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Twenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise performance during the Wingate anaerobic test (WAnT). Thus, pre-exercise hypocapnic hyperventilation may be a useful means of stressing the anaerobic energy system during training, ultimately improving anaerobic exercise performance. However, it remains unclear whether a shorter (e.g., 5 min) pre-exercise hypocapnic hyperventilation is sufficient to reduce the aerobic metabolic rate during high-intensity exercise. We therefore compared the effects of 5-min and 20-min pre-exercise hypocapnic hyperventilation on aerobic metabolism during the 30-s WAnT. Ten healthy young males and one female performed the WAnT following 20 min of spontaneous breathing (control trial) or 5 or 20 min of voluntary hypocapnic hyperventilation. Both the 5-min and 20-min hyperventilation reduced end-tidal CO2 partial pressure (an index of arterial CO2 partial pressure) to ∼23 mmHg, whereas it remained unchanged during the spontaneous breathing. The peak, mean and minimum power outputs during the WAnT did not differ among the three trials. Oxygen uptake during the WAnT was lower in both the 5-min (1493 ± 257 mL min−1) and 20-min (1397 ± 447 mL min−1) hyperventilation trials than during the control trial (1847 ± 286 mL min−1), and was similar in the two hyperventilation trials. These results suggest that 5 min of pre-exercise hypocapnic hyperventilation reduces aerobic metabolism during the 30-s WAnT to a level similar to that seen with the 20-min hyperventilation. Moreover, exercise performance was unaffected, which implies anaerobic metabolism was enhanced. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study? The lack of useful small‐animal models for studying exercise hyperpnoea makes it difficult to investigate the underlying mechanisms of exercise‐induced ventilatory abnormalities in various disease states. What is the main finding and its importance? We developed an anaesthetized‐rat model for studying exercise hyperpnoea, using a respiratory equilibrium diagram for quantitative characterization of the respiratory chemoreflex feedback system. This experimental model will provide an opportunity to clarify the major determinant mechanisms of exercise hyperpnoea, and will be useful for understanding the mechanisms responsible for abnormal ventilatory responses to exercise in disease models. Abstract: Exercise‐induced ventilatory abnormalities in various disease states seem to arise from pathological changes of respiratory regulation. Although experimental studies in small animals are essential to investigate the pathophysiological basis of various disease models, the lack of an integrated framework for quantitatively characterizing respiratory regulation during exercise prevents us from resolving these problems. The purpose of this study was to develop an anaesthetized‐rat model for studying exercise hyperpnoea for quantitative characterization of the respiratory chemoreflex feedback system. In 24 anaesthetized rats, we induced muscle contraction by stimulating bilateral distal sciatic nerves at low and high voltage to mimic exercise. We recorded breath‐by‐breath respiratory gas analysis data and cardiorespiratory responses while running two protocols to characterize the controller and plant of the respiratory chemoreflex. The controller was characterized by determining the linear relationship between end‐tidal CO2 pressure ( P ETC O 2) and minute ventilation ( V ̇ E), and the plant by the hyperbolic relationship between V ̇ E and P ETC O 2. During exercise, the controller curve shifted upward without change in controller gain, accompanying increased oxygen uptake. The hyperbolic plant curve shifted rightward and downward depending on exercise intensity as predicted by increased metabolism. Exercise intensity‐dependent changes in operating points ( V ̇ E and P ETC O 2) were estimated by integrating the controller and plant curves in a respiratory equilibrium diagram. In conclusion, we developed an anaesthetized‐rat model for studying exercise hyperpnoea, using systems analysis for quantitative characterization of the respiratory system. This novel experimental model will be useful for understanding the mechanisms responsible for abnormal ventilatory responses to exercise in disease models. [ABSTRACT FROM AUTHOR]

New FindingsWhat is the central question of this study? By manipulating recovery intensity and exercise duration during high-intensity interval training (HIIT), we tested the hypothesis that fast inputs contribute more than metabolic stimuli to respiratory frequency (fR) regulation. What is the main finding and its importance? Respiratory frequency, but not tidal volume, responded rapidly and in proportion to changes in workload during HIIT, and was dissociated from some markers of metabolic stimuli in response to both experimental manipulations, suggesting that fast inputs contribute more than metabolic stimuli to fR regulation. Differentiating between fR and tidal volume may help to unravel the mechanisms underlying exercise hyperpnoea. Given that respiratory frequency (fR) has been proposed as a good marker of physical effort, furthering the understanding of how fR is regulated during exercise is of great importance. We manipulated recovery intensity and exercise duration during high-intensity interval training (HIIT) to test the hypothesis that fast inputs (including central command) contribute more than metabolic stimuli to fR regulation. Seven male cyclists performed an incremental test, a 10 and a 20 min continuous time trial (TT) as preliminary tests. Subsequently, recovery intensity and exercise duration were manipulated during HIIT (30 s work and 30 s active recovery) by performing four 10 min and one 20 min trial (recovery intensities of 85, 70, 55 and 30% of the 10 min TT mean workload; and 85% of the 20 min TT mean workload). The work intensity of the HIIT sessions was self-paced by participants to achieve the best performance possible. When manipulating recovery intensity, fR, but not tidal volume (VT), showed a fast response to the alternation of the work and recovery phases, proportional to the extent of workload variations. No association between fR and gas exchange responses was observed. When manipulating exercise duration, fR and rating of perceived exertion were dissociated from VT, carbon dioxide output and oxygen uptake responses. Overall, the rating of perceived exertion was strongly correlated with fR (r = 0.87; P < 0.001) but not with VT. These findings may reveal a differential control of fR and VT during HIIT, with fast inputs appearing to contribute more than metabolic stimuli to fR regulation. Differentiating between fR and VT may help to unravel the mechanisms underlying exercise hyperpnoea. [ABSTRACT FROM AUTHOR]

Key points Hypoglycaemia is counteracted by release of hormones and an increase in ventilation and CO2 sensitivity to restore blood glucose levels and prevent a fall in blood pH., The full counter-regulatory response and an appropriate increase in ventilation is dependent on carotid body stimulation., We show that the hypoglycaemia-induced increase in ventilation and CO2 sensitivity is abolished by preventing adrenaline release or blocking its receptors., Physiological levels of adrenaline mimicked the effect of hypoglycaemia on ventilation and CO2 sensitivity., These results suggest that adrenaline, rather than low glucose, is an adequate stimulus for the carotid body-mediated changes in ventilation and CO2 sensitivity during hypoglycaemia to prevent a serious acidosis in poorly controlled diabetes., Abstract Hypoglycaemia in vivo induces a counter-regulatory response that involves the release of hormones to restore blood glucose levels. Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea that maintains arterial CO2 levels and prevents respiratory acidosis in the face of increased metabolism. It is unclear whether the carotid body is directly stimulated by low glucose or by a counter-regulatory hormone such as adrenaline. Minute ventilation was recorded during infusion of insulin-induced hypoglycaemia (8-17 mIU kg−1 min−1) in Alfaxan-anaesthetised male Wistar rats. Hypoglycaemia significantly augmented minute ventilation (123 ± 4 to 143 ± 7 ml min−1) and CO2 sensitivity (3.3 ± 0.3 to 4.4 ± 0.4 ml min−1 mmHg−1). These effects were abolished by either β-adrenoreceptor blockade with propranolol or adrenalectomy. In this hypermetabolic, hypoglycaemic state, propranolol stimulated a rise in [ABSTRACT FROM AUTHOR]

Aim We hypothesized that hydrogen sulphide ( H2 S), acting specifically in the anteroventral preoptic region ( AVPO - an important integrating site of thermal and cardiorespiratory responses to hypoxia in which H2 S synthesis has been shown to be increased under hypoxic conditions), modulates the hypoxic ventilatory response. Methods To test this hypothesis, we measured pulmonary ventilation ( [ABSTRACT FROM AUTHOR]

One hundred years ago in this journal, Krogh and Lindhard published a seminal paper highlighting the importance of the brain in the control of breathing during exercise. This symposium report reviews the historical developments that have taken place since 1913, and attempts to place the detailed neurocircuitry thought to underpin exercise hyperpnoea into context by focusing on key structures that might form the command network. With the advent of enhanced neuroimaging and functional neurosurgical techniques, a unique window of opportunity has recently arisen to target potential circuits in humans. Animal studies have identified a priori sites of interest in mid-brain structures, in particular the subthalamic locomotor region (subthalamic nucleus, STN) and the periaqueductal grey (PAG), which have now been recorded from in humans during exercise. When all data are viewed in an integrative manner, the PAG, in particular the lateral PAG, and aspects of the dorsal lateral PAG, appear to be key communicating circuitry for 'central command'. Moreover, the PAG also fulfils many requirements of a command centre. It has functional connectivity to higher centres (dorsal lateral prefrontal cortex) and the basal ganglia (in particular, the STN), and receives a sensory input from contracting muscle, but, importantly, it sends efferent information to brainstem nuclei involved in cardiorespiratory control. [ABSTRACT FROM AUTHOR]

Airway dysfunction is prevalent in elite endurance athletes and when left untreated may impact upon both health and performance. There is now concern that the intensity of hyperpnoea necessitated by exercise at an elite level may be detrimental for an athlete's respiratory health. This article addresses the evidence of causality in this context with the aim of specifically addressing whether airway dysfunction in elite athletes should be classified as an occupational lung disease. The approach used highlights a number of concerns and facilitates recommendations to ensure airway health is maintained and optimized in this population. We conclude that elite athletes should receive the same considerations for their airway health as others with potential and relevant occupational exposures. [ABSTRACT FROM AUTHOR]

Previously, we undertook simultaneous recording of ventilation and pulmonary gas exchange in mice and revealed that dopamine D2 receptors participate in exercise hyperpnoea via behavioural control of ventilation with unchanged pulmonary gas exchange. Here, we examined the hypothesis that D1 receptors also contribute to exercise hyperpnoea using a D1 receptor antagonist (SCH 23390; SCH) that crosses the blood-brain barrier, with the same recording technique and protocol as in the previous study. The respiratory responses of mice injected with saline or SCH (50 μg (kg body weight)−1, i.p.) were compared during constant-load exercise at 6 m min−1. Each mouse was set in an airtight treadmill chamber equipped with a differential pressure transducer and open-circuit system with a mass spectrometer. At rest, SCH-injected mice had significantly reduced respiratory frequency, minute ventilation and pulmonary gas exchange compared with saline-injected mice. Ventilation during hyperoxic gas inhalation and hypercapnic ventilatory responses between groups were similar. Abrupt increases and sequential declines to the steady-state level were produced by treadmill exercise in both groups of mice. Treatment with SCH lowered the increased levels of respiratory frequency, tidal volume and minute ventilation during the steady state, as well as reducing the O2 uptake, CO2 output and body temperature throughout treadmill exercise. These data suggest that D1 receptors contribute to a resting ventilation level and exercise hyperpnoea during the steady state in parallel with metabolic changes. Notably, the metabolic control of D1 receptors was important for maintenance of the steady state, and D1 receptors in hypothalamic nuclei could be involved in this modulation. [ABSTRACT FROM AUTHOR]

Aim The neural structures responsible for the coupling between ventilatory control and pulmonary gas exchange during exercise have not been fully identified. Suprapontine mechanisms have been hypothesized but not formally evidenced. Because the involvement of a premotor circuitry in the compensation of inspiratory mechanical loads has recently been described, we looked for its implication in exercise-induced hyperpnea. Methods Electroencephalographical recordings were performed to identify inspiratory premotor potentials (i PPM) in eight physically fit normal men during cycling at 40 and 70% of their maximal oxygen consumption ( [ABSTRACT FROM AUTHOR]

Aim: It has been suggested that the medullary raphe (MR) plays a key role in the physiological responses to hypoxia. As opioid μ-receptors have been found in the MR, we studied the putative role of opioid μ-receptors in the rostral MR (rMR) region on ventilation in normal and 7% hypoxic conditions. Methods: We measured pulmonary ventilation () and the body temperatures (Tb) of male Wistar rats before and after the selective opioid μ-receptor antagonist CTAP ( d-Phe-Cys-Tyr- d-Trp-Arg-Thr-Pen-Thr-NH2, cyclic, 0.1 μg per 0.1 μL) was microinjected into the rMR during normoxia or after 60 min of hypoxia. Results: The animals treated with intra-rMR CTAP exhibited an attenuation of the ventilatory response to hypoxia (430 ± 86 mL kg−1 min−1) compared with the control group (790 ± 82 mL kg−1 min−1) ( P < 0.05). No differences in the Tb were observed between groups during hypoxia. Conclusion: These data suggest that opioids acting on μ-receptors in the rMR exert an excitatory modulation of hyperventilation induced by hypoxia. [ABSTRACT FROM AUTHOR]

The author reflects on advances in understanding the mechanisms that regulate breathing during exercise. He discusses a concept developed by French physiologist Claude Bernard which assumes that living organisms tend to maintain constant the composition of their internal environment. He also offers information on the work of physiologist C. Gordon Douglas on exercise hyperpnoea.

We investigated whether heat‐induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot‐water immersion and a water‐perfused garment covering their upper body (both 41°C) until esophageal temperature (Tes) reached 39°C or volitional termination. In each trial, participants breathed normally (normal‐breathing) or voluntarily controlled minute ventilation (VE) at a level equivalent to that observed after 5 min of heating (controlled‐breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end‐expiratory and inspiratory lung volumes were measured. During normal‐breathing, VE increased as Tes rose above 38.0 ± 0.3°C, whereas controlled‐breathing diminished the increase in VE (VE at Tes = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min−1 during normal‐ and controlled‐breathing, respectively, P < 0.001). During normal‐breathing, end‐tidal CO2 pressure and MCAV decreased with rising Tes, but controlled‐breathing diminished these reductions (at Tes = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec−1, both P < 0.001). The work of breathing correlated positively with changes in VE (P < 0.001) and was lower during controlled‐ than normal‐breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min−1, respectively, at heating termination, P = 0.013). End‐expiratory and inspiratory lung volumes did not differ between trials (P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat‐induced hyperventilation increases the work of breathing without affecting end‐expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing. We demonstrated that heat‐induced hyperventilation is accompanied by increased work of breathing without an effect of end‐expiratory lung volume, and that this hyperventilation can be voluntarily suppressed, which diminishes the increase in the work of breathing as well as the reductions in arterial CO2 pressure and cerebral blood flow occurring during passive heating. [ABSTRACT FROM AUTHOR]