scholarly journals Impact of pulmonary system limitations on locomotor muscle fatigue in patients with COPD

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.

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 ◽  
...  

2017 ◽  
Vol 41 (S1) ◽  
pp. S628-S628
Author(s):  
T. Jukur ◽  
V. Kiviniemi ◽  
J. Veijola

ObjectiveThe cerebellum plays a critical role in cognition and behavior. Altered function of the cerebellum has been related to schizophrenia and psychosis but it is not known how this applies to spontaneous resting state activity in young people with familial risk for psychosis.MethodsWe conducted resting-state functional MRI (R-fMRI) in 72 (29 male) young adults with a history of psychosis in one or both parents (FR) but without their own psychosis, and 72 (29 male) similarly healthy control subjects without parental psychosis. Both groups in the Oulu Brain and Mind Study were drawn from the Northern Finland Birth Cohort 1986. Participants were 20–25 years old. Parental psychosis was established using the Care Register for Health Care. R-fMRI data pre-processing was conducted using independent component analysis with 30 and 70 components. A dual regression technique was used to detect between- group differences in the cerebellum with p b 0.05 threshold corrected for multiple comparisons.ResultsFR participants demonstrated statistically significantly increased activity compared to control subjects in the anterior lobe of the right cerebellum in the analysis with 70 components. The volume of the increased activity was 73 mm3. There was no difference between the groups in the analysis with 30 components (Fig. 1).ConclusionThe finding suggests that increased activity of the anterior lobe of the right cerebellum may be associated with increased vulnerability to psychosis. The finding is novel, and needs replication to be confirmed.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2018 ◽  
Vol 314 (2) ◽  
pp. H180-H187 ◽  
Author(s):  
U. W. Iepsen ◽  
G. W. Munch ◽  
C. K. Ryrsø ◽  
N. H. Secher ◽  
P. Lange ◽  
...  

Sympathetic vasoconstriction is blunted in exercising muscle (functional sympatholysis) but becomes attenuated with age. We tested the hypothesis that functional sympatholysis is further impaired in chronic obstructive pulmonary disease (COPD) patients. We determined leg blood flow and calculated leg vascular conductance (LVC) during 1) femoral-arterial Tyramine infusion (evokes endogenous norepinephrine release, 1 µmol·min−1·kg leg mass−1), 2) one-legged knee extensor exercise with and without Tyramine infusion [10 W and 20% of maximal workload (WLmax)], 3) ATP (0.05 µmol·min−1·kg leg mass−1) and Tyramine infusion, and 4) incremental ATP infusions (0.05, 0.3, and 3.0 µmol·min−1·kg leg mass−1). We included 10 patients with moderate to severe COPD and 8 age-matched healthy control subjects. Overall, leg blood flow and LVC were lower in COPD patients during exercise ( P < 0.05). Tyramine reduced LVC in both groups at 10-W exercise (COPD: −3 ± 1 ml·min−1·mmHg−1and controls: −3 ± 1 ml·min−1·mmHg−1, P < 0.05) and 20% WLmax(COPD: −4 ± 1 ml·min−1·mmHg−1and controls: −3 ± 1 ml·min−1·mmHg−1, P < 0.05) with no difference between groups. Incremental ATP infusions induced dose-dependent vasodilation with no difference between groups, and, in addition, the vasoconstrictor response to Tyramine infused together with ATP was not different between groups (COPD: −0.03 ± 0.01 l·min−1·kg leg mass−1vs. controls: −0.04 ± 0.01 l·min−1·kg leg mass−1, P > 0.05). Compared with age-matched healthy control subjects, the vasodilatory response to ATP is intact in COPD patients and their ability to blunt sympathetic vasoconstriction (functional sympatholysis) as evaluated by intra-arterial Tyramine during exercise or ATP infusion is maintained.NEW & NOTEWORTHY The ability to blunt sympathetic vasoconstriction in exercising muscle and ATP-induced dilation in chronic obstructive pulmonary disease patients remains unexplored. Chronic obstructive pulmonary disease patients demonstrated similar sympathetic vasoconstriction in response to intra-arterial Tyramine during exercise and ATP-induced vasodilation compared with age-matched healthy control subjects.


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.


1984 ◽  
Vol 70 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Nicola Conte ◽  
Maurizio Cecchettin ◽  
Paolo Manente ◽  
Maria Antonia Monco ◽  
Ferruccio Salandin ◽  
...  

Serum immunoreactive calcitonin (iCT) assay was performed in 92 patients suffering from different kinds of cancer of the lung and in 42 healthy control subjects. Gel filtration of serum of patients suffering from microcytoma was carried out on Sephadex G75 to study the forms of circulating iCT. The obtained results (pg/ml M ± SE) were: 1) normal subjects, 73 ± 3; 2) epidermoidal cancer, 105 ± 19; 3) adenocarcinoma, 116 ± 47; 4) anaplastic carcinoma with large cells, 156 ± 74; 5) microcytoma, 354 ± 74; 6) chronic obstructive bronchitis, 38 ± 6. Gel filtration of serum of patients with microcytoma demonstrated the same behavior as in normal subjects. We can conclude that iCT increases significantly in microcytoma with extensive disease (84 % of cases): in this condition, the iCT assay can be useful as a marker in follow-up of disease.


2013 ◽  
Vol 115 (5) ◽  
pp. 634-642 ◽  
Author(s):  
Markus Amann ◽  
Stuart Goodall ◽  
Rosie Twomey ◽  
Andrew W. Subudhi ◽  
Andrew T. Lovering ◽  
...  

The development of muscle fatigue is oxygen (O2)-delivery sensitive [arterial O2 content (CaO2) × limb blood flow ( QL)]. Locomotor exercise in acute hypoxia (AH) is, compared with sea level (SL), associated with reduced CaO2 and exaggerated inspiratory muscle work (Winsp), which impairs QL, both of which exacerbate fatigue individually by compromising O2 delivery. Since chronic hypoxia (CH) normalizes CaO2 but exacerbates Winsp, we investigated the consequences of a 14-day exposure to high altitude on exercise-induced locomotor muscle fatigue. Eight subjects performed the identical constant-load cycling exercise (138 ± 14 W; 11 ± 1 min) at SL (partial pressure of inspired O2, 147.1 ± 0.5 Torr), in AH (73.8 ± 0.2 Torr), and in CH (75.7 ± 0.1 Torr). Peripheral fatigue was expressed as pre- to postexercise percent reduction in electrically evoked potentiated quadriceps twitch force (ΔQtw,pot). Central fatigue was expressed as the exercise-induced percent decrease in voluntary muscle activation (ΔVA). Resting CaO2 at SL and CH was similar, but CaO2 in AH was lower compared with SL and CH (17.3 ± 0.5, 19.3 ± 0.7, 20.3 ± 1.3 ml O2/dl, respectively). Winsp during exercise increased with acclimatization (SL: 387 ± 36, AH: 503 ± 53, CH: 608 ± 67 cmH2O·s−1·min−1; P < 0.01). Exercise at SL did not induce central or peripheral fatigue. ΔQtw,pot was significant but similar in AH and CH (21 ± 2% and 19 ± 3%; P = 0.24). ΔVA was significant in both hypoxic conditions but smaller in CH vs. AH (4 ± 1% vs. 8 ± 2%; P < 0.05). In conclusion, acclimatization to severe altitude does not attenuate the substantial impact of hypoxia on the development of peripheral fatigue. In contrast, acclimatization attenuates, but does not eliminate, the exacerbation of central fatigue associated with exercise in severe AH.


2007 ◽  
Vol 30 (3) ◽  
pp. 27
Author(s):  
Véronique Pepin ◽  
Didier Saey ◽  
Claude H. Côté ◽  
Pierre LeBlanc ◽  
François Maltais

Background: Contractile fatigue of the quadriceps occurs in a significant proportion of patients with COPD after constant-load cycling exercise. Dynamic hyperinflation, by altering cardiac output during exercise, could contribute to fatigue susceptibility in this population. The purpose of this study was to compare operational lung volumes during constant workrate exercise between COPD patients who do and those who do not develop contractile fatigue of the quadriceps (fatiguers vs non-fatiguers). Methods: Sixty-two patients with COPD (FEV1: 46±16%) completed a constant-load cycling test at 80% of the peak workrate achieved during progressive cycle ergometry. Ventilatory parameters were monitored breath-by-breath, while inspiratory capacity maneuvers were obtained every other minute during constant-load cycling. Quadriceps twitch force was measured with magnetic stimulation of the femoral nerve before and after the test. Muscle fatigue was defined as a post-exercise reduction in quadriceps twitch force of more than 15% of the resting value. Results: Forty patients (65%) developed muscle fatigue after constant-load cycling. No significant differences were found between fatiguers and non-fatiguers with respect to age, body mass index, resting lung function, peak oxygen consumption, and endurance time to constant-load exercise. Change in inspiratory capacity from rest to end-exercise (DIC) was similar between both subgroups (DIC: 0.56±0.32L vs 0.56±0.47L for fatiguers and non-fatiguers respectively, P=0.99). Conclusion: Susceptibility to muscle fatigue could not be predicted by exercise duration or by the degree of dynamic hyperinflation in patients with COPD.


2008 ◽  
Vol 104 (3) ◽  
pp. 879-888 ◽  
Author(s):  
Lee M. Romer ◽  
Michael I. Polkey

It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O2and CO2transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles.


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