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This book surveys the research evidence into exercise-induced fatigue and discusses how knowledge of fatigue can be applied in sport and exercise contexts. The book examines the different \"types\" of fatigue and the difficulties of identifying which types are prevalent during different types of exercise. It introduces the fundamental science of fatigue, focusing predominantly on physiological and neuromuscular aspects, and explores key topics in detail, such as energy depletion, lactic acid, dehydration, electrolytes and minerals, and the perception of fatigue.-- From publisher's description.

Running is generally considered a symmetrical activity that involves harmonized functions of upper and lower limbs. However, asymmetry can occur under certain conditions, such as fatigue, as lower limbs perform distinct functional tasks. While running, trunk muscles play a crucial role in transmitting loads between the upper and lower limbs, yet the impact of trunk muscle fatigue on the dominant and nondominant legs has not been well addressed. This study investigated the effects of trunk muscle fatigue on ground reaction force characteristics on dominant and nondominant legs in novice runners. Thirty participants were asked to run along a runway at 3.3 m · s−1 before and after a trunk muscle fatigue protocol. Ground reaction force data were collected bilaterally, and subsequent asymmetries were calculated. Trunk muscle fatigue had different effects on the dominant and nondominant legs. In the dominant leg peak medial force increased, while the nondominant leg showed reduced peak lateral force, peak braking force and peak negative free moment and increased medio-lateral impulse. Trunk muscle fatigue increased asymmetries in peak lateral force, peak braking force and decreased asymmetry in peak negative free moment. These findings suggest that trunk muscle fatigue, due to its different effects on dominant and nondominant legs, deteriorates running asymmetry and may increase injury risk in novice runners. Strengthening and improving the endurance of trunk muscles is recommended for novice runners to prevent strength reduction-related changes in running mechanics and mitigate injury risk.

Skeletal muscle fatigue is accompanied by the accumulation of metabolites, such as adenosine diphosphate (ADP), inorganic phosphate (Pi), and protons (H+). However, we lack a comprehensive understanding of the contribution of these metabolic changes to the development of muscle fatigue during intense exercise and the underlying mechanisms. To address this gap, we collected data from young adults performing a dynamic (0.75 Hz) plantar flexion exercise to task failure (642 ± 104 s), including in vivo concentrations of metabolites and H+ measured by 31P magnetic resonance spectroscopy as well as muscle activation signals obtained via electromyography. Using these data, we developed and validated a human skeletal muscle model. Our model‐based simulations suggested that to continue the plantar flexion exercise at the required power output, muscle activation should progressively increase. In the absence of this increased activation, we observed a reduction in force‐generating capacity due to metabolite‐mediated inhibition of actin–myosin cross‐bridge cycling. Our simulations also showed that Pi reduced force production by 30% when we increased it 50% above the concentrations measured experimentally. A parameter sensitivity analysis suggested that force generation is strongly dependent on the rate of Pi release from the actin–myosin complex, and Pi inhibits force by increasing the rate of actin–myosin detachment. In addition, we proposed an alternative mechanism through which H+ might reduce muscle force generation during exercise. In contrast, elevated ADP levels did not significantly affect force generation. This study provides insight into the impact of metabolite accumulation on force generation and muscle fatigue development. What is the central question of this study? Force generation in skeletal muscles is driven by ATP hydrolysis and thereby results in the accumulation of its metabolite byproducts, such as ADP, Pi and H+, which can lead to muscle fatigue during intense exercise: what are the individual contributions of each of these metabolites to muscle fatigue development and the underlying mechanisms? What is the main finding and its importance? Using 31P‐MRS and electromyography data from exercising humans and a computational model, we demonstrate that Pi accumulation inhibits force generation by hindering actin–myosin cross‐bridge cycling during intense exercise. The developed skeletal muscle model helps in understanding the role of metabolite accumulation in muscle fatigue development.

This study investigated the effect of respiratory muscle fatigue on cardiovascular function, locomotor muscle fatigue and exercise performance in young and master athletes, a model of successful ageing. Ten young male (YA, 27.4 ± 4.4 years) and 11 male master endurance athletes (MA, 65.0 ± 5.1 years) performed, on separate days, two constant workload cycling tests at 90% of peak power to exhaustion (CWT) following a fatiguing inspiratory loading task at 60% (ILT60%) and a sham task at 2% (ILT2%) of their maximal inspiratory pressure. On a third day, the sham task was replicated but CWT was interrupted at the time equal to that performed during CWTILT60% (CWTILT2%–ISO). Quadriceps fatigue was assessed by changes in maximal voluntary isometric contraction (MVC), potentiated twitch force (QTSINGLE) and voluntary activation (VA) from 15 s to 15 min post‐exercise. Mean arterial pressure (MAP) was measured using finger pulse photoplethysmography. Blood flow (Q̇L) and limb vascular conductance (LVC) were measured using Doppler ultrasound. During ILT60%, MA demonstrated reduced Q̇L (P = 0.036), a greater increase in MAP (P < 0.001) and a larger decrease in LVC (P = 0.044) compared to YA. During CWTILT60%, MA experienced a larger decrease in time to exhaustion (−39.7 ± 14.0%) than YA (−15.5 ± 13.9%, P = 0.010). Exercise‐induced reductions in MVC and QTSINGLE (both P < 0.039) were also more pronounced during CWTILT60% compared to CWTILT2%–ISO in MA. Ageing exacerbates the adverse effects of respiratory muscle fatigue on limb vascular function and locomotor muscle fatigue during subsequent exercise, resulting in greater impairments in exercise performance. What is the central question of this study? What is the effect of respiratory muscle fatigue on cardiovascular function, locomotor muscle fatigue and exercise performance in young and master athletes? What is the main finding and its importance? Ageing exacerbates the respiratory metaboreflex – the pressor response triggered by respiratory muscle fatigue – resulting in greater increase in mean arterial pressure and reduction in limb vascular conductance. Similar pre‐existing respiratory muscle fatigue accelerates locomotor muscle fatigue and more significantly impairs exercise performance in master athletes compared to younger counterparts. This underscores the respiratory system's growing contribution in limiting exercise capacity with advancing age.

Muscle fatigue is a temporary decline in the force and power capacity of skeletal muscle resulting from muscle activity. Because control of muscle is realized at the level of the motor unit (MU), it seems important to consider the physiological properties of motor units when attempting to understand and predict muscle fatigue. Therefore, we developed a phenomenological model of motor unit fatigue as a tractable means to predict muscle fatigue for a variety of tasks and to illustrate the individual contractile responses of MUs whose collective action determines the trajectory of changes in muscle force capacity during prolonged activity. An existing MU population model was used to simulate MU firing rates and isometric muscle forces and, to that model, we added fatigue-related changes in MU force, contraction time, and firing rate associated with sustained voluntary contractions. The model accurately estimated endurance times for sustained isometric contractions across a wide range of target levels. In addition, simulations were run for situations that have little experimental precedent to demonstrate the potential utility of the model to predict motor unit fatigue for more complicated, real-world applications. Moreover, the model provided insight into the complex orchestration of MU force contributions during fatigue, that would be unattainable with current experimental approaches.

Muscle length changes may evoke alternating activity and consequently reduce local fatigue and pain during prolonged static bending. The aim of this study was to assess whether a postural intervention involving intermittent trunk extensor muscle length changes (INTERMITTENT) can delay muscle fatigue during prolonged static bending when compared to a near-isometric condition (ISOMETRIC) or when participants were allowed to voluntarily vary muscle length (VOLUNTARY). These three conditions were completed by 11 healthy fit male participants, in three separate sessions of standing with 30 ± 3 degrees trunk inclination until exhaustion. Conventional and high-density electromyography (convEMG and HDsEMG, respectively) were measured on the left and right side of the spine, respectively. The endurance time for INTERMITTENT was 33.6% greater than ISOMETRIC (95% CI: [3.8, 63.5]; p = 0.027) and 29.4% greater than VOLUNTARY (95% CI: [7.0, 51.7]; p = 0.010), but not different between ISOMETRIC and VOLUNTARY. The convEMG and HDsEMG amplitude coefficient of variation was significantly greater for INTERMITTENT versus ISOMETRIC. The rate of change in convEMG and HDsEMG spectral content did not reveal significant differences between conditions as found in endurance time. Additional regression analyses between endurance time and rate of change in convEMG (p > 0.05) and HDsEMG (R2 = 0.39–0.65, p = 0.005–0.039) spectral content indicated that HDsEMG better reflects fatigue development in low-level contractions. In conclusion, imposed intermittent trunk extensor muscle length changes delayed muscle fatigue development when compared to a near-isometric condition or when participants were allowed to voluntarily vary muscle length, possibly due to evoking alternating activity between/within trunk extensor muscles.

Calcium (Ca2+) release from the sarcoplasmic reticulum is central to excitation–contraction coupling and plays a critical role in the development of skeletal muscle fatigue. Altered Ca2+ dynamics may affect not only contractile function but also neuromuscular excitability. This study examined the effects of pharmacological modulation of Ca2+ channels on fatigue development and spinal reflex activity in rats. Using the Hoffmann reflex (H-reflex) as an indicator of motoneuron excitability, we evaluated the effects of Ca2+ channel blockers (Amiloride, Nifedipine) and an activator ((−)-Bay K8644) on the reflex responses of the plantar muscle before and after fatigue induction. The ratio of the maximum H-reflex to maximum M-wave (Hmax/Mmax) was used to assess alterations in spinal excitability. Compared with the control, both Amiloride and Nifedipine markedly reduce the Hmax/Mmax ratio (77% and 60%, respectively), whereas (−)-Bay K8644 elicited a robust 129% increase. These findings demonstrate that pharmacological modulation of Ca2+ channels has distinct and divergent effects on spinal excitability during fatigue. These results highlight the close interaction between intramuscular Ca2+ regulation and reflex pathways and suggest potential strategies for enhancing muscle performance through targeted Ca2+ channel modulation.

Muscle fatigue, the transient decrease in muscle power, leads to low levels of physical activity and an inability to perform activities of daily living. Altered muscle coordination in response to fatigue may contribute to impaired physical performance. We sought to determine whether lower extremity muscle coordination during gait changes differently depending on susceptibility to fatigue (i.e., fatigability). Thirty-one older adults completed muscle power testing before and after a 30-min walk, with the change in power used to categorize participants as more or less fatigable. We used non-negative matrix factorization to identify muscle modules from electromyography (EMG) from the 2nd minute as our measure of baseline muscle coordination. Changes in muscle coordination were determined by computing the variance in the 30th minute’s EMG accounted for by the baseline modules across all muscles (tVAF) and in individual muscles (mVAF). We compared tVAF between the 2nd and 30th minutes of the walk in individuals who were more and less fatigable. We used mVAF to explore the contribution of changes in individual muscle activity to tVAF. There was a decrease in tVAF overall in response to the walk (p < 0.001; 92.3 ± 1.6 % vs. 89.0 ± 4.3 %) but this did not differ between groups (interaction p = 0.66). There were significant associations between mVAF and tVAF for knee extensor, knee flexor, and ankle dorsiflexor muscles. Our results suggest that muscle coordination changes over the course of a walk in older adults but that this change does not differ between more and less fatigable older adults.

This study investigates the effects of a fatiguing exercise on lower limb electro-myographic activities and co-contraction in overweight females compared with normal weight females during running. Forty-eight females were divided into two groups. The first group included individuals with a normal body-mass-index. The second group comprised individuals classified as overweight/obese based on body-mass-index. Electromyography data from the tibialis anterior, gastrocnemius medialis, vastus lateralis, vastus medialis, rectus femoris, biceps femoris, and semitendinosus muscles were collected during running at constant speed using a surface electromyography system before and after a running induced fatigue. The results indicated significant main effects of the \"Group\" on tibialis anterior muscle activities during the loading phase (P = 0.040). Furthermore, the results showed significant main effects of \"Fatigue\" on rectus femoris (P = 0.028) and semitendinosus (P = 0.007) muscle activities during the loading phase. Paired-wise comparison demonstrated significantly greater rectus femoris and semitendinosus activities during the loading phase after the fatigue protocol. The results demonstrated significant main effects of \"Fatigue\" for general knee muscular co-contraction during early stance phase (P < 0.001). Paired-wise comparison demonstrated significantly greater general knee muscular co-contraction during early stance phase at post-test compared with pre-test. No significant main effect of \"Group\" and group-by-fatigue interactions were found for general and direct knee co-contraction during early stance phase (P > 0.05). Overall, our findings indicate that both fatigue and being overweight result in running pattern differences, but these occur through different mechanisms at a neuromuscular level. Neuromuscular responses to fatigue during running in overweight adults and in normal weight adults can be evaluated together, in order to optimize the modality of treatment and rehabilitation processes in overweight adults to reduce and/or prevent the risk of running related injury.