scholarly journals The role of pulmonary CO2 flow in the control of the phase i ventilatory response to exercise in humans

1995 ◽  
Vol 71 (4) ◽  
pp. 287-294 ◽  
Author(s):  
Paolo Cerretelli ◽  
Bruno Grassi ◽  
Lei Xi ◽  
Federico Schena ◽  
Claudio Marconi ◽  
...  
Keyword(s):  
Phase I ◽  
Ventilatory Response ◽  
Co2 Flow ◽  
Response To Exercise ◽  
Exercise In Humans

scholarly journals The role of pulmonary CO2 flow in the control of the phase I ventilatory response to exercise in humans

1996 ◽  
Vol 72 (3) ◽  
pp. 285-285
Author(s):  
Paolo Cerretelli ◽  
Bruno Grassi ◽  
Lei Xi ◽  
Federico Schena ◽  
Claudio Marconi ◽  
...  
Keyword(s):  
Phase I ◽  
Ventilatory Response ◽  
Co2 Flow ◽  
Response To Exercise ◽  
Exercise In Humans

Control of breathing at the start of exercise as influenced by posture

1983 ◽  
Vol 55 (5) ◽  
pp. 1460-1466 ◽  
Author(s):  
D. Weiler-Ravell ◽  
D. M. Cooper ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Stroke Volume ◽  
Phase I ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Co2 Output ◽  
End Tidal ◽  
Response To Exercise ◽  
Initial Change

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Opioid antagonism alters blood glucose homeostasis during exercise in humans

1994 ◽  
Vol 76 (6) ◽  
pp. 2452-2460 ◽  
Author(s):  
M. S. Hickey ◽  
S. W. Trappe ◽  
A. C. Blostein ◽  
B. A. Edwards ◽  
B. Goodpaster ◽  
...  
Keyword(s):  
Serum Insulin ◽  
Insulin Response ◽  
Serum Glucose ◽  
Endogenous Opioid ◽  
Hormonal Responses ◽  
Blood Glucose Homeostasis ◽  
The Difference ◽  
Response To Exercise ◽  
Exercise In Humans

In an attempt to clarify the role of endogenous opioid peptides in substrate mobilization and hormonal responses to dynamic exercise, eight trained cyclists completed exercise trials at 90% of maximal O2 consumption (VO2max) until exhaustion and at 70% VO2max for 90 min. Trials were conducted after intravenous administration of the opiate antagonist naloxone (NAL, 0.1 mg/kg bolus + 0.1 mg.kg-1.h-1) or volume-matched saline (SAL) at each intensity. Serum glucose was maintained at significantly higher levels at 60 and 90 min of exercise in the 70%-NAL than in the 70%-SAL trial and at all points during exercise and at 30 and 60 min of recovery in the 90%-NAL than in the 90%-SAL trial. The serum insulin response to exercise was not altered by NAL administration at either intensity. Serum C-peptide was approximately 50% higher at 60 and 90 min of exercise in the 70%-NAL than in the 70%-SAL trial but was significantly lower during exercise in the 90%-NAL than in the 90%-SAL trial. The plasma glucagon response to exercise at 70% VO2max was not altered by NAL administration but was significantly elevated in the 90%-NAL vs. the 90%-SAL trial. Plasma epinephrine was 50–150% (approximately 2–3 nM) higher during exercise from 30 to 90 min of exercise in the 70%-NAL than in the 70%-SAL trial and was higher at termination (4.9 +/- 2.1 vs. 2.7 +/- 1.7 nM) in the 90%-NAL than in the 90%-SAL trial, although the difference in the 90% trial was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Elevated extracellular potassium prior to muscle contraction reduces onset and steady-state exercise hyperemia in humans

2018 ◽  
Vol 125 (2) ◽  
pp. 615-623 ◽  
Author(s):  
Janée D. Terwoord ◽  
Christopher M. Hearon ◽  
Gary J. Luckasen ◽  
Jennifer C. Richards ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Steady State ◽  
Voluntary Contraction ◽  
Extracellular Potassium ◽  
Handgrip Exercise ◽  
Exercise Hyperemia ◽  
Forearm Vascular Conductance ◽  
Response To Exercise ◽  
Exercise In Humans ◽  
Hyperemic Response

The increase in interstitial potassium (K+) during muscle contractions is thought to be a vasodilatory signal that contributes to exercise hyperemia. To determine the role of extracellular K+ in exercise hyperemia, we perfused skeletal muscle with K+ before contractions, such that the effect of any endogenously-released K+ would be minimized. We tested the hypothesis that local, intra-arterial infusion of potassium chloride (KCl) at rest would impair vasodilation in response to subsequent rhythmic handgrip exercise in humans. In 11 young adults, we determined forearm blood flow (FBF) (Doppler ultrasound) and forearm vascular conductance (FVC) (FBF/mean arterial pressure) during 4 min of rhythmic handgrip exercise at 10% of maximal voluntary contraction during 1) control conditions, 2) infusion of KCl before the initiation of exercise, and 3) infusion of sodium nitroprusside (SNP) as a control vasodilator. Infusion of KCl or SNP elevated resting FVC similarly before the onset of exercise (control: 39 ± 6 vs. KCl: 81 ± 12 and SNP: 82 ± 13 ml·min−1·100 mmHg−1; both P < 0.05 vs. control). Infusion of KCl at rest diminished the hyperemic (ΔFBF) and vasodilatory (ΔFVC) response to subsequent exercise by 22 ± 5% and 30 ± 5%, respectively (both P < 0.05 vs. control), whereas SNP did not affect the change in FBF ( P = 0.74 vs. control) or FVC ( P = 0.61 vs. control) from rest to steady-state exercise. These findings implicate the K+ ion as an essential vasodilator substance contributing to exercise hyperemia in humans. NEW & NOTEWORTHY Our findings support a significant and obligatory role for potassium signaling in the local vasodilatory and hyperemic response to exercise in humans.

scholarly journals Ventilatory response to exercise of elite soccer players

2014 ◽  
Vol 9 ◽  
Author(s):  
Adriano Di Paco ◽  
Giosuè A. Catapano ◽  
Guido Vagheggini ◽  
Stefano Mazzoleni ◽  
Matteo Levi Micheli ◽  
...  
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lung Function Test ◽  
Peak Oxygen Uptake ◽  
Forced Expiratory Volume ◽  
Soccer Players ◽  
Ventilatory Parameters ◽  
Response To Exercise

Background: The purpose of this study was to evaluate the role of ventilatory parameters in maximal exercise performance in elite soccer players. Methods: From September 2009 to December 2012, 90 elite soccer players underwent evaluation of lung function test and ergospirometry by means of an incremental symptom-limited treadmill test. Results were analyzed according to i) maximal exercise velocity performed (Hi-M: high-performers, >18.65 km/h; Lo-M: low-performers, <18.65 km/h) and ii) usual role in the team. Results: Hi-M showed higher peak minute ventilation (V_ Epeak: 158.3 ± 19.5 vs 148.0 ± 18.54 L/min, p = 0.0203), and forced expiratory volume at first second (5.28 ± 0.50 vs 4.89 ± 0.52 liters, p < 0.001) than Lo-M, independently of playing role. Moreover, a significant correlation between peak oxygen uptake and V_ E (r = 0.57, p < 0.001) was found. Conclusions: Ventilatory response plays a role in the assessment of exercise capacity in elite soccer players.

Dynamics of ventilatory response to exercise in humans

1981 ◽  
Vol 51 (1) ◽  
pp. 194-203 ◽  
Author(s):  
F. M. Bennett ◽  
P. Reischl ◽  
F. S. Grodins ◽  
S. M. Yamashiro ◽  
W. E. Fordyce
Keyword(s):  
Cross Correlation ◽  
Ventilatory Response ◽  
Slow Component ◽  
Binary Sequence ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Fast Component ◽  
Pseudorandom Binary Sequence ◽  
Response To Exercise ◽  
Exercise In Humans

The dynamics of the ventilatory response to moderate exercise on a bicycle ergometer have been studied in humans. The work load was varied between 25 and 100 W as a pseudorandom binary sequence (PRBS) that enabled the impulse responses to be calculated by cross-correlation techniques. The response of all five subjects exhibited a bimodal response, i.e., a fast component that was followed after a delay by a slow component. The fast component accounted for a relatively small proportion of the total response. Also, it was demonstrated that to identify the rapid component it was necessary to excite the respiratory system with an input containing highfrequency components; this result was used to reconcile the findings from this study with those of previous investigation.

scholarly journals The role of spinal cord transmission in the ventilatory response to exercise in man.

1984 ◽  
Vol 355 (1) ◽  
pp. 85-97 ◽  
Author(s):  
L Adams ◽  
H Frankel ◽  
J Garlick ◽  
A Guz ◽  
K Murphy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ventilatory Response ◽  
Response To Exercise

Antioxidants attenuate the plasma cytokine response to exercise in humans

2003 ◽  
Vol 94 (3) ◽  
pp. 1025-1032 ◽  
Author(s):  
Theodoros Vassilakopoulos ◽  
Maria-Helena Karatza ◽  
Paraskevi Katsaounou ◽  
Androniki Kollintza ◽  
Spyros Zakynthinos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Potential Contribution ◽  
Bicycle Exercise ◽  
Tnf Α ◽  
Before And After ◽  
Plasma Cytokines ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Exercise In Humans

Exercise increases plasma TNF-α, IL-1β, and IL-6, yet the stimuli and sources of TNF-α and IL-1β remain largely unknown. We tested the role of oxidative stress and the potential contribution of monocytes in this cytokine (especially IL-1β) response in previously untrained individuals. Six healthy nonathletes performed two 45-min bicycle exercise sessions at 70% ofV˙o 2 max before and after a combination of antioxidants (vitamins E, A, and C for 60 days; allopurinol for 15 days; and N-acetylcysteine for 3 days). Blood was drawn at baseline, end-exercise, and 30 and 120 min postexercise. Plasma cytokines were determined by ELISA and monocyte intracellular cytokine level by flow cytometry. Before antioxidants, TNF-α increased by 60%, IL-1β by threefold, and IL-6 by sixfold secondary to exercise ( P < 0.05). After antioxidants, plasma IL-1β became undetectable, the TNF-α response to exercise was abolished, and the IL-6 response was significantly blunted ( P < 0.05). Exercise did not increase the percentage of monocytes producing the cytokines or their mean fluorescence intensity. We conclude that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process.

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