Lower Leg High-Intensity Resistance Training and Peripheral Hemodynamic Adaptations

1996 ◽  
Vol 21 (3) ◽  
pp. 209-217 ◽  
Author(s):  
Vernon Bond Jr. ◽  
Arthur T. Johnson ◽  
Paul Vaccaro ◽  
Paul Wang ◽  
Richard G. Adams ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Intensity ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Lower Leg ◽  
Muscle Volume ◽  
Flow Limitation ◽  
Leg Muscle ◽  
Calf Muscles ◽  
Blood Flow Limitation

High-intensity resistance (HIR) training has been associated with muscle hypertrophy and decreased microvascular density that might produce a blood flow limitation. The effect of HIR training on lower leg maximal blood flow and minimum vascular resistance (Rmin) during reactive hyperemia were investigated in 7 healthy males. The gastrocnemius-soleus muscles of one leg were trained using maximal isokinetic concentric contractions for 4 weeks; the nontrained leg was the control. Lower leg blood flow was measured by venous occlusion plethysmography. Lower leg muscle volume was determined using magnetic resonance imaging. Peak isokinetic torque increased in both the trained (T) and nontrained (NT) legs (p <.05). Lower leg muscle volume increased by 2% in the T leg only (p <.05). In the T leg, maximal blood flow decreased and Rmin increased (p <.05); no hemodynamic change was detected in the NT leg. It is concluded that HIR training of the calf muscles is associated with a decrease in hyperemia-induced blood flow; thereby, indicating a blood flow limitation to the calf muscles. Key words: Isokinetic strength training, reactive hyperemia

Peak calf blood flow estimates are higher with Dohn than with Whitney plethysmograph

1996 ◽  
Vol 81 (3) ◽  
pp. 1418-1422 ◽  
Author(s):  
D. N. Proctor ◽  
J. R. Halliwill ◽  
P. H. Shen ◽  
N. E. Vlahakis ◽  
M. J. Joyner
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Calf Blood Flow ◽  
Absolute Flow ◽  
Wide Range ◽  
Before And After ◽  
The Mean ◽  
Highly Correlated

Estimates of calf blood flow with venous occlusion plethysmography vary widely between studies, perhaps due to the use of different plethysmographs. Consequently, we compared calf blood flow estimates at rest and during reactive hyperemia in eight healthy subjects (four men and four women) with two commonly used plethysmographs: the mercury-in-silastic (Whitney) strain gauge and Dohn air-filled cuff. To minimize technical variability, flow estimates were compared with a Whitney gauge and a Dohn cuff on opposite calves before and after 10 min of bilateral femoral arterial occlusion. To account for any differences between limbs, a second trial was conducted in which the plethysmographs were switched. Resting flows did not differ between the plethysmographs (P = 0.096), but a trend toward lower values with the Whitney was apparent. Peak flows averaged 37% lower with the Whitney (27.8 +/- 2.8 ml.dl-1.min-1) than with the Dohn plethysmograph (44.4 +/- 2.8 ml.dl-1.min-1; P < 0.05). Peak flow expressed as a multiple above baseline was also lower with the Whitney (10-fold) than with the Dohn plethysmograph (14.5-fold; P = 0.02). Across all flows at rest and during reactive hyperemia, estimates were highly correlated between the plethysmographs in all subjects (r2 = 0.96-0.99). However, the mean slope for the Whitney-Dohn relationship was only 60 +/- 2%, indicating that over a wide range of flows the Whitney gauge estimate was 40% lower than that for the Dohn cuff. These results demonstrate that the same qualitative results can be obtained with either plethysmograph but that absolute flow values will generally be lower with Whitney gauges.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Effect of active muscle mass during ischemic exercise on peak lower leg vascular conductance

2005 ◽  
Vol 98 (3) ◽  
pp. 765-771 ◽  
Author(s):  
Aaron J. Polichnowski ◽  
Ellen K. Heyer ◽  
Alexander V. Ng
Keyword(s):  
Blood Flow ◽  
Muscle Mass ◽  
Plantar Flexion ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Lower Leg ◽  
Isokinetic Dynamometer ◽  
Active Muscle ◽  
Vascular Conductance ◽  
The Right

Uncertainty exists as to whether a period of passive arterial occlusion (PAO) or ischemic exercise (IE) results in peak lower leg vascular conductance (LVC). This uncertainty is due to the different body positions, active muscle mass, and occlusion times used for PAO or IE. The purpose of this study was to examine whether 10 min of PAO elicits a similar LVC compared with ischemic dorsiflexion (IDF), ischemic plantar flexion (IPF), and ischemic plantar-dorsiflexion (IPDF). Ten subjects (5 women, 27 ± 9 yr, 68 ± 3 kg) were studied on 3 days over 1 wk in a semireclined position with the right foot attached to an isokinetic dynamometer. Mean arterial pressure (Finapres) and lower leg blood flow (LBF, venous occlusion plethysmography) were measured at rest and after PAO and IE. PAO was administered randomly on 1 of the 3 days and before IE. IE protocols consisted of maximal isokinetic dorsiflexion and/or plantar flexion at 120 and 60°/s, respectively. In a second experiment, an additional eight subjects (4 women, 29 ± 12 yr, 77 ± 12 kg) were studied to examine the effect of isokinetic speed during IDF on peak LBF and LVC. Peak LVC (ml·min−1·100 ml−1·mmHg−1) was similar among IPF (0.590 ± 0.16), IPDF (0.532 ± 0.17), and PAO (0.511 ± 0.18), and significantly lower after IDF (0.334 ± 0.15). No differences in peak LBF and LVC were observed after IDF using different isokinetic speeds. We conclude that 10 min of PAO, IPF, and IPDF performed in a similar posture are adequate stimuli to elicit peak LVC.

scholarly journals Scaling of maximal oxygen uptake by lower leg muscle volume in boys and men

2006 ◽  
Vol 100 (6) ◽  
pp. 1851-1856 ◽  
Author(s):  
Keith Tolfrey ◽  
Alan Barker ◽  
Jeanette M. Thom ◽  
Christopher I. Morse ◽  
Marco V. Narici ◽  
...  
Keyword(s):  
Body Size ◽  
Confidence Interval ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Lower Leg ◽  
Muscle Volume ◽  
Fat Free Mass ◽  
Percentage Body Fat ◽  
Leg Muscle

The aim of this study was to critically examine the influence of body size on maximal oxygen uptake (V̇o2 max) in boys and men using body mass (BM), estimated fat-free mass (FFM), and estimated lower leg muscle volume (Vol) as the separate scaling variables. V̇o2 max and an in vivo measurement of Vol were assessed in 15 boys and 14 men. The FFM was estimated after percentage body fat had been predicted from population-specific skinfold measurements. By using nonlinear allometric modeling, common body size exponents for BM, FFM, and Vol were calculated. The point estimates for the size exponent (95% confidence interval) from the separate allometric models were: BM 0.79 (0.53–1.06), FFM 1.00 (0.78–1.22), and Vol 0.64 (0.40–0.88). For the boys, substantial residual size correlations were observed for V̇o2 max/BM0.79 and V̇o2 max/FFM1.00, indicating that these variables did not correctly partition out the influence of body size. In contrast, scaling by Vol0.64 led to no residual size correlation in boys or men. Scaling by BM is confounded by heterogeneity of body composition and potentially substantial differences in the mass exponent between boys and men. The FFM is precluded as an index of involved musculature because Vol did not represent a constant proportion of FFM [Vol∝FFM1.45 (95% confidence interval, 1.13–1.77)] in the boys (unlike the men). We conclude that Vol, as an indicator of the involved muscle mass, is the most valid allometric denominator for the scaling of V̇o2 max in a sample of boys and men heterogeneous for body size and composition.

scholarly journals Intercostal muscle blood flow limitation in athletes during maximal exercise

2009 ◽  
Vol 587 (14) ◽  
pp. 3665-3677 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Dimitris Athanasopoulos ◽  
Helmut Habazettl ◽  
Wolfgang M. Kuebler ◽  
Harrieth Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Maximal Exercise ◽  
Muscle Blood Flow ◽  
Flow Limitation ◽  
Intercostal Muscle ◽  
Blood Flow Limitation

Inhibition of vascular ATP-sensitive K+channels does not affect reactive hyperemia in human forearm

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Adaptive Response ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Hyperemic Response

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

scholarly journals Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans

1996 ◽  
Vol 271 (4) ◽  
pp. H1594-H1598 ◽  
Author(s):  
P. F. Banitt ◽  
P. Smits ◽  
S. B. Williams ◽  
P. Ganz ◽  
M. A. Creager
Keyword(s):  
Blood Flow ◽  
Katp Channel ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Katp Channels ◽  
Venous Occlusion ◽  
Membrane Hyperpolarization ◽  
Flow Response ◽  
Hyperemic Flow ◽  
Basal Flow

Activation of ATP-sensitive potassium (KATP) channels present on vascular smooth muscle cells causes membrane hyperpolarization and vasodilation. The purpose of this study was to determine whether KATP channels contribute to reactive hyperemia in humans. Accordingly, we studied the effect of tolbutamide, a KATP channel inhibitor, on reactive hyperemic forearm blood flow. Forearm blood flow was measured by venous occlusion plethysmography. Forearm ischemia was produced by inflating a sphygmomanometric cuff on the arm to suprasystolic pressures for 5 min. After cuff release, forearm blood flow was measured during the reactive hyperemic phase for 5 min. Tolbutamide (1 mM blood concentration, n = 6) did not affect basal (2.4 +/- 0.2 to 2.2 +/- 0.1 ml.100 ml-1.min-1) or peak reactive hyperemic forearm blood flow (21.9 +/- 3.8 to 22.6 +/- 2.9 ml.100 ml-1.min-1, each P = NS), but it significantly attenuated total hyperemic volume (12.6 +/- 1.7 vs. 9.2 +/- 1.8 ml/100 ml, P < 0.02). Vehicle (n = 6) did not affect basal flow, peak reactive hyperemic flow, or total hyperemia. To determine whether adenosine or endothelium-derived nitric oxide contribute to reactive hyperemia via KATP channels, adenosine (1.5-500 micro grams/min, n = 6) and acetylcholine (30 micrograms/min, n = 6) were infused before and during tolbutamide coinfusion. Tolbutamide did not significantly alter the forearm blood flow response to either adenosine or acetylcholine. In conclusion, KATP channels contribute to vasodilation during reactive hyperemia in humans.

Intrinsic control of colonic blood flow and oxygenation

1980 ◽  
Vol 238 (6) ◽  
pp. G478-G484
Author(s):  
P. R. Kvietys ◽  
T. Miller ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Reactive Hyperemia ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Colonic Blood Flow ◽  
O2 Extraction ◽  
O2 Delivery

In a denervated autoperfused dog colon preparation, arterial perfusion pressure, venous outflow pressure, blood flow, and arteriovenous O2 difference were measured during graded arterial pressure alterations, arterial occlusion, venous pressure elevation, venous occlusion, and local intra-arterial infusion of adenosine. As perfusion pressure was reduced from 100 to 30 mmHg, colonic blood flow decreased and arteriovenous O2 difference increased. Although blood flow was not autoregulated O2 delivery was maintained within 10% of control between 70 to 100 mmHg and then decreased with further reduction in perfusion pressure. Arterial occlusion (15, 30, and 60 s) resulted in a postocclusion reactive hyperemia; the magnitude of the hyperemia was directly related to the duration of occlusion. Venous occlusion resulted in a postocclusion reactive hypoemia. Elevation of venous pressure from 0 to 20 mmHg increased vascular resistance, O2 extraction, and the capillary filtration coefficient, but decreased O2 delivery. Infusion of adenosine decreased vascular resistance and O2 extraction, but increased O2 delivery. These data suggest that both metabolic and myogenic mechanisms are involved in the control of colonic blood flow and oxygenation.

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