Blood flow variation in human muscle during electrically stimulated exercise bouts

2002 ◽  
Vol 83 (7) ◽  
pp. 936-941 ◽  
Author(s):  
Marc Vanderthommen ◽  
Jean-Claude Depresseux ◽  
Luc Dauchat ◽  
Christian Degueldre ◽  
Jean-Louis Croisier ◽  
...  
2014 ◽  
Vol 30 ◽  
pp. e102-e103
Author(s):  
A. Skouroliakou ◽  
I. Seferis ◽  
C. Michail ◽  
I. Sianoudis ◽  
D. Mathes ◽  
...  
Keyword(s):  

2014 ◽  
Vol 306 (10) ◽  
pp. E1198-E1204 ◽  
Author(s):  
David M. Gundermann ◽  
Dillon K. Walker ◽  
Paul T. Reidy ◽  
Michael S. Borack ◽  
Jared M. Dickinson ◽  
...  

Restriction of blood flow to a contracting muscle during low-intensity resistance exercise (BFR exercise) stimulates mTORC1 signaling and protein synthesis in human muscle within 3 h postexercise. However, there is a lack of mechanistic data to provide a direct link between mTORC1 activation and protein synthesis in human skeletal muscle following BFR exercise. Therefore, the primary purpose of this study was to determine whether mTORC1 signaling is necessary for stimulating muscle protein synthesis after BFR exercise. A secondary aim was to describe the 24-h time course response in muscle protein synthesis and breakdown following BFR exercise. Sixteen healthy young men were randomized to one of two groups. Both the control (CON) and rapamycin (RAP) groups completed BFR exercise; however, RAP was administered 16 mg of the mTOR inhibitor rapamycin 1 h prior to BFR exercise. BFR exercise consisted of four sets of leg extension exercise at 20% of 1 RM. Muscle biopsies were collected from the vastus lateralis before exercise and at 3, 6, and 24 h after BFR exercise. Mixed-muscle protein fractional synthetic rate increased by 42% at 3 h postexercise and 69% at 24 h postexercise in CON, whereas this increase was inhibited in the RAP group. Phosphorylation of mTOR (Ser2448) and S6K1 (Thr389) was also increased in CON but inhibited in RAP. Mixed-muscle protein breakdown was not significantly different across time or groups. We conclude that activation of mTORC1 signaling and protein synthesis in human muscle following BFR exercise is inhibited in the presence of rapamycin.


2007 ◽  
Vol 293 (5) ◽  
pp. H2928-H2936 ◽  
Author(s):  
Kathryn L. Walker ◽  
Natasha R. Saunders ◽  
Dennis Jensen ◽  
Jennifer L. Kuk ◽  
Suzi-Lai Wong ◽  
...  

We tested the hypothesis that vasoregulatory mechanisms completely counteract the effects of sudden changes in arterial perfusion pressure on exercising muscle blood flow. Twelve healthy young subjects (7 female, 5 male) lay supine and performed rhythmic isometric handgrip contractions (2 s contraction/ 2 s relaxation 30% maximal voluntary contraction). Forearm blood flow (FBF; echo and Doppler ultrasound), mean arterial blood pressure (arterial tonometry), and heart rate (ECG) were measured. Moving the arm between above the heart (AH) and below the heart (BH) level during contraction in steady-state exercise achieved sudden ∼30 mmHg changes in forearm arterial perfusion pressure (FAPP). We analyzed cardiac cycles during relaxation (FBFrelax). In an AH-to-BH transition, FBFrelax increased immediately, in excess of the increase in FAPP (∼69% vs. ∼41%). This was accounted for by pressure-related distension of forearm resistance vasculature [forearm vascular conductance (FVCrelax) increased by ∼19%]. FVCrelax was restored by the second relaxation. Continued slow decreases in FVCrelax stabilized by 2 min without restoring FBFrelax. In a BH-to-AH transition, FBFrelax decreased immediately, in excess of the decrease in FAPP (∼37% vs. ∼29%). FVCrelax decreased by ∼14%, suggesting pressure-related passive recoil of resistance vessels. The pattern of FVCrelax was similar to that in the AH-to-BH transition, and FBFrelax was not restored. These data support rapid myogenic regulation of vascular conductance in exercising human muscle but incomplete flow restoration via slower-acting mechanisms. Local arterial perfusion pressure is an important determinant of steady-state blood flow in the exercising human forearm.


2005 ◽  
Vol 90 (5) ◽  
pp. 715-726 ◽  
Author(s):  
Leonardo F. Ferreira ◽  
Allison J. Harper ◽  
Dana K. Townsend ◽  
Barbara J. Lutjemeier ◽  
Thomas J. Barstow

2015 ◽  
Vol 118 (6) ◽  
pp. 783-793 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Helmut Habazettl ◽  
Zafeiris Louvaris ◽  
Vasileios Andrianopoulos ◽  
Harrieth Wagner ◽  
...  

Heterogeneity in the distribution of both blood flow (Q̇) and O2 consumption (V̇o2) has not been assessed by near-infrared spectroscopy in exercising normal human muscle. We used near-infrared spectroscopy to measure the regional distribution of Q̇ and V̇o2 in six trained cyclists at rest and during constant-load exercise (unloaded pedaling, 20%, 50%, and 80% of peak Watts) in both normoxia and hypoxia (inspired O2 fraction = 0.12). Over six optodes over the upper, middle, and lower vastus lateralis, we recorded 1) indocyanine green dye inflow after intravenous injection to measure Q̇; and 2) fractional tissue O2 saturation (StiO2) to estimate local V̇o2-to-Q̇ ratios (V̇o2/Q̇). Varying both exercise intensity and inspired O2 fraction provided a (directly measured) femoral venous O2 saturation range from about 10 to 70%, and a correspondingly wide range in StiO2. Mean Q̇-weighted StiO2 over the six optodes related linearly to femoral venous O2 saturation in each subject. We used this relationship to compute local muscle venous blood O2 saturation from StiO2 recorded at each optode, from which local V̇o2/Q̇ could be calculated by the Fick principle. Multiplying regional V̇o2/Q̇ by Q̇ yielded the corresponding local V̇o2. While six optodes along only in one muscle may not fully capture the extent of heterogeneity, relative dispersion of both Q̇ and V̇o2 was ∼0.4 under all conditions, while that for V̇o2/Q̇ was minimal (only ∼0.1), indicating in fit young subjects 1) a strong capacity to regulate Q̇ according to regional metabolic need; and 2) a likely minimal impact of heterogeneity on muscle O2 availability.


Sensors ◽  
2015 ◽  
Vol 15 (10) ◽  
pp. 25507-25519 ◽  
Author(s):  
Wataru Iwasaki ◽  
Hirofumi Nogami ◽  
Satoshi Takeuchi ◽  
Masutaka Furue ◽  
Eiji Higurashi ◽  
...  

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S63
Author(s):  
R. S. Richardson ◽  
B. Saltin ◽  
J. Bangsbo ◽  
T. Graham ◽  
L. B. Rowell

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