Increased hypoxic ventilatory response during 8 weeks at 3800 m altitude

Hupperets, Maarten; Hopkins, Susan R.; Pronk, Marieke; Tiemessen, Ivo; Garcia, Nathalie; Wagner, Peter D.; Powell, Frank L.

doi:10.1016/j.resp.2004.06.011

Cited by 33 publications

(31 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They found a significant decrease in the excitability of both excitatory and inhibitory cortical circuits. The cortical changes observed correlated with the level of AMS and the authors suggested this was linked to the respiratory alkalosis which develops 3–5 d after being exposed to hypoxia (70, 71). A modified bicarbonate ion concentration is a result of respiratory alkalosis and this may subsequently change the properties of neuronal membranes and several characteristics of Na + channels, with the net effect being a reduced neuronal excitability (72, 73).…”

Section: Introductionmentioning

confidence: 92%

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Goodall

Twomey

Amann

2014

Fatigue: Biomedicine, Health & Behavior

View full text Add to dashboard Cite

Purpose To outline how hypoxia profoundly affects neuronal functionality and thus compromise exercise-performance. Methods Investigations using electroencephalography (EEG) and transcranial magnetic stimulation (TMS) detecting neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH) were evaluated. Results At rest during very early hypoxia (<1-h), slowing of cerebral neuronal activity is evident despite no change in corticospinal excitability. As time in hypoxia progresses (3-h), increased corticospinal excitability becomes evident; however, changes in neuronal activity are unknown. Prolonged exposure (3–5 d) causes a respiratory alkalosis which modulates Na+ channels, potentially explaining reduced neuronal excitability. Locomotor exercise in AH exacerbates the development of peripheral-fatigue; as the severity of hypoxia increases, mechanisms of peripheral-fatigue become less dominant and CNS hypoxia becomes the predominant factor. The greatest central-fatigue in AH occurs when SaO2 is ≤75%, a level that coincides with increasing impairments in neuronal activity. CH does not improve the level of peripheral-fatigue observed in AH; however, it attenuates the development of central-fatigue paralleling increases in cerebral O2 availability and corticospinal excitability. Conclusions The attenuated development of central-fatigue in CH might explain, the improvements in locomotor exercise-performance commonly observed after acclimatisation to high altitude.

show abstract

Section: Introductionmentioning

confidence: 92%

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Goodall

Twomey

Amann

2014

Fatigue: Biomedicine, Health & Behavior

View full text Add to dashboard Cite

show abstract

“…In the literature, HVD has also been referred to as ventilatory “roll-off” of the HVR or hypoxic ventilatory “depression,” although we explicitly recommend against this latter terminology for reasons explained below. HVD occurs when hypoxemia is sustained for at least 3 to 5 min in adult animals (321) and can persist for as long as 8 weeks in humans during sustained hypoxia at high altitude (167, 350, 351). Thus, this time domain bridges the temporal gap between short-term time domains of the HVR (e.g., STP) and long-term time domains [e.g., VAH and hypoxic desensitization (HD), see later].…”

Section: Physiological and Molecular Responses To Brief Hypoxic Exposmentioning

confidence: 99%

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Pamenter

Powell

2016

Comprehensive Physiology

Self Cite

104

101

View full text Add to dashboard Cite

Ventilatory responses to hypoxia vary widely depending on the pattern and length of hypoxic exposure. Acute, prolonged, or intermittent hypoxic episodes can increase or decrease breathing for seconds to years, both during the hypoxic stimulus, and also after its removal. These myriad effects are the result of a complicated web of molecular interactions that underlie plasticity in the respiratory control reflex circuits and ultimately control the physiology of breathing in hypoxia. Since the time domains of the physiological hypoxic ventilatory response (HVR) were identified, considerable research effort has gone toward elucidating the underlying molecular mechanisms that mediate these varied responses. This research has begun to describe complicated and plastic interactions in the relay circuits between the peripheral chemoreceptors and the ventilatory control circuits within the central nervous system. Intriguingly, many of these molecular pathways seem to share key components between the different time domains, suggesting that varied physiological HVRs are the result of specific modifications to overlapping pathways. This review highlights what has been discovered regarding the cell and molecular level control of the time domains of the HVR, and highlights key areas where further research is required. Understanding the molecular control of ventilation in hypoxia has important implications for basic physiology and is emerging as an important component of several clinical fields.

show abstract

“…Other rats such as Wistars (Tucks) do exhibit a blunted hypoxic response (Wach et al , 1989). Nevertheless, the present findings in rats are relevant, since other species, including humans, exhibit attenuated hypoxic responses following CHH (White et al , 1987; Weil, 1994; Zabka et al , 2001; Hupperets et al , 2004). …”

Section: Discussionmentioning

confidence: 75%

Respiratory modulation of sympathetic activity is attenuated in adult rats conditioned with chronic hypobaric hypoxia

Hsieh

Jacono

Siegel

2015

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

Respiratory modulation of sympathetic nerve activity (SNA) depends on numerous factors including prior experience. Exposing naïve adult, rats (Sprague-Dawley) to acute intermittent hypoxia (AIH) enhances respiratory-modulation of splanchnic SNA (sSNA); whereas conditioning to chronic hypobaric hypoxia (CHH) attenuated modulation. We hypothesized that AIH in CHH rats would restore respiratory modulation of SNA. In anesthetized, CHH-conditioned (0.5 atm, 2 wks) rats (n=16), we recorded phrenic and sSNA before during and after AIH (8% O2 for 45s every 5min for 1h). At baseline, sSNA was not modulated with respiration. The sSNA was not recruited during a single brief exposure of hypoxia nor after 10 repetitive exposures. Further, the sSNA chemoresponse was not restored 1h after completing AIH. Thus, CHH-conditioning blocked the short-term plasticity expressed in sympatho-respiratory efferent activities and this was associated with reduced respiratory modulation of sympathetic activity and with attenuation of the sympatho-respiratory chemoresponse.

show abstract

Increased hypoxic ventilatory response during 8 weeks at 3800 m altitude

Cited by 33 publications

References 14 publications

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Acute and chronic hypoxia: implications for cerebral function and exercise tolerance

Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis

Respiratory modulation of sympathetic activity is attenuated in adult rats conditioned with chronic hypobaric hypoxia

Contact Info

Product

Resources

About