TEMPERAMENT AND RACE. By S. D. Proteus and Majorie E. Babcock. Boston: Richard Badger, 1926. 364 pp. $3.00

Johnson, Guy B.

doi:10.1093/sf/5.3.540

Cited by 6 publications

(9 citation statements)

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“…In hypoxia, twitch transdiaphragmatic pressure 10 min into recovery fell significantly more than after normoxic exercise, thus confirming greater fatigue in hypoxia (Vogiatzis et al 2007). At this time, diaphragmatic pressures remain low and represent what is happening during exercise (Johnson et al 1993. The workload sustained by the respiratory muscles is a critical determinant of the degree of diaphragmatic fatigue (Babcock et al 2002).…”

Section: Effect Of Respiratory Loading and Metabolic Acidosis On Diapmentioning

confidence: 87%

“…In healthy subjects of varying fitness, diaphragmatic fatigue is thought to be affected by the magnitude of diaphragmatic work, the degree of arterial hypoxaemia and the competition for blood flow between the diaphragm and the locomotor muscles (Babcock et al , 2002Romer & Polkey, 2008). Accordingly, an imbalance of muscle force output versus blood flow or O 2 transport availability to the diaphragm that favours fatigue appears to occur during high-intensity endurance exercise (Johnson et al 1993) when the diaphragm must compete with locomotor muscles for its share of the available cardiac output (Harms et al 1997(Harms et al , 1998(Harms et al , 2000 or when arterial O 2 saturation drops below ∼90% (Babcock et al 1995;Vogiatzis et al 2006Vogiatzis et al , 2007.…”

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confidence: 99%

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Contribution of respiratory muscle blood flow to exercise‐induced diaphragmatic fatigue in trained cyclists

Vogiatzis

Athanasopoulos

Boushel

et al. 2008

The Journal of Physiology

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We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O 2 fractions (F IO 2 ) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each F IO 2 (63 ± 1, 78 ± 1 and 87 ± 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 ± 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 ± 3.5% reduction) and hyperoxic (26.6 ± 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 ± 1.2 l min −1 and 100.4 ± 8.7 ml (100 ml) −1 min −1 , respectively) were significantly different compared with normoxia (28.4 ± 1.9 l min −1 and 94.4 ± 5.2 ml (100 ml) −1 min −1 , respectively) and hyperoxia (27.8 ± 1.6 l min −1 and 95.1 ± 7.8 ml (100 ml) −1 min −1 , respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 ± 8.5, 49.9 ± 5.9 and 52.9 ± 5.9 ml (100 ml) −1 min −1 , respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in P aO 2 , thus further compromising O 2 supply to the respiratory muscles.

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Section: Effect Of Respiratory Loading and Metabolic Acidosis On Diapmentioning

confidence: 87%

mentioning

confidence: 99%

Contribution of respiratory muscle blood flow to exercise‐induced diaphragmatic fatigue in trained cyclists

Vogiatzis

Athanasopoulos

Boushel

et al. 2008

The Journal of Physiology

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“…The inability to preserve perfusion to locomotor muscles at maximal exercise appears associated with both the plateau in cardiac output and increased sympathetic vasoconstrictor activity (Gonzalez-Alonso & Calbet, 2003;Mortensen et al 2005). The latter is thought to be secondary to fatigue of the respiratory muscles , taking place only during heavy exercise (Babcock et al 1995;Johnson et al 1993Johnson et al , 1996. Increased vasoconstriction could also account for the observed reduction in intercostal muscle blood flow as intercostals muscle vascular conductance was also reduced above ∼80% WR max .…”

Section: Discussionmentioning

confidence: 99%

“…When the intensity of exercise exceeds 80-85%V O 2 ,max , inspiratory (Johnson et al 1993(Johnson et al , 1996 and expiratory (Taylor et al 2006) muscle fatigue is exhibited in subjects with varying degrees of fitness levels including highly trained endurance athletes (Vogiatzis et al 2006(Vogiatzis et al , 2007. Conversely, exercise at lower intensities attenuates respiratory muscle fatigue, thus preventing the activation of the sympathetic vasoconstrictor efferent output to the locomotor muscles (Wetter et al 1999).…”

Section: Intercostal and Quadriceps Muscle Blood Flow During Exercisementioning

confidence: 99%

Intercostal muscle blood flow limitation in athletes during maximal exercise

Vogiatzis

Athanasopoulos

Habazettl

et al. 2009

The Journal of Physiology

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We investigated whether, during maximal exercise, intercostal muscle blood flow is as high as during resting hyperpnoea at the same work of breathing. We hypothesized that during exercise, intercostal muscle blood flow would be limited by competition from the locomotor muscles. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle perfusion were measured simultaneously in ten trained cyclists by near-infrared spectroscopy using indocyanine green dye. Measurements were made at several exercise intensities up to maximal (WR max ) and subsequently during resting isocapnic hyperpnoea at minute ventilation levels up to those at WR max . During resting hyperpnoea, intercostal muscle blood flow increased linearly with the work of breathing (R 2 = 0.94) to 73.0 ± 8.8 ml min −1 (100 g) −1 at the ventilation seen at WR max (work of breathing ∼550-600 J min −1 ), but during exercise it peaked at 80% WR max (53.4 ± 10.3 ml min −1 (100 g) −1 ), significantly falling to 24.7 ± 5.3 ml min −1 (100 g)at WR max . At maximal ventilation intercostal muscle vascular conductance was significantly lower during exercise (0.22 ± 0.05 ml min −1 (100 g) −1 mmHg −1 ) compared to isocapnic hyperpnoea (0.77 ± 0.13 ml min −1 (100 g) −1 mmHg −1 ). During exercise, both cardiac output and vastus lateralis muscle blood flow also plateaued at about 80% WR max (the latter at 95.4 ± 11.8 ml min −1 (100 g) −1 ). In conclusion, during exercise above 80% WR max in trained subjects, intercostal muscle blood flow and vascular conductance are less than during resting hyperpnoea at the same minute ventilation. This suggests that the circulatory system is unable to meet the demands of both locomotor and intercostal muscles during heavy exercise, requiring greater O 2 extraction and likely contributing to respiratory muscle fatigue.

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“…Fatigue is defined as a reduction in skeletal muscle force-and/or velocity-generating capacity after exposure to load that is reversible with rest (NHLBI, 1990). It is well known that the respiratory muscles fatigue in response to the substantive ventilatory work associated with heavy exercise (Johnson et al 1993;Taylor et al 2006). There are several physiological consequences of fatiguing contractions of inspiratory and expiratory muscles.…”

Section: Introductionmentioning

confidence: 99%

Influence of inspiratory resistive loading on expiratory muscle fatigue in healthy humans

Peters

Welch

Dominelli

et al. 2017

Experimental Physiology

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What is the central question of this study? This study is the first to measure objectively both inspiratory and expiratory muscle fatigue after inspiratory resistive loading to determine whether the expiratory muscles are activated to the point of fatigue when specifically loading the inspiratory muscles. What is the main finding and its importance? The absence of abdominal muscle fatigue suggests that future studies attempting to understand the neural and circulatory consequences of diaphragm fatigue can use inspiratory resistive loading without considering the confounding effects of abdominal muscle fatigue. Expiratory resistive loading elicits inspiratory as well as expiratory muscle fatigue, suggesting parallel coactivation of the inspiratory muscles during expiration. It is unknown whether the expiratory muscles are likewise coactivated to the point of fatigue during inspiratory resistive loading (IRL). The purpose of this study was to determine whether IRL elicits expiratory as well as inspiratory muscle fatigue. Healthy male subjects (n = 9) underwent isocapnic IRL (60% maximal inspiratory pressure, 15 breaths min , 0.7 inspiratory duty cycle) to task failure. Abdominal and diaphragm contractile function was assessed at baseline and at 3, 15 and 30 min post-IRL by measuring gastric twitch pressure (P ) and transdiaphragmatic twitch pressure (P ) in response to potentiated magnetic stimulation of the thoracic and phrenic nerves, respectively. Fatigue was defined as a significant reduction from baseline in P or P . Throughout IRL, there was a time-dependent increase in cardiac frequency and mean arterial blood pressure, suggesting activation of the respiratory muscle metaboreflex. The P was significantly lower than baseline (34.3 ± 9.6 cmH O) at 3 (23.2 ± 5.7 cmH O, P < 0.001), 15 (24.2 ± 5.1 cmH O, P < 0.001) and 30 min post-IRL (26.3 ± 6.0 cmH O, P < 0.001). The P was not significantly different from baseline (37.6 ± 17.1 cmH O) at 3 (36.5 ± 14.6 cmH O), 15 (33.7 ± 12.4 cmH O) and 30 min post-IRL (32.9 ± 11.3 cmH O). Inspiratory resistive loading elicits objective evidence of diaphragm, but not abdominal, muscle fatigue. Agonist-antagonist interactions for the respiratory muscles appear to be more important during expiratory versus inspiratory loading.

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TEMPERAMENT AND RACE. By S. D. Proteus and Majorie E. Babcock. Boston: Richard Badger, 1926. 364 pp. $3.00

Cited by 6 publications

References 0 publications

Contribution of respiratory muscle blood flow to exercise‐induced diaphragmatic fatigue in trained cyclists

Contribution of respiratory muscle blood flow to exercise‐induced diaphragmatic fatigue in trained cyclists

Intercostal muscle blood flow limitation in athletes during maximal exercise

Influence of inspiratory resistive loading on expiratory muscle fatigue in healthy humans

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