Maximal strength training and increased work efficiency: contribution from the trained muscle bed

Maximal strength training (MST) reduces pulmonary oxygen uptake (V̇o2) at a given submaximal exercise work rate (i.e., efficiency). However, whether the increase in efficiency originates in the trained skeletal muscle, and therefore the impact of this adaptation on muscle blood flow and arterial-venous oxygen difference (a-vO2diff), is unknown. Thus five trained subjects partook in an 8-wk MST intervention consisting of half-squats with an emphasis on the rate of force development during the concentric phase of the movement. Pre- and posttraining measurements of pulmonary V̇o2 (indirect calorimetry), single-leg blood flow (thermodilution), and single-leg a-vO2diff (blood gases) were performed, to allow the assessment of skeletal muscle V̇o2 during submaximal cycling [237 ± 23 W; ∼60% of their peak pulmonary V̇o2 (V̇o2peak)]. Pulmonary V̇o2peak (∼4.05 l/min) and peak work rate (∼355 W), assessed during a graded exercise test, were unaffected by MST. As expected, following MST there was a significant reduction in pulmonary V̇o2 during steady-state submaximal cycling (∼237 W: 3.2 ± 0.1 to 2.9 ± 0.1 l/min). This was accompanied by a significant reduction in single-leg V̇o2 (1,101 ± 105 to 935 ± 93 ml/min) and single-leg blood flow (6,670 ± 700 to 5,649 ± 641 ml/min), but no change in single-leg a-vO2diff (16.7 ± 0.8 to 16.8 ±0.4 ml/dl). These data confirm an MST-induced reduction in pulmonary V̇o2 during submaximal exercise and identify that this change in efficiency originates solely in skeletal muscle, reducing muscle blood flow, but not altering muscle a-vO2diff.

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One-arm maximal strength training improves work economy and endurance capacity but not skeletal muscle blood flow

Journal of Sports Sciences ◽

10.1080/02640414.2010.529454 ◽

2011 ◽

Vol 29 (2) ◽

pp. 161-170 ◽

Cited By ~ 4

Author(s):

Ole J. Kemi ◽

Oivind Rognmo ◽

Brage H. Amundsen ◽

Stig Stordahl ◽

Russel S. Richardson ◽

...

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Strength Training ◽

Muscle Blood Flow ◽

Endurance Capacity ◽

Maximal Strength ◽

Skeletal Muscle Blood Flow ◽

Work Economy

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Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

Journal of Applied Physiology ◽

10.1152/japplphysiol.01211.2004 ◽

2005 ◽

Vol 98 (4) ◽

pp. 1463-1468 ◽

Cited By ~ 15

Author(s):

Jay T. Williams ◽

Mollie P. Pricher ◽

John R. Halliwill

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Oxygen Consumption ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Muscle Blood Flow ◽

Causal Link ◽

Skeletal Muscle Blood Flow ◽

Leg Blood Flow ◽

Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

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α-Adrenergic receptor regulation of skeletal muscle blood flow during exercise in heart failure patients with reduced ejection fraction

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00345.2018 ◽

2019 ◽

Vol 316 (5) ◽

pp. R512-R524 ◽

Cited By ~ 5

Author(s):

Zachary Barrett-O’Keefe ◽

Joshua F. Lee ◽

Stephen J. Ives ◽

Joel D. Trinity ◽

Melissa A. H. Witman ◽

...

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Ejection Fraction ◽

Adrenergic Receptor ◽

Muscle Blood Flow ◽

Skeletal Muscle Blood Flow ◽

Reduced Ejection Fraction ◽

Leg Blood Flow ◽

Related Increase

Patients suffering from heart failure with reduced ejection fraction (HFrEF) experience impaired limb blood flow during exercise, which may be due to a disease-related increase in α-adrenergic receptor vasoconstriction. Thus, in eight patients with HFrEF (63 ± 4 yr) and eight well-matched controls (63 ± 2 yr), we examined changes in leg blood flow (Doppler ultrasound) during intra-arterial infusion of phenylephrine (PE; an α1-adrenergic receptor agonist) and phentolamine (Phen; a nonspecific α-adrenergic receptor antagonist) at rest and during dynamic single-leg knee-extensor exercise (0, 5, and 10 W). At rest, the PE-induced reduction in blood flow was significantly attenuated in patients with HFrEF (−15 ± 7%) compared with controls (−36 ± 5%). During exercise, the controls exhibited a blunted reduction in blood flow induced by PE (−12 ± 4, −10 ± 4, and −9 ± 2% at 0, 5, and 10 W, respectively) compared with rest, while the PE-induced change in blood flow was unchanged compared with rest in the HFrEF group (−8 ± 5, −10 ± 3, and −14 ± 3%, respectively). Phen administration increased leg blood flow to a greater extent in the HFrEF group at rest (+178 ± 34% vs. +114 ± 28%, HFrEF vs. control) and during exercise (36 ± 6, 37 ± 7, and 39 ± 6% vs. 13 ± 3, 14 ± 1, and 8 ± 3% at 0, 5, and 10 W, respectively, in HFrEF vs. control). Together, these findings imply that a HFrEF-related increase in α-adrenergic vasoconstriction restrains exercising skeletal muscle blood flow, potentially contributing to diminished exercise capacity in this population.

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Effects of hyperthyroidism on muscle blood flow during exercise in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.1.h330 ◽

1995 ◽

Vol 268 (1) ◽

pp. H330-H335 ◽

Cited By ~ 5

Author(s):

R. M. McAllister ◽

J. C. Sansone ◽

M. H. Laughlin

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Citrate Synthase ◽

Muscle Blood Flow ◽

Left Ventricular ◽

Submaximal Exercise ◽

Treadmill Running ◽

Exercise Intolerance ◽

Blood Flows

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6–12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25–60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1–2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50–150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.

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Dynamic regulation of leg vasomotor tone in patients with chronic heart failure

Journal of Applied Physiology ◽

10.1152/jappl.1991.71.3.1070 ◽

1991 ◽

Vol 71 (3) ◽

pp. 1070-1075 ◽

Cited By ~ 10

Author(s):

M. J. Sullivan ◽

F. R. Cobb

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Cardiac Output ◽

Chronic Heart Failure ◽

Left Ventricular ◽

Work Rate ◽

Vasomotor Tone ◽

Leg Blood Flow ◽

Leg Exercise

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.

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Role of α1-adrenergic vasoconstriction in the regulation of skeletal muscle blood flow with advancing age

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01016.2008 ◽

2009 ◽

Vol 296 (2) ◽

pp. H497-H504 ◽

Cited By ~ 28

Author(s):

D. Walter Wray ◽

Steven K. Nishiyama ◽

Russell S. Richardson

Keyword(s):

Blood Flow ◽

Muscle Blood Flow ◽

Knee Extensor ◽

The Elderly ◽

Work Rate ◽

Leg Blood Flow ◽

Vasoconstrictor Response ◽

Leg Exercise ◽

Exercise Induced ◽

Induced Changes

α1-Adrenergic vasoconstriction during dynamic leg exercise is diminished in younger individuals, although the extent of this exercise-induced “sympatholysis” in the elderly remains uncertain. Thus, in nine young (25 ± 1 yr) and six older (72 ± 2 yr) healthy volunteers, we evaluated changes in leg blood flow (ultrasound Doppler) during blood flow-adjusted intra-arterial infusion of phenylephrine (PE; a selective α1-adrenergic agonist) at rest and during knee-extensor leg exercise at 20, 40, and 60% of maximal work rate (WRmax). To probe the potential contributors to exercise-induced changes in α1-adrenergic receptor sensitivity, exercising leg O2 consumption (V̇o2) and lactate efflux were also evaluated ( n = 10). At rest, the PE-induced vasoconstriction (i.e., decrease in leg blood flow) was diminished in older (−37 ± 3%) compared with young (−54 ± 4%) subjects. During exercise, the magnitude of α1-adrenergic vasoconstriction in the active leg decreased in both groups. However, compared with young, older subjects maintained a greater vasoconstrictor response to PE at 40% WRmax (−14 ± 3%, older; −7 ± 2%, young) and 60% WRmax (−11 ± 3%, older; −4 ± 3%, young). It is possible that this observation may be attributed to lower absolute work rates in the older group, because, for a similar absolute work rate (≈10 W) and leg V̇o2 (≈0.36 l/min), vasoconstriction to PE was not different between groups (−14 ± 3%; older; −17 ± 5%, young). Together, these data challenge the concept of reduced sympatholysis in the elderly, suggesting instead that the inhibition of α1-adrenergic vasoconstriction in the exercising leg is associated with work performed and, therefore, more closely related to the rate of oxidative metabolism than to age per se.

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Hyperbaric hyperoxia reduces exercising forearm blood flow in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00165.2011 ◽

2011 ◽

Vol 300 (5) ◽

pp. H1892-H1897 ◽

Cited By ~ 19

Author(s):

Darren P. Casey ◽

Michael J. Joyner ◽

Paul L. Claus ◽

Timothy B. Curry

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Forearm Blood Flow ◽

Muscle Blood Flow ◽

Hyperbaric Hyperoxia ◽

Exercise Hyperemia ◽

Forearm Vascular Conductance ◽

Forearm Exercise ◽

The Impact ◽

Hyperemic Response

Hypoxia during exercise augments blood flow in active muscles to maintain the delivery of O2 at normoxic levels. However, the impact of hyperoxia on skeletal muscle blood flow during exercise is not completely understood. Therefore, we tested the hypothesis that the hyperemic response to forearm exercise during hyperbaric hyperoxia would be blunted compared with exercise during normoxia. Seven subjects (6 men/1 woman; 25 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Forearm blood flow (FBF; in ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC; in ml·min−1·100 mmHg−1) was calculated from FBF and blood pressure (in mmHg; brachial arterial catheter). Studies were performed in a hyperbaric chamber with the subjects supine at 1 atmospheres absolute (ATA) (sea level) while breathing normoxic gas [21% O2, 1 ATA; inspired Po2 (PiO2) ≈ 150 mmHg] and at 2.82 ATA while breathing hyperbaric normoxic (7.4% O2, 2.82 ATA, PiO2 ≈ 150 mmHg) and hyperoxic (100% O2, 2.82 ATA, PiO2 ≈ 2,100 mmHg) gas. Resting FBF and FVC were less during hyperbaric hyperoxia compared with hyperbaric normoxia ( P < 0.05). The change in FBF and FVC (Δ from rest) during exercise under normoxia (204 ± 29 ml/min and 229 ± 37 ml·min−1·100 mmHg−1, respectively) and hyperbaric normoxia (203 ± 28 ml/min and 217 ± 35 ml·min−1·100 mmHg−1, respectively) did not differ ( P = 0.66–0.99). However, the ΔFBF (166 ± 21 ml/min) and ΔFVC (163 ± 23 ml·min−1·100 mmHg−1) during hyperbaric hyperoxia were substantially attenuated compared with other conditions ( P < 0.01). Our data suggest that exercise hyperemia in skeletal muscle is highly dependent on oxygen availability during hyperoxia.

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Ischaemia and insulin, but not ischaemia and contraction, act synergistically in stimulating muscle glucose uptake in vivo in humans

Clinical Science ◽

10.1042/cs20080087 ◽

2008 ◽

Vol 116 (2) ◽

pp. 157-164 ◽

Cited By ~ 1

Author(s):

Marlies Bosselaar ◽

Paul Smits ◽

Cees J. Tack

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Muscle Contraction ◽

Glucose Uptake ◽

Muscle Blood Flow ◽

In Vitro Models ◽

Skeletal Muscle Glucose Uptake ◽

The Impact

Ischaemia, like muscle contraction, has been reported to induce skeletal muscle glucose uptake in in vitro models. This stimulating effect appears independent of insulin and is probably mediated by activation of AMPK (AMP-activated protein kinase). In the present study, we hypothesized that in vivo in humans ischaemia- and insulin-induced glucose uptake are additive, and that the combined impact of ischaemia and contraction on glucose uptake is of a similar magnitude when each is applied separately. We assessed the effects of ischaemia with and without euglycaemic–hyperinsulinaemia (clamp; protocol 1) and with and without muscle contraction (protocol 2) on muscle FGU (forearm glucose uptake) in healthy subjects. Furthermore, we assessed the impact of ischaemia on FBF (forearm blood flow; plethysmography). In protocol 1, ischaemia increased FGU from 0.6±0.1 at baseline to 5.5±1.9 μmol·min−1·dl−1, and insulin increased FGU to 1.6±0.3 μmol·min−1·dl−1 (P<0.05 for both). The combination of ischaemia+insulin increased FGU to 15.5±2.2 μmol·min−1·dl−1 (P<0.05 compared with each stimulus alone). Maximal FBF obtained after ischaemia was similar with and without hyperinsulinaemia. In protocol 2, isometric contraction increased FGU from 0.3±0.1 to 2.7±0.8 μmol·min−1·dl−1 (P<0.05), but FGU was not significantly different from ischaemia compared with ischaemia+contraction. However, combined ischaemia+contraction resulted in a greater increase in FBF. In summary, ischaemia and insulin independently stimulate skeletal muscle glucose uptake in vivo in humans, whereas ischaemia and contraction do not. The observed differential effects of these stimuli on glucose uptake appear to be unrelated to changes in muscle blood flow.

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Neural control of glucose uptake by skeletal muscle after central administration of NMDA

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.268.2.r492 ◽

1995 ◽

Vol 268 (2) ◽

pp. R492-R497 ◽

Cited By ~ 1

Author(s):

C. H. Lang ◽

M. Ajmal ◽

A. G. Baillie

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Glucose Uptake ◽

Neural Control ◽

Plasma Insulin ◽

Regional Blood Flow ◽

Muscle Blood Flow ◽

Whole Body ◽

Glucose Disposal ◽

Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

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