Our concern in these studies was with the cardiovascular consequences of reflexes from fatiguing inspiratory muscles in the human. We recently demonstrated that induction of inspiratory muscle fatigue in healthy subjects by means of voluntary hyperpnoea against resistance caused a gradual increase in muscle sympathetic nerve activity (MSNA) in the resting limb (St Croix et al. 2000). This finding, taken together with the finding of increased neural activity in type IV afferents from the diaphragm during fatiguing contractions of this muscle in the anaesthetized rat (Hill, 1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue.2. In six healthy human subjects at rest, we measured leg blood flow (« Q L ) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3-10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P M ) and a prolonged duty cycle (T I /T TOT = 0.7); and (ii) 60 % maximal P M and a T I /T TOT of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P CO 2 was maintained by increasing the inspired CO 2 fraction (F I,CO 2 ) as needed. Both trials caused a 25-40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation.3. « Q L and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, « Q L subsequently decreased (_30 %) and LVR increased (50-60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4-13 mmHg) and heart rate (+16-20 beats min _1 ) increased during fatiguing diaphragm contractions.4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 w eupnoea), « Q L , MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in « Q L .5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and « Q L increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume.6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effec...

The purpose of this review is to outline the physiological responses associated with the diving response, its functional significance, and its cardiorespiratory control. This review is separated into four major sections. Section one outlines the diving response and its physiology. Section two provides support for the hypothesis that the primary role of the diving response is the conservation of oxygen. The third section describes how the diving response is controlled and provides a model that illustrates the cardiorespiratory interaction. Finally, the fourth section illustrates potential adaptations that result after regular exposure to an asphyxic environment. The cardiovascular and endocrine responses associated with the diving response and apnea are bradycardia, vasoconstriction, and an increase in secretion of suprarenal catecholamines. These responses require the integration of both the cardiovascular system and the respiratory system. The primary role of the diving response is likely to conserve oxygen for sensitive brain and heart tissue and to lengthen the time before the onset of serious hypoxic damage. We suggest that future research should be focused towards understanding the role of altered ventilatory responses in human breath-hold athletes as well as in patients suffering from sleep-disordered breathing.

Constant cerebral blood flow (CBF) is vital to human survival. Originally thought to receive steady blood flow, the brain has shown to experience increases in blood flow during exercise. Although increases have not consistently been documented, the overwhelming evidence supporting an increase may be a result of an increase in brain metabolism. While an increase in metabolism may be the underlying causative factor for the increase in CBF during exercise, there are many modulating variables. Arterial blood gas tensions, most specifically the partial pressure of carbon dioxide, strongly regulate CBF by affecting cerebral vessel diameter through changes in pH, while carbon dioxide reactivity increases from rest to exercise. Muscle mechanoreceptors may contribute to the initial increase in CBF at the onset of exercise, after which exercise-induced hyperventilation tends to decrease flow by pial vessel vasoconstriction. Although elite athletes may benefit from hyperoxia during intense exercise, cerebral tissue is well protected during exercise, and cerebral oxygenation does not appear to pose a limiting factor to exercise performance. The role of arterial blood pressure is important to the increase in CBF during exercise; however, during times of acute hypotension such as during diastole at high-intensity exercise or post-exercise hypotension, cerebral autoregulation may be impaired. The impairment of an increase in cardiac output during exercise with a large muscle mass similarly impairs the increase in CBF velocity, suggesting that cardiac output may play a key role in the CBF response to exercise. Glucose uptake and CBF do not appear to be related; however, there is growing evidence to suggest that lactate is used as a substrate when glucose levels are low. Traditionally thought to have no influence, neural innervation appears to be a protective mechanism to large increases in cardiac output. Changes in middle cerebral arterial velocity are independent of changes in muscle sympathetic nerve activity, suggesting that sympathetic activity does not alter medium-sized arteries (middle cerebral artery).CBF does not remain steady, as seen by apparent increases during exercise, which is accomplished by a multi-factorial system, operating in a way that does not pose any clear danger to cerebral tissue during exercise under normal circumstances.

The purpose of this study was to compare the mechanics of breathing including the measurement of expiratory flow limitation, end-expiratory lung volume, end-inspiratory lung volume, and the work of breathing in endurance-trained men (n = 8) and women (n = 10) during cycle exercise. Expiratory flow limitation was assessed by applying a negative expiratory pressure at the mouth. End-expiratory lung volume and end-inspiratory lung volume were determined by having subjects perform inspiratory capacity manoeuvres. Transpulmonary pressure, taken as the difference between oesophageal and airway opening pressure, was plotted against volume and integrated to determine the work of breathing. Expiratory flow limitation occurred in nine females (90%) and three males (43%) during the final stage of exercise. Females had a higher relative end-expiratory lung volume (42 ± 8 versus 35 ± 5% forced vital capacity (FVC)) and end-inspiratory lung volume (88 ± 5 versus 82 ± 7% FVC) compared to males at maximal exercise (P < 0.05). Women also had a higher work of breathing compared to men across a range of ventilations. On average, women had a work of breathing that was twice that of men at ventilations above 90 l min −1 . These data suggest that expiratory flow limitation may be more common in females and that they experience greater relative increases in end-expiratory lung volume and end-inspiratory lung volume at maximal exercise compared to males. The higher work of breathing in women is probably attributed to their smaller lung volumes and smaller diameter airways. Collectively, these findings suggest that women utilize a greater majority of their ventilatory reserve compared to men and this is associated with a higher cost of breathing.

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We hypothesized that inspiratory muscle training (IMT) would attenuate the sympathetically mediated heart rate (HR) and mean arterial pressure (MAP) increases normally observed during fatiguing inspiratory muscle work. An experimental group (Exp, n = 8) performed IMT 6 days per week for 5 weeks at 50% of maximal inspiratory pressure (MIP), while a control group (Sham, n = 8) performed IMT at 10% MIP. Pre-and post-training, subjects underwent a eucapnic resistive breathing task (RBT) (breathing frequency = 15 breaths min −1 , duty cycle = 0.70) while HR and MAP were continuously monitored. Following IMT, MIP increased significantly (P < 0.05) in the Exp group (−125 ± 10 to −146 ± 12 cmH 2 O; mean ± S.E.M.) but not in the Sham group (−141 ± 11 to −148 ± 11 cmH 2 O). Prior to IMT, the RBT resulted in significant increases in HR (Sham: 59 ± 2 to 83 ± 4 beats min −1 ; Exp: 62 ± 3 to 83 ± 4 beats min −1 ) and MAP (Sham: 88 ± 2 to 106 ± 3 mmHg; Exp: 84 ± 1 to 99 ± 3 mmHg) in both groups relative to rest. Following IMT, the Sham group observed similar HR and MAP responses to the RBT while the Exp group failed to increase HR and MAP to the same extent as before (HR: 59 ± 3 to 74 ± 2 beats min −1 ; MAP: 84 ± 1 to 89 ± 2 mmHg). This attenuated cardiovascular response suggests a blunted sympatho-excitation to resistive inspiratory work. We attribute our findings to a reduced activity of chemosensitive afferents within the inspiratory muscles and may provide a mechanism for some of the whole-body exercise endurance improvements associated with IMT.

Study design: Experts opinions consensus.Objective: To develop a common strategy to document remaining autonomic neurologic function following spinal cord injury (SCI). Background and Rationale: The impact of a specific SCI on a person's neurologic function is generally described through use of the International Standards for the Neurological Classification of SCI. These standards document the remaining motor and sensory function that a person may have; however, they do not provide information about the status of a person's autonomic function. Methods: Based on this deficiency, the American Spinal Injury Association (ASIA) and the International Spinal Cord Society (ISCoS) commissioned a group of international experts to develop a common strategy to document the remaining autonomic neurologic function. Results: Four subgroups were commissioned: bladder, bowel, sexual function and general autonomic function. On-line communication was followed by numerous face to face meetings. The information was then presented in a summary format at a course on Measurement in Spinal Cord Injury, held on June 24, 2006. Subsequent to this it was revised online by the committee members, posted on the websites of both ASIA and ISCoS for comment and re-revised through webcasts. Topics include an overview of autonomic anatomy, classification of cardiovascular, respiratory, sudomotor and thermoregulatory function, bladder, bowel and sexual function. Conclusion: This document describes a new system to document the impact of SCI on autonomic function. Based upon current knowledge of the neuroanatomy of autonomic function this paper provides a framework with which to communicate the effects of specific spinal cord injuries on cardiovascular, broncho-pulmonary, sudomotor, bladder, bowel and sexual function.

Rock climbing has increased in popularity as both a recreational physical activity and a competitive sport. Climbing is physiologically unique in requiring sustained and intermittent isometric forearm muscle contractions for upward propulsion. The determinants of climbing performance are not clear but may be attributed to trainable variables rather than specific anthropometric characteristics.