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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.

Background Heat stress during aerobic exercise training may offer an additional stimulus to improve cardiovascular function and performance in a cool-temperate environment. However, there is a paucity of information on the additive effects of high-intensity interval exercise (HIIE) and acute heat stress. We aimed to determine the effects of HIIE in combination with acute heat stress on cardiovascular function and exercise performance. Methods Twelve active (peak O 2 consumption [VO 2peak ]: 47 ± 8 ml·O 2 /min/kg) young adults were counterbalanced to six sessions of HIIE in hot (HIIE-H, 30 ± 1 °C, 50 ± 5% relative humidity [RH]) or temperate conditions (HIIE-T, 20 ± 2 °C, 15 ± 10% RH). Resting heart rate (HR), HR variability (HRV), central (cBP) and peripheral blood pressure (pBP), peripheral mean arterial pressure (pMAP), pulse wave velocity (PWV), VO 2peak , and 5-km treadmill time-trial were measured pre- and post-training. Results Resting HR and HRV were not significantly different between groups. However, expressed as percent change from baseline, cSBP (HIIE-T: + 0.9 ± 3.6 and HIIE-H: -6.6 ± 3.0%, p  = 0.03) and pSBP (HIIE-T: -2.0 ± 4.6 and HIIE-H: -8.4 ± 4.7%, p  = 0.04) were lower in the heat group. Post-training PWV was also significantly lower in the heat group (HIIE-T: + 0.4% and HIIE-H: -6.3%, p  = 0.03). Time-trial performance improved with training when data from both groups were pooled, and estimated VO 2peak was not significantly different between groups (HIIE-T: 0.7% and HIIE-H: 6.0%, p  = 0.10, Cohen’s d = 1.4). Conclusions The addition of acute heat stress to HIIE elicited additive adaptations in only cardiovascular function compared to HIIE alone in active young adults in temperate conditions, thus providing evidence for its effectiveness as a strategy to amplify exercise-induced cardiovascular adaptations.

Heightened muscle sympathetic nerve activity (MSNA) contributes to impaired vasodilatory capacity and vascular dysfunction associated with aging and cardiovascular disease. The contribution of elevated MSNA to the vasodilatory response during passive leg movement (PLM) is not fully understood. This study tested the hypothesis that elevated MSNA diminishes the vasodilatory response to PLM in healthy young males (n = 11, 25 ± 2 yr). Post exercise circulatory occlusion (PECO) following 2 min of isometric handgrip (HG) exercise performed at 25% (ExPECO 25%) and 40% (ExPECO 40%) maximum voluntary contraction was used to incrementally engage the metaboreceptors and augment MSNA. Control trials were performed without PECO (ExCON 25% and ExCON 40%) to account for changes due to HG exercise. PLM was performed 2 min after exercise and hemodynamics were assessed. MSNA was recorded by microneurography in the peroneal nerve (n = 8). Measures of MSNA (i.e., burst incidences) increased during ExPECO 25% (+15 ± 5 burst/100 bpm) and ExPECO 40% (+22 ± 4 burst/100 bpm) and returned to pre‐HG levels during ExCON trials. Leg vascular conductance (vasodilation) during PLM was reduced by 16% and 44% during ExPECO 25% and ExPECO 40%, respectively. These findings indicate elevated MSNA attenuates the vasodilatory response to PLM and the magnitude of reduction in vasodilation during PLM is graded with the degree of sympathoexcitation.

Exercise‐induced hyperemia in calf muscles was recently shown to be quantifiable with high‐resolution magnetic resonance imaging (MRI). However, processing of the MRI data to obtain muscle‐perfusion maps is time‐consuming. This study proposes to substantially accelerate the mapping of muscle perfusion using a deep‐learning method called artificial neural network (NN). Forty‐eight MRI scans were acquired from 21 healthy subjects and patients with peripheral artery disease (PAD). For optimal training of NN, different training‐data sets were compared, investigating the effect of data diversity and reference perfusion accuracy. Reference perfusion was estimated by tracer kinetic model fitting initialized with multiple values (multigrid model fitting). Result: The NN method was much faster than tracer kinetic model fitting. To generate a perfusion map of matrix 128 × 128 on a same computer, multigrid model fitting took about 80 min, single‐grid or regular model fitting about 3 min, while the NN method took about 1 s. Compared to the reference values, NN trained with a diverse group gave estimates with mean absolute error (MAE) of 15.9 ml/min/100g and correlation coefficient (R) of 0.949, significantly more accurate than regular model fitting (MAE 22.3 ml/min/100g, R 0.889, p < .001). Conclusion: the NN method enables rapid perfusion mapping, and if properly trained, estimates perfusion with accuracy comparable to multigrid model fitting. A recent study reported the potential of using DCE MRI method to map muscle perfusion after stimulation of exercise. This current study proposed a deep learning method to enable rapid processing of the data so that perfusion maps can be obtained online.

Impaired O 2 transport to skeletal muscle potentially contributes to the decline in aerobic capacity with aging. Thus, we examined whether (1) skeletal muscle oxidative capacity decreases with age and (2) O 2 availability or mitochondrial capacity limits the maximal rate of mitochondrial ATP synthesis in vivo in sedentary elderly individuals. We used 31 P-magnetic resonance spectroscopy ( 31 P-MRS) to examine the PCr recovery kinetics in six young (26 ± 10 years) and six older (69 ± 3 years) sedentary subjects following 4 min of dynamic plantar flexion exercise under different fractions of inspired O 2 (FiO 2 , normoxia 0.2; hyperoxia 1.0). End-exercise pH was not significantly different between old (7.04 ± 0.10) and young (7.05 ± 0.04) and was not affected by breathing hyperoxia (old 7.08 ± 0.08, P  > 0.05 and young 7.05 ± 0.03). Likewise, end-exercise PCr was not significantly different between old (19 ± 4 mM) and young (24 ± 5 mM) and was not changed in hyperoxia. The PCr recovery time constant was significantly longer in the old (36 ± 9 s) compared to the young in normoxia (23 ± 8 s, P  < 0.05) and was not significantly altered by breathing hyperoxia in both the old (35 ± 9 s) and young (29 ± 10 s) groups. Therefore, this study reveals that the muscle oxidative capacity of both sedentary young and old individuals is independent of O 2 availability and that the decline in oxidative capacity with age is most likely due to limited mitochondrial content and/or mitochondrial dysfunction and not O 2 availability.

The primary goal of this study was to evaluate arterial transit time (ATT) in exercise‐stimulated calf muscles as a promising indicator of muscle function. Following plantar flexion, ATT was measured by dynamic contrast‐enhanced (DCE) MRI in young and elderly healthy subjects and patients with peripheral artery disease (PAD). In the young healthy subjects, gastrocnemius ATT decreased significantly (P < 0.01) from 4.3 ± 1.5 to 2.4 ± 0.4 sec when exercise load increased from 4 lbs to 16 lbs. For the same load of 4 lbs, gastrocnemius ATT was lower in the elderly healthy subjects (3.2 ± 1.1 sec; P = 0.08) and in the PAD patients (2.4 ± 1.2 sec; P = 0.02) than in the young healthy subjects. While the sensitivity of the exercise‐stimulated ATT is diagnostically useful, it poses a challenge for arterial spin labeling (ASL), a noncontrast MRI method for measuring muscle perfusion. As a secondary goal of this study, we assessed the impact of ATT on ASL‐measured perfusion with ASL data of multiple post labeling delays (PLDs) acquired from a healthy subject. Perfusion varied substantially with PLD in the activated gastrocnemius, which can be attributed to the ATT variability as verified by a simulation. In conclusion, muscle ATT is sensitive to exercise intensity, and it potentially reflects the functional impact of aging and PAD on calf muscles. For precise measurement of exercise‐stimulated muscle perfusion, it is recommended that ATT be considered when quantifying muscle ASL data. Magnetic resonance imaging enables accurate measurement of arterial transit time (ATT) in exercise‐stimulated calf muscles. This study aims to evaluate the potential value of exercise‐stimulated ATT in assessing muscle function. It was found that the measured ATT varied significantly between exercises of different intensities in young healthy subjects, and between different subject groups.

Anthocyanins and bromelain have gained significant attention due to their antioxidative and anti-inflammatory properties. Both have been shown to improve endothelial function, blood pressure (BP) and oxygen utility capacity in humans; however, the combination of these two and the impacts on endothelial function, BP, total antioxidant capacity (TAC) and oxygen utility capacity have not been previously investigated. The purpose of this study was to investigate the impacts of a combined anthocyanins and bromelain supplement (BE) on endothelial function, BP, TAC, oxygen utility capacity and fatigability in healthy adults. Healthy adults (n 18, age 24 (sd 4) years) received BE or placebo in a randomised crossover design. Brachial artery flow-mediated dilation (FMD), BP, TAC, resting heart rate, oxygen utility capacity and fatigability were measured pre- and post-BE and placebo intake. The BE group showed significantly increased FMD, reduced systolic BP and improved oxygen utility capacity compared with the placebo group (P < 0·05). Tissue saturation and oxygenated Hb significantly increased following BE intake, while deoxygenated Hb significantly decreased (P < 0·05) during exercise. Additionally, TAC was significantly increased following BE intake (P < 0·05). There were no significant differences for resting heart rate, diastolic BP or fatigability index. These results suggest that BE intake is an effective nutritional therapy for improving endothelial function, BP, TAC and oxygen utility capacity, which may be beneficial to support vascular health in humans.

Investigations of training effects on exercise energy cost have yielded conflicting results. The purpose of the present study was to compare quadriceps energy cost and oxidative capacity between endurance-trained and sedentary subjects during a heavy dynamic knee extension exercise. We quantified the rates of ATP turnover from oxidative and anaerobic pathways with 31 P-MRS, and we measured simultaneously pulmonary oxygen uptake in order to assess both total ATP production [i.e., energy cost (EC)] and O 2 consumption (O 2 cost) scaled to power output. Seven sedentary (SED) and seven endurance-trained (TRA) subjects performed a dynamic standardized rest-exercise-recovery protocol at an exercise intensity corresponding to 35% of maximal voluntary contraction. We showed that during a dynamic heavy exercise, the O 2 cost and EC were similar in the SED and endurance-trained groups. For a given EC, endurance-trained subjects exhibited a higher relative mitochondrial contribution to ATP production at the muscle level (84 ± 12% in TRA and 57 ± 12% in SED; P  < 0.01) whereas the anaerobic contribution was reduced (18 ± 12% in TRA and 44 ± 11% in SED; P  < 0.01). Our results obtained in vivo illustrate that on the one hand the beneficial effects of endurance training are not related to any reduction in EC or O 2 cost and on the other hand that this similar EC was linked to a change regarding the contribution of anaerobic and oxidative processes to energy production, i.e., a greater aerobic energy contribution associated with a concomitant reduction of the anaerobic energy supply.

Introduction Given that we have reached a point in the field of muscle energetics where absolute measurements are warranted to take the area forward, we designed an ergometer, including two force and two displacement transducers, allowing dynamic and isometric knee extension within a MR system and accurate measurements of power output. Methods On the basis of repeated measurements, the force and displacement transducers accuracy was 1% for values ranging from 0 to 394 N and 4% for values ranging from 0 to 20 cm. In addition, measurements were not affected by magnetic field. MRS experiments in exercising muscle were conducted in eight subjects. They performed two standardized dynamic alternate leg extension exercises (25 and 35% of MVC) while the corresponding metabolic changes were measured using 31 P-MRS. Results The mean power output produced during both exercises were 63 ± 16 and 81 ± 15 W while the eccentric work was reduced i.e. 12 ± 14 and 21 ± 6 W for the moderate and heavy exercise respectively. The corresponding metabolic changes were significant with a 20–40% PCr depletion and an end of exercise pH ranging from 0.02 to 0.70 pH units. Conclusion Overall, the present ergometer allows quadriceps exercise in a MR system and should be useful for future metabolic studies for which reliable and absolute quantification of power output is warranted.

Electromyostimulation (EMS) is commonly used as part of training programs. However, the exact effects at the muscle level are largely unknown and it has been recently hypothesized that the beneficial effect of EMS could be mediated by an improved muscle perfusion. In the present study, we investigated rates of changes in pulmonary oxygen consumption and muscle deoxygenation during a standardized exercise performed after an EMS warm-up session. We aimed at determining whether EMS could modify pulmonary O 2 uptake and muscle deoxygenation as a result of improved oxygen delivery. Nine subjects performed a 6-min heavy constant load cycling exercise bout preceded either by an EMS session (EMS) or under control conditions (CONT). and heart rate (HR) were measured while deoxy-(HHb), oxy-(HbO 2 ) and total haemoglobin/myoglobin (Hb tot ) relative contents were measured using near infrared spectroscopy. EMS significantly increased ( P  < 0.05) the Hb tot resting level illustrating a residual hyperaemia. The EMS priming exercise did not affect either the HHb time constant (17.7 ± 14.2 s vs. 13.1 ± 2.3 s under control conditions) or the kinetics (time-constant = 18.2 ± 5.2 s vs. 15.4 ± 4.6 s under control conditions). Likewise, the other parameters were unchanged. Our results further indicated that EMS warm-up improved muscle perfusion through a residual hyperaemia. However, neither nor [HHb] kinetics were modified accordingly. These results suggest that improved O 2 delivery by residual hyperaemia induced by EMS does not accelerate the rate of aerobic metabolism during heavy exercise at least in trained subjects.