Portrait of Dr Mark Burnley

Dr Mark Burnley

Senior Lecturer

About

Dr Mark Burnley received a BSc (Hons) in Sport Science from the Chelsea School, University of Brighton in 1998, and commenced a PhD in Exercise Physiology in the same year.  He received his doctorate in 2001 and completed a PGCert in Academic Practice in 2002.  

After a year spent teaching at Brighton, Mark joined Aberystwyth University as a founding member of the department of Sport and Exercise Science, where he remained for 10 years teaching human and equine physiology and biomechanics.  

His PhD thesis examined the effect of prior exercise on the pulmonary oxygen uptake response to high-intensity exercise, and he continued to investigate the kinetics of oxygen uptake and the physiology of high-intensity exercise tolerance throughout his time at Aberystwyth.  

He joined the School of Sport and Exercise Sciences at the University of Kent in September 2012.

Research interests

Endurance physiology, specifically the oxygen uptake and metabolic responses to exercise and the power-duration relationship.

Specifically, what fascinates me is why such a large fraction of the exercise intensity spectrum is both non-steady state and unsustainable (i.e., beyond about 20-30% of peak force or power).  

My research has been, and continues to be, focused on why this is the case, what role the oxygen uptake response plays in exercise tolerance, and how the oxygen uptake response can be altered acutely to increase/reduce that tolerance.  This research also has major implications for the design and interpretation of a range of tests used to determined VO2max and critical power.

Mark’s current research interest is the physiological basis of the critical power concept and its relationship to the neuromuscular fatigue process.

Teaching

Publications

Article

  • Pethick, J., Winter, S. and Burnley, M. (2020). Physiological Evidence that the Critical Torque Is a Phase Transition Not a Threshold. Medicine and Science in Sports and Exercise [Online]. Available at: https://doi.org/10.1249/MSS.0000000000002389.
    Introduction: Distinct physiological responses to exercise occur in the heavy and severe-intensity domains, which are separated by the critical power or critical torque (CT). However, how the transition between these intensity domains actually occurs is not known. We tested the hypothesis that CT is a sudden threshold, with no gradual transition from heavy- to severe-intensity behavior within the confidence limits associated with the CT.
    Methods: Twelve healthy participants performed four exhaustive severe-intensity trials for the determination of CT, and four 30-minute trials in close proximity to CT (one or two standard errors above or below each participant’s CT estimate; CT–2, CT–1, CT+1, CT+2). Muscle O2 uptake (mV[Combining Dot Above]O2), rectified EMG and torque variability and complexity were monitored throughout each trial, and maximal voluntary contractions with femoral nerve stimulation were performed before and after each trial to determine central and peripheral fatigue responses.
    Results: The rates of change in fatigue-related variables, mV[Combining Dot Above]O2, EMG amplitude and torque complexity were significantly faster in the severe trials compared to CT–2. For example, the fall in maximal voluntary contraction (MVC) torque was –1.5 ± 0.8 N.m.min-1 in CT–2 vs. –7.9 ± 2.5 N.m.min-1 in the lowest severe-intensity trial (S1; P < 0.05). Individual analyses showed a low frequency of severe responses even in the circa-CT trials ostensibly above the CT, but also the rare appearance of severe-intensity responses in all circa-CT trials.
    Conclusion: These data demonstrate that the transition between heavy- and severe-intensity exercise occurs gradually rather than suddenly.
  • Pethick, J., Winter, S. and Burnley, M. (2019). Relationship between muscle metabolic rate and muscle torque complexity during fatiguing intermittent isometric contractions in humans. Physiological Reports [Online] 7. Available at: https://dx.doi.org/10.14814/phy2.14240.
    To test the hypothesis that a system’s metabolic rate and the complexity of fluctuations in the output of that system are related, thirteen healthy participants performed intermittent isometric knee extensor contractions at intensities where a rise in metabolic rate would (40% maximal voluntary contraction, MVC) and would not (20% MVC) be expected. The contractions had a 60% duty factor (6 sec contraction, 4 sec rest) and were performed until task failure or for 30 min, whichever occurred sooner. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Muscle metabolic rate was determined using near‐infrared spectroscopy. At 40% MVC, task failure occurred after (mean ± SD) 11.5 ± 5.2 min, whereas all participants completed 30 min of contractions at 20% MVC. Muscle metabolic rate increased significantly after 2 min at 40% MVC (2.70 ± 1.48 to 4.04 ± 1.23 %·s‐1, P < 0.001), but not at 20% MVC. Similarly, complexity decreased significantly at 40% MVC (ApEn, 0.53 ± 0.19 to 0.15 ± 0.09; DFA α, 1.37 ± 0.08 to 1.60 ± 0.09; both P < 0.001), but not at 20% MVC. The rates of change of torque complexity and muscle metabolic rate at 40% MVC were significantly correlated (ApEn, ρ = −0.63, P = 0.022; DFA, ρ = 0.58, P = 0.037). This study demonstrated that an inverse relationship exists between muscle torque complexity and metabolic rate during high‐intensity contractions.
  • Pethick, J., Winter, S. and Burnley, M. (2019). Fatigue reduces the complexity of knee extensor torque during fatiguing sustained isometric contractions. European Journal of Sport Science [Online]. Available at: https://doi.org/10.1080/17461391.2019.1599450.
    The temporal structure, or complexity, of muscle torque output reflects the adaptability of motor control to changes in task demands. This complexity is reduced by neuromuscular fatigue during intermittent isometric contractions. We tested the hypothesis that sustained fatiguing isometric contractions would result in a similar loss of complexity. To that end, nine healthy participants performed, on separate days, sustained isometric contractions of the knee extensors at 20% MVC to task failure and at 100% MVC for 60 s. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling were quantified by calculating approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central and peripheral fatigue were quantified using maximal voluntary contractions (MVCs) with femoral nerve stimulation. Fatigue reduced the complexity of both submaximal (ApEn from 1.02 ± 0.06 to 0.41 ± 0.04, P < 0.05) and maximal contractions (ApEn from 0.34 ± 0.05 to 0.26 ± 0.04, P < 0.05; DFA α from 1.41 ± 0.04 to 1.52 ± 0.03, P < 0.05). The losses of complexity were accompanied by significant global, central and peripheral fatigue (all P < 0.05). These results demonstrate that a fatigue-induced loss of torque complexity is evident not only during fatiguing intermittent isometric contractions, but also during sustained fatiguing contractions.
  • Pethick, J., Whiteaway, K., Winter, S. and Burnley, M. (2019). Prolonged depression of knee extensor torque complexity following eccentric exercise. Experimental Physiology [Online] 104:100-111. Available at: https://doi.org/10.1113/EP087295.
    Neuromuscular fatigue reduces the temporal structure, or complexity, of muscle torque output. Exercise-induced muscle damage reduces muscle torque output for considerably longer than
    high-intensity fatiguing contractions. We hypothesised that muscle damaging eccentric exercise would lead to a persistent decrease in torque complexity, whereas fatiguing exercise would not. Ten healthy participants performed five isometric contractions (6 s contraction, 4 s rest) at 50% maximal voluntary contraction (MVC) before, immediately after, 10, 30 and 60 minutes, and 24 hours after eccentric (muscle damaging) and isometric (fatiguing) exercise. These contractions were also repeated 48 hours and one week after eccentric exercise. Torque and surface EMG signals were sampled throughout each test. Complexity and fractal scaling were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis ? exponent (DFA ?). Global, central and peripheral perturbations were quantified using MVCs with femoral nerve stimulation. Complexity decreased following both eccentric (ApEn, mean (SD), from 0.39 (0.10) to 0.20 (0.12), P < 0.001) and isometric exercise (from 0.41 (0.13) to 0.09 (0.04); P < 0.001). After eccentric exercise ApEn and DFA ? required 24 hours to recover to baseline levels, but only 10 minutes following isometric exercise. MVC torque remained reduced (from 233.6 (74.2) to 187.5 (64.7) N.m) 48 hours after eccentric exercise, with such changes only evident up to 60 minutes following isometric exercise (MVC torque, from 246.1 (77.2) to 217.9 (71.8) N.m). The prolonged depression in maximal muscle torque output is therefore accompanied by a prolonged reduction in torque complexity.
  • Jones, A., Burnley, M., Black, M., Poole, D. and Vanhatalo, A. (2019). The maximal metabolic steady state: redefining the ‘gold standard’. Physiological Reports [Online] 7. Available at: https://doi.org/10.14814/phy2.14098.
    The maximal lactate steady state (MLSS) and the critical power (CP) are two widely used indices of the highest oxidative metabolic rate that can be sustained during continuous exercise and are often considered to be synonymous. However, while perhaps having similarities in principle, methodological differences in the assessment of these parameters typically result in MLSS occurring at a somewhat lower power output or running speed and exercise at CP being sustainable for no more than approximately 20–30 min. This has led to the view that CP overestimates the ‘actual’ maximal metabolic steady state and that MLSS should be considered the ‘gold standard’ metric for the evaluation of endurance exercise capacity. In this article we will present evidence consistent with the contrary conclusion: i.e., that (1) as presently defined, MLSS naturally underestimates the actual maximal metabolic steady state; and (2) CP alone represents the boundary between discrete exercise intensity domains within which the dynamic cardiorespiratory and muscle metabolic responses to exercise differ profoundly. While both MLSS and CP may have relevance for athletic training and performance, we urge that the distinction between the two concepts/metrics be better appreciated and that comparisons between MLSS and CP, undertaken in the mistaken belief that they are theoretically synonymous, is discontinued. CP represents the genuine boundary separating exercise in which physiological homeostasis can be maintained from exercise in which it cannot, and should be considered the gold standard when the goal is to determine the maximal metabolic steady state.
  • Burnley, M. (2018). Peripheral Fatigue: Has Another “Threshold” Bitten the Dust?. Exercise and Sport Sciences Reviews [Online] 46:204. Available at: https://doi.org/10.1249/JES.0000000000000169?.
  • Pethick, J., Winter, S. and Burnley, M. (2018). Effects of ipsilateral and contralateral fatigue and muscle blood flow occlusion on the complexity of knee extensor torque output in humans. Experimental Physiology [Online] 103:956-967. Available at: http://dx.doi.org/10.1113/EP086960.
    Neuromuscular fatigue reduces the temporal structure, or complexity, of torque output during muscular contractions. To determine whether the fatigue-induced loss of torque complexity could be accounted for by central or peripheral factors, nine healthy participants performed four experimental trials involving intermittent isometric contractions of the knee extensors at 50% of the maximal voluntary contraction (MVC) torque. These trials involved: 1) two bouts of contractions to failure using the right leg separated by 3 min recovery (IPS); 2) the same protocol but with cuff occlusion during the 3-min recovery (IPS-OCC); 3) contractions of the left leg to failure, followed 1 min later by contractions of the right leg to failure (CONT); and 4) the same protocol but with cuff occlusion applied to the left leg throughout both the recovery period and right leg contractions (CONT-OCC). Supramaximal electrical stimulation during MVCs was used to determine the degree of central and peripheral fatigue, whilst complexity was determined using Approximate Entropy (ApEn) and Detrended Fluctuation Analysis ? exponent (DFA ?). Neuromuscular fatigue was consistently associated with a loss of torque complexity in all conditions (e.g., IPS bout 1 ApEn from [mean {plus minus} SD]: 0.46 {plus minus} 0.14 to 0.12 {plus minus} 0.06 [P < 0.001]). In IPS-OCC, occlusion abolished the recovery from fatigue and torque complexity remained at the values observed at task failure in the preceding bout (IPS-OCC bout 2, first minute: 0.14 {plus minus} 0.03, P < 0.001). Prior contralateral contractions, with or without blood flow occlusion, had no effect on torque complexity.
  • Pethick, J., Winter, S. and Burnley, M. (2017). Caffeine Ingestion Attenuates Fatigue-induced Loss of Muscle Torque Complexity. Medicine & Science in Sports & Exercise [Online] 50:236-245. Available at: http://dx.doi.org/10.1249/MSS.0000000000001441.
    Purpose: We tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. Methods: Eleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction (MVC), with a 60% duty factor (6 s contraction, 4 s rest), 60 min after ingesting 6 mg·kg?1 caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) ? scaling exponent. Global, central and peripheral fatigue were quantified using MVCs with femoral nerve stimulation. Results: Caffeine ingestion increased endurance by 30 ± 16% (mean ± SD, P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA ?; both P < 0.01), as global, central and peripheral fatigue developed (all P < 0.01). Complexity decreased significantly more slowly following caffeine ingestion (ApEn, -0.04 ± 0.02 vs. –0.06 ± 0.01, P = 0.004; DFA ?, 0.03 ± 0.02 vs. 0.04 ± 0.03, P = 0.024), as did the rates of global (-18.2 ± 14.1 vs. –23.0 ± 17.4 N.m.min?1, P = 0.004) and central (-3.5 ± 3.4 vs. –5.7 ± 3.9 %·min?1, P = 0.02) but not peripheral (-6.1 ± 4.1 vs. –7.9 ± 6.3 N.m.min?1, P = 0.06) fatigue. Conclusion: Caffeine ingestion slowed the fatigue-induced loss of torque complexity and increased the time to task failure during intermittent isometric contractions, most likely through central mechanisms.
  • Burnley, M. and Jones, A. (2016). Power-duration relationship: physiology, fatigue and the limits of human performance. European Journal of Sport Science [Online] 18:1-12. Available at: http://dx.doi.org/10.1080/17461391.2016.1249524.
    The duration that exercise can be maintained decreases as the power requirements increase. In this review we describe the power-duration (PD) relationship across the full range of attainable power outputs in humans. We show that a remarkably small range of power outputs are sustainable (power outputs below the critical power, CP). We also show that the origin of neuromuscular fatigue differs considerably depending on the exercise intensity domain in which exercise is performed. In the moderate domain (below the lactate threshold, LT), fatigue develops slowly and is predominantly of central origin (residing in the central nervous system). In the heavy domain (above LT but below CP), both central and peripheral (muscle) fatigue are observed. In this domain, fatigue is frequently correlated with the depletion of muscle glycogen. Severe-intensity exercise (above the CP) is associated with progressive derangements of muscle metabolic homeostasis and consequent peripheral fatigue. To counter these effects, muscle activity increases progressively, as does pulmonary oxygen uptake (VO2), with task failure being associated with the attainment of VO2max. Although the loss of homeostasis and thus fatigue develop more rapidly the higher the power output is above CP, the metabolic disturbance and the degree of peripheral fatigue reach similar values at task failure. We provide evidence that the failure to continue severe-intensity exercise is a physiological phenomenon involving multiple interacting mechanisms which indicate a mismatch between neuromuscular power demand and instantaneous power supply. Valid integrative models of fatigue must account for the PD relationship and its physiological basis.
  • Pethick, J., Winter, S. and Burnley, M. (2016). Loss of knee extensor torque complexity during fatiguing isometric muscle contractions occurs exclusively above the critical torque. American Journal of Physiology: Regulatory Integrative and Comparative Physiology [Online] 310:R1144-R1153. Available at: http://dx.doi.org/10.1152/ajpregu.00019.2016.
    The complexity of knee extensor torque time series decreases during fatiguing isometric muscle contractions. We hypothesised that, due to peripheral fatigue, this loss of torque complexity would occur exclusively during contractions above the critical torque (CT). Nine healthy participants performed isometric knee extension exercise (6 s contraction, 4 s rest) on 6 occasions for 30 min or to task failure, whichever occurred sooner. Four trials were performed above CT (trials S1-S4, S1 being the lowest intensity), and two were performed below CT (at 50% and 90% of CT). Global, central and peripheral fatigue were quantified using maximal voluntary contractions (MVCs) with femoral nerve stimulation. The complexity of torque output was determined using approximate entropy (ApEn) and the Detrended Fluctuation Analysis ? scaling exponent (DFA ?). The MVC torque was reduced in trials below CT (by [Mean ± SEM] 19 ± 4% in 90%CT), but complexity did not decrease (ApEn for 90%CT: from 0.82 ± 0.03 to 0.75 ± 0.06, 95% paired-samples confidence intervals, 95% CI = –0.23, 0.10; DFA ? from 1.36 ± 0.01 to 1.32 ± 0.03, 95% CI –0.12, 0.04). Above CT, substantial reductions in MVC torque occurred (of 49 ± 8% in S1), and torque complexity was reduced (ApEn for S1: from 0.67 ± 0.06 to 0.14 ± 0.01, 95% CI = –0.72, –0.33; DFA ? from 1.38 ± 0.03 to 1.58 ± 0.01, 95% CI 0.12, 0.29). Thus, in these experiments, the fatigue-induced loss of torque complexity occurred exclusively during contractions performed above the CT.
  • Poole, D., Burnley, M., Vanhatalo, A., Rossiter, H. and Jones, A. (2016). Critical Power: An Important Fatigue Threshold in Exercise Physiology. Medicine and Science in Sports and Exercise [Online] 48:2320-2334. Available at: http://dx.doi.org/10.1249/MSS.0000000000000939.
    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[spacing dot above]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[spacing dot above]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.
  • Pethick, J., Winter, S. and Burnley, M. (2015). Fatigue reduces the complexity of knee extensor torque fluctuations during maximal and submaximal intermittent isometric contractions in man. Journal of Physiology [Online] 593:2085-2096. Available at: http://dx.doi.org/10.1113/jphysiol.2015.284380.
    Neuromuscular fatigue increases the amplitude of fluctuations in torque output during isometric contractions, but the effect of fatigue on the temporal structure, or complexity, of these fluctuations is not known. We hypothesised that fatigue would result in a loss of temporal complexity and a change in fractal scaling of the torque signal during isometric knee extensor exercise. Eleven healthy participants performed a maximal test (5 min of intermittent maximal voluntary contractions, MVCs), and a submaximal test (contractions at a target of 40% MVC performed until task failure), each with a 60% duty factor (6 s contraction, 4 s rest). Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified by calculating approximate entropy (ApEn), sample entropy (SampEn) and the detrended fluctuation analysis (DFA) scaling exponent ?. Fresh submaximal contractions were more complex than maximal contractions (mean ± SEM, submaximal vs. maximal: ApEn 0.65 ± 0.09 vs. 0.15 ± 0.02; SampEn 0.62 ± 0.09 vs. 0.14 ± 0.02; DFA ? 1.35 ± 0.04 vs. 1.55 ± 0.03; all P < 0.005). Fatigue reduced the complexity of submaximal contractions (ApEn to 0.24 ± 0.05; SampEn to 0.22 ± 0.04; DFA ? to 1.55 ± 0.03; all P < 0.005) and maximal contractions (ApEn to 0.10 ± 0.02; SampEn to 0.10 ± 0.02; DFA ? to 1.63 ± 0.02; all P < 0.01). This loss of complexity and shift towards Brownian-like noise suggests that as well as reducing the capacity to produce torque, fatigue reduces the neuromuscular system's adaptability to external perturbations.
  • Burnley, M., Vanhatalo, A. and Jones, A. (2012). Distinct profiles of neuromuscular fatigue during muscle contractions below and above the critical torque in humans. Journal of Applied Physiology [Online] 113:215-223. Available at: http://dx.doi.org/10.1152/japplphysiol.00022.2012.
    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.
  • Burnley, M., Vanhatalo, A., Fulford, J. and Jones, A. (2010). Similar metabolic perturbations during all-out and constant force exhaustive exercise in humans: a 31P magnetic resonance spectroscopy study. Experimental Physiology [Online] 95:798-807. Available at: http://dx.doi.org/10.1113/expphysiol.2010.052688.
    It is not possible to attain a metabolic steady state during exercise above the so-called critical force or critical power. We tested the hypothesis that the muscle metabolic perturbations at the end of a bout of maximal isometric contractions, which yield a stable end-test force (equal to the critical force), would be similar to that at task failure following submaximal contractions performed above the critical force. Eight healthy subjects (four female) performed isometric single knee-extension exercise in the bore of a 1.5 T superconducting magnet on two occasions. Following familiarization, subjects performed the following exercises: (1) 60 maximal contractions (3 s contraction, 2 s rest); and (2) submaximal contractions (the same contraction regime performed at 54 ± 8% maximal voluntary contraction) to task failure. Phosphocreatine (PCr), inorganic phosphate (Pi) and diprotonated phosphate (H2PO4?) concentrations and pH were determined using 31P magnetic resonance spectroscopy throughout both tests. During the maximal contractions, force production fell from 213 ± 33 N to reach a plateau in the last 30 s of the test at 100 ± 20 N. The muscle metabolic responses at the end of each test were substantial, but not different between conditions: [PCr] was reduced (to 21 ± 12 and 17 ± 7% of baseline for maximal and submaximal contractions, respectively; P = 0.17), [Pi] was elevated (to 364 ± 98 and 363 ± 135% of baseline, respectively; P = 0.98) and pH reduced (to 6.64 ± 0.16 and 6.69 ± 0.17, respectively; P = 0.43). The [H2PO4?] was also elevated at the end of both tests (to 607 ± 252 and 556 ± 269% of baseline, respectively; P = 0.22). These data suggest that the exercise-induced metabolic perturbations contributing to force depression in all-out exercise are the same as those contributing to task failure during submaximal contractions.
  • Burnley, M. (2009). Estimation of critical torque using intermittent isometric maximal voluntary contractions of the quadriceps in humans. Journal of Applied Physiology [Online] 106:975-983. Available at: http://dx.doi.org/10.1152/japplphysiol.91474.2008.
    To determine whether the asymptote of the torque-duration relationship (critical torque) could be estimated from the torque measured at the end of a series of maximal voluntary contractions (MVCs) of the quadriceps, eight healthy men performed eight laboratory tests. Following familiarization, subjects performed two tests in which they were required to perform 60 isometric MVCs over a period of 5 min (3 s contraction, 2 s rest), and five tests involving intermittent isometric contractions at ?35–60% MVC, each performed to task failure. Critical torque was determined using linear regression of the torque impulse and contraction time during the submaximal tests, and the end-test torque during the MVCs was calculated from the mean of the last six contractions of the test. During the MVCs voluntary torque declined from 263.9 ± 44.6 to 77.8 ± 17.8 N·m. The end-test torque was not different from the critical torque (77.9 ± 15.9 N·m; 95% paired-sample confidence interval, ?6.5 to 6.2 N·m). The root mean squared error of the estimation of critical torque from the end-test torque was 7.1 N·m. Twitch interpolation showed that voluntary activation declined from 90.9 ± 6.5% to 66.9 ± 13.1% (P < 0.001), and the potentiated doublet response declined from 97.7 ± 23.0 to 46.9 ± 6.7 N·m (P < 0.001) during the MVCs, indicating the development of both central and peripheral fatigue. These data indicate that fatigue during 5 min of intermittent isometric MVCs of the quadriceps leads to an end-test torque that closely approximates the critical torque.
  • DiMenna, F., Wilkerson, D., Burnley, M. and Jones, A. (2008). Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline. Journal of Applied Physiology [Online] 105:538-546. Available at: http://dx.doi.org/10.1152/japplphysiol.90357.2008.
    It has been suggested that the slower O2 uptake (V?o2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that “priming” exercise would significantly reduce the phase II time constant (?) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak V?o2 from a moderate-intensity baseline (90% GET) on three occasions in each of the “unprimed” and “primed” conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II V?o2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean ± SD ?, 42 ± 15 vs. 33 ± 8 s; P < 0.05), but were not accelerated by priming exercise (42 ± 17 s; P > 0.05). The amplitude of the V?o2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (V?o2 slow component: from 0.47 ± 0.09 to 0.27 ± 0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51 ± 35 to 26±43% of baseline; P < 0.05 for both comparisons). These results indicate that the slower phase II V?o2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced V?o2 slow component may be linked to changes in muscle fiber activation.

Conference or workshop item

  • Winter, S., Burnley, M., Forrest, S. and Challis, J. (2015). Complexity of isometric force production is associated with time to achieve steady state when moving to a new force level. In: 25th International Society of Biomechanics Conference.
  • Burnley, M. and Winter, S. (2009). Quadriceps activation at different hip and knee joint angles. In: 33rd Annual Meeting of the American Society of Biomechanics.

Thesis

  • Pethick, J. (2016). The Effects of Neuromuscular Fatigue on the Complexity of Isometric Torque Output in Humans.
    The temporal structure, or complexity, of torque output is thought to reflect the adaptability of motor control and has important implications for system function, with high values endowing greater adaptability in response to alterations in task demand. The aim of this thesis was to investigate the effect of neuromuscular fatigue on the complexity of isometric muscle torque output. It was hypothesised that neuromuscular fatigue would lead to a reduction in the complexity of muscle torque output, as measured by approximate entropy (ApEn), sample entropy (SampEn) and the detrended fluctuation analysis (DFA) ? scaling exponent. The first experimental study (Chapter 4) demonstrated that muscle torque complexity was significantly reduced during both maximal and submaximal intermittent fatiguing contractions, with the values at task failure indicative of increasingly Brownian noise (DFA ? > 1.50). It was subsequently shown in the second study (Chapter 5) that this reduction in complexity occurred exclusively during contractions performed above the critical torque. It was next demonstrated, in the third study (Chapter 6), that pre-existing fatigue significantly reduced torque complexity and time to task failure, but still resulted in consistent values of complexity at task failure regardless of the time taken to reach that point. In the fourth study (Chapter 7) caffeine ingestion was found to slow the rate of reduction in torque complexity with fatigue, seemingly through both central and peripheral mechanisms. Finally, in the fifth study (Chapter 8) eccentric exercise decreased the complexity of torque output, with values only recovering to baseline levels after 24 hours recovery, in comparison to only 10 minutes recovery following isometric exercise. These results demonstrate that torque complexity is significantly perturbed by neuromuscular fatigue. This thesis has thus provided substantial evidence that the complexity of motor control during force production becomes less complex, and that muscles become less adaptable, with neuromuscular fatigue.

Forthcoming

  • Hoskin, L. (2019). The Effect of Exercise Priming on V̇O2 Kinetics, Muscle Torque Complexity and Exercise Tolerance During Intermittent Isometric Contractions.
    Exercise priming can alter V̇O2 kinetics and improve the performance of subsequent exhaustive heavy exercise. During fatiguing isometric exercise there is a reduction in the
    complexity of muscle torque output, which correlates with metabolic changes observed in the same exercise domain. This study aims to investigate the effect of exercise priming on V̇O2
    kinetics, muscle torque complexity and exercise tolerance during intermittent isometric exercise.
    Five males and five females (25 ± 6 years, 171.4 ± 9.3 cm, 69.2 ± 12.0 kg) completed three experimental trials in a randomised order. The trials consisted of a six-minute priming exercise bout or rest period, followed by 20 minutes of rest, before completing a second exhaustive exercise bout. Participants performed intermittent isometric contractions of the knee extensors at 40% maximal voluntary contraction (MVC) with a duty cycle of 0.6. Participants' rate of perceived exertion (RPE) and muscle oxygen consumption were measured at regular intervals throughout the exercise.
    There was no difference in the time to task failure between primed and non-primed exercise. There was a higher EMG amplitude at the start of the primed exhaustive bout compared to the non-primed exercise bout. The V̇O2 response to exhaustive exercise was not different between the primed and non-primed conditions. Peripheral fatigue was present at the onset of exercise following priming and a significant loss of muscle torque complexity with priming.
    There was no improvement in performance of subsequent intermittent isometric contractions with prior exercise, nor was there change in the V̇O2 response. Loss of complexity could be attributed to the increase in arEMG at the onset of the exhaustive exercise, more specifically an increase in motor unit recruitment with the development of fatigue. These results suggest that there is some effect of high-intensity prior exercise on exhaustive isometric contractions of the knee extensors.
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