Diaphragm fatigue during exercise at high altitude: the role of hypoxia and workload

Guðjónsdóttir, Marta; Appendini, Lorenzo; Baderna, Paolo; Purro, Andrea; Patessio, A; Vilianis, G; Pastorelli, Marcello; Sigurdsson, Stefan; Donner, Claudio F.

doi:10.1183/09031936.01.17406740

Cited by 25 publications

(30 citation statements)

References 28 publications

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“…Using this technique we found no evidence of exercise-induced central activation failure of the diaphragm. This finding is in agreement with one previous study (Gudjonsdottir et al 2001), although more recent evidence using transcranial magnetic stimulation suggests that central "supraspinal" diaphragm fatigue may occur in response to maximal incremental exercise (Verin et al 2004). …”

Section: 22supporting

confidence: 93%

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

Romer

Miller

Haverkamp

et al. 2007

Respiratory Physiology & Neurobiology

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We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed 6 incremental exercise tests. For 3 trials, subjects exercised with proportional assist ventilation (PAV). For the remaining 3 trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (Pmus) was reduced with PAV (−35.9 ± 2.3% vs. placebo; P < 0.05). Furthermore, V̇O 2 and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak workload, however, was not different between placebo and PAV (324 ± 4 vs. 326 ± 4 W; P > 0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise performance.

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Section: 22supporting

confidence: 93%

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

Romer

Miller

Haverkamp

et al. 2007

Respiratory Physiology & Neurobiology

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“…Additionally, it has been reported that approximately 50% of highly trained individuals exhibit arterial hypoxaemia during high-intensity exercise (Powers et al 1988;Dempsey & Wagner, 1999) and that hypoxaemia worsens the degree of diaphragmatic fatigue (Babcock et al 1995a). However, prior studies did not investigate individuals naturally demonstrating EIAH, and the employment of hypoxic challenge caused not only hypoxaemia but also a higher respiratory muscle effort because of the additional hypoxic stimulus to ventilation (Babcock et al 1995a;Cibella et al 1996;Gudjonsdottir et al 2001). This makes it difficult to isolate the effect of hypoxaemia per se on fatigue.…”

Section: Discussionmentioning

confidence: 91%

“…It has been shown that hypoxaemia superimposed on high-intensity exercise hastens diaphragmatic fatigue during exercise (Babcock et al 1995a(Babcock et al , 1995b Gudjonsdottir et al 2001). However, hypoxaemia also stimulates ventilation, so that this strategy created not only hypoxaemia but also increased respiratory muscle load, making the role of hypoxaemia difficult to isolate.…”

Section: Respiratory Muscle Loading During the Hi And Lo Testsmentioning

confidence: 99%

“…It has been hypothesized that exercise-induced diaphragmatic fatigue is dependent on several factors namely: (a) high diaphragmatic workload ) (b) arterial hypoxaemia (Babcock et al 1995a;Gudjonsdottir et al 2001) and (c) competition for blood flow between the diaphragm and the locomotor muscles associated with an increased production of metabolic byproducts by the active musculature (Fregosi & Dempsey, 1986;Johnson et al 1996). More recently, Babcock et al (2002) have shown that in healthy subjects diaphragmatic fatigue during high-intensity whole-body exercise depends on the relationship between the magnitude of work incurred by the diaphragm and the adequacy of its blood and/or oxygen supply.…”

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confidence: 99%

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Effects of exercise‐induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes

Vogiatzis¹,

Georgiadou²,

Giannopoulou³

et al. 2006

The Journal of Physiology

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Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists (V O 2 max : 70.0 ± 1.6 ml kg -1 min -1 ; mean ± S.E.M.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation (S a,O 2 ): 92 ± 1%) and one hyperoxic (F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume (V T ) and breathing frequency (f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P di,tw ) during recovery. Hyperoxic exercise at 90% WR max induced significantly (P = 0.022) greater post-exercise reduction in P di,tw (15 ± 2%) than did normoxic exercise at 80% WR max (9 ± 2%), despite the similar mean ventilation (123 ± 8 and 119 ± 8 l min -1 , respectively), breathing pattern (V T : 2.53 ± 0.05 and 2.61 ± 0.05 l, f : 49 ± 2 and 46 ± 2 breaths min -1 , respectively), mean changes in P di during exercise (37.1 ± 2.4 and 38.2 ± 2.8 cmH 2 O, respectively) and end-exercise arterial lactate (12.1 ± 1.4 and 10.8 ± 1.1 mmol l -1 , respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S a,O 2 tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.

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“…The factors limiting exercise at altitude may be different from those that limit exercise at sea level and may include diffusion limitation of V O 2 in the alveolus, the work of ventilation, respiratory muscle fatigue, and the possible steal of blood from limb locomotor muscles to respiratory muscles (8,10,30). The perception of dyspnea is also increased during exercise at altitude (5), which may lead to the premature ending of exercise.…”

Section: Discussionmentioning

confidence: 99%

Effect of exercise on cerebral perfusion in humans at high altitude

Imray

Myers²,

Pattinson³

et al. 2005

Journal of Applied Physiology

113

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Society. Effect of exercise on cerebral perfusion in humans at high altitude. J Appl Physiol 99: 699 -706, 2005. First published May 26, 2005 doi:10.1152/japplphysiol.00973.2004.-The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m, mean (SD) cerebral oxygenation (rSO2%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) (P Ͻ 0.0001) and at maximal oxygen uptake (V O2 max) to 69.8 (SD 3.1) (P Ͻ 0.02). In contrast, at each of the high altitudes studied, rSO2 was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m (P Ͻ 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m (P Ͻ 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m (P Ͻ 0.01), and at V O2 max to 61.2 (SD 3.3) at 3,610 m (P Ͻ 0.0001), to 59.4 (SD 2.6) at 4,750 m (P Ͻ 0.0001), and to 58.0 (SD 3.0) at 5,260 m (P Ͻ 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise (P ϭ not significant) and rise at V O2 max, following the changes in arterial oxygen saturation and end-tidal CO 2. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at V O2 max, but at high altitude peaked at 30% of V O2 max and then fell progressively at higher levels of exercise. The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and highaltitude cerebral edema. maximal oxygen uptake; cerebral oxygenation; cerebral blood flow; cerebrovascular resistance; cerebral oxygen delivery ALTERED CEREBRAL FUNCTION on ascent to altitude was part of the first description of mountain sickness in 1913 (40), and acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) have been shown to be potentially serious clinical conditions that may occur on acute exposure to altitudes above 2,500 -3,000 m. Exercise at altitude causes further decreases in arterial oxygenation and so may exacerbate cerebral hypoxia. However, the fall in arterial saturation that occurs during exercise at high altitude (14) might not affect cerebral oxygenation to the same extent as it does in peripheral tissues due to a compensatory increase in cerebral blood flow (24). Nevertheless, avoidance of strenuous exercise during ascent, and on arrival at altitude, is standard advice for reducing the risk of AMS and HACE. Evidence from clinical studies is conflicting. Higher AMS symptom scores were found in subjects exercising four times a day for 30 min at 50% of their altitude-specific maximal oxygen consumption (V O 2 max ), compared with no exercise, in a chamber study at simulated altitude of 4,800 m (41). Another study of mountaineers, however, showed that physical fitness and exercise intensity during ascent to 4,559 m were of minor importance for the development of AMS (3). It is also possible that other neurological conditions falling outside the usual def...

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Diaphragm fatigue during exercise at high altitude: the role of hypoxia and workload

Cited by 25 publications

References 28 publications

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

Effects of exercise‐induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes

Effect of exercise on cerebral perfusion in humans at high altitude

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