Skeletal muscle strength during exposure to hypobaric hypoxia

Young, Albert G.; Wright, James D.; Knapik, Joseph J.; Cymerman, Allen

doi:10.1249/00005768-198025000-00005

Cited by 16 publications

(7 citation statements)

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“…Despite these changes in cortical excitability, acute hypoxia had no effect on MVC force, confirming previous results on finger abduction (19), hand grip (6), elbow flexion (14,41) and knee extension (9,14,20,47) force. Also, voluntary activation was not altered during acute hypoxia.…”

supporting

confidence: 88%

The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation

Szubski¹,

Burtscher²,

Löscher³

2006

Journal of Applied Physiology

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Szubski, Christoph, Martin Burtscher, and Wolfgang N. Lö scher. The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation. J Appl Physiol 101: 1673-1677, 2006. First published August 17, 2006 doi:10.1152/japplphysiol.00617.2006.-The effects of acute hypoxia on motor cortex excitability, force production, and voluntary activation were studied using single-and double-pulse transcranial magnetic stimulation techniques in 14 healthy male subjects. Electrical supramaximal stimulations of the right ulnar nerve were performed, and transcranial magnetic stimulations were delivered to the first dorsal interosseus motor cortex area during short-term hypoxic (HX) and normoxic (NX) condition. M waves, voluntary activation, F waves, resting motor threshold (rMT), recruitment curves (100 -140% of rMT), and short-interval intracortical inhibition and intracortical facilitation were measured. Moreover, motor-evoked potentials (MEPs) and cortical silent periods were determined during brief isometric maximum right index finger abductions. Hypoxia was induced by breathing a fraction of inspired oxygen of 12% via a face mask. M waves, voluntary activation, and F waves did not differ between NX and HX. The rMT was significantly lower in HX (55.79 Ϯ 9.40%) than in NX (57.50 Ϯ 10.48%) (P Ͻ 0.01), whereas MEP recruitment curve, short-interval intracortical inhibition, intracortical facilitation, maximum right index finger abduction, and MEPs were unaffected by HX. In contrast, the cortical silent periods in HX (158.21 Ϯ 33.96 ms) was significantly shortened compared with NX (169.42 Ϯ 39.69 ms) (P Ͻ 0.05). These data demonstrate that acute hypoxia results in increased cortical excitability and suggest that acute hypoxia alters motor cortical ion-channel function and GABAergic transmission. transcranial magnetic stimulation; voluntary activation; cortical silent period STUDIES OF HYPOXIA-INDUCED CHANGES in central nervous system function have primarily focused on behavioral parameters and revealed impairments in psychomotor skills (25, 43) and cognitive performances (24,29,32). In addition to these deteriorations in performance, evidence of slowed visual and auditory reaction time has been demonstrated in experimental conditions corresponding to an altitude of ϳ6,100 m (15, 16).Numerous in vitro studies on central neurons strongly suggested that reduced arterial oxygen saturation impairs central nervous system function (34). In particular, the cerebral neuron excitability critically depends on sufficient O 2 supply, but hypoxia may not only compromise ion channels but also signaling pathways and neurotransmitter function (22,35). So far, most of our knowledge about the processes underlying hypoxia-induced alterations of neuronal excitability and synaptic neurotransmission has been gained from in vitro patchclamped studies.As yet, in vivo studies addressing the functional consequences of reduced O 2 supply to the neuromuscular system have primarily focused on effects on muscle force generation (13), endu...

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confidence: 88%

The effects of short-term hypoxia on motor cortex excitability and neuromuscular activation

Szubski¹,

Burtscher²,

Löscher³

2006

Journal of Applied Physiology

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“…Since hypoxia decreased the peak work rate and maximum O 2 consumption observed during cycling, this means that the constant load cycling exercise was carried out at an elevated relative intensity of exercise, which in turn would be expected to increase the rate of accumulation of fatigue-causing metabolites (27). However, our present findings and those of others (11,21,22,39,48) show that MVC or force output in response to supramaximal motor nerve stimulation in the rested muscle was not influenced by hypoxia; thus isolated submaximal quadriceps exercise was conducted at equivalent levels of both absolute and relative force outputs. We conclude that a significant portion of hypoxic effects on exercise-induced peripheral fatigue does not require an increase in the relative exercise intensity.…”

Section: Relevance To Hypoxic Effects During Whole Body Exercisecontrasting

confidence: 66%

“…Given that a changing Ca O 2 induced by breathing various FI O 2 also had significant effects on maximal peak exercise capacity during whole body exercise, the observed effect of changing Ca O 2 on peripheral limb fatigue might be attributed at least in part to changes in relative work intensity (2, 43). Different relative work intensities might be expected to influence the rate of accumulation of muscle metabolites (27) and therefore influence peripheral muscle fatigue.We tested this hypothesis by using isolated submaximal isometric contractions of the quadriceps muscle, since maximal force output of locomotor muscle under baseline resting conditions is not affected by breathing various FI O 2 levels (0.110 -0.123, equivalent to an altitude of 4,000 -5,050 m) (11,21,22,39,48). Accordingly, repeated quadriceps muscle contractions at the same absolute force output with variations in FI O 2 would also be carried out at the same relative work intensity.…”

mentioning

confidence: 99%

“…We tested this hypothesis by using isolated submaximal isometric contractions of the quadriceps muscle, since maximal force output of locomotor muscle under baseline resting conditions is not affected by breathing various FI O 2 levels (0.110 -0.123, equivalent to an altitude of 4,000 -5,050 m) (11,21,22,39,48). Accordingly, repeated quadriceps muscle contractions at the same absolute force output with variations in FI O 2 would also be carried out at the same relative work intensity.…”

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confidence: 99%

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Effect of arterial oxygenation on quadriceps fatigability during isolated muscle exercise

Katayama

Amann²,

Pegelow³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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.-The effect of various levels of oxygenation on quadriceps muscle fatigability during isolated muscle exercise was assessed in six male subjects. Twitch force (Qtw) was assessed using supramaximal magnetic femoral nerve stimulation. In experiment 1, maximal voluntary contraction (MVC) and Qtw of resting quadriceps muscle were measured in normoxia [inspired O2 fraction (FIO 2 ) ϭ 0.21, percent arterial O2 saturation (Sp O 2 ) ϭ 98.4%, estimated arterial O2 content (CaO 2 ) ϭ 20.8 ml/dl], acute hypoxia (FIO 2 ϭ 0.11, Sp O 2 ϭ 74.6%, CaO 2 ϭ 15.7 ml/dl), and acute hyperoxia (FIO 2 ϭ 1.0, Sp O 2 ϭ 100%, CaO 2 ϭ 22.6 ml/dl). No significant differences were found for MVC and Qtw among the three FIO 2 levels. In experiment 2, the subjects performed three sets of nine, intermittent, isometric, unilateral, submaximal quadriceps contractions (62% MVC followed by 1 MVC in each set) while breathing each FIO 2 . Qtw was assessed before and after exercise, and myoelectrical activity of the vastus lateralis was obtained during exercise. The percent reduction of twitch force (potentiated Qtw) in hypoxia (Ϫ27.0%) was significantly (P Ͻ 0.05) greater than in normoxia (Ϫ21.4%) and hyperoxia (Ϫ19.9%), as were the changes in intratwitch measures of contractile properties. The increase in integrated electromyogram over the course of the nine contractions in hypoxia (15.4%) was higher (P Ͻ 0.05) than in normoxia (7.2%) or hyperoxia (6.7%). These results demonstrate that quadriceps muscle fatigability during isolated muscle exercise is exacerbated in acute hypoxia, and these effects are independent of the relative exercise intensity. hypoxia; magnetic femoral nerve stimulation; hyperoxia ; hypoxemia; quadriceps twitch force WE AND OTHERS HAVE RECENTLY SHOWN that high-intensity whole body exercise to exhaustion caused significant peripheral limb muscle fatigue and that the level of arterial O 2 content (Ca O 2 ) via changes in inspired O 2 fraction (FI O 2 ) is a significant determinant of the rate at which peripheral muscle fatigue is developed during exercise (2,43,46). In these studies, evidence for the effects of Ca O 2 on peripheral fatigue was obtained via measures of quadriceps force output using supramaximal magnetic stimulation obtained pre-vs. postexercise and also by the rate of rise of quadriceps muscle electromyogram (EMG) during the exercise. The latter measurement presumably indicates the rate of motor unit recruitment in response to peripheral fatigue development (2, 46). Given that a changing Ca O 2 induced by breathing various FI O 2 also had significant effects on maximal peak exercise capacity during whole body exercise, the observed effect of changing Ca O 2 on peripheral limb fatigue might be attributed at least in part to changes in relative work intensity (2, 43). Different relative work intensities might be expected to influence the rate of accumulation of muscle metabolites (27) and therefore influence peripheral muscle fatigue.We tested this hypothesis by using isolated submaximal isometric contractions of th...

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“…These changes culminated in the first revision of the questionnaire (ESQ-II), which was then evaluated by Sampson and Kobrick (45) in two separate field studies examining the effects of prolonged overseas flight on health and physical performance (52,55), and the effects of continued load-carrying over several days (56).…”

Section: Evolution Of the Environmental Symptoms Questionnairementioning

confidence: 99%