Invited review: The speed-duration relationship across the animal kingdom.

The parameters of the hyperbolic speed-duration relationship (the asymptote critical speed, CS, and the curvature constant, D') provide estimates of the maximal steady state speed (CS) and the distance an animal can run, swim, or fly at speeds above CS before it is forced to slow down or stop (D'). The speed-duration relationship has been directly studied in humans, horses, mice and rats. The technical difficulties with treadmill running in dogs and the relatively short greyhound race durations means that, perhaps surprisingly, it has not been assessed in dogs. The endurance capabilities of lizards, crabs and salamanders has also been measured, and the speed-duration relationship can be calculated from these data. These analyses show that 1) raising environmental temperature from 25 °C to 40 °C in lizards can double the CS with no change in D'; 2) that lungless salamanders have an extremely low critical speed due, most likely, to O2 diffusion limitations associated with cutaneous respiration; and 3) the painted ghost crab possesses the highest endurance parameter ratio (D'/CS) yet recorded (470 s), allowing it to maintain high speeds for extended periods. Although the speed-duration relationship has not been measured in fish, the sustainable swimming speed has been quantified in a range of species and is conceptually similar to the maximal steady state in humans. The high aerobic power of birds and low metabolic cost of transport during flight permits the extreme feats of endurance observed in bird migrations. However, the parameters of the avian speed-duration relationship have not been quantified.

The Application of non-linear methods to quantify changes to movement dynamics during running: A scoping review.

The aim of this scoping review was to evaluate research approaches that quantify changes to non-linear movement dynamics during running in response to fatigue, different speeds, and fitness levels. PubMed and Scopus were used to identify appropriate research articles. After the selection of eligible studies, study details and participant characteristics were extracted and tabulated to identify methodologies and findings. Twenty-seven articles were included in the final analysis. To evaluate non-linearities in the time series, a range of approaches were identified including motion capture, accelerometery, and foot switches. Common methods of analysis included measures of fractal scaling, entropy, and local dynamic stability. Conflicting findings were evident when studies examined non-linear features in fatigued states when compared to non-fatigued. More pronounced alterations to movement dynamics are evident when running speed is changed markedly. Greater fitness levels resulted in more stable and predictable running patterns. The mechanisms by which these changes are underpinned require further examination. These could include the physiological demand of running, biomechanical constraints of the runner, and the attentional demands of the task. Moreover, the practical implications are yet to be elucidated. This review has identified gaps in the literature which should be addressed for further understanding of the field.

Functional threshold power and the (manufactured) critical power controversy.

We read with concern yet another communication from Dotan regarding the critical power (CP) concept which contains a litany of factual errors, false statements, and dated physiological interpretations. Space does not permit us to rebut every incorrect point made about our work (Wong et al., 2022) and the wider field in which it sits, but we will address what we consider to be some of the more egregious errors in his letter. We would first note, however, that our paper was not actually focused on the critical power concept.

Different categories of VO2 kinetics in the 'extreme' exercise intensity domain.

The aim of this study was to classify potential sub-zones within the extreme exercise domain. Eight well-trained male cyclists participated in this study. The upper boundary of the severe exercise domain (Pupper-bound) was estimated by constant-work-rate tests. Then three further extreme-work-rate tests were performed in discrete regions within the extreme domain: extreme-1) at a work-rate greater than the Pupper-bound providing an 80-110-s time to task failure; extreme-2) a 30-s maximal sprint; and extreme-3) a 4-s maximal sprint. Different functions were used to describe the behaviour of the V˙O2 kinetics over time. V˙O2 on-kinetics during extreme-1 exercise was best described by a single-exponential model (R2 ≥ 0.97; SEE ≤ 0.10; p < 0.001), and recovery V˙O2 decreased immediately after the termination of exercise. In contrast, V˙O2 on-kinetics during extreme-2 exercise was best fitted by a linear function (R2 ≥ 0.96; SEE ≤ 0.16; p < 0.001), and V˙O2 responses continued to increase during the first 10-20 s of recovery. During the extreme-3 exercise, V˙O2 could not be modelled due to inadequate data, and there was an M-shape recovery V˙O2 response with an exponential decay at the end. The V˙O2 response to exercise across the extreme exercise domain has distinct features and must therefore be characterised with different fitting strategies in order to describe the responses accurately.

The effect of hypertonic saline evoked muscle pain on neurophysiological changes and exercise performance in the contralateral limb.

Non-local muscle pain may impair endurance performance through neurophysiological mechanisms, but these are relatively unknown. This study examined the effects of muscle pain on neuromuscular and neurophysiological responses in the contralateral limb. On separate visits, nine participants completed an isometric time to task failure (TTF) using the right knee extensors after intramuscular injection of isotonic saline (CTRL) or hypertonic saline (HYP) into the left vastus lateralis. Measures of neuromuscular fatigue were taken before, during and after the TTF using transcranial magnetic stimulation (TMS) and peripheral nerve stimulation. Mean pain intensity was greater in the left leg in HYP (3.3 ± 1.9) compared to CTRL (0.4 ± 0.7; P < 0.001) which was combined with a reduced TTF by 9.8% in HYP (4.54 ± 0.56 min) compared to CTRL (5.07 ± 0.77 min; P = 0.005). Maximum voluntary force was not different between conditions (all P > 0.05). Voluntary activation was lower in HYP compared to CTRL (P = 0.022). No difference was identified between conditions for doublet amplitude (P > 0.05). Furthermore, no difference in MEP·Mmax-1 or the TMS silent period between conditions was observed (all P > 0.05). Non-local pain impairs endurance performance of the contralateral limb. This impairment in performance is likely due to the faster attainment of the sensory tolerance limit from a greater amount of sensory feedback originating from the non-exercising, but painful, left leg.

The effect of elevated muscle pain on neuromuscular fatigue during exercise.

PURPOSE: Muscle pain can impair exercise performance but the mechanisms for this are unknown. This study examined the effects of muscle pain on neuromuscular fatigue during an endurance task. METHODS: On separate visits, twelve participants completed an isometric time-to-task failure (TTF) exercise of the right knee extensors at ~ 20% of maximum force following an intramuscular injection of isotonic saline (CTRL) or hypertonic saline (HYP) into the vastus lateralis. Measures of neuromuscular fatigue were taken before, during and after the TTF using transcranial magnetic stimulation (TMS) and peripheral nerve stimulation. RESULTS: The mean pain intensity was 57 ± 10 in HYP compared to 38 ± 18 in CTRL (P < 0.001). TTF was reduced in HYP (4.36 ± 0.88 min) compared to CTRL (5.20 ± 0.39 min) (P = 0.003). Maximum voluntary force was 12% lower at minute 1 (P = 0.003) and 11% lower at minute 2 in HYP (P = 0.013) compared to CTRL. Voluntary activation was 4% lower at minute 1 in HYP compared to CTRL (P = 0.006) but not at any other time point (all P > 0.05). The TMS silent period was 9% longer at 100 s during the TTF in HYP compared to CTRL (P = 0.026). CONCLUSION: Muscle pain reduces exercise performance through the excacerbation of neuromuscular fatigue that is central in origin. This appears to be from inhibitory feedback from group III/IV nociceptors which acts to reduce central motor output.

Functional threshold power is not a valid marker of the maximal metabolic steady state.

Functional Threshold Power (FTP) has been considered a valid alternative to other performance markers that represent the upper boundary of the heavy intensity domain. However, such a claim has not been empirically examined from a physiological perspective.This study examined the blood lactate and VO2 response when exercising at and 15 W above the FTP (FTP+15W). Thirteen cyclists participated in the study. The VO2 was recorded continuously throughout FTP and FTP+15W, with blood lactate measured before the test, every 10 minutes and at task failure. Data were subsequently analysed using two-way ANOVA. The time to task failure at FTP and FTP+15W were 33.7 ± 7.6 and 22.0 ± 5.7 minutes (p < 0.001), respectively. The VO2peak was not attained when exercising at FTP+15W (VO2peak: 3.61 ± 0.81 vs FTP+15W 3.33 ± 0.68 L·min-1, p < 0.001). The VO2 stabilised during both intensities. However, the end test blood lactate corresponding to FTP and FTP+15W was significantly different (6.7 ± 2.1 mM vs 9.2 ± 2.9 mM; p < 0.05). The VO2 response corresponding to FTP and FTP+15W suggests that FTP should not be considered a threshold marker between heavy and severe intensity.

Physiological complexity: influence of ageing, disease and neuromuscular fatigue on muscle force and torque fluctuations.

NEW FINDINGS: What is the topic of this review? Physiological complexity in muscle force and torque fluctuations, specifically the quantification of complexity, how neuromuscular complexityis altered by perturbations and the potential mechanism underlying changes in neuromuscular complexity. What advances does it highlight? The necessity to calculate both magnitude- and complexity-based measures for the thorough evaluation of force/torque fluctuations. Also the need for further research on neuromuscular complexity, particularly how it relates to the performance of functional activities (e.g. manual dexterity, balance, locomotion). ABSTRACT: Physiological time series produce inherently complex fluctuations. In the last 30 years, methods have been developed to characterise these fluctuations, and have revealed that they contain information about the function of the system producing them. Two broad classes of metrics are used: (1) those which quantify the regularity of the signal (e.g. entropy metrics); and (2) those which quantify the fractal properties of the signal (e.g. detrended fluctuation analysis). Using these techniques, it has been demonstrated that ageing results in a loss of complexity in the time series of a multitude of signals, including heart rate, respiration, gait and, crucially, muscle force or torque output. This suggests that as the body ages, physiological systems become less adaptable (i.e. the systems' ability to respond rapidly to a changing external environment is diminished). More recently, it has been shown that neuromuscular fatigue causes a substantial loss of muscle torque complexity, a process that can be observed in a few minutes, rather than the decades it requires for the same system to degrade with ageing. The loss of torque complexity with neuromuscular fatigue appears to occur exclusively above the critical torque (at least for tasks lasting up to 30 min). The loss of torque complexity can be exacerbated with previous exercise of the same limb, and reduced by the administration of caffeine, suggesting both peripheral and central mechanisms contribute to this loss. The mechanisms underpinning the loss of complexity are not known but may be related to altered motor unit behaviour as the muscle fatigues.

Fatigue-induced changes in knee-extensor torque complexity and muscle metabolic rate are dependent on joint angle.

PURPOSE: Joint angle is a significant determinant of neuromuscular and metabolic function. We tested the hypothesis that previously reported correlations between knee-extensor torque complexity and metabolic rate ([Formula: see text]) would be conserved at reduced joint angles (i.e. shorter muscle lengths). METHODS: Eleven participants performed intermittent isometric knee-extensor contractions at 50% maximum voluntary torque for 30 min or until task failure (whichever occurred sooner) at joint angles of 30º, 60º and 90º of flexion (0º = extension). Torque and surface EMG were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and detrended fluctuation analysis (DFA) α. [Formula: see text] was determined using near-infrared spectroscopy. RESULTS: Time to task failure/end increased as joint angle decreased (P < 0.001). Over time, complexity decreased at 90º and 60º (decreased ApEn, increased DFA α, both P < 0.001), but not 30º. [Formula: see text] increased at all joint angles (P < 0.001), though the magnitude of this increase was lower at 30º compared to 60º and 90º (both P < 0.01). There were significant correlations between torque complexity and [Formula: see text] at 90º (ApEn, r = - 0.60, P = 0.049) and 60º (ApEn, r = - 0.64, P = 0.035; DFA α, ρ = 0.68, P = 0.015). CONCLUSION: The lack of correlation between [Formula: see text] and complexity at 30º was likely due to low relative task demands, given the similar kinetics of [Formula: see text] and torque complexity. An inverse correlation between [Formula: see text] and knee-extensor torque complexity occurs during high-intensity contractions at intermediate, but not short, muscle lengths.

A non-linear analysis of running in the heavy and severe intensity domains.

PURPOSE: Altered movement complexity, indicative of system dysfunction, has been demonstrated with increased running velocity and neuromuscular fatigue. The critical velocity (CV) denotes a metabolic and neuromuscular fatigue threshold. It remains unclear whether changes to complexity during running are coupled with the exercise intensity domain in which it is performed. The purpose of this study was to examine whether movement variability and complexity differ exclusively above the CV intensity during running. METHODS: Ten endurance-trained participants ran at 95%, 100%, 105% and 115% CV for 20 min or to task failure, whichever occurred first. Movement at the hip, knee, and ankle were sampled throughout using 3D motion analysis. Complexity of kinematics in the first and last 30 s were quantified using sample entropy (SampEn) and detrended fluctuation analysis (DFA-α). Variability was determined using standard deviation (SD). RESULTS: SampEn decreased during all trials in knee flexion/extension and it increased in hip internal/external rotation, whilst DFA-α increased in knee internal/external rotation. SD of ankle plantar/dorsiflexion and inversion/eversion, knee internal/external rotation, and hip flexion/extension and abduction/adduction increased during trials. Hip flexion/extension SampEn values were lowest below CV. DFA-α was lower at higher velocities compared to velocities below CV in ankle plantar/dorsiflexion, hip flexion/extension, hip adduction/abduction, hip internal/external rotation. In hip flexion/extension SD was highest at 115% CV. CONCLUSIONS: Changes to kinematic complexity over time are consistent between heavy and severe intensity domains. The findings suggest running above CV results in increased movement complexity and variability, particularly at the hip, during treadmill running.

Prolonged depression of knee-extensor torque complexity following eccentric exercise.

NEW FINDINGS: What is the central question of this study? Does eccentric exercise leading to prolonged knee-extensor torque depression also result in a prolonged loss of knee-extensor torque complexity? What is the main finding and its importance? The recovery of the loss of torque complexity after eccentric exercise took 24 h, whereas after acute muscle fatigue it took 10 min. The depression of torque complexity after eccentric exercise was prolonged. ABSTRACT: 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 hypothesized 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 and 10, 30 and 60 min and 24 h after eccentric (muscle-damaging) and isometric (fatiguing) exercise. These contractions were also repeated 48 h and 1 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 α exponent (DFA α). Global, central and peripheral perturbations were quantified using MVCs with femoral nerve stimulation. Complexity decreased after 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 α required 24 h to recover to baseline levels, but after isometric exercise they required only 10 min. The MVC torque remained reduced [from 233.6 (74.2) to 187.5 (64.7) N m] 48 h after eccentric exercise, with such changes evident only up to 60 min after 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.

Effects of ipsilateral and contralateral fatigue and muscle blood flow occlusion on the complexity of knee-extensor torque output in humans.

NEW FINDINGS: What is the central question of this study? We addressed the question "what role do central and peripheral fatigue mechanisms play in the fatigue-induced loss of isometric torque complexity?" What is the main finding and its importance? When the contralateral limb is fatigued, the complexity of isometric torque output is unaffected even if the blood flow to the contralateral limb is occluded, which suggests that neither central fatigue nor afferent feedback from ischaemic muscle influences the complexity of torque output in an otherwise fresh muscle. ABSTRACT: 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 torque. These trials involved: (i) two bouts of contractions to failure using the right leg separated by 3 min recovery (IPS); (ii) the same protocol but with cuff occlusion during the 3 min recovery (IPS-OCC); (iii) contractions of the left leg to failure, followed 1 min later by contractions of the right leg to failure (CONT); and (iv) 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 maximal voluntary contractions was used to determine the degree of central and peripheral fatigue, whilst complexity was determined using approximate entropy (ApEn) and detrended fluctuation analysis α exponent (DFA α). Neuromuscular fatigue was consistently associated with a loss of torque complexity in all conditions [e.g. IPS bout 1, ApEn from (mean ± SD) 0.46 ± 0.14 to 0.12 ± 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 ± 0.03, P < 0.001). Prior contralateral contractions, with or without blood flow occlusion, had no effect on torque complexity.

Loss of knee extensor torque complexity during fatiguing isometric muscle contractions occurs exclusively above the critical torque.

The complexity of knee extensor torque time series decreases during fatiguing isometric muscle contractions. We hypothesized that because of 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 of contraction, 4 s of rest) on six 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-α scaling exponent (DFA-α). The MVC torque was reduced in trials below CT [by 19 ± 4% (means ± SE) 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 (CIs), 95% CI = -0.23, 0.10; DFA-α 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-α 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.

Fatigue reduces the complexity of knee extensor torque fluctuations during maximal and submaximal intermittent isometric contractions in man.

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 α. 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 α 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 α 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 α 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.

No sex differences in oxygen uptake or extraction kinetics in the moderate or heavy exercise intensity domains.

The integrative response to exercise differs between sexes, with oxidative energy contribution purported as a potential mechanism. The present study investigated whether this difference was evident in the kinetics of oxygen uptake (V̇o2) and extraction (HHb + Mb) during exercise. Sixteen adults (8 males, 8 females, age: 27 ± 5 yr) completed three experimental visits. Incremental exercise testing was performed to obtain lactate threshold and V̇o2peak. Subsequent visits involved three 6-min cycling bouts at 80% of lactate threshold and one 30-min bout at a work rate of 30% between the lactate threshold and power at V̇o2peak. Pulmonary gas exchange and near-infrared spectroscopy of the vastus lateralis were used to continuously sample V̇o2 and HHb + Mb, respectively. The phase II V̇o2 kinetics were quantified using monoexponential curves during moderate and heavy exercise. Slow component amplitudes were also quantified for the heavy-intensity domain. Relative V̇o2peak values were not different between sexes (P = 0.111). Males achieved ∼30% greater power outputs (P = 0.002). In the moderate- and heavy-intensity domains, the relative amplitude of the phase II transition was not different between sexes for V̇o2 (∼24 and ∼40% V̇o2peak, P ≥ 0.179) and HHb + Mb (∼20 and ∼32% ischemia, P ≥ 0.193). Similarly, there were no sex differences in the time constants for V̇o2 (∼28 s, P ≥ 0.385) or HHb + Mb (∼10 s, P ≥ 0.274). In the heavy-intensity domain, neither V̇o2 (P ≥ 0.686) or HHb + Mb (P ≥ 0.432) slow component amplitudes were different between sexes. The oxidative response to moderate- and heavy-intensity exercises did not differ between males and females, suggesting similar dynamic responses of oxidative metabolism during intensity-matched exercise.NEW & NOTEWORTHY This study demonstrated no sex differences in the oxidative response to moderate- and heavy-intensity cycling exercise. The change in oxygen uptake and deoxyhemoglobin were modeled with monoexponential curve fitting, which revealed no differences in the rate of oxidative energy provision between sexes. This provides insight into previously reported sex differences in the integrative response to exercise.