Sumatriptan reduces exercise capacity in healthy males: a peripheral effect of 5-hydroxytryptamine agonism?

2000 ◽  
Vol 98 (6) ◽  
pp. 643-648 ◽  
Author(s):  
Gerald P. MCCANN ◽  
Helen CAHILL ◽  
Stephen KNIPE ◽  
Douglas F. MUIR ◽  
Paul D. MACINTYRE ◽  
...  

5-Hydroxytryptamine (5-HT; serotonin) has been implicated in the perception of exercise-induced fatigue. Sumatriptan is a selective 5-HT1B/D receptor agonist which does not cross the blood–brain barrier. The aim of the present study was to determine the effect of sumatriptan on exercise capacity. Ten healthy male subjects (mean age 28.4±10.8 years) performed a maximal treadmill exercise test according to the Bruce protocol with expired gas analysis on two occasions. Either 6 mg of sumatriptan or placebo was administered subcutaneously in a randomized, double-blind, placebo-controlled, cross-over design. Exercise time was greater after placebo compared with sumatriptan [914 and 879 s respectively; 95% confidence interval (CI) of difference 12.1 s, 59.1 s; P = 0.008]. There was no significant effect on peak oxygen consumption (placebo, 50.6±6.3 ml·min-1·kg-1; sumatriptan, 51.7±7.6 ml·min-1·kg-1). Sumatriptan administration resulted in decreases in both heart rate (sumatriptan, 188±14 beats/min, placebo, 196±12 beats/min; 95% CI of difference 12.6, 2.6; P = 0.008) and respiratory exchange ratio (sumatriptan, 1.23±0.06; placebo, 1.26±0.07; 95% CI of difference 0.05, 0.01; P = 0.01) at peak exercise. There were no significant differences in blood pressure, heart rate or submaximal oxygen consumption between sumatriptan and placebo treatments at any stage of exercise. Thus sumatriptan reduces maximal exercise capacity in normal males. The failure to demonstrate any haemodynamic or cardiorespiratory effect suggests that sumatriptan enhances perception of fatigue by a peripheral mechanism affecting 5-HT modulation.

Author(s):  
Claudia Baratto ◽  
Sergio Caravita ◽  
Andrea Faini ◽  
Giovanni Battista Perego ◽  
Michele Senni ◽  
...  

Background. Survivors from COVID-19 pneumonia can present with persisting multisystem involvement (lung, pulmonary vessels, heart, muscle, red blood cells) that may negatively affect exercise capacity. Methods. We sought to determine the extent and the determinants of exercise limitation in COVID-19 patients at the time of hospital discharge. Results. Eighteen consecutive patients with COVID-19 and 1:1 age-, sex-, and body mass index- matched controls underwent: spirometry, echocardiography, cardiopulmonary exercise test and exercise echocardiography for the study of pulmonary circulation. Arterial blood was sampled at rest and during exercise in COVID-19 patients. COVID-19 patients lie roughly on the same oxygen consumption isophlets than controls both at rest and during submaximal exercise, thanks to supernormal cardiac output (p<0.05). Oxygen consumption at peak exercise was reduced by 30% in COVID-19 (p<0.001), due to a peripheral extraction limit. Additionally, within COVID-19 patients, hemoglobin content was associated with peak oxygen consumption (R2=0.46, p=0.002)Respiratory reserve was not exhausted (median [IRQ], 0.59 [0.15]) in spite of moderate reduction of forced vital capacity (79±40%)Pulmonary artery pressure increase during exercise was not different between patients and controls. Ventilatory equivalents for carbon dioxide were higher in COVID-19 patients than in controls (39.5 [8.5] vs 29.5 [8.8], p<0.001), and such an increase was mainly explained by increased chemosensitivity. Conclusions. When recovering from COVID-19, patients present with reduced exercise capacity and augmented exercise hyperventilation. Peripheral factors, including anemia and reduced oxygen extraction by peripheral muscles were the major determinants of deranged exercise physiology. Pulmonary vascular function seemed unaffected, despite restrictive lung changes.


1995 ◽  
Vol 79 (6) ◽  
pp. 1870-1877 ◽  
Author(s):  
O. Bauerle ◽  
M. Younes

The progression of chronic obstructive pulmonary disease (COPD) is generally associated with decreased exercise capacity. Differences in forced expired volume in 1 s (FEV1) among patients account for only a fraction of the variability in maximal oxygen consumption (VO2max). We hypothesized that variability in ventilatory response to exercise and in inspiratory mechanics and body mass index contributes importantly to variability in VO2max in this disease. We analyzed the files of 53 patients with established diagnosis of COPD who underwent a recent symptom-limited exercise test. We used inspiratory capacity and maximum inspiratory flow as measures of variability in inspiratory mechanics. The minute ventilation (VE) at the subject's VO2max was divided by the predicted in a normal subject at the same VO2 to obtain a ratio (VE,max/VE,pred). The ventilatory response during exercise provided the best correlation with peak VO2 (r = 0.62). FEV1 and inspiratory capacity also correlated with peak oxygen consumption but not as well as the ventilatory response (r = 0.49 and r = 0.46, respectively). Maximum inspiratory flow and body mass index showed only weak positive correlations (r = 0.23, not significant). The stepwise analysis generated the following equation: VO2max (%predicted) = (77.26 x VE,pred/VE,max) + [0.45 x FEV1 (%predicted)] - 23.66; r = 0.76, P < 0.001. We conclude that variability in the ventilatory response during exercise is one of the main determinants of variability in exercise capacity in COPD patients.


2018 ◽  
pp. 413-436
Author(s):  
Andrew Kao

The chapter Cardiopulmonary Exercise Testing focuses on the opportunities provided by cardiopulmonary exercise (CPX) testing. The coordination of 5 organ systems is described in normal exercise physiology to understand abnormal exercise findings. From a few measured expired gas analysis parameters, most of the important exercise variables can be derived, including the peak oxygen consumption (peak VO2). The contribution of both the aerobic and anaerobic phases of exercise to total exercise capacity are described, including the methods for determination of the anaerobic threshold. The calculation of the normative values of peak VO2 are included, and a suggested template of a CPX report is included. The use of CPX testing in the determination of prognosis in heart failure patients is included.


2003 ◽  
Vol 94 (3) ◽  
pp. 991-996 ◽  
Author(s):  
Luke A. Garske ◽  
Michael G. Brown ◽  
Stephen C. Morrison

Acetazolamide (Acz) is used at altitude to prevent acute mountain sickness, but its effect on exercise capacity under hypoxic conditions is uncertain. Nine healthy men completed this double-blind, randomized, crossover study. All subjects underwent incremental exercise to exhaustion with an inspired O2 fraction of 0.13, hypoxic ventilatory responses, and hypercapnic ventilatory responses after Acz (500 mg twice daily for 5 doses) and placebo. Maximum power of 203 ± 38 (SD) W on Acz was less than the placebo value of 225 ± 40 W ( P < 0.01). At peak exercise, arterialized capillary pH was lower and Po 2 higher on Acz ( P < 0.01). Ventilation was 118.6 ± 20.0 l/min at the maximal power on Acz and 102.4 ± 20.7 l/min at the same power on placebo ( P < 0.02), and Borg score for leg fatigue was increased on Acz ( P < 0.02), with no difference in Borg score for dyspnea. Hypercapnic ventilatory response on Acz was greater ( P < 0.02), whereas hypoxic ventilatory response was unchanged. During hypoxic exercise, Acz reduced exercise capacity associated with increased perception of leg fatigue. Despite increased ventilation, dyspnea was not increased.


1979 ◽  
Vol 57 (s5) ◽  
pp. 393s-396s ◽  
Author(s):  
L. A. Salako ◽  
A. O. Falase ◽  
A. Fadeke Aderounmu

1. The β-adrenoreceptor-blocking effects of pindolol were compared with those of propranolol and a placebo in a double-blind cross-over trial involving nine hypertensive African patients. 2. Heart rate, systolic blood pressure and diastolic blood pressure were measured at rest and immediately after exercise before and at intervals up to 6 h after oral administration of the drugs. In addition, plasma pindolol and propranolol concentrations were determined at the same intervals. 3. Pindolol diminished systolic blood pressure at rest and after exercise and antagonized exercise-induced tachycardia, but had no effect on resting heart rate. Propranolol diminished systolic blood pressure predominantly after exercise and reduced both resting and exercise heart rate. Both drugs had no effect on diastolic pressure. 4. The mean plasma concentration reached a peak at 2 h for each drug and this coincided with the interval at which maximal β-adrenoreceptor-blocking effect was observed.


2018 ◽  
Vol 33 (3) ◽  
pp. 428-438 ◽  
Author(s):  
Marguerite Harvey ◽  
Kathryn L Weston ◽  
William K Gray ◽  
Ailish O’Callaghan ◽  
Lloyd L Oates ◽  
...  

Objectives: To investigate whether people with Parkinson’s disease can exercise at a high-intensity across a 12-week intervention and to assess the impact of the intervention on cardiorespiratory fitness. Design: This is a randomized, controlled, feasibility study with waiting list control. Assessors were blinded to group allocation. Setting: The intervention took place at an exercise centre and assessments at a district general hospital. Subjects: This study included 20 people with idiopathic Parkinson’s disease. Intervention: A total of 36 exercise sessions over 12 weeks, with each session lasting ~45 minutes, were conducted. Main measures: The main measures were maximal heart rates achieved during exercise, recruitment rate, attendance, drop-out, change in peak oxygen consumption, cardiac output, cognitive function and quality of life. The study was considered technically feasible if participants achieved ⩾85% of maximal heart rate during exercise. Results: There were 12 male and 8 female participants; they had a mean age of 68.5 years (standard deviation 6.825). Two participants were of Hoehn and Yahr stage I, 11 stage II and 7 stage III. In all, 17 participants completed the intervention. The median (interquartile range) proportion of repetitions delivered across the intervention which met our high-intensity criterion was 80% (67% to 84%). Mean peak heart rate was 88.8% of maximal. Peak oxygen consumption increased by 2.8 mL kg−1 min−1 in the intervention group and 1.5 mL kg−1 min−1 in the control group after 12 weeks of exercise. We estimate that a fully powered randomized controlled trial would require 30 participants per group. Conclusion: High-intensity interval exercise is feasible in people with Parkinson’s disease. Improvements in cardiorespiratory function are promising.


1982 ◽  
Vol 243 (5) ◽  
pp. H830-H836 ◽  
Author(s):  
R. J. Ferguson ◽  
A. W. Taylor ◽  
P. Cote ◽  
J. Charlebois ◽  
Y. Dinelle ◽  
...  

Cardiovascular and skeletal muscle adaptations were studied before and after 6 mo of physical training in patients with coronary artery disease and exertional angina pectoris. Symptom-limited exercise capacity increased by 41% (470 +/- 30 to 665 +/- 35 kg.m.min-1; n = 29, P less than 0.001) with training as did skeletal muscle succinate dehydrogenase activity (1.75 +/- 0.24 to 3.31 +/- 0.24 IU; n = 23, P less than 0.001) and the areas of muscle fibers (type I from 43.6 +/- 3.3 to 54.4 +/- 3.3 micrometers 2 X 10(2); n = 21, P less than 0.05 and type II from 43.9 +/- 2.4 to 57.2 +/- 5.1 micrometers 2 X 10(2); P less than 0.01). At the same submaximal exercise intensity (mean 355 +/- 100 km.m.min-1), plasma catecholamines (1.31 +/- 0.14 to 1.07 +/- 0.09 ng.ml-1; n = 13, P less than 0.05), heart rate (115 +/- 3 to 97 +/- 3 beats/min; n = 29, P less than 0.001), and systolic blood pressure (171 +/- 4 to 143 +2- 4 mmHg; n = 29, P less than 0.001) were significantly reduced after training. Maximal coronary sinus blood flow (192 +/- 10 to 208 +/- 9 ml.min-1; n = 29, P less than 0.05) and left ventricular oxygen consumption (23.2 +/- 1.5 to 25.8 +/- 1.6 ml.min-1; n = 24, P less than 0.05) were increased by 8 and 11%, respectively, after training. The improvement in exercise capacity with training in patients with exercise is secondary to a reduction in myocardial oxygen requirements during subangina levels of exercise and partly to a small increase in maximal myocardial oxygen consumption. The skeletal muscle adaptations with training were not related to other indices of training such as the reduced exercise heart rate or increased symptom-limited exercise capacity.


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