Neural regulation of cardiovascular response to exercise: role of central command and peripheral afferents

During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discusse

Physiological modeling of isoprene dynamics in exhaled breath

Human breath contains a myriad of endogenous volatile organic compounds (VOCs) which are reflective of ongoing metabolic or physiological processes. While research into the diagnostic potential and general medical relevance of these trace gases is conducted on a considerable scale, little focus has been given so far to a sound analysis of the quantitative relationships between breath levels and the underlying systemic concentrations. This paper is devoted to a thorough modeling study of the end-tidal breath dynamics associated with isoprene, which serves as a paradigmatic example for the class of low-soluble, blood-borne VOCs. Real-time measurements of exhaled breath under an ergometer challenge reveal characteristic changes of isoprene output in response to variations in ventilation and perfusion. Here, a valid compartmental description of these profiles is developed. By comparison with experimental data it is inferred that the major part of breath isoprene variability during exercise conditions can be attributed to an increased fractional perfusion of potential storage and production sites, leading to higher levels of mixed venous blood concentrations at the onset of physical activity. In this context, various lines of supportive evidence for an extrahepatic tissue source of isoprene are presented. Our model is a first step towards new guidelines for the breath gas analysis of isoprene and is expected to aid further investigations regarding the exhalation, storage, transport and biotransformation processes associated with this important compound.Comment: 14 page

Physiological modeling of isoprene dynamics in exhaled breath

Human breath contains a myriad of endogenous volatile organic compounds (VOCs) which are reflective of ongoing metabolic or physiological processes. While research into the diagnostic potential and general medical relevance of these trace gases is conducted on a considerable scale, little focus has been given so far to a sound analysis of the quantitative relationships between breath levels and the underlying systemic concentrations. This paper is devoted to a thorough modeling study of the end-tidal breath dynamics associated with isoprene, which serves as a paradigmatic example for the class of low-soluble, blood-borne VOCs. Real-time measurements of exhaled breath under an ergometer challenge reveal characteristic changes of isoprene output in response to variations in ventilation and perfusion. Here, a valid compartmental description of these profiles is developed. By comparison with experimental data it is inferred that the major part of breath isoprene variability during exercise conditions can be attributed to an increased fractional perfusion of potential storage and production sites, leading to higher levels of mixed venous blood concentrations at the onset of physical activity. In this context, various lines of supportive evidence for an extrahepatic tissue source of isoprene are presented. Our model is a first step towards new guidelines for the breath gas analysis of isoprene and is expected to aid further investigations regarding the exhalation, storage, transport and biotransformation processes associated with this important compound.Comment: 14 page

THE EFFECT OF NORMOBARIC HYPOXIA AND METABOREFLEX IN THE CARDIOVASCULAR ADJUSTMENTS TO EXERCISE

INTRODUCTION It is well established that both hypoxia and metaboreflex have a great impact on the cardiovascular system, exerting both contrasting and complementary effects on heart rate (HR), cardiac output (CO), ventilation (VE), stroke volume (SV) and systemic vascular resistance (SVR). However, evidence on the interaction between hypoxia and metaboreflex when concomitantly active is still lacking. The aim of my study was to better elucidate this topic, focusing on hemodynamic parameters that have never been studied in the past in this context (like SV, BP, and SVR). To reach this goal, I performed 2 series of experiments in which were evaluated the effects of a previous dynamic exercise bout in hypoxia (Experiment 1) and the simultaneous exposure to hypoxia (Experiment 2) on metaboreflex activation. MATERIALS AND METHODS Experiment 1 was conducted recruiting 17 well-trained subjects (7 females, 10 males) that underwent a cardiopulmonary exercise test (CPET) to asses their fitness. Then, the athletes performed a 10-minute rectangular exercise bout on a cycle ergometer in normoxia and in normobaric hypoxia at two different levels of fraction of inspired oxygen (15,5% and 13,5 % of FiO2 ) in three separate days after randomization. Each exercise session was followed by a metaboreflex-activating protocol in normoxia that consisted of 2 sessions called post-exercise muscle ischemia (PEMI) and control exercise recovery (CER). PEMI and CER both included 3 minutes of rest and 3 minutes of exercise at 30% of the maximum wattage (Wmax) reached during the CPET. After the exercise, PEMI was followed by a 3-minute application of an inflatable thigh cuff to induce a temporary occlusion of the arterial and venous vascular bed and 3 minutes of rest. Regarding CER, the exercise was followed by 6 minutes of resting without occlusion and was used as control. In experiment 2, 11 moderately-fit male subjects were recruited. After CPET, the subjects underwent a PEMI/CER session in normoxia and hypoxia (13,5 % of FiO2 ) in 2 separate days. The variables analyzed in experiment 1 and 2 were SV, CO, HR, ventricular filling rate (VFR, a measure of cardiac diastolic function/preload) and ventricular ejection rate (VER a measure of cardiac inotropism) by means of impedance cardiography, mean BP by manual sphygmomanometer and SVR indirectly from CO and BP according to Poiseuille's law. Moreover, I measured cerebral tissue oxygenation (COX) and peripheral hemoglobin saturation (SPO2) by means of near-infrared spectroscopy (NIRS) throughout all the experimental sessions to check if the hypoxia was effective.    RESULTS In both experiments 1 and 2, I evidenced a significant reduction of SV, CO and VFR response during metaboreflex activation when the hypoxic stimulus was applied while SVR response was increased preventing BP from dropping as a consequence of SV reduction. DISCUSSION My results demonstrate that hypoxia can impair SV response to metaboreflex activation. This mechanism is likely related to a reduced left ventricular (LV) preload as VFR decreased when the hypoxic stimulus was applied. Two possible explanations could be proposed to explain my results. Firstly, hypoxia could have stimulated nitric oxide (NO) production in the venous vascular bed with a consequent venodilation and reduced venous return to the heart, impairing the recruitment of the Frank-Starling mechanism to increase SV. Secondly, hypoxia has a vasoconstrictor effect on the pulmonary arterial bed that could have increased right ventricular (RV) afterload, reducing the amount of blood returning to the LV from the pulmonary vascular bed and impairing LV preload. Moreover, SVR response increased both in experiments 1 and 2, counterbalancing the potential BP drop that could have taken place as a consequence of SV reduction. Thus, it can be speculated that metaboreflex activation overcame the vasodilatory effect of hypoxia-mediated NO production on peripheral arteries.

Using near infrared spectroscopy and heart rate variability to detect mental overload

Mental workload is a key factor influencing the occurrence of human error, especially during piloting and remotely operated vehicle (ROV) operations, where safety depends on the ability of pilots to act appropriately. In particular, excessively high or low mental workload can lead operators to neglect critical information. The objective of the present study is to investigate the potential of functional Near Infrared Spectroscopy (fNIRS) – a non-invasive method of measuring prefrontal cortex activity – in combination with measurements of heart rate variability (HRV), to predict mental workload during a simulated piloting task, with particular regard to task engagement and disengagement. Twelve volunteers performed a computer-based piloting task in which they were asked to follow a dynamic target with their aircraft, a task designed to replicate key cognitive demands associated with real life ROV operating tasks. In order to cover a wide range of mental workload levels, task difficulty was manipulated in terms of processing load and difficulty of control – two critical sources of workload associated with piloting and remotely operating a vehicle. Results show that both fNIRS and HRV are sensitive to different levels of mental workload; notably, lower prefrontal activation as well as a lower LF/HF ratio at the highest level of difficulty, suggest that these measures are suitable for mental overload detection. Moreover, these latter measurements point towards the existence of a quadratic model of mental workload

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 171

This bibliography lists 186 reports, articles, and other documents introduced into the NASA scientific and technical information system in August 1977

Intra-Renal Hemodynamic Changes After Habitual Physical Activity in Patients with Chronic Kidney Disease

Background: Chronic Kidney Disease (CKD) is considered a silent epidemic with a continuously growing prevalence around the world. Due to uremia many functional and morphological abnormalities occur in almost all systems. Mostly affected, the cardiovascular system, leads to diminished cardiac function that affects patients’ functional capacity and physical activity levels, reducing survival and increasing all-cause mortality. Systematic exercise training ameliorates uremia induced body deficits and significantly improves the survival of CKD patients. Intradialytic exercise training has been recommended as a complementary therapeutic modality equally important to hemodialysis. Methods: The aim of this systematic review is to provide an update on recent advances in our understanding of how exercise training improves functionality of the cardiovascular system through the hemodynamic changes induced by habitual or intradialytic and/or home-based exercise training programs. Results: Systematic exercise training induces beneficial adaptive responses and influences many sensitive physiological biomarkers, such as oxidative stress biomarkers that are implicated in the development of atherosclerosis. Additionally, exercise training decreases the cardiovascular risk by improving the autonomic nervous system activity and the left ventricular function and by reducing nontraditional risk factors such as epicardial adipose tissue. It seems that all these central and peripheral adaptations to exercise training significantly contribute to improvements in functional capacity and exercise tolerance among CKD patients and result in the risk reduction of CKD-associated disorders. Conclusion: Exercise training could serve as a complimentary therapeutic strategy in CKD patients while health care providers should motivate patients to engage in any type of exercise training programs

The effects diabetes has on the neurovascular system during exercise

The autonomic nervous system is responsible for the involuntary control of most visceral organs. This system greatly influences the neurovascular and cardiovascular systems while at rest and during exercise. Central command, the baroreflex, and the exercise pressor reflex are the three systems that are responsible for the distribution of blood during exercise. Specifically, the exercise pressor reflex plays a dominant role during exercise because it is influenced by metabolic and mechanical factors that affect the vasculature health. Diabetes mellitus is a metabolic disease that can alter the way these systems function within the body. The effects of neural damage and exercise-induced hypoglycemia have been thought to be the sources behind the changes seen in the exercise pressor reflex. Currently, not a lot of research has been done on the exact mechanisms behind the changes of the exercise pressor reflex in diabetes; therefore, the explanations to these alterations are unknown. Thus, the purpose of this report is to develop a hypothesis for the effects of diabetes on the autonomic control of exercise, specifically the exercise pressor reflex.Kinesiology and Health Educatio

Vagal modulation of the heart and central hemodynamics during dynamic handgrip exercise and forearm occlusion following forearm exercise training

The purpose was to examine the cardiovascular response to an acute bout of handgrip exercise before and after non-dominant arm exercise training. 19 people participated in 16 sessions of exercise training and 16 participants acted as controls (age: 20±1yrs). Blood flow measurements were taken at rest and following 3-min of forearm occlusion (RHBF) using plethysmography. Pneumotachometer, ECG, and blood pressure data were continuously collected during three testing conditions (spontaneous breathing (SB1: 5min), handgrip exercise (0.5hz) at 60%MVC with 50mmHg of pressure on the arm (H60+50mmHg: 5 min), and forearm occlusion (FAO: 3min)). Data were analyzed for respiratory rate, mean R-R interval, standard deviation of normal RR intervals (SDNN), normalized units of low- (0-0.15 hz) frequency power (LFnu), and mean arterial pressure (MAP). There was no main effect of group or arm. There was a main effect of test condition such that respiratory rate (+3.10±5.40breaths/min), LFnu (+19.06±14.73%), and MAP increased (+24.51±21.15mmHg) and mean R-R (-247.11±129.70msec) and SDNN (-45.16±40.65msec) decreased significantly during H60+50mmHg (non-dominant arm; p\u3c0.05). Respiratory rate (-0.10±4.84breaths/min), SDNN (-9.50±57.14msec), and LFnu (-1.64±18.34%) recovered to SB1 levels during. Mean R-R (46.11±106.57msec) and MAP (16.65±15.84mmHg) remained elevated above SB1 (p\u3c0.05). There were positive linear associations between forearm circumference and Mean R-R and MAP during H60+50mmHg; and MAP during FAO. There was a negative linear association with forearm circumference and Mean R-R during FAO. There was no significant main effect or interaction with handgrip exercise training on any of the variables. There was a decrease in vascular resistance during RHBF (0.80±1.08 mmHg/ ml/100ml/min, p\u3c0.05) in the arm that underwent exercise training. In conclusion, we found elevated MAP during FAO, which is indicative of significant EPR activity during exercise. Uniquely, we found linear associations between forearm circumference and the cardiovascular response to H60+50mmHg and FAO suggesting variation in the predominant mechanism of cardiovascular control. We did not see an attenuation of cardiovascular responses to H60+50mmHg and FAO with exercise training. However, we did see a decrease in forearm vascular resistance during the reactive hyperemia condition in the exercise-trained arm

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: A systematic review

Exercise performance is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension, exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects as well as in patients with pulmonary hypertension (PH) maximal performance during progressive ramp exercise and endurance of submaximal constant load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH-patients these improvements were mediated by a better arterial, muscular and cerebral oxygenation along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with pulmonary hypertension, alterations in the inspiratory PO2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen delivery to the muscles and the brain, by effects on cardiovascular and respiratory control and by alterations in pulmonary gas exchange. The understanding of these physiologic mechanisms helps counselling individuals planning altitude or air travel and prescribing oxygen therapy to patients with pulmonary hypertension