European Journal of Applied Physiology最新文献

Purpose: The aim of this pilot study was to evaluate differences in vasti muscle motor unit (MU) firing between individuals with current patellofemoral pain (PFP) and asymptomatic controls during submaximal isometric knee extension contractions in both single-joint (knee extension) and multi-joint (leg press) exercises.

Methods: Ten individuals with PFP and ten age- and gender-matched asymptomatic controls performed submaximal isometric contractions (10-70% maximum voluntary isometric contraction; MVIC) during single-joint and multi-joint exercises. High-density surface electromyography assessed MU discharge properties of the vastus medialis (VM) and vastus lateralis (VL), while torque steadiness was quantified using the coefficient of variation of torque.

Results: Neural drive to the vasti muscles was comparable between groups across both exercises however, individuals with PFP exhibited reduced torque steadiness during single-joint compared to multi-joint exercises. This reduction in torque steadiness was accompanied by increased MU discharge rate variability at higher torque levels (50-70% MVIC), particularly for the VL muscle at 70% MVIC. For those with PFP, their pain intensity was also higher during single-joint exercises, which may have further contributed to the aforementioned neuromuscular impairments. Additionally, MU firing-torque relationships revealed neuromuscular adjustments in people with PFP, indicated by significantly lower cross-correlation values during multi-joint exercises compared to the asymptomatic controls.

Conclusion: Physically active people with PFP exhibit reduced torque steadiness, increased discharge rate variability, and potentially altered MU firing-torque relationships during single-joint knee extension exercise. These MU adaptations likely reflect neuromuscular adjustments to ongoing PFP, helping to sustain force production despite impaired motor control and potentially mitigating pain during multi-joint exercises.

Mass is a fundamental physical property of all tissues in the human body, including skeletal muscle. Surprisingly intramuscular mass is almost ubiquitously ignored in models of muscle contraction. Here we demonstrate that that muscle mass plays an important role in the dynamics of the tissue deformation in the human biceps brachii and brachialis. Twenty-one subjects held a vibrating dumbbell that generated 10 Hz oscillations within the muscle. Because of tissue inertia, strain-wave propagations developed that we tracked with B-mode ultrasonography: the velocity of these waves increased with increased tension in the muscle. A complementary study in ten participants measured the myoelectric activity in this experimental paradigm and determined that the tonic vibration reflex was minimal for this low frequency set-up, and thus were not the cause of the strain-wave propagations. These experimental results show that muscle mass has a significant effect on the internal dynamics of contraction in human muscle. It is suggested that models of human muscle contraction should re-evaluate whether the inclusion of muscle mass is important for the accurate prediction of muscle force.

Humans optimize muscle activation strategies to minimize energy costs at faster movement velocities. However, empirical evidence on the relationship between joint power and motor unit control strategies is lacking. Therefore, we investigated whether the range of motion and movement velocity influence the association between concentric ankle joint power and motor unit discharge rates in the tibialis anterior muscle. Eleven males performed submaximal concentric ankle dorsiflexion at 5°/s and 20°/s. High-density surface electromyography was recorded from the tibialis anterior muscle and decomposed at the two movement velocities to extract motor unit behavioral data. Ankle power and HD-sEMG from each movement velocity were separated into the first (INI) and second half (END) of the concentric motion. The results showed that the ankle power during INI at 20°/s (3.1 ± 0.7 W/kg) was greater when compared to END at 20°/s (1.8 ± 0.5 W/kg) and to both INI and END at 5°/s (0.5 ± 0.1 W/kg, p < 0.001). The relative increase in discharge rate slope from 5°/s to 20°/s was greater during INI (5.4 ± 1.0 a.u.) when compared to END (2.1 ± 1.0 a.u., p < 0.0001). Moreover, we found significant associations between ankle power and average discharge rate (r = 0.53, p < 0.005) and discharge rate slopes (r=-0.41, p < 0.005) during INI at 20°/s, but not at 5°/s. Our results demonstrate that neural drive modulation in dynamic contractions is determined by the increase in power required to execute movements, demanding specific motor unit control strategies at the start of concentric actions. Moreover, only movements performed at 20°/s demonstrated significant relation between concentric power and motor unit rate coding.

Claude Bernard (1813-1878) studied medicine in Paris from 1834 to 1843. During his studies, he attended the physiology lectures at Collège de France provided by François Magendie (1783-1855). Magendie was the world's leading experimental physiologist, and Bernard became his assistant in 1841. Bernard's training in vivisection, anatomy and physiology was the foundation for his success as an experimental physiologist. Bernard's first years of independent research were not successful, but his dexterity in vivisection allowed him to collect pancreatic juice from living dogs in 1848. With fresh pancreatic juice available, he demonstrated the lipolytic action of the fluid. Bernard's first successful finding had been made. The young chemist Barreswil had established a method for the measurement of glucose in Paris in1845 and became Bernard's collaborator. In 1848, they reported that the liver contained sugar, whereas other tissues did not. Bernard continued these studies and established the glucogenic function of the liver the same year. This finding transformed the existing view of animal metabolism. Serendipity helped in his next big achievement, enabling him to isolate glycogen. Bernard made always double determinations of sugar but during an experiment in 1855, he was unable to make both the determinations of sugar in the liver on the same day. Bernard had perfused a liver with cold water to remove all glucose but found much glucose in the liver the next day. Bernard acknowledged the surprising result and systematically investigated the formation of glucose in water-perfused livers, finding that the "glucose forming" material was insoluble in alcohol and sensitive to heat. Finally, in 1857, Bernard described a method for isolating glycogen and characterized it as "animal starch", which could produce sugar. The method Bernard used to isolate glycogen is still used, with some minor modifications. Bernard's legendary status is unquestionable. He characterised glycogen and introduced the concept of the constancy of the internal environment (la fixité du milieu intérieur), which today is known as homeostasis. His fame also survives through the book "An introduction to the study of experimental medicine" published in 1865. The book is still worth reading and should be read in all courses on the theory of science. In this review we discuss the findings that directed Bernard toward the isolation of glycogen.

Purpose: This study introduces the Ramp Above Critical Level Endurance Test (RACLET), a novel method for evaluating critical power model parameters, and tests its reliability and concurrent validity.

Methods: Twenty-three participants completed several RACLET and time-to-exhaustion tests (TTE). The RACLET is based on the proportionnality between the decline in maximal power (fatigability) and the work done above the critical power and involves a decreasing power ramp with intermittent maximal sprints, inducing moderate fatigue without exhaustion.

Results: The test demonstrated reliability for the initial power ([Formula: see text]) and critical power ([Formula: see text]) (ICC > 0.97), and for the time constant (τ) (ICC = 0.70). The concurrent validity against TTE for [Formula: see text] and [Formula: see text] showed systematic errors of 1.7% and 3.0%, respectively, and for τ and maximum work above the critical power, systematic errors were approximately 10%. The RACLET predictive capacity for time-to-exhaustion showed a systematic error of -0.6% and a random error of 10.3%.

Conclusion: These results suggest that the RACLET is a reliable, valid, and efficient alternative to traditional critical power testing methods, offering comparable accuracy with a single test without inducing exhaustion. This approach could be particularly beneficial for populations in which exhaustive testing is challenging or impractical.

Purpose: Ischemia-reperfusion injury (IRI) poses a major challenge in cardiovascular therapy due to inflammation and oxidative stress. Ischemic postconditioning (IPoC) offers cardioprotection against IRI, but its efficacy may be compromised by chronic methadone use. This study examined the impact of IPoC on inflammatory and oxidative biomarkers in methadone-treated rats subjected to myocardial IRI.

Methods: Twenty-four male Wistar rats were divided into four groups: IRI, methadone-treated IRI (IRI-M), IPoC-treated IRI (IRI-IPoC), and methadone-treated IPoC-IRI (IRI-M-IPoC). Inflammatory proteins (IL-1β, IL-6, TNF-α), oxidative markers (SOD, GPx, TAS), and MDA levels were measured using commercial kits. Gene expression of inflammatory and antioxidant (NRF2, SOD, and GPx) was measured using Real-time PCR assay.

Results: IPoC significantly reduced the expression of inflammatory genes (IL-1β, IL-6, TNF-α, NF-κB) and enhanced antioxidant responses (NRF2, SOD, GPx) in rats subjected to myocardial IRI. Methadone-treated rats (IRI-M) exhibited elevated inflammatory markers and suppressed antioxidant gene expression. The combination group (IRI-M-IPoC) showed partial restoration of antioxidant activity and moderate reduction in inflammation, but these effects were significantly weaker than those observed in the IPoC-only group.

Conclusion: IPoC effectively reduces myocardial IRI by modulating inflammation and oxidative stress. However, chronic methadone use impairs these protective effects, likely through redox imbalance and enhanced inflammatory signaling. These findings confirm the need for optimized therapeutic strategies, potentially including antioxidant support, for patients on opioid maintenance therapy. Further research is warranted to clarify the molecular interplay between opioids and conditioning interventions.

Purpose: Anabolic-Androgenic Steroid (AAS) use has been shown to impact the expression of myogenic growth factors. Very little of this research has been performed with human subjects, and none with athletes. This study investigated the effects of AAS use and iron sport training style on myogenic expression of the genes coding for insulin-like growth factor 1 (IGF1), myogenin (MYOG), and myoblast determination protein 1 (MyoD).

Methods: Fifty-two male iron sport athletes were classified as powerlifters (n = 21), body builders (n = 19), or strongmen (n = 12), and as AAS users (n = 18) or non-users (n = 34) via self-reported data. Saliva samples were collected to be analyzed for expression levels of IGF1, MYOG, and MyoD. Expression levels were analyzed via a 2 (AAS use) x 3 (iron sport) factorial multivariate analysis of variance (MANOVA).

Results: There was no mean vector difference on any combination of dependent variables (Pillai's Trace = 0.087, F(6, 86) = 0.653, p = .688, η_p² = 0.044), and no significant main effects for AAS use (Pillai's Trace = 0.126, F(3, 42) = 2.026, p = .125, η_p² = 0.126), or iron sport (Pillai's Trace = 0.181, F(6, 86) = 1.422, p = .215, η_p² = 0.090).

Conclusion: Neither AAS use nor iron sport training facilitate meaningful changes in myogenic growth factor expression relative to each other. Future researchers should investigate the effects of variables such as training age, length of AAS history, or expression of myogenic inhibitors such as myostatin.

Vascular dynamics in the eyes and brain under microgravity have gained attention due to the Spaceflight-Associated Neuro-Ocular Syndrome (SANS). We explored how changes in gravitational vectors, circadian rhythm, and sleep regulate cerebral blood flow (CBF) and eye perfusion. Hypothesizing that the eye lacks the capacity to autoregulate, we expected increases in blood flow or volume to drive choroidal engorgement in SANS, and circadian and sleep-related changes to further influence these dynamics. Lower-body negative pressure (LBNP) was investigated as a countermeasure for posterior ciliary artery velocity (PCAv) changes. 16 participants were examined in seated, supine, lateral, and prone positions to assess blood flow in the internal carotid and vertebral artery, and PCAv and middle cerebral artery velocity (MCAv) via ultrasonography. CBF and PCAv were stable in-between horizontal positions, and both lowest in a seated position: CBF (supine, 1036 ± 231 vs. seated, 889 ± 177 ml∙min^- 1; P = 0.0019), PCAv (supine, 7.24 ± 1.8 vs. seated, 5.46 ± 1.3 cm∙sec^- 1; P = 0.0012). CBF conductance was lower in the seated position (P = 0.0303), but after correcting for intraocular pressure and hydrostatic columns, PCA conductance remained stable (P = 0.0876). Oxygen delivery was higher in the supine position (supine, 212 ± 54 vs. seated, 182 ± 41 ml∙min^- 1; P = 0.0022), but unchanged between horizontal positions (both P > 0.29). No diurnal changes were observed (all P > 0.15). Sleep decreased MCAv (P < 0.0001), heart rate (P = 0.0019), and mean arterial pressure (P = 0.0019). LBNP unexpectedly increased PCAv (P = 0.0358) and ocular perfusion pressure (P = 0.0156). In conclusion, CBF and PCA velocity change similarly with postural changes on Earth, and low-level LBNP was ineffective in lowering PCAv.