Peripheral Physiological Systems Research Articles

Hindbrain adrenergic/noradrenergic control of integrated endocrine and autonomic stress responses.

Hindbrain adrenergic/noradrenergic nuclei facilitate endocrine and autonomic responses to physical and psychological challenges. Neurons that synthesize adrenaline and noradrenaline target hypothalamic structures to modulate endocrine responses while descending spinal projections regulate sympathetic function. Furthermore, these neurons respond to diverse stress-related metabolic, autonomic, and psychosocial challenges. Accordingly, adrenergic and noradrenergic nuclei are integrative hubs that promote physiological adaptation to maintain homeostasis. However, the precise mechanisms through which adrenaline- and noradrenaline-synthesizing neurons sense interoceptive and exteroceptive cues to coordinate physiological responses have yet to be fully elucidated. Additionally, the regulatory role of these cells in the context of chronic stress has received limited attention. This mini-review consolidates reports from pre-clinical rodent studies on the organization and function of brainstem adrenaline and noradrenaline cells to provide a framework for how these nuclei coordinate endocrine and autonomic physiology. This includes identification of hindbrain adrenaline- and noradrenaline-producing cell groups and their role in stress responding through neurosecretory and autonomic engagement. Although temporally and mechanistically distinct, the endocrine and autonomic stress axes are complementary and interconnected. Therefore, the interplay between brainstem adrenergic/noradrenergic nuclei and peripheral physiological systems is necessary for integrated stress responses and organismal survival.

Integrative pathways linking close family ties to health: A neurochemical perspective.

The quality of one's familial life, for better or worse, has been linked to physical health. Such associations are evident across a number of acute and chronic conditions and highlight the widespread impact that close relationships have on physical health. However, the field currently lacks a complete understanding of the integrative biological pathways underlying the association between close relationships and disease risk. This article reviews the main peripheral biological and central nervous system pathways linking positive and negative familial relationship processes to physical health outcomes. It emphasizes the role of neurochemical pathways in mediating the influence of social relationships on health-relevant peripheral physiological systems using the oxytocin system as a model. Such neurochemical approaches are an important step toward a more integrative understanding of complex biological pathways and has novel theoretical and intervention implications. (PsycINFO Database Record

Hot flushes

Vasomotor symptoms, such as hot flushes and night sweats, are considered to be the cardinal symptoms of menopause, and are experienced by most women. The physiology of hot flushes is not fully understood, and is likely to reflect the interplay between multiple central and peripheral physiological systems. Reproductive hormones play an integral role, as evidenced by the onset of vasomotor symptoms during the dramatic reproductive hormone changes of the menopausal transition, and by the efficacy of exogenous oestrogen in the treatment of hot flushes. Menopausal hormone therapy with oestrogen, and with or without a progestogen, is the most widely studied and most effective treatment option for the relief of menopause-related vasomotor symptoms. It is also considered to be the standard of care for women with moderate to severe vasomotor symptoms.

Memory-updating abrogates extinction of learned immunosuppression

When memories are recalled, they enter a transient labile phase in which they can be impaired or enhanced followed by a new stabilization process termed reconsolidation. It is unknown, however, whether reconsolidation is restricted to neurocognitive processes such as fear memories or can be extended to peripheral physiological functions as well. Here, we show in a paradigm of behaviorally conditioned taste aversion in rats memory-updating in learned immunosuppression. The administration of sub-therapeutic doses of the immunosuppressant cyclosporin A together with the conditioned stimulus (CS/saccharin) during retrieval blocked extinction of conditioned taste aversion and learned suppression of T cell cytokine (interleukin-2; interferon-γ) production. This conditioned immunosuppression is of clinical relevance since it significantly prolonged the survival time of heterotopically transplanted heart allografts in rats. Collectively, these findings demonstrate that memories can be updated on both neural and behavioral levels as well as on the level of peripheral physiological systems such as immune functioning.

Memory reconsolidation prevents extinction of learned immunosuppression

When memories are recalled, they enter a transient labile phase in which they can be impaired or enhanced followed by a new stabilization process termed reconsolidation. It is unknown, however, whether reconsolidation is restricted to neurocognitive processes such as fear memories or can be extended to peripheral physiological functions as well. Bidirectional interaction between the brain and peripheral immune system, together with the fact that immune functions can be modified by associative learning processes provide a unique opportunity to test this assumption. Employing an established paradigm of behaviorally-conditioned taste aversion in rats, we here demonstrate reconsolidation in “learned immunosuppression”. The administration of sub-therapeutic doses of the calcineurin inhibitor and immunosuppressant cyclosporin A (CsA) together with the conditioned stimulus (CS/saccharine) during evocation blocked the extinction of conditioned taste aversion and learned suppression of T cell cytokine (interleukin-2; interferon-gamma) production. In contrast, reconsolidation of learned immunosuppression could not be induced by administering sub-therapeutic CsA as a reminder cue outside the reconsolidation window, 8 hours after CS exposure. This reconsolidated immunosuppression is of clinical relevance since it significantly prolonged the survival time of heterotopically-transplanted heart allografts in rats. Collectively, these findings demonstrate that memories can reconsolidate on peripheral physiological systems such as immune functioning; they might pave the way for the systematic integration of conditioning paradigms as supportive therapy in pharmacological regimens.

Biomarkers of stress in behavioural medicine

In recent years, a growing interest has emerged in behavioural medicine to examine the role of acute and chronic stress as a predisposing and contributing factor to physical health and illness. For a deeper understanding of these associations, research is in need of biological markers for alterations in biological stress systems. This review will summarize a selection of important recent findings in this area of research. We will focus on essential peripheral stress-sensitive physiological systems, that is, the hypothalamic-pituitary-adrenal axis, the autonomic nervous system, and the immune system. We will present findings on commonly used stress biomarkers (cortisol, alpha-amylase, pro-inflammatory cytokines) regarding alterations in basal activity and stress-dependent reactivity in these systems, and discuss selected findings on intervention-induced changes of these biomarkers. This review will highlight new developments and guide readers in their choice of suitable study designs and outcomes in behavioural medicine. The reviewed studies included here encourage optimism that the employment of stress biomarkers in behavioural medicine has the potential to significantly improve our understanding of physical health and illness.

Hyperthermia effects on brain function and exercise capacity

Abstract Hyperthermia has been demonstrated as an important factor limiting endurance per-formance in a hot environment in both human and animal studies. While temperature can affect individual peripheral physiological systems such as muscle contraction characteristics directly, a dominant role for central mechanisms for exercise impairment has been proposed over the past two decades. Exercise-induced hyperthermia may have a direct effect on the central nervous system such as brain temperature, cerebral blood flow, brain activity, cognitive function, brain neurotransmission and neuromuscular activity. In turn, these changes may affect not only the physiological capacity for exercise, but also the athlete’s perception of heat stress, motivation for exercise or pacing strategy. The purpose of this review is to focus on the central mechanisms underlying human limits to exercise in heat. Specifically, the effects of hyperthermia on brain physiology and function will be summarized, along with the potential impact of these changes on regulating exercise capacity.

What do we know about serotonin?

The present review focuses on what is known of basic serotonin physiology in the human body. Here, we describe serotonin biochemistry and metabolism and summarize the results of studies that have contributed significantly to our understanding of serotonin physiology. We report the well-established role of serotonin in cardiovascular, gastrointestinal, and circulatory physiology. Emphasis is placed on the role of serotonin in peripheral physiological systems rather than in the central nervous system. A brief overview is provided on the emerging role of serotonin in novel areas such as bone pathways and glucose uptake. We also report a select few animal studies and animal models that have provided worthwhile contributions to the understanding of serotonin in human physiology. In addition, we summarize the results of large-scale genetic studies on serotonin and serotonin transporter genes, performed in relation to behavioral and mood disorders.

Why does exercise terminate at the maximal lactate steady state intensity?

Objective:The purpose of this study was to measure physiological responses during exercise performed until exhaustion at the exercise intensity corresponding to the maximal lactate steady state (MLSS) in order to...

Medically unexplained symptoms and between-group differences in 24-h ambulatory recording of stress physiology

People with medically unexplained symptoms (MUS) often have a comorbid history of stress and negative affect. Although the verbal-cognitive and (peripheral) physiological stress systems have shown a great degree of independence, at the same time it is claimed that chronic stress and negative affect can result in a disregulated physiological stress system, which may lead to MUS. Previous studies could not demonstrate a straightforward between subject relationship between MUS and stress physiology, supporting the view of independence. The aim of the current study was to further explore this relationship using an improved methodology based on ecologically valid 24-h real-life ambulatory recordings. Seventy-four participants (19 male; 55 female) with heterogeneous MUS were compared with 71 healthy controls (26 male; 45 females). Momentary experienced somatic complaints and mood, heart rate, cardiac autonomic activity, respiration and saliva cortisol were monitored using electronic diary and ambulatory registration devices. Participants with MUS reported much more momentary complaints and negative affect as compared to controls. Although MUS seemed to be associated with elevated heart rate and reduced low and very-low frequency heart period variability, these effects disappeared after controlling for differences in sports behaviour. No group differences were found for cardiac autonomic activity, respiration, end-tidal CO2 and saliva cortisol. Our 24-h real-life ambulatory study did not support the existence of a connection between MUS and disregulated peripheral stress physiology. Future studies may instead focus on central measures to reveal potential abnormalities such as deviant central processing of visceral signals in MUS patients.

The Role of Information Processing Between the Brain and Peripheral Physiological Systems in Pacing and Perception of Effort

This article examines how pacing strategies during exercise are controlled by information processing between the brain and peripheral physiological systems. It is suggested that, although several different pacing strategies can be used by athletes for events of different distance or duration, the underlying principle of how these different overall pacing strategies are controlled is similar. Perhaps the most important factor allowing the establishment of a pacing strategy is knowledge of the endpoint of a particular event. The brain centre controlling pace incorporates knowledge of the endpoint into an algorithm, together with memory of prior events of similar distance or duration, and knowledge of external (environmental) and internal (metabolic) conditions to set a particular optimal pacing strategy for a particular exercise bout. It is proposed that an internal clock, which appears to use scalar rather than absolute time scales, is used by the brain to generate knowledge of the duration or distance still to be covered, so that power output and metabolic rate can be altered appropriately throughout an event of a particular duration or distance. Although the initial pace is set at the beginning of an event in a feedforward manner, no event or internal physiological state will be identical to what has occurred previously. Therefore, continuous adjustments to the power output in the context of the overall pacing strategy occur throughout the exercise bout using feedback information from internal and external receptors. These continuous adjustments in power output require a specific length of time for afferent information to be assessed by the brain's pace control algorithm, and for efferent neural commands to be generated, and we suggest that it is this time lag that crates the fluctuations in power output that occur during an exercise bout. These non-monotonic changes in power output during exercise, associated with information processing between the brain and peripheral physiological systems, are crucial to maintain the overall pacing strategy chosen by the brain algorithm of each athlete at the start of the exercise bout.

From Catastrophic to Complex System Control of Exercise-Metabolic Signalling Between Peripheral Physiological Systems and the Brain, and the Conscious Perception of these Signalling Processes

From Catastrophic to Complex System Control of Exercise-Metabolic Signalling Between Peripheral Physiological Systems and the Brain, and the Conscious Perception of these Signalling Processes

From Catastrophic to Complex System Control of Exercise - Electrophysiological and Piezoelectric Information Processing Between the Brain and Peripheral Physiological Systems

From Catastrophic to Complex System Control of Exercise - Electrophysiological and Piezoelectric Information Processing Between the Brain and Peripheral Physiological Systems

From Catastrophic to Complex System Control of Exercise - Electrophysiological and Piezoelectric Information Processing Between the Brain and Peripheral Physiological Systems

From Catastrophic to Complex System Control of Exercise - Electrophysiological and Piezoelectric Information Processing Between the Brain and Peripheral Physiological Systems

From Catastrophic to Complex System Control of Exercise-Metabolic Signalling Between Peripheral Physiological Systems and the Brain, and the Conscious Perception of these Signalling Processes

From Catastrophic to Complex System Control of Exercise-Metabolic Signalling Between Peripheral Physiological Systems and the Brain, and the Conscious Perception of these Signalling Processes

Metabolic setpoint control mechanisms in different physiological systems at rest and during exercise

Using a number of different homeostatic control mechanisms in the brain and peripheral physiological systems, metabolic activity is continuously regulated at rest and during exercise to prevent catastrophic system failure. Essential for the function of these regulatory processes are baseline “setpoint” levels of metabolic function, which can be used to calculate the level of response required for the maintenance of system homeostasis after system perturbation, and to which the perturbed metabolic activity levels are returned to at the end of the regulatory process. How these setpoint levels of all the different metabolic variables in the different peripheral physiological systems are created and maintained, and why they are similar in different individuals, has not been well explained. In this article, putative system regulators of metabolic setpoint levels are described. These include that: (i) innate setpoint values are stored in a certain region of the central nervous system, such as the hypothalamus; (ii) setpoint values are created and maintained as a response to continuous external perturbations, such as gravity or “zeitgebers”, (iii) setpoint values are created and maintained by complex system dynamical activity in the different peripheral systems, where setpoint levels are regulated by the ongoing feedback control activity between different peripheral variables; (iv) human anatomical and biomechanical constraints contribute to the creation and maintenance of metabolic setpoints values; or (v) a combination of all these four different mechanisms occurs. Exercise training and disease processes can affect these metabolic setpoint values, but the setpoint values are returned to pre-training or pre-disease levels if the training stimulus is removed or if the disease process is cured. Further work is required to determine what the ultimate system regulator of metabolic setpoint values is, why some setpoint values are more stringently protected by homeostatic regulatory mechanisms than others, and the role of conscious decision making processes in determining the regulation of metabolic setpoint values.

Physiological effects of emotional odors

Advances in neuromaging have provided new and exciting knowledge concerning how odors come to activate emotional systems in the brain. Often neglected are the concomitant changes that follow this activation throughout the body. Odor‐induced emotional changes in peripheral physiological systems will be critically discussed including changes in respiration, muscle tone, skin conductance and heart rate. Multidimensional patterning of these responses may prove especially valuable in identifying subtle emotional response. Research to date, however, contains few examples of successful response patterning related to odors.

The Psychobiology of Stress

Stressful life experience can have significant effects on a variety of physiological systems, including the autonomic nervous system, the hypothalamic-pituitary-adrenal axis, and the immune system. These relationships can be bidirectional; for example, immune cell products can act on the brain, altering mood and cognition, potentially contributing to depression. Although acute physiological alterations may be adaptive in the short term, chronic or repeated provocation can result in damage to health. The central dogma in the field of stress research assumes a stereotyped physiological response to all stressors (the generality model). However, increasing evidence suggests that specific stressful conditions and the specific way an organism appraises these conditions can elicit qualitatively distinct emotional and physiological responses (the integrated specificity model). For example, appraisals of threat (vs. challenge), uncontrollability, and negative social evaluation have been shown to provoke specific psychobiological responses. Emotional responses appear to have specific neural substrates, which can result in differentiated alterations in peripheral physiological systems, so that it is incorrect to presume a uniform stress response.

Structural changes in nuclear chromatin in rat pituitary after chronic stress of low intensity.

Acute, intense sources of "psychogenic" stress clearly modify the structure and function of the hypophysis, and there are concomitant changes in many peripheral physiological systems. Less dramatic sources of stress yield more equivocal results. An experiment is reported in which nuclear morphology of adenohypophyseal cells from 49 male rats exposed to a chronic, low-intensity stressor was examined both by conventional histological and computer-assisted-image-processing methods. The hypothesis tested was that an unequivocal pattern of morphological changes in the nucleus and nuclear chromatin would be revealed by image processing. Rats were killed after living for a year in a relatively low-stress environment, "crowded" in groups of five animals per cage. The control condition was a minimal stress environment of two rats per cage. Results suggested few signs of pathology from peripheral measures of hypophyseal activity, and direct light microscopic examination of the gland revealed no differences between the two groups. Analysis of computer-enhanced images of the pars distalis nuclei from the adenohypophysis, on the other hand, generated findings that were statistically and biologically significant. Nuclear size increased in the stress condition, the number of chromatin and area occupied by the particles increased, and the position of chromatin shifted toward the periphery of the nucleus. Perhaps more important, optical density analysis indicated that chromatin was less tightly packed in the experimental animals. Implications are that chronic, low-intensity stress modulates nuclear structural changes from a dormant to an active state that portend changes in the peripheral systems influenced by the hypophysis.