European Journal of Applied Physiology最新文献

Breaking the sub-2-hour marathon barrier under record-eligible conditions requires the coordinated contribution of physiological, biomechanical, psychological, environmental, nutritional, and technological factors. Achieving such a feat demands aerobic power (VO₂_max ≈ 75-85 mL·kg⁻¹·min⁻¹), running economy (≤ 190 mL·kg⁻¹·km⁻¹ at 21 km·h⁻¹), fractional utilization (90-94% VO₂_max, near the maximum metabolic steady state), favourable anthropometry (e.g., low body mass), efficient neuromuscular coordination, and cognitive endurance to sustain near-threshold effort for ~ 2 h. Technological innovations, particularly carbon-fiber-plated footwear ("supershoes") together with refined pacing strategies, optimized nutrition (carbohydrate intake ~ 60-100 g·h⁻¹; caffeine 3-6 mg·kg⁻¹), and advantageous environmental conditions (~ 10 °C, < 60% RH, low wind) have further narrowed the remaining gap. This narrative review extends previous integrative perspectives by incorporating recent advances in thermoregulation, emerging AI-assisted training applications, and cognitive performance into a conceptual systems-oriented perspective on the determinants of record-eligible sub-2-hour marathon performance. It synthesizes multidisciplinary evidence to propose a conceptual model illustrating how physiological, mechanical, cognitive, and technological domains interact to constrain or enhance endurance capacity. The INEOS 1:59 Challenge (1:59:40) and Kelvin Kiptum's world record (2:00:35) exemplify the proximity of this frontier, while ongoing innovations in real-time monitoring and predictive analytics are expected to refine performance optimization further. Collectively, these developments suggest that achieving an officially ratified sub-2-hour marathon is increasingly plausible, provided that physiological, environmental, and technological systems are co-optimized within ethical and regulatory boundaries.

Purpose: To compare the acute effects of high-load (HL) and low-load (LL) resistance exercise (RE) on circulating monocytes, their subpopulations, and intracellular expression of immunoregulatory markers (IL-10, IL-1β, TLR4, TLR6, and HSP27) in trained postmenopausal women.

Methods: Thirteen trained postmenopausal women completed two RE protocols (7 exercises): HL (90% 1RM, 6 reps, 3-min rest) and LL (50% 1RM, 20 reps, 90-s rest), in a randomized crossover design. Blood samples were collected PRE, POST, and 1H. Flow cytometry quantified monocyte subsets and the proportion of cells expressing the target markers.

Results: Circulating monocyte percentages increased significantly (P < 0.001), with a more sustained elevation after LL (P = 0.016). No major changes were seen in the overall distribution of monocyte subsets, but the intermediate-to-classical monocyte ratio decreased (P < 0.001), indicating a relative increase in classical monocytes. In non-classical monocytes, the proportion of cells expressing IL-10 (P = 0.005), total HSP27 (P = 0.016), and phosphorylated HSP27 (P < 0.001) decreased, while the proportion of IL-1β-expressing cells remained unchanged. The IL-1β to IL-10 ratio increased at 1H (P = 0.009). No changes were detected in the proportion of cells expressing TLR4 or TLR6.

Conclusion: Both HL and LL RE induced acute immunomodulatory responses with similar patterns. Load magnitude appears less influential than the RE stimulus itself in shaping monocyte-mediated immune changes.

Background: Prior studies have shown that ingestion of exogenous ketone esters (KE) significantly increases cerebral blood flow and skeletal muscle oxygenation in humans. This pilot study tested the hypothesis that KE may also lower exercise pressor responses and improve cardiovagal baroreflex sensitivity (cBRS) in individuals with metabolic syndrome (MetS).

Methods: Twenty individuals (ten with MetS and ten matched controls) completed a three visit, single-blind, placebo-controlled, matched-pairs pilot study involving a cardiometabolic prescreening and two randomized experimental trials. In the experimental trials, cardiovagal baroreflex sensitivity (cBRS), heart rate variability (HRV), and exercise pressor responses to 2 min of isometric handgrip exercise (HG) were evaluated at baseline, and during a 105-min period following ingestion of a commercially available KE or a taste- and volume-matched placebo.

Results: Main effects of condition and group by time interactions were observed for BP responses to HG (all p ≤ 0.050). The main effect of condition was explained by lower blood pressure values during HG in the KE trial compared to the placebo trial. The cBRS of all sequences (cBRS_all) and all up-ramping sequences (cBRS_up) were also attenuated in the KE condition compared to placebo (time by condition interaction: F ≥ 2.42, p ≤ 0.007), independent of group, and the normalized low- to high-frequency (LF/HF) HRV ratio decreased in both conditions (F = 0.176, p ≤ 0.031), but remained higher in the KE condition independent of group (p = 0.023).

Conclusions: This study provides preliminary evidence that acute exogenous ketosis may reduce blood pressure responses to acute exercise and attenuate spontaneous baroreflex gain in individuals with MetS (NCT05651243).

Purpose: This study compared the effects of different muscle activity patterns on blood pressure and lower leg edema during interrupted sitting in overweight and obese men.

Design: Randomized four-arm cross-over experimental study.

Methods: Eighteen overweight and obese men (21.0 ± 1.2 years; 28.8 ± 2.2 kg/m²) took part. The four interventions were uninterrupted sitting for 8.5 h (SIT) and interruptions in sitting with 30-min walking at 4 km/h (ONE), sitting with 3-min walking at 4 km/h (WALK) or squatting (SQUAT) every 45 min for 10 times. Blood pressure was measured every 45 min. Lower leg volume was measured using water displacement method at the beginning and immediately after the experiment to examine lower leg edema. Thigh muscle electromyogram (EMG) amplitude and EMG activity duration were used to predict the effects on blood pressure and lower leg edema in generalized linear mixed effects models.

Results: Mean systolic blood pressure was reduced by 2.54 mmHg (95% CI - 4.47 to - 0.62, P = 0.010) in WALK relative to SIT. The changes of lower leg volumes were reduced by 70.34 ml (- 112.78 to - 27.91, P = 0.002) in WALK and 62.49 ml (- 104.92 to - 20.06, P = 0.005) in SQUAT relative to SIT. Increased thigh muscle EMG amplitude was associated with lower systolic blood pressure (- 1.02 mmHg [- 1.79 to - 0.25], P = 0.010). Longer EMG activity duration was associated with decreased lower leg edema (- 1.02 ml [- 1.83 to - 0.21], P = 0.015).

Conclusion: Frequent interruptions to prolonged sitting confer distinct health benefits through specific muscle activity patterns, providing potential targets for interventions.

Purpose: Circulating cell-free DNA (cfDNA) is recognized as a relevant biomarker for monitoring the effects of various physiological and pathophysiological factors. To identify the effect of body temperature, we investigated the kinetics of cfDNA in response to two forms of heating.

Methods: In a randomized crossover design, twelve healthy young males cycled at 60% of their maximum oxygen uptake (VO_2max) (exertional heating) and conducted lower-body immersion in hot water (43-44°C) (exogenous heating) until their rectal temperature (T_re) reached 39°C. EDTA blood samples were collected at each time point T_re increased and decreased by 0.5°C, to determine the concentrations of cfDNA, epinephrine (Epi), norepinephrine (NE), prolactin (PRL), as well as subjective sensation, and heart rate.

Results: Linear mixed model analyses revealed a strong significant interaction effect for cfDNA (T_re × heating modality, F (6, 135.95) = 7.51, P < 0.001), with a significant 1.76-fold increase of cfDNA in response to exogenous heating and a 5.72-fold increase in response to exertional heating (P < 0.05). Significant interaction effects were detected for NE (F (6, 109.80) = 8.0683, P < 0.001), and PRL (F (6, 120.92) = 2.2746, P = 0.041), but not Epi. Repeated measures correlation (r_rm) showed strong correlations between cfDNA and core temperature in exertional heating (r_rm = 0.89), as well as exogenous heating (r_rm = 0.75).

Conclusion: Our findings demonstrate that an increase in rectal temperature induces physiological stress, which triggers the release of cfDNA, however, at a significantly lower level than exertional heating, suggesting that mechanical stress has a greater influence on the release.

Purpose: This study aimed to investigate bilateral motor control and connectivity between supplementary motor area (SMA) and primary motor cortex (M1) in younger, middle-aged, and older healthy adults.

Methods: 32 younger (mean age 22.8 ± 5.3 years), 18 middle-aged (47.6 ± 6.5 years), and 23 older (75.8 ± 6.7 years) adults were tested. Bilateral motor control was assessed using the Purdue pegboard. Dual-site transcranial magnetic stimulation (TMS) was used to measure SMA-M1 connectivity at different conditioning stimulation intensities.

Results: Older adults had significantly poorer motor performance than younger and middle-aged in all pegboard subtests. Notably, there were no conclusive differences in motor performance between younger and middle-aged adults. There was no conclusive evidence supporting age-related and intensity-related differences in SMA-M1 connectivity between younger, middle-aged, and older adults. There was also no conclusive evidence to support clear associations between SMA-M1 connectivity and bilateral motor control.

Conclusion: Age-related declines in bilateral motor functioning was found in older, but not middle-aged adults. The bilateral motor functioning of middle-aged adults is more young-like than old-like. The lack of conclusive age- and intensity-related differences in SMA-M1 connectivity, and lack of conclusive association with bilateral motor performance, might be due to high inter-individual variability in SMA-M1 connectivity. Potential factors contributing to this variability include SMA and M1 morphometry, the structural connectivity between these regions, and the localisation of SMA.

The time-variability of physiological and kinematic variables, extracted at mesoscopic and macroscopic levels, respectively, has shown potential in detecting changes in exercise workload and associated fatigue effects. However, the sensitivity of microscopic variables -such as muscle oxygen saturation, which reflect the dynamics of muscle metabolism-remains unexplored. This study aimed to compare the time-variability structure of the tissular saturation index (TSI) during a graded maximal exercise performed until exhaustion. Nineteen participants started running at 8 km/h with the speed increasing by 1 km/h every 100 s until they could not keep the prescribed velocity. The time-variability of TSI, recorded from the quadriceps, was analyzed using Detrended fluctuation analysis (DFA) and Sample entropy (SampEn) over the first and last 2048 recorded data points (corresponding to 204 s each). Wilcoxon test and Cohen's d were used to compare the initial and final parts of the test. Results revealed a significant decrease in the Hurst (H) exponent (from H = 0.84 ± 0.21 to H = 0.49 ± 0.10; p < 0.01; d = -1.57) and a corresponding increase in SampEn (from 1.12 ± 0.20 to 1.40 ± 0.13; p < 0.01; d = 1.17). These findings indicate a shift towards uncorrelated white-noise as exhaustion approached, suggesting reduced efficacy of oxygen transportation with increasing workloads. The time-variability of muscle oxygen saturation appears to be a) a promising measure for assessing exercise intensity, and b) allow the study of physiological network interactions extracted from different levels (from microscopic to macroscopic).

Purpose: Exercise-induced cardiac adaptation is well-studied in male athletes. However, evidence for longitudinal adaptation, particularly in females, is limited. This study compared cardiac adaptation between elite female and male rowers across a competitive season.

Methods: Ten females (19 ± 0.9 years) and 11 males (20 ± 1.7 years) were assessed across 21 weeks at early (ES), mid- (MS), and late season (LS). Echocardiography (2D, 3D, strain), peak oxygen consumption (V̇O₂peak), weekly training volume (sessions) and intensity (minutes in heart rate zones) were documented. Bayesian two-way repeated measures ANOVA assessed sex and training effects.

Results: Training volume was comparable between sexes; however, females spent less time at maximal heart rate intensity. An interaction effect for V̇O₂peak demonstrated the highest value at LS in females (55.8 ± 1.6 mL kg min^-1) and MS in males (64.1 ± 1.6 mL kg min^-1). Females had smaller left ventricular (LV) 2D mass and volume with no training-induced response in either sex. A sex-specific interaction was observed for 3D LV mass: females peaked at MS (221.2 ± 20.6 g) compared to males at LS (301.9 ± 20.9 g). Females also had smaller LV diameter, wall thickness and right heart dimensions. Across the season, most females (67%) exhibited eccentric hypertrophy, whilst males (89%) showed concentric hypertrophy. However, classifications varied throughout the season. No sex or training effects were observed for strain.

Conclusion: Whilst sex strongly influences cardiac morphology in elite rowers, sex-specific adaptation in 3D LV mass and LV geometry changes emphasise cardiac plasticity with training in athletes.

Whether high-intensity exercise training can effectively mitigate orthostatic-induced post-exercise hypotension (PEH) has not been satisfactory resolved to date. We therefore examined whether 2 weeks of high-intensity exercise training can effectively mitigate the orthostatic-induced PEH by conducting comparisons pre- and post-training at the same absolute and relative workloads. Eleven healthy men underwent 2 weeks of high-intensity exercise training within the severe intensity domain (i.e., above critical power) for 15 min per session for 14 daily consecutive sessions. Assessment of orthostatic-induced PEH was conducted at pre- and post-training (both absolute and relative workloads) across seated and standing recovery postures. The exercise intensities for the PEH trials were conducted at 10% above critical power, followed by a 1-h recovery across seated and standing postures. Post-training, PEH assessment was performed at the same absolute and relative power output (i.e., 10% above the post-intervention critical power) as pre-training. Two weeks of high-intensity exercise training significantly increased $\dot{V}$ O_2max, resting ejection fraction, and fractional shortening velocity (all P < 0.01), thereby confirming an increased training status. Consequently, the reduction of systolic, diastolic, and mean arterial blood pressures from baseline were smaller following 2 weeks of high-intensity exercise training in both absolute and relative workloads during the recovery across seated and standing postures (all P < 0.01). We conclude that 2 weeks of high-intensity exercise training was able to mitigate the orthostatic-induced PEH with both absolute and relative workloads in healthy Asian men.

People with Down syndrome (DS) have a depressed heart rate (HR) and blood pressure (BP) response to exercise. We tested the hypothesis that people with DS, compared to controls (CON), would have more blunted HR and BP responses to isometric rather than dynamic cycling exercise. Twenty-eight individuals with DS and 14 controls (16-40 years) completed a 6-min cycling exercise at 50% body weight and 2-min handgrip isometric exercise at 30% maximum voluntary contraction (MVC). HR and BP were sampled via a single-lead system and finger photoplethysmography, respectively. Hemodynamic responses to both exercises were tested with linear mixed models. Individuals with DS showed a blunted HR increase to handgrip (DS: difference (d)_60s-rest= 3, 95% CI: -10 to 4 bpm, p = 0.989; CON: d_60s-rest = 16, 95%CI: 6 to 26 bpm, p < 0.001) but not cycling exercise (DS: d_60-rest = 21, 95%CI: 6 to 26 bpm, p < 0.001). Exercise-induced increases in mean arterial pressure were smaller in people with DS during handgrip (DS: d_60s-rest = 7, 95% CI: 3-12 mmHg, p < 0.001; CON: d_60s-rest = 15, 95% CI: 12 to 22 mmHg, p < 0.001) but not during cycling exercise (DS: d_60s-rest = 13, 95% CI: 7 to 18 mmHg, p < 0.001; CON: d_60s-rest= 8, 95% CI:1 to 16 mmHg). Controlling for group differences in resting BP, fitness, %peak HR and MVC did not change results. People with DS exhibited a blunted hemodynamic response to isometric, but not dynamic cycling exercise, suggesting that HR and BP control differ between these two exercise modes in this population.