% and SR Ca2+ release rate decreased to 85 +/- 2% of initial levels. Glycogen noticeably recovered after 4 h recovery with CHO (59 +/- 5% initial) and the SR Ca2+ release rate returned to pre-exercise levels. However, in the absence of CHO during the first 4 h recovery, glycogen and the SR Ca2+ release rate remained unchanged (29 +/- 2% and 77 +/- 8%, respectively), with both parameters becoming normal after the remaining 18 h recovery with CHO. Leg muscle glycogen decreased to a lesser extent (71 +/- 10% initial), with no effects on the SR Ca2+ release rate. Interestingly, transmission electron microscopy (TEM) analysis revealed that the specific pool of intramyofibrillar glycogen, representing 10-15% of total glycogen, was highly significantly correlated with the SR Ca2+ release rate. These observations strongly indicate that low glycogen and especially intramyofibrillar glycogen, as suggested by TEM, modulate the SR Ca2+ release rate in highly trained subjects. Thus, low glycogen during exercise may contribute to fatigue by causing a decreased SR Ca2+ release rate.
To analyse the slow component of oxygen uptake (VO2) in professional cyclists and to determine whether this phenomenon is due to altered neuromuscular activity, as assessed by surface electromyography (EMG).
The following variables were measured during 20 minute cycle ergometer tests performed at about 80% of VO2MAX in nine professional road cyclists (mean (SD) age 26 (2) years; VO2max 72.6 (2.2) ml/kg/min): heart rate (HR), gas exchange variables (VO2, ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen and carbon dioxide (VE/VO2 and VE/VCO2 respectively), respiratory exchange ratio (RER), and end tidal PO2 and PCO2 (PETO2 and PETCO2 respectively)), blood variables (lactate, pH, and [HCO3-]) and EMG data (root mean from square voltage (rms-EMG) and mean power frequency (MPF)) from the vastus lateralis muscle.
The mean magnitude of the slow component (from the end of the third minute to the end of exercise) was 130 (0.04) ml in 17 minutes or 7.6 ml/min. Significant increases from three minute to end of exercise values were found for the following variables: VO2 (p<0.01), HR (p<0.01), VE (p<0.05), fb (p<0.01), VE/VO2 (p<0.05), VE/VCO2 (p<0.01), PETO2 (p<0.05), and blood lactate (p<0.05). In contrast, rms-EMG and MPF showed no change (p>0.05) throughout the exercise tests.
A significant but small VO2 slow component was shown in professional cyclists during constant load heavy exercise. The results suggest that the primary origin of the slow component is not neuromuscular factors in these subjects, at least for exercise intensities up to 80% of VO2MAX.
The effects of prolonged cycling on neuromuscular parameters were studied in nine endurance-trained subjects during a 5-h exercise sustained at 55% of the maximal aerobic power. Torque during maximal voluntary contraction (MVC) of the quadriceps muscle decreased progressively throughout the exercise (P < 0.01) and was 18% less at the end of exercise compared with the preexercise value. Peak twitch torque, contraction time, and total area of mechanical response decreased significantly (P < 0.05) after the first hour of exercise. In contrast, changes in M-wave characteristics were significant only after the fourth hour of the exercise. Significant reductions (P < 0.05) in electromyographic activity normalized to the M wave occurred after the first hour for the vastus lateralis muscle but only at the end of the exercise for the vastus medialis muscle. Muscle activation level, assessed by the twitch interpolation technique, decreased by 8% (P < 0.05) at the end of the exercise. The results suggest that the time course is such that the contractile properties are significantly altered after the first hour, whereas excitability and central drive are more impaired toward the latter stages of the 5-h cycling exercise.
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.
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.
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.
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.
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.
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.
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.
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 .
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.
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.
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.
Key points:
The mechanisms for the age-related increase in fatigability during dynamic exercise remain elusive. We tested whether age-related impairments in muscle oxidative capacity would result in a greater accumulation of fatigue causing metabolites, inorganic phosphate (Pi ), hydrogen (H+ ), and diprotonated phosphate (H2 PO4- ), in the muscle of old compared with young adults during a dynamic knee extension exercise. The age-related increase in fatigability (reduction in mechanical power) of the knee extensors was closely associated with a greater accumulation of metabolites within the working muscle but could not be explained by age-related differences in muscle oxidative capacity. These data suggest that the increased fatigability in old adults during dynamic exercise is primarily determined by age-related impairments in skeletal muscle bioenergetics that result in a greater accumulation of metabolites.
Abstract:
The purpose of this study was to determine whether the increased fatigability in old adults during dynamic exercise is associated with age-related differences in skeletal muscle bioenergetics. Phosphorus nuclear magnetic resonance spectroscopy (31 P-MRS) was used to quantify concentrations of high-energy phosphates and pH in the knee extensors of 7 young (22.7 ± 1.2 years, 6 women) and 8 old adults (76.4 ± 6.0 years, 7 women). Muscle oxidative capacity was measured from the phosphocreatine (PCr) recovery kinetics (kPCr ) following a 24-s maximal voluntary isometric contraction (MVC). The fatiguing exercise consisted of 120 maximal velocity contractions (1 contraction per 2-s) against a load equivalent to 20% of the MVC. The PCr recovery kinetics did not differ between young and old adults (0.023 ± 0.007 s-1 vs. 0.019 ± 0.004 s-1 , respectively). Fatigability (reductions in mechanical power) of the knee extensors was ∼1.8-fold greater with age and was accompanied by a greater decrease in pH (young = 6.73 ± 0.09, Old = 6.61 ± 0.04) and increases in concentrations of inorganic phosphate ([Pi ], young = 22.7 ± 4.8 mM, Old = 32.3 ± 3.6 mM) and diprotonated phosphate ([H2 PO4- ], young = 11.7 ± 3.6 mM, Old = 18.6 ± 2.1 mM) at the end of the exercise in old compared with young adults. The age-related increase in power loss during the fatiguing exercise was strongly associated with intracellular pH (r = -0.837), [Pi ] (r = 0.917), and [H2 PO4- ] (r = 0.930) at the end of the exercise. These data suggest that the age-related increase in fatigability during dynamic exercise has a bioenergetic basis and is explained by an increased accumulation of metabolites within the muscle. This article is protected by copyright. All rights reserved.
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 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.