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

2006 ◽  
Vol 290 (2) ◽  
pp. R365-R375 ◽  
Author(s):  
Lee M. Romer ◽  
Hans C. Haverkamp ◽  
Andrew T. Lovering ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (V̇o2 peak) = 56.4 ± 2.8 ml·kg−1·min−1; mean ± SE]. Subjects exercised on a cycle ergometer at ≥90% V̇o2 peak to exhaustion (13.2 ± 0.8 min), during which time arterial O2 saturation (SaO2) fell from 97.7 ± 0.1% at rest to 91.9 ± 0.9% (range 84–94%) at end exercise, primarily because of changes in blood pH (7.183 ± 0.017) and body temperature (38.9 ± 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 (FiO2) = 0.25–0.31] that prevented EIAH (SaO2 = 97–99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1–100 Hz). Immediately after exercise at FiO2 0.21, the mean force response across 1–100 Hz decreased 33 ± 5% compared with only 15 ± 5% when EIAH was prevented ( P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at FiO2 0.21 (SaO2 = 95.3 ± 0.7%), the decrease in evoked force was exacerbated by 35% ( P < 0.05) in response to further desaturation induced via FiO2 0.17 (SaO2 = 87.8 ± 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (−6 ± 1% ΔSaO2 from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.

2007 ◽  
Vol 293 (5) ◽  
pp. R2036-R2045 ◽  
Author(s):  
Markus Amann ◽  
David F. Pegelow ◽  
Anthony J. Jacques ◽  
Jerome A. Dempsey

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 (FiO2) = 0.15, arterial hemoglobin saturation (SaO2) = 81 ± 1%; 8.6 ± 0.5 min, 273 ± 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (SaO2 = 95 ± 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 SaO2, were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of SaO2 ( P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Qtw,pot) decreased by 30 ± 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 ± 4%; P = 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 SaO2 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 ± 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (−22 ± 3%; P = 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.


2008 ◽  
Vol 104 (5) ◽  
pp. 1442-1451 ◽  
Author(s):  
Bryan J. Taylor ◽  
Lee M. Romer

High-intensity exercise (≥90% of maximal O2 uptake) sustained to the limit of tolerance elicits expiratory muscle fatigue (EMF). We asked whether prior EMF affects subsequent exercise tolerance. Eight male subjects (means ± SD; maximal O2 uptake = 53.5 ± 5.2 ml·kg−1·min−1) cycled at 90% of peak power output to the limit of tolerance with (EMF-EX) and without (CON-EX) prior induction of EMF and for a time equal to that achieved in EMF-EX but without prior induction of EMF (ISO-EX). To induce EMF, subjects breathed against an expiratory flow resistor until task failure (15 breaths/min, 0.7 expiratory duty cycle, 40% of maximal expiratory gastric pressure). Fatigue of abdominal and quadriceps muscles was assessed by measuring the reduction relative to prior baseline values in magnetically evoked gastric twitch pressure (Pgatw) and quadriceps twitch force (Qtw), respectively. The reduction in Pgatw was not different after resistive breathing vs. after CON-EX (−27 ± 5 vs. −26 ± 6%; P = 0.127). Exercise time was reduced by 33 ± 10% in EMF-EX vs. CON-EX (6.85 ± 2.88 vs. 9.90 ± 2.94 min; P < 0.001). Exercise-induced abdominal and quadriceps muscle fatigue was greater after EMF-EX than after ISO-EX (−28 ± 9 vs. −12 ± 5% for Pgatw, P = 0.001; −28 ± 7 vs. −14 ± 6% for Qtw, P = 0.015). Perceptual ratings of dyspnea and leg discomfort (Borg CR10) were higher at 1 and 3 min and at end exercise during EMF-EX vs. during ISO-EX ( P < 0.05). Percent changes in limb fatigue and leg discomfort (EMF-EX vs. ISO-EX) correlated significantly with the change in exercise time. We propose that EMF impaired subsequent exercise tolerance primarily through an increased severity of limb locomotor muscle fatigue and a heightened perception of leg discomfort.


2014 ◽  
Vol 39 (2) ◽  
pp. 266-269 ◽  
Author(s):  
Paolo B. Dominelli ◽  
Glen E. Foster ◽  
Giulio S. Dominelli ◽  
William R. Henderson ◽  
Michael S. Koehle ◽  
...  

Exercise-induced arterial hypoxemia (EIAH) occurs in some healthy humans at sea-level, whereby the most aerobically trained individuals develop the most severe hypoxemia. A female competitive runner completed 2 maximal exercise tests. Maximal oxygen consumption increased by 15% between testing days, but the degree of hypoxemia remained similar (PaO2, SaO2; 82 and 80 mm Hg; 93.8% and 92.8%; first and second test, respectively). Our case indicates that EIAH does not necessarily worsen with aerobic training.


2017 ◽  
Vol 595 (15) ◽  
pp. 5227-5244 ◽  
Author(s):  
Paolo B. Dominelli ◽  
Yannick Molgat-Seon ◽  
Donald E. G. Griesdale ◽  
Carli M. Peters ◽  
Jean-Sébastien Blouin ◽  
...  

1987 ◽  
Vol 62 (3) ◽  
pp. 1227-1230 ◽  
Author(s):  
P. Y. Lo ◽  
G. A. Dudley

The purpose of this study was to determine the influence of endurance-type exercise training on alterations of the ammonia content of blood in exercising humans. Seven females and four males trained 6 days/wk for 7 wk alternating days of continuous cycling (40 min) and interval running (five 5-min bouts). The NH3 content of blood was determined before and during cycle ergometer (CE) exercise (4 min) at power outputs (PO) of 119, 172, and 241 W pretraining and of 163, 230, and 271 W posttraining. These PO for each occasion represent relative work loads of approximately 65, 90, and 115% of peak CE maximum O2 uptake (PCE VO2), respectively. Training increased (P less than 0.05) PCE VO2 approximately 32% (2.72 +/- 0.25 to 3.56 +/- 0.29 l/min or 38.5 +/- 1.9 to 51.2 +/- 2.3 ml X kg-1 X min-1). Both pre- and posttraining the NH3 content of blood increased (P less than 0.05) with increasing intensity of exercise. Training did not influence the measure of these responses during exercise at the same relative intensity. During exercise at the same absolute PO, approximately 168 or 235 W, however, increases in blood NH3 were less (P less than 0.05) after training. The results indicate that the magnitude of increase in blood NH3 during exercise is determined by the energy requirement of the absolute work load, relative to an individual's aerobic power.


2005 ◽  
Vol 37 (Supplement) ◽  
pp. S296 ◽  
Author(s):  
Lee M. Romer ◽  
Andrew T. Lovering ◽  
Hans C. Haverkamp ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S296
Author(s):  
Lee M. Romer ◽  
Andrew T. Lovering ◽  
Hans C. Haverkamp ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S381-S382
Author(s):  
Bryan J. Taylor ◽  
Stephen C. How ◽  
Lee M. Romer ◽  
Alison McConnell

2010 ◽  
Vol 299 (1) ◽  
pp. R314-R324 ◽  
Author(s):  
Markus Amann ◽  
Mark S. Regan ◽  
Majd Kobitary ◽  
Marlowe W. Eldridge ◽  
Urs Boutellier ◽  
...  

We examined the effects of respiratory muscle work [inspiratory (Wr-insp); expiratory (Wr-exp)] and arterial oxygenation (SpO2) on exercise-induced locomotor muscle fatigue in patients with chronic obstructive pulmonary disease (COPD). Eight patients (FEV, 48 ± 4%) performed constant-load cycling to exhaustion (Ctrl; 9.8 ± 1.2 min). In subsequent trials, the identical exercise was repeated with 1) proportional assist ventilation + heliox (PAV); 2) heliox (He:21% O2); 3) 60% O2 inspirate (hyperoxia); or 4) hyperoxic heliox mixture (He:40% O2). Five age-matched healthy control subjects performed Ctrl exercise at the same relative workload but for 14.7 min (≈best COPD performance). Exercise-induced quadriceps fatigue was assessed via changes in quadriceps twitch force (Qtw,pot) from before to 10 min after exercise in response to supramaximal femoral nerve stimulation. During Ctrl, absolute workload (124 ± 6 vs. 62 ± 7 W), Wr-insp (207 ± 18 vs. 301 ± 37 cmH2O·s·min−1), Wr-exp (172 ± 15 vs. 635 ± 58 cmH2O·s·min−1), and SpO2 (96 ± 1% vs. 87 ± 3%) differed between control subjects and patients. Various interventions altered Wr-insp, Wr-exp, and SpO2 from Ctrl (PAV: −55 ± 5%, −21 ± 7%, +6 ± 2%; He:21% O2: −16 ± 2%, −25 ± 5%, +4 ± 1%; hyperoxia: −11 ± 2%, −17 ± 4%, +16 ± 4%; He:40% O2: −22 ± 2%, −27 ± 6%, +15 ± 4%). Ten minutes after Ctrl exercise, Qtw,pot was reduced by 25 ± 2% ( P < 0.01) in all COPD and 2 ± 1% ( P = 0.07) in healthy control subjects. In COPD, ΔQtw,pot was attenuated by one-third after each interventional trial; however, most of the exercise-induced reductions in Qtw,pot remained. Our findings suggest that the high susceptibility to locomotor muscle fatigue in patients with COPD is in part attributable to insufficient O2 transport as a consequence of exaggerated arterial hypoxemia and/or excessive respiratory muscle work but also support a critical role for the well-known altered intrinsic muscle characteristics in these patients.


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