American journal of physiology. Regulatory, integrative and comparative physiology最新文献

This study examined how successive sets of high-intensity leg press (LP) resistance exercise impact the cerebral pressure-flow relationship in untrained males and eumenorrheic females not taking oral contraceptives and assessed how the menstrual cycle (MC) phase influences the cerebral pressure-flow relationship and cerebral hemodynamics (middle cerebral artery blood velocity, MCAv; via transcranial Doppler ultrasound) during and after LP exercise in females. Young adults (11M;11F) performed three sets of leg-press exercises at 90% of their one-repetition maximum. Data from males and females in the early follicular phase were pooled together. Directional sensitivity of the cerebral pressure-flow relationship was calculated as the ratio of the rate of changes in MCAv and mean arterial pressure (MAP) (ΔMCAv_T/ΔMAP_T) per transition between eccentric and concentric muscular contractions during each repetition of LP exercise. ΔMCAv_T/ΔMAP_T was higher during concentric than eccentric phases (P < 0.001) in males and early follicular (EF) phase in females. There were no effects of successive leg press sets on any systemic or cerebral hemodynamic measures. The MC phase affected directional sensitivity and cerebral hemodynamics, with greater responses in the mid-luteal (ML) phase than the EF phase. We observed a MAP direction by MC phase interaction on relative directional sensitivity, with greater sensitivity during concentric contractions in the ML phase (P = 0.02). Our results suggest that successive sets of LP exercises do not impact the cerebral pressure-flow relationship or cerebral hemodynamics during and immediately following LP exercise. The MC phase appears to influence the cerebral pressure-flow relationship and cerebral hemodynamics both during and following LP exercise, mediated by vasoprotective effects of increased estrogen concentration in the ML phase compared with the EF phase.NEW & NOTEWORTHY Successive sets of high-intensity bilateral leg press exercises do not appear to affect cerebral or systemic hemodynamic measures, given adequate recovery time. The menstrual cycle phase impacts the directional sensitivity of the cerebral pressure-flow relationship during high-intensity bilateral leg press exercises. During high-intensity bilateral leg press exercises, the cerebrovasculature appears to be more pressure passive in the mid-luteal phase of the menstrual cycle.

Important inputs originating in the forebrain circumventricular organs and also in the central amygdala (CeA) trigger essential water deprivation (WD)-induced behaviors, such as thirst and sodium appetite. Together with the secretion of the neurohypophysial peptides arginine vasopressin (AVP) and oxytocin (OT), these behavioral responses seek to maintain the normalcy of extracellular fluid (ECF) osmolality and volume. Within this context, the main hypothesis tested by the present study was that CeA type 1 cannabinoid receptors (CB1Rs) were essential for the maintenance of body fluid homeostasis, particularly in response to WD challenge. We found that CeA CB1R knockdown increased spontaneous and WD-induced hypertonic saline intake, without significantly impacting water ingestion. In euhydrated rats, despite unaltered urinary volume, CB1R knockdown reduced urinary osmolality, and diminished urinary nitrate concentrations, suggesting reduced renal sodium excretion. No relevant changes were induced by CeA CB1R knockdown on urinary parameters following WD-induced rehydration, which is consistent with unaltered AVP and OT mRNA transcription and hormone release under the same experimental conditions. Taken together, the present data support the notion that CeA CB1Rs participate in both spontaneous and WD-induced NaCl intake, without significantly affecting neuroendocrine output. Given the well-described facilitatory CeA role on natriorexigenic responses, and the reported interplay between CB1Rs and γ-aminobutyric acid (GABA) within the CeA, the present findings suggest that CB1Rs may indirectly regulate sodium appetite through effects on CeA GABAergic neurotransmission.NEW & NOTEWORTHY CeA CB1R knockdown increased spontaneous and WD-induced hypertonic saline intake, without significantly impacting water ingestion. In euhydrated rats, despite unaltered urinary volume, CB1R knockdown reduced urinary osmolality, and diminished urinary nitrate concentrations, suggesting reduced renal sodium excretion. No relevant changes were induced by CeA CB1R knockdown on urinary parameters following WD-induced rehydration, which is consistent with unaltered AVP and OT mRNA transcription and hormone release under the same experimental conditions.

Cardiovascular responses to exercise are exaggerated in patients with chronic kidney disease (CKD). Enhanced sympathetic activation is thought to play a role with the exercise pressor reflex (EPR), a reflex originating in contracting muscle, modulating this response. Previous studies suggest an overactive EPR in patients with CKD as indicated by muscle sympathetic overactivation during static handgrip exercise. However, the role of the EPR could not be fully elucidated due to experimental constraints inherent to humans. The purpose of this study was to specifically test EPR function in a CKD animal model. Male Sprague-Dawley rats were assigned to a diet containing 0.25% adenine to induce CKD or a control diet. Mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to activation of the EPR, including its functional components, the mechanoreflex and metaboreflex, were assessed in decerebrate, unanesthetized animals after feeding 10-14 wk. Plasma creatinine was significantly higher in CKD rats compared with controls (1.80 ± 0.78 vs. 0.34 ± 0.02 mg·dL^-1, P = 0.017). MAP and RSNA responses to muscle contraction (i.e., EPR activation) were potentiated in CKD rats compared with controls (Δ = 36 ± 19 vs. 17 ± 8 mmHg, P = 0.014 and Δ = 159 ± 62 vs. 64 ± 54%, P = 0.004, respectively). Similarly, the pressor and sympathetic responses to passive muscle stretch (i.e., mechanoreflex stimulation) were significantly higher in CKD than in control animals. Intra-arterial capsaicin administration (i.e., metaboreflex activation) induced an augmented pressor response in CKD rats, compared with controls. Our findings suggest that the EPR, stimulated by the mechanoreflex and metaboreflex, is exaggerated in CKD.NEW & NOTEWORTHY The current investigation identifies that activation of the exercise pressor reflex (EPR) by hindlimb muscle contraction generates exaggerated pressor responses in a chronic kidney disease (CKD) animal model. This hypertensive response is accompanied by sympathetic overactivation during EPR stimulation, with both the muscle mechanoreflex activated by passive muscle stretch and the muscle metaboreflex stimulated by intra-arterial capsaicin administration, contributing to the heightened pressor effect. These findings suggest augmented EPR, mechanoreflex, and metaboreflex function in CKD.

Previous studies have suggested that, during prolonged cold exposure, shivering thermogenesis may gradually be attenuated, supposedly reflecting a state of central fatigue (aka 'thermoregulatory fatigue') provoked by extended shivering activity, that precipitates hypothermia. The purpose of this study was to revisit the validity of this notion. Twelve noncold-acclimatized men participated in three ∼10-h sessions, during which they performed repeatedly three 120-min cold-water immersions. To induce discrete amounts of heat-producing thermoeffector output, presumptively leading to distinct levels of fatigue during each session, subjects were submersed, within each session, in either severely (15°C), moderately (20°C), or slightly (28°C) cold water. The cold-induced elevation in thermogenic rate was similar across the three repeated immersions performed within the 15°C (∼130 W·m²) and 20°C (∼100 W·m²) sessions (P ≥ 0.43). In the 28°C-session, the metabolic heat production was augmented by ∼7% in the second and third immersions compared with the first immersion (P = 0.01). No intrasession differences were noted with regards to the body-core cooling rate, the cold-induced drop in skin temperature and forearm cutaneous vascular conductance, or the stress-hormone (salivary α-amylase and cortisol concentrations) and thermoperceptual responses (P > 0.05). The present findings, therefore, demonstrate that the ability to generate heat remains intact during prolonged iterative exposure to a high-heat loss environment in a single day, regardless of the severity of cold stressor. The intermittent application of slight cold stress (i.e., 28°C water) appears to mediate metabolic sensitization, reflecting either the circadian rhythmicity of heat-producing thermoeffector activity, or perhaps the rapid induction of metabolic adaptation.NEW & NOTEWORTHY The study evaluated whether centrally mediated thermoregulatory fatigue is provoked by prolonged exposure to uncompensable cold. Regardless of the severity of cold stressor, the ability to produce endogenous heat remains intact during prolonged iterative exposure to a high-heat loss environment.

Several forebrain and brainstem neurochemical circuitries interact with peripheral, neural, and humoral signals to collaboratively maintain both the volume and osmolality of extracellular fluids. Over the past decades, much progress has been made in understanding the complex mechanisms underlying the neuroendocrine control of hydromineral homeostasis. Classical experiments performed by Dr. Antunes-Rodrigues in the early 1960s, such as lesions of hypothalamic and extra-hypothalamic areas and drug microinfusions, associated with behavioral analysis and electrolytes/hormones measurements, were crucial to elucidate several aspects of the regulation of hydromineral balance. Fifty years after this pioneering research, the use of immunohistochemistry shifted methodological efforts to the central nervous system, in an attempt to elucidate how neurons (and lately, also glial cells) receive and interpret sensory signals originating from the periphery. This report focuses on the main findings obtained by Dr. Antunes-Rodrigues and colleagues using immunohistochemistry as an important tool in the first two decades of this century to elucidate the brain specific neurochemical circuits underlying functional mechanisms by which osmotic and volume challenges could impact hormonal and behavioral responses.

Purpose: Chronic anxiety is commonly associated with poor sleep patterns, which may contribute to an increased risk of cardiovascular disease (CVD) through mechanisms like oxidative stress, vascular dysfunction, and poor blood pressure control. As sleep disturbances, particularly poor sleep quality and/or regularity, have been independently linked to CVD development, this study explored whether sleep quality/regularity in young adults with chronic anxiety are associated with early indicators of CVD risk, specifically oxidative stress, vascular function, and blood pressure control. Methods: Twenty-eight young (24±4 years) participants with a prior clinical diagnosis of generalized anxiety disorder (GAD) or elevated GAD symptoms (GAD7>10) had their sleep quality (total sleep time (TST) and sleep efficiency (SE)) and regularity (via TST/SE standard deviations (SD)) assessed for seven consecutive days. Various precursors to CVD development such as oxidative stress, brachial artery function, microvascular function, and blood pressure control (exercise pressor responses and cardiovagal baroreflex sensitivity (cBRS)), were also evaluated. Pearson's correlations were utilized to determine potential relationships between sleep quality/regularity and CVD precursors. Results: Both sleep irregularity variables (SE-SD (r=0.61; p<0.01) and TST-SD (r=0.39; p=0.04)), but neither of the sleep quality variables, were positively correlated with oxidative stress. TST-SD alone was significantly associated with lower brachial artery function (r=-0.44; p=0.02) and cBRS (r=0.43; p=0.02), with TST-SD median splits further highlighting these differences. Conclusions: The study found that irregular TST in individuals with chronic anxiety was significantly associated with higher oxidative stress, lower brachial artery function, and blunted blood pressure control (lower cBRS), key precursors of CVD.

Obesity is increasingly prevalent worldwide, and climate change is exacerbating water shortages, leading to dehydration. Both obesity and dehydration cause increased arterial pressure (AP), fluid electrolytic imbalance, and neuroinflammation. Thus, the present study aimed to verify the changes in the cardiovascular system, hydroelectrolytic balance and microglia and neuronal activation in rats fed with a high-fat diet (HFD) in response to 24 h of water deprivation (WD) and the possible mechanisms involved. Male Holtzman rats (290-310 g) were fed with a standard diet (SD, 10% calories from fat) or HFD (46% calories from fat) for 6 weeks before the WD experiments. Compared to WD SD rats, WD HFD rats presented a greater c-Fos immunolabelling in the subfornical organ (SFO) and supraoptic nucleus and greater microglial activation in SFO. WD-induced water intake was lower in HFD rats than in SD rats. WD HFD rats presented greater anti-diuresis and lesser natriuresis than WD SD rats. Renal denervation did not change the anti-diuresis or natriuresis observed in WD HFD or SD-fed rats. The lower water intake in WD HFD rats might be due to neuroinflammation and/or decreased urinary output. The increase in AP after WD was similar between HFD and SD, but it is more dependent on AT1 receptor activation in HFD rats. Overall, HFD rats seem less responsive to fluid and electrolyte balance responses to WD, highlighting the need for strategies to prevent dehydration in obese individuals, particularly during rising drought conditions worldwide.