High frequency diaphragmatic fatigue detected with paired stimuli in humans

Babcock, Mark A.; Pegelow, David F.; Taha, Basel; Dempsey, Jerome A.

doi:10.1097/00005768-199804000-00006

Cited by 33 publications

(26 citation statements)

References 18 publications

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“…The inconsistent decreases in transdiaphragmatic twitch pressure after maximal incremental exercise (−15% across stimulus frequencies) were less than the reductions typically observed after sustained, high-intensity exercise (−20 to 32%) (Johnson et al 1993;Babcock et al 1998). That maximal incremental exercise did not elicit significant diaphragm fatigue points to the critical importance of exercise duration and intensity in defining the fatigability of the diaphragm and its role in exercise performance.…”

Section: Inspiratory Muscle Fatigue-mentioning

confidence: 89%

“…We used single (nonpotentiated and potentiated) and paired stimuli (interstimulus intervals: 100 ms [10 Hz], 20 ms [50 Hz] and 10 ms [100 Hz]) to discriminate between low and high frequency fatigue (Yan et al 1993;Polkey et al 1997;Babcock et al 1998). For paired stimuli the two stimulators were synchronized by a separate module (BiStim Module, Jali Medical Inc., Newton, MA).…”

Section: Diaphragm Fatiguementioning

confidence: 99%

“…Exercise-induced diaphragm fatigue occurs in healthy individuals following heavy intensity (>85% maximal O 2 uptake [V̇O 2max ]), constant-load exercise performed to the limit of tolerance (Johnson et al 1993;Babcock et al 1998). There is mounting evidence that a metaboreflex effect from fatiguing respiratory muscles increases sympathetic outflow in the resting limb Derchak et al 2002) and compromises perfusion of both resting (Sheel et al 2001;Sheel et al 2002) and exercising (Harms et al 1997;Rodman et al 2003) limb muscle, thereby limiting its ability to perform work during heavy exercise.…”

Section: Introductionmentioning

confidence: 99%

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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: Inspiratory Muscle Fatigue-mentioning

confidence: 89%

Section: Diaphragm Fatiguementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…In normoxia, it has been shown that a relative exercise intensity of Ͼ85% of V O 2max sustained to exhaustion is necessary to elicit diaphragm fatigue (11,40). Furthermore, a work rate Ͼ80% of V O 2max is needed in order for the relief of inspiratory muscle work to significantly increase limb blood flow and limb O 2 transport (66).…”

Section: Conditions Under Which Respiratory Muscle Work Might Be Expementioning

confidence: 99%

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Amann¹,

Pegelow²,

Jacques³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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122

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Our aim was to isolate the independent effects of 1) inspiratory muscle work (Wb) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O2 fraction (FIO 2 ) ϭ 0.15, arterial hemoglobin saturation (SaO 2 ) ϭ 81 Ϯ 1%; 8.6 Ϯ 0.5 min, 273 Ϯ 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (SaO 2 ϭ 95 Ϯ 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO 2 , were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of SaO 2 (P ϭ 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Qtw,pot) decreased by 30 Ϯ 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 Ϯ 4%; P ϭ 0.0007). This effect of Wb on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of reduced SaO 2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 15 Ϯ 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (Ϫ22 Ϯ 3%; P ϭ 0.034). We conclude that both arterial hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, Wb has no effect on peripheral fatigue. work of breathing; arterial oxygen content; altitude; limb blood flow; expiratory flow limitation ON THE BASIS OF STUDIES that mimicked the work of breathing (W b ) obtained during heavy and maximum exercise (1, 2) and unloaded the W b in maximal exercise (34), it has been estimated that the oxygen cost of breathing or the cardiac output devoted to the respiratory muscles approximates 10 -16% of maximal O 2 consumption (V O 2max ) or maximal cardiac output in healthy trained and untrained subjects. More direct microsphere measurements of blood flow distribution during maximal exercise in equines also showed that ϳ15-16% of cardiac output was distributed to the inspiratory and expiratory muscles of the chest wall and abdomen (47). One mechanism protecting blood flow to the respiratory muscles in heavy exercise may be the respiratory muscle metaboreflex, which has been shown to cause sympathetically mediated vasoconstriction of the exercising limb vasculature during heavy exercise in the face of developing inspiratory or expiratory muscle fatigue (32,56,57,59).We (4 -6) and others (48, 53, 62) have shown previously that whole body exercise in acute hypoxia significantly increases the rate of develo...

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“…We used magnetic stimulation of the femoral nerve to determine a force-frequency relationship for the quadriceps (2,30,33,34,40). The technique was highly reproducible between and within days, which was critical to our ability to detect systematic effects of exercise-induced hypoxemia on quadriceps fatigue.…”

Section: Technical Considerationsmentioning

confidence: 99%

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

Romer

Haverkamp²,

Lovering³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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116

126

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-The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O 2 uptake (V O2 peak) ϭ 56.4 Ϯ 2.8 ml⅐kg Ϫ1 ⅐min Ϫ1 ; mean Ϯ SE]. Subjects exercised on a cycle ergometer at Ն90% V O2 peak to exhaustion (13.2 Ϯ 0.8 min), during which time arterial O 2 saturation (SaO 2 ) fell from 97.7 Ϯ 0.1% at rest to 91.9 Ϯ 0.9% (range 84 -94%) at end exercise, primarily because of changes in blood pH (7.183 Ϯ 0.017) and body temperature (38.9 Ϯ 0.2°C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (FIO 2 ) ϭ 0.25-0.31] that prevented EIAH (Sa O 2 ϭ 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at FI O 2 0.21, the mean force response across 1-100 Hz decreased 33 Ϯ 5% compared with only 15 Ϯ 5% when EIAH was prevented (P Ͻ 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at FIO 2 0.21 (SaO 2 ϭ 95.3 Ϯ 0.7%), the decrease in evoked force was exacerbated by 35% (P Ͻ 0.05) in response to further desaturation induced via FI O 2 0.17 (SaO 2 ϭ 87.8 Ϯ 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O 2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (Ϫ6 Ϯ 1% ⌬Sa O 2 from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism. magnetic stimulation; low-and high-frequency fatigue; quadriceps twitch force; voluntary activation; peripheral fatigue; central fatigue EXERCISE-INDUCED ARTERIAL HYPOXEMIA (EIAH), defined as a reduced arterial HbO 2 saturation below preexercise levels, occurs during sustained, heavy-intensity exercise to exhaustion in a significant number of healthy subjects (9). The desaturation is attributable primarily to a reduced arterial O 2 partial pressure (Pa O 2 ) in some highly fit subjects (17, 22, 52) or, more universally, to a rightward shift of the O 2 dissociation curve because of a time-and intensity-dependent metabolic acidosis and an increase in body temperature (42,50). EIAH has a detrimental effect on maximal O 2 uptake (V O 2 max ) (16, 41) and endurance exercise performance (36, 37).Multiple "peripheral" and "central" mechanisms have been proposed to explain how arterial hypoxemia limits endurance exercise performance. There is potential for reduced O 2 transport to cause limb muscle fatigue during heavy exercise via an effect of hypoxia on Ca 2ϩ uptake and Ca 2ϩ release by the sarcoplasmic reticulum (10). Changes in the intracellular environment may impair Ca 2ϩ cycling and other excitation/ contraction processes. Alternatively, an inability of the sarcolemma and T tubule to conduct repetitive action potentials may indirectly reduce Ca 2ϩ cycling. The possibility that such peripheral processes are involved in exercise limitation during hypoxemia is suggested by the finding that...

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High frequency diaphragmatic fatigue detected with paired stimuli in humans

Abstract: We interpret these data to mean that high frequency fatigue as well as low frequency fatigue were present in the diaphragm after intense whole body endurance exercise.

Cited by 33 publications

References 18 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

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

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