Journal of applied physiology最新文献

The primary aim of the study was to assess differences in strength performance, neuromuscular fatigue, and perceived exertion across phases of the menstrual cycle [MC; early follicular (eFP), late follicular (lFP), and mid-luteal phase (mLP)] and oral contraceptives [OCs; active pill phase (aPP) and nonactive pill phase (nPP)]. The secondary aim was to analyze the influence of fluctuating serum 17β-estradiol and progesterone concentrations on these parameters in naturally menstruating women. Thirty-four women (21 with a natural MC and 13 using OCs) completed three or two experimental sessions, respectively. Mean propulsive velocity (MPV_mean) and total number of repetitions (REP_total) were assessed during a power [3 × 8 at 60% 1RM (one-repetition maximum)] and hypertrophy squat loading (3 sets to failure at 70% 1RM), respectively. Changes in bench press and squat MPV at 60% 1RM in response to the loadings were used as surrogates for nonlocal and local fatigue, respectively. Total blood lactate accumulation (BLA_A) and markers of perceived exertion were assessed in each session. No significant differences between any of the MC or OC phases were observed for MPV_mean, REP_total, nonlocal and local fatigue, and markers of perceived exertion (all P > 0.050). A higher intraindividual 17β-estradiol concentration was significantly associated with a lower MPV_mean (P = 0.019). BLA_A was significantly higher in the lFP than in the mLP (P = 0.019) and negatively associated with the intraindividual progesterone concentration (P = 0.005). Although 17β-estradiol may negatively influence the MPV, it appears that fluctuations of both sex hormones across the MC and OC phases are not prominent enough to induce significant or practically relevant changes in the assessed parameters.NEW & NOTEWORTHY Although a high intraindividual 17β-estradiol concentration was associated with a lower movement velocity, markers of strength performance and surrogates for nonlocal and local fatigue remained unaffected by MC and OC phases. Blood lactate accumulation was significantly reduced in the mLP. Furthermore, our findings suggest that the impact of the MC phases varies greatly among individuals. Individuals with high fluctuations in sex hormone concentrations may experience relevant changes in the assessed parameters.

The molecular mechanisms that drive muscle adaptations after eccentric exercise training are multifaceted and likely impacted by age. Previous studies have reported that many genes and proteins respond differently in young and older muscles following training. Keratin 18 (Krt18), a cytoskeletal protein involved in force transduction and organization, was found to be upregulated after muscles performed repeated bouts of eccentric contractions, with higher levels observed in young muscle compared with older muscle. Therefore, the purpose of this study was to determine if Krt18 mediates skeletal muscle adaptations following eccentric exercise training. The anterior crural muscles of Krt18 knockout (KO) and wild-type (WT) mice were subjected to either a single bout or repeated bouts of eccentric contractions, with isometric torque assessed across the initial and final bouts. Functionally, Krt18 KO and WT mice did not differ prior to performing any eccentric contractions (P ≥ 0.100). Muscle strength (tetanic isometric torques) and the ability to adapt to eccentric exercise training were also consistent across strains at all time points (P ≥ 0.169). Stated differently, immediate strength deficits and the recovery of strength following a single bout or multiple bouts of eccentric contractions were similar between Krt18 KO and WT mice. In summary, the absence of Krt18 does not impede the muscle's ability to adapt to repeated eccentric contractions, suggesting it is not essential for exercise-induced remodeling.NEW & NOTEWORTHY The molecular processes that underlie the changes in skeletal muscle following eccentric exercise training are complex and involve multiple factors. Our findings indicate that Krt18 may not play a significant role in muscle adaptations following eccentric exercise training, likely due to its low expression in skeletal muscle. These results underscore the complexity of the molecular mechanisms that contribute to muscle plasticity and highlight the need for further research in this area.

This cross-sectional study aims to elucidate the neural mechanisms underlying the control of knee extension forces in individuals with anterior cruciate ligament reconstruction (ACLR). Eleven soccer players with ACLR and nine control players performed unilateral isometric knee extensions at 10% and 30% of their maximum voluntary force (MVF). Simultaneous recordings of high-density surface electromyography (HDEMG) and force output were conducted for each lower limb, and HDEMG data from the vastus lateralis (VL) and vastus medialis (VM) muscles were decomposed into individual motor unit spike trains. Force steadiness was estimated using the coefficient of variation of force. An intramuscular coherence analysis was adopted to estimate the common synaptic input (CSI) converging to each muscle. A factor analysis was applied to investigate the neural strategies underlying the control of synergistic motor neuron clusters, referred to as motor unit modes. Force steadiness was similar between lower limbs. However, motor neurons innervating the VL on the reconstructed side received a lower proportion of CSI at low-frequency bandwidths (<5 Hz) compared with the unaffected lower limbs (P < 0.01). Furthermore, the reconstructed side demonstrated a higher proportion of motor units associated with the neural input common to the synergistic muscle, as compared with the unaffected lower limbs (P < 0.01). These findings indicate that the VL muscle of reconstructed lower limbs contribute marginally to force steadiness and that a plastic rearrangement in synergistic clusters of motor units involved in the control of knee extension forces is evident following ACLR.NEW & NOTEWORTHY Chronic quadriceps dysfunction is common after anterior cruciate ligament reconstruction (ACLR). We investigated voluntary force control strategies by estimating common inputs to motor neurons innervating the vastii muscles. Our results showed attenuated common inputs to the vastus lateralis and plastic rearrangements in functional clusters of motor neurons modulating knee extension forces in the reconstructed limb. These findings suggest neuroplastic adjustments following ACLR that may occur to fine-tune the control of quadriceps forces.

Brain hypoperfusion is associated with cognitive impairment. Higher cerebrovascular impedance modulus (Z) may contribute to brain hypoperfusion. We tested hypotheses that patients with amnestic mild cognitive impairment (aMCI) (i.e., those who have a high risk of developing Alzheimer's disease) have higher Z than age-matched cognitively normal individuals, and that high Z is correlated with brain hypoperfusion. Fifty-eight patients with aMCI (67 ± 7 yr) and 25 cognitively normal subjects (CN, 65 ± 6 yr) underwent simultaneous measurements of carotid artery pressure (CAP, via applanation tonometry) and middle cerebral arterial blood velocity (CBV, via transcranial Doppler). Z was quantified using cross-spectral and transfer function analyses between dynamic changes in CBV and CAP. Patients with aMCI exhibited higher Z than NC (1.18 ± 0.34 vs. 1.01 ± 0.35 mmHg/cm/s, P = 0.044) in the frequency range from 0.78 to 4.29 Hz. The averaged Z in the frequency range (0.78-3.13 Hz) of high coherence (>0.9) was inversely correlated with total cerebral blood flow measured with 2-D Doppler ultrasonography normalized by the brain tissue mass (via structural MRI) across both patients with aMCI and NC (r = -0.311, P = 0.007), and in patients with aMCI alone (r = -0.306, P = 0.007). Our findings suggest that patients with aMCI have higher cerebrovascular impedance than cognitively normal older adults and that increased cerebrovascular impedance is associated with brain hypoperfusion.NEW & NOTEWORTHY This is the first study to compare cerebrovascular impedance between patients with amnestic mild cognitive impairment (aMCI) and age-matched cognitively normal individuals. Patients with aMCI had higher cerebrovascular impedance modulus than age-matched cognitively normal individuals, which was correlated with brain hypoperfusion. These results suggest the presence of cerebrovascular dysfunction in the dynamic regulation of cerebral blood flow in older adults who have high risks of Alzheimer's disease.