Journal of applied physiology最新文献

An initial bout of eccentric exercise (EE) is known to protect against exercise-induced muscle damage (EIMD) following the performance of a subsequent bout of similar volume and intensity, a phenomenon known as the repeated bout effect (RBE). We examined whether aspects of motor unit (MU) behavior and reticulospinal tract (RST) drive are neural components of this protective effect. Twenty-three participants (6 females; age 26 ± 5 yr) performed two bouts of EE (10 repetitions × 10 sets) with the dorsiflexors separated by 3 wk. Maximal voluntary isometric torque (MVIC), muscle soreness (DOMS), MU behavior (quantified from MUs identified via high-density electromyography decomposition), and RST drive (visual-auditory vs. visual-startle reaction time) were recorded at baseline, 24, 48, and 72 h postexercise. Symptoms of EIMD were elevated following bout 1; MVIC was reduced, and perceived soreness was increased. Despite comparable work performed (∼1,300 J; P = 0.721), MVIC (P < 0.001) and soreness (P < 0.001) recovered quicker following bout 2. The attenuated symptoms of EIMD were coupled with reduced variability in MU discharge rate (P = 0.001) and torque (P < 0.001). MU adjustments were not accompanied by any change in RST drive (-8 ms; P = 0.634). Lower MU discharge variability and an attenuated increase in firing rate in bout 2 support a neural contribution to the RBE. The present study cannot infer whether such adaptations actively protect against muscle damage or merely reflect the reduced mechanical and nociceptive disturbance. Nonetheless, we confirm that MU adjustments are involved in the RBE phenomenon.NEW & NOTEWORTHY Unfamiliar eccentric exercise causes muscle damage, but repeating the same exercise later substantially reduces symptoms-an adaptive phenomenon known as the repeated bout effect (RBE). We investigated the neural contributions to this response. We observed lower motor unit discharge variability and smaller increases in firing rate after the repeated bout. These findings provide evidence that motor unit-level neural adjustments are a critical component of the RBE, offering a new perspective on this protective adaptation.

Acute kidney injury (AKI) contributes to excess hospital admissions observed during heatwaves. We tested the hypothesis that water spray and fan use would modulate biomarkers of AKI risk in older adults exposed to 3 h of very hot and dry heat. On each of 3 days (randomized), older adults (12 males/8 females; 66-84 yr) were exposed to 3 h of heating (47°C, 15% relative humidity) with no cooling intervention (control), water spray, or fan use. We assessed core temperature, fluid loss, biomarkers of AKI risk (AKIRISK score), and kidney function (plasma creatinine and cystatin C). The increase in core temperature was 1.3 ± 0.5°C (means ± SD) in control, 1.0 ± 0.2°C in water spray, and 1.9 ± 0.7°C in the fan trial. Fluid loss was 0.9 ± 0.2% in control, 0.4 ± 0.2% in water spray, and 1.5 ± 0.4% in fan. Compared with control, the AKIRISK score at end-heating was -0.18 [95% CI: -0.35, -0.02] lower in water spray (P = 0.047) and 0.26 [0.09, 0.44] higher in fan (P = 0.002). Repeated-measures correlations demonstrated positive associations between end-heating core temperature (r = 0.77; P < 0.001) and fluid loss (r = 0.48; P = 0.001), both relative to the end-heating AKIRISK score. Compared with control, end-heating plasma creatinine was not different (P = 0.43), but plasma cystatin C was 0.07 [-0.13, -0.01] mg/L lower (P = 0.025) in water spray. Compared with control, end-heating creatinine was 0.08 [0.03, 0.12] mg/dL higher (P < 0.001), and cystatin C was 0.07 [0.01, 0.13] mg/L higher (P = 0.026) in the fan trial. These findings suggest that in very hot and dry conditions, water spray can attenuate, whereas fans elevate heat-related increases in AKI risk biomarkers.NEW & NOTEWORTHY Acute kidney injury contributes to the increased mobility and mortality reported during heatwaves. Air conditioning is protective but may not be available to all; thus, there is a need to identify non-air-conditioning-dependent cooling strategies. We show that water spray mitigates, but fans elevate heat-related increases in biomarkers of acute kidney injury in older adults exposed to 3 h of very hot and dry conditions.

Hypertension affects over 30% of adults worldwide, significantly increasing the risk of cardiovascular, cerebrovascular, and renal diseases. Although regular physical activity is a well-established strategy for lowering blood pressure, additional therapeutic approaches may help individuals who struggle to achieve target blood pressure levels. Hot water immersion is garnering attention due to its potential cardiovascular benefits. Historically practiced for therapeutic and cultural purposes, hot water immersion induces physiological responses that share key similarities with physical activity. Accumulating evidence suggests that hot water immersion may contribute to blood pressure reduction. Although small-scale studies report promising acute and chronic blood-pressure-lowering effects, critical gaps remain in the literature. This review summarizes current evidence on the antihypertensive effects of hot water immersion, outlining key areas for future research. Hot water immersion may emerge as an accessible and culturally relevant adjunct therapy for hypertension management.

Consuming cold fluids during heat stress can alter sweating responses; however, it remains unclear why chemical activation of cold-sensitive transient receptor potential melastatin 8 (TRPM8) with menthol only induces a cold sensation. Animal models propose that complete cold transduction with TRPM8 chemical stimulation must be combined with physical cooling to impact thermoeffector responses. To address this, 12 participants (5 females and 7 males; 22 ± 5 yr; 79.5 ± 15.0 kg; 1.8 ± 0.1 m) conducted four passive heating protocols in random order where, within trial, they consumed 3.2 mL/kg body mass of either 1) 37°C water, 2) 1.5°C water, 3) 37°C menthol solution (0.05%), or 4) 1.5°C menthol solution (0.05%); 5 min before heating, and following a 0.5°C and 1.0°C increase in rectal temperature. Forearm sweating onset was attenuated with 1.5°C compared with 37°C (+0.16°C, P = 0.001) and delayed with menthol (+0.15°C, P = 0.03), but not at the forehead (main effect of temperature: +0.08°C, P = 0.17, menthol: +0.09°C, P = 0.17). Sudomotor thermosensitivity at the forearm and forehead was attenuated with 1.5°C compared with 37°C (-0.62 mg/cm²/min/°C, P = 0.02) but not affected by menthol (-0.11 mg/cm²/min/°C, P = 0.55). A small attenuation in forearm (-0.05 mg/cm²/min) and forehead (-0.08 mg/cm²/min) sweat rate was observed with 1.5°C combined with menthol, following a 0.5°C (P < 0.04), but not a 1.0°C (P > 0.09) rise in rectal temperature; 1.5°C water alone, nor 37°C water with or without menthol, altered sweating during passive heat stress (P ≥ 0.55). Collectively, chemical stimulation of TRPM8 within the gastrointestinal tract could alter thermoregulatory sweating, but only when paired with physical cooling, and the effect is small.NEW & NOTEWORTHY Chemical stimulation of TRPM8 channels during heat stress provides alterations in thermal perception without impacting sweating. However, evidence to date in humans has not considered the impact of fluid temperature, which may be needed to fully induce cold transduction. We provide evidence that coadministration of a TRPM8 agonist with physical cold stimulation is required to alter sudomotor output during heat stress; however, this effect is small.

This study investigated the acute effects of passive stretching on microvascular oxygen partial pressure ([Formula: see text]) and hypoxia-inducible factor-1α (HIF-1α) expression in rat skeletal muscle, focusing on stretch intensity and duration. Twenty male Wistar rats were assigned to either a stretch or sham group. In study 1, the soleus muscle was passively stretched at varying intensities by changing its length from the optimal length (L_O) by 2, 4, 6, 8, and 10 mm, whereas [Formula: see text] was simultaneously measured. In a separate experiment, the muscle was stretched from L_O to 8 mm and maintained in the stretched position for 2 h, whereas in the sham group it was kept at L_O throughout. After stretching, the muscle was rapidly frozen, and HIF-1α mRNA was quantified by real-time PCR. Passive stretching induced an acute, intensity-dependent decrease in [Formula: see text]. Values during high-intensity stretches (6-10 mm) were significantly lower than in the sham group (25 ± 9 vs. 39 ± 7 mmHg, 8 mm vs. L_O; P < 0.05). Sustained 8 mm stretching caused a rapid decline in [Formula: see text] within 40 s, followed by a stable low plateau for 2 h (time F = 11.2; group F = 17.9; interaction F = 2.10; P < 0.01). Interestingly, 2 h of stretching reduced HIF-1α mRNA expression. These findings demonstrate that passive stretching elicits an intensity-dependent and sustained reduction in microvascular Po₂, which may suppress HIF-1α mRNA expression in skeletal muscle.NEW & NOTEWORTHY The intramuscular oxygen dynamics during stretching remain unclear. Real-time changes in Po₂ during passive stretching were investigated using phosphorescence quenching. Microvascular Po₂ decreased in an intensity-dependent manner and remained low during prolonged stretching. The decline reached a plateau about 2 min after stretch onset. Moreover, 2 h of sustained stretching downregulated HIF-1α mRNA. Collectively, these findings indicate that passive stretching induces acute, intensity-dependent microvascular hypoxia that persists and alters hypoxia-related transcriptional responses in skeletal muscle.

Motoneurons adapt to both resistance and endurance training in reduced animal preparations, with adaptations seemingly more apparent in higher-threshold neurons, but similar evidence in humans is lacking. We compared identified motor unit (MU) discharge patterns from decomposed electromyography signals acquired during triangular dorsiflexion contractions up to 70% of maximal voluntary force (MVF) between resistance-trained, endurance-trained, and untrained individuals (n = 23 per group). We estimated the contribution of intrinsic motoneuron properties and the proportion of excitatory, inhibitory, and neuromodulatory inputs to motoneuron discharge across contraction intensities in each group. Participants also performed a "sombrero" task (triangular contractions superimposed onto sustained ones) designed to challenge inhibitory control of dendritic persistent inward currents (PICs). Both trained groups demonstrated higher MU discharge rates with greater ascending discharge rate modulation during higher contraction forces (≥50% MVF), which were accompanied by more linear MU discharge patterns with steeper slopes after PIC-induced acceleration. The lack of differences in discharge rate hysteresis (triangular contractions) and the discharge rate characteristics during sombrero contractions suggests that neuromodulatory input is not different between groups. Conversely, since resistance-compared with endurance-trained individuals exhibited steeper PIC-induced acceleration during lower contraction forces (≤50% MVF), there is a possibility of enhanced PIC activation at onset. Collectively, the greater discharge rates and more linear but steeper MU discharge patterns in the trained groups suggest a more reciprocal (i.e., push-pull) excitation-inhibition coupling during higher contraction forces, leading to enhanced net excitatory synaptic input to the motor pool, which might underpin greater force production of trained individuals.NEW & NOTEWORTHY Physical training alters intrinsic motoneuron properties in reduced animal preparations, especially in neurons recruited at high excitation levels. Here, we show that individuals with a history of resistance or endurance training exhibit higher discharge rates that are more linear during forceful contractions. This likely reflects a more reciprocal/push-pull excitation-inhibition coupling, leading to greater net excitation to the motor pool that may contribute to greater force production observed in trained individuals.

Older adults expend more metabolic energy than young adults during walking (worse walking economy). Amid the numerous physiological changes that accompany advanced aging, the mechanisms governing the age-related decline in walking economy remain unestablished. Due to conflicting evidence, we studied whether older adults produce lower-limb joint moments less economically than young adults, independent of an age-related difference in muscle coactivation. Eight older adults (71.6 ± 6.0 yr) and 13 young adults (23.1 ± 4.7 yr) repeatedly produced hip and ankle moment cycles on a dynamometer following visual feedback and an audible metronome. We instructed participants to produce moments with peak net torque values of 20 and 30 Nm at a 0.75 Hz cycle frequency and a 0.5 duty cycle. Overall, young and older adults did not coactivate their antagonist muscles differently during the moment production trials. At the hip, older adults expended more metabolic power than young adults despite producing lower moment amplitudes. At the ankle, older adults expended more metabolic power than young adults while producing nondifferent moment production cycles. Because older adults produced lower-limb joint moments less economically than young adults, interventions aimed at prolonging youthful walking economy into advanced age may need to directly address changing muscle-tendon unit physiology.NEW & NOTEWORTHY The mechanisms governing the age-related decline in walking economy are elusive. Here, we demonstrate that older adults produce lower-limb joint moment profiles less economically than young adults. Therefore, less economical muscle-tendon unit force production in older versus young adults likely contributes to their greater metabolic energy expenditure during walking.

The triceps surae, composed of the soleus (SOL) and medial (MG) and lateral (LG) gastrocnemii, are anatomically-derived synergists which act as a functional unit to plantarflex the ankle. However, anatomical differences suggest that each muscle is capable of generating distinct torques at the ankle, raising the possibility that each can be independently controlled to suit the needs of a given task. This possibility was explored by investigating the activation patterns of the triceps surae during two balance tasks that use different neuromechanical control strategies to maintain equilibrium. High-density surface EMG was recorded from the triceps surae of 14 healthy young adults during multiple trials of dual- and single-legged standing. Newly developed analyses examined how each muscle tuned its activity with center of pressure (COP) movement throughout 2-D space. During dual-legged standing, only the SOL and MG were active and both tuned their activity uniformly with anteroposterior COP movement. By contrast, during single-legged standing, each muscle showed robust activation and significantly different directional tuning, with the LG most active before medial COP movement, while SOL and MG were most active before lateral COP movement. Further analyses demonstrated the LG could be activated entirely independent of the SOL and MG, and vice versa, with independent activation of each muscle causing different angular deflections of the COP during single-, but not dual-legged standing. These observations reveal a sophisticated level of neural control, whereby the nervous system exploits subtle differences between highly similar muscles to tune stabilizing torques in a task-dependent manner.

We tested the hypothesis that excess cardiac activation (ECA) generates increased cardiovascular circuit flow at the onset of exercise. 30 participants (14 female) performed 30s of right-legged knee extension/flexion exercise at 50% one-legged WR_PEAK to assess the normal cardiovascular adjustment at the onset of single leg exercise (control; CON). ECA in isolation was accomplished in separate trials by initiating exercise with both the right leg and the occluded left leg (each at 50% one-legged WR_PEAK) to generate additional muscle mass activation of autonomic cardiac control without allowing the exercising left leg circulation to add to the cardiovascular circuit. Central (finger photoplethysmography) and peripheral (Doppler ultrasound) hemodynamics were measured continuously. ECA increased cardiac activation vs. CON (Δ heart rate; 35.3 ±8.4 vs. 24.5 ±8.7 beats/min, P < 0.0001), which elevated Δ Q̇ (4.62 ±1.62 vs. 3.48 ±1.51 L/min, P < 0.001) as Δ stroke volume was not different between conditions. ECA increased Δ mean arterial pressure (11.9 ±5.8 vs. 5.5 ±5.6 mmHg, P < 0.0001) via Δ Q̇ as Δ total vascular conductance was also greater during ECA (36.6 ±18.3 vs. 31.3 ±15.1 mL/min/mmHg, P = 0.0120). Δ exercising leg blood flow (LBF; 2594.3 ±639.6 vs. 2425.1 ±550.9 mL/min, P = 0.0179) but not Δ leg vascular conductance was greater in ECA vs. CON. These findings demonstrate that excess exercise-induced cardiac activation can create a greater increase in Q̇ and exercising leg perfusion at exercise onset without a change in exercising leg vasodilation magnitude during sub-maximal knee flexion/extension exercise.