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

Abstract

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.

Fatigue and Exhaustion in Hypoxia: The Role of Cerebral Oxygenation

“…3). Increased respiratory work, either by voluntarily increasing the tidal integral of transdiaphragmatic pressure or by hypoxiainduced hyperventilation, exacerbates diaphragm fatigue during exercise (Babcock et al, 1995;Vogiatzis et al, 2008). Diaphragm fatigue (and other respiratory muscle fatigue) is accompanied by metabolite accumulation and activation of unmyelinated group IV phrenic afferents (respiratory metaboreceptors) ; these in turn increase sympathetic nerve activity (St Croix et al, 2000) and activate the respiratory muscle metaboreflex (Hussain et al, 1991;Sheel et al, 2001Sheel et al, , 2002.…”

The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases

“…If the patient is breathing pure O 2 , real shunting is the only cause of hypoxaemia contributing to QS/QT. The value is normally zero, since significant shunting does not occur in normal lungs [1,26], but due to (random) errors, the calculation may reveal a value of perhaps 2-3%. Of interest, Thebesian venous drainage directly into the cavity of the left ventricle should add poorly saturated venous blood to arterial and act as a shunt.…”

The use of near-infrared spectroscopy in understanding skeletal muscle physiology: recent developments

“…erector spinae, intercostal, multifidus, paravertebral, serratus anterior) were also investigated during cycling, back extension and bending forward. So far, NIRS has been applied for studying exercise-induced muscle damage [11,20], ergonomics/biomechanics [21], heterogeneity of muscle O 2 supply/demand [12,22], muscle activation [11,23], priming exercise [19,24], respiratory muscle blood flow/fatigue [25,26], the role of the brain in muscle fatigue [27,28], the time course of oxidative metabolism [6,29] and the effect of exercise training [30]. Owing to the restriction of the allocated space, this review article neglects an in-depth discussion of the 160 studies published in the last four years.…”