scholarly journals Exercise induced changes in T1, T2 relaxation times and blood flow in the lower extremities in healthy subjects

2013 ◽  
Vol 15 (S1) ◽  
Author(s):  
Juliet Varghese ◽  
Debbie Scandling ◽  
Chikako Ono ◽  
Ashish Aneja ◽  
William A Kay ◽  
...  
2018 ◽  
Vol 52 (4) ◽  
pp. 446-454 ◽  
Author(s):  
Christoph Centner ◽  
Denise Zdzieblik ◽  
Patrick Dressler ◽  
Bruno Fink ◽  
Albert Gollhofer ◽  
...  

2019 ◽  
Vol 63 (3) ◽  
pp. 309-313
Author(s):  
Carolina P.B. Gracitelli ◽  
Nubia Vanessa Lima de Faria ◽  
Izabela Almeida ◽  
Diego Torres Dias ◽  
Julia Maggi Vieira ◽  
...  

1988 ◽  
Vol 75 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Richard L. Hughson

1. The blood flow in the forearm and the calf of six healthy volunteers was measured at rest and after exercise by impedance plethysmography using pulsatile (QZp) and venous occlusion (QZocc) methods, and by venous occlusion strain gauge plethysmography (Qsg). 2. At rest, the impedance QZp method gave values slightly higher than those of Qsg. In the forearm, the ratio QZp to Qsg was 1.26 in the supine position and 1.97 in the upright sitting position. For the calf muscle, the ratios were 1.08 in the supine position and 1.23 in the upright position. 3. Immediately after exercise, Qsg increased from resting values of approximately 2–4 ml min−1 100 ml−1 to mean values of 16–25 ml min−1 100 ml−1 in upright and supine arm or leg exercise. In contrast, the QZp values after exercise increased to only 3.1–4.6 ml min−1 100 ml−1. QZocc likewise failed to show increases in flow except in the supine leg exercise, where flow increased to 8.7 ml min−1 100 ml−1. 4. In an additional subject, it was shown that electrode position had no significant effect on the QZp blood flow measurement after exercise. 5. The failure of QZp to accurately follow the change in Qsg with exercise was probably due in part to pulsatile venous outflow. In addition, changes in microvessel packed cell volume and shear rate may influence the observed QZp. It is concluded that impedance plethysmography is not valid for estimation of limb blood flow during reactive hyperaemia after exercise.


2016 ◽  
Vol 120 (8) ◽  
pp. 843-854 ◽  
Author(s):  
K. J. Smith ◽  
K. W. Wildfong ◽  
R. L. Hoiland ◽  
M. Harper ◽  
N. C. Lewis ◽  
...  

Cerebral blood flow (CBF) is temporally related to exercise-induced changes in partial pressure of end-tidal carbon dioxide (PetCO2); hyperoxia is known to enhance this relationship. We examined the hypothesis that preventing PetCO2 from rising (isocapnia) during submaximal exercise with and without hyperoxia [end-tidal Po2 (PetO2) = 300 mmHg] would attenuate the increases in CBF. Additionally, we aimed to identify the magnitude that breathing, per se, influences the CBF response to normoxic and hyperoxic exercise. In 14 participants, CBF (intra- and extracranial) measurements were measured during exercise [20, 40, 60, and 80% of maximum workload (Wmax)] and during rest while ventilation (V̇e) was volitionally increased to mimic volumes achieved during exercise (isocapnic hyperpnea). While V̇e was uncontrolled during poikilocapnic exercise, during isocapnic exercise and isocapnic hyperpnea, V̇e was increased to prevent PetCO2 from rising above resting values (∼40 mmHg). Although PetCO2 differed by 2 ± 3 mmHg during normoxic poikilocapnic and isocapnic exercise, except for a greater poikilocapnic compared with isocapnic increase in blood velocity in the posterior cerebral artery at 60% Wmax, the between condition increases in intracranial (∼12-15%) and extracranial (15–20%) blood flow were similar at each workload. The poikilocapnic hyperoxic increases in both intra- and extracranial blood-flow (∼17–29%) were greater compared with poikilocapnic normoxia (∼8–20%) at intensities >40% Wmax ( P < 0.01). During both normoxic and hyperoxic conditions, isocapnia normalized both the intracranial and extracranial blood-flow differences. Isocapnic hyperpnea did not alter CBF. Our findings demonstrate a differential effect of PetCO2 on CBF during exercise influenced by the prevailing PetO2.


1983 ◽  
Vol 55 (6) ◽  
pp. 1916-1923 ◽  
Author(s):  
A. W. Bell ◽  
J. R. Hales ◽  
R. B. King ◽  
A. A. Fawcett

Radioactive microspheres were used to measure cardiac output and blood flow to most major tissues in sheep at rest and during treadmill exercise (3- to 6-fold increase in metabolic rate for 30 min) in thermoneutral (TN) [dry bulb temperature (Tdb) = 16 degrees C, wet bulb temperature (Twb) = 12 degrees C] and mildly hot (MH) (Tdb = 40 degrees C, Twb = 23 degrees C) environments. During exercise, rectal temperature increased more under MH than under TN conditions; exercise-induced changes in the major central cardiovascular parameters were unaffected by MH. Exercise in TN caused mild hypocapnia, and in MH, severe respiratory alkalosis. Skin blood flow in the torso decreased during exercise in TN and MH. Extremity skin blood flow was increased by heat but not exercise. Exercise-induced increases in flows to respiratory muscles and upper respiratory tract tissues were greatly enhanced in MH. Exercise caused large increases in blood flow to fore- and hindlimb muscles, which were less in MH than in TN. Effects of MH on exercise-induced changes in flow to these and other tissues (e.g., abdominal viscera and adipose tissue) are discussed in terms of the conflicting requirements of energy expenditure and body temperature regulation during exercise in sheep and other species, particularly humans.


2003 ◽  
Vol 44 (5) ◽  
pp. 2126 ◽  
Author(s):  
John V. Lovasik ◽  
He´le`ne Kergoat ◽  
Charles E. Riva ◽  
Benno L. Petrig ◽  
Martial Geiser

1997 ◽  
Vol 82 (4) ◽  
pp. 1107-1111 ◽  
Author(s):  
Seiji Maeda ◽  
Takashi Miyauchi ◽  
Michiko Sakane ◽  
Makoto Saito ◽  
Shinichi Maki ◽  
...  

Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto Saito, Shinichi Maki, Katsutoshi Goto, and Mitsuo Matsuda. Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans? J. Appl. Physiol. 82(4): 1107–1111, 1997.—Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide that potentiates contractions to norepinephrine in human vessels. We previously reported that the circulating plasma concentration of ET-1 is significantly increased after exercise (S. Maeda, T. Miyauchi, K. Goto, and M. Matsuda. J. Appl. Physiol. 77: 1399–1402, 1994). To study the roles of ET-1 during and after exercise, we investigated whether endurance exercise affects the production of ET-1 in the circulation of working muscles and nonworking muscles. Male athletes performed one-leg cycle ergometer exercise of 30-min duration at intensity of 110% of their individual ventilatory threshold. Plasma concentrations of ET-1 in both sides of femoral veins (veins in the working leg and nonworking leg) and in the femoral artery (artery in the nonworking leg) were measured before and after exercise. The plasma ET-1 concentration in the femoral vein in the nonworking leg was significantly increased after exercise, whereas that in femoral vein in the working leg was not changed. The arteriovenous difference in ET-1 concentration was significantly increased after exercise in the circulation of the nonworking leg but not of the working leg, which suggests that the production of ET-1 was increased in the circulation of the nonworking leg by exercise. The present study also demonstrated that the plasma norepinephrine concentrations were elevated by exercise in the femoral veins of both the working and nonworking legs, suggesting that the sympathetic nerve activity was augmented in both legs during exercise. Therefore, the present study demonstrates the possibility that the increase in production of ET-1 in nonworking muscles may cause vasoconstriction and hence decrease blood flow in nonworking muscles through its direct vasoconstrictive action or through an indirect effect of ET-1 to enhance vasoconstrictions to norepinephrine and that these responses may be helpful in increasing blood flow in working muscles. We propose that endogenous ET-1 contributes to the exercise-induced redistribution of blood flow in muscles.


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