Early Leg Blood Flow Adjustment During Dynamic Foot Plantarflexions in Upright and Supine Body Position

Leyk, Dieter; Essfeld, D; Baum, K; Stegemann, J.

doi:10.1055/s-2007-1021086

Cited by 45 publications

(52 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although there is an immediate increase in blood flow to active skeletal muscle with the onset of exercise (1,10,11,15,17,19,20), the mechanism(s) by which this rapid increase in blood flow occurs has remained elusive. The muscle pump theory has been proposed as a rapid, local mechanism by which blood flow to active skeletal muscle can be regulated.…”

Section: Discussionmentioning

confidence: 99%

Muscle blood flow response to contraction: influence of venous pressure

Valić

Buckwalter²,

Clifford³

2005

Journal of Applied Physiology

View full text Add to dashboard Cite

The skeletal muscle pump is thought to be at least partially responsible for the immediate muscle hyperemia seen with exercise. We hypothesized that increases in venous pressure within the muscle would enhance the effectiveness of the muscle pump and yield greater postcontraction hyperemia. In nine anesthetized beagle dogs, arterial inflow and venous outflow of a single hindlimb were measured with ultrasonic transit-time flow probes in response to 1-s tetanic contractions evoked by electrical stimulation of the sciatic nerve. Venous pressure in the hindlimb was manipulated by tilting the upright dogs to a 30°angle in the head-up or head-down positions. The volume of venous blood expelled during contractions was 2.2 Ϯ 0.2, 1.6 Ϯ 0.2, and 1.4 Ϯ 0.2 ml with the head-up, horizontal, and head-down positions, respectively. Although altering hindlimb venous pressure influenced venous expulsion during contraction, the increase in arterial inflow was similar regardless of position. Moreover, the volume of blood expelled was a small fraction of the cumulative arterial volume after the contraction. These results suggest that the muscle pump is not a major contributor to the hyperemic response to skeletal muscle contraction. exercise; hyperemia; muscle pump; vasodilation; dog IT IS WELL KNOWN THAT, DURING EXERCISE, there is an elevation in blood flow to exercising skeletal muscle. The muscle pump is hypothesized to elevate skeletal muscle blood flow by mechanical factors (16). As the muscle contracts, it compresses the veins within the muscle and expels the venous contents toward the heart. On relaxation, it is hypothesized that the muscle fibers that are tethered to the walls of the veins open the lumen of the compliant vessels and create low pressure (7, 9). Because the venous circulation contains one-way valves, oneway flow is ensured, and the enhanced arteriovenous pressure gradient results in an increase in arterial inflow to skeletal muscle (7).Studies employing both human and animal models have shown that skeletal muscle blood flow is significantly elevated within 1 s after the release of a brief tetanic contraction (1,15,19). Despite this rapid blood flow response in vivo, direct observations of arteriolar diameter reveal that dilation of the skeletal muscle arterioles occurs more slowly (4, 6, 21). Because activation of the muscle pump is temporally compatible with the immediate increase in blood flow seen at the onset of exercise, this observation has been used as prima facie evidence that the muscle pump must be responsible for the rapid increase in skeletal muscle blood flow with the initiation of exercise (16).Fundamental to the muscle pump theory of blood flow control is that muscular contraction lowers venous pressure within the active muscle, thus widening the arteriovenous pressure gradient. However, the relationship between venous pressure within the muscle before contraction and the ability of the muscle pump to produce skeletal muscle hyperemia is a question open for investigation (8). In the present stu...

show abstract

Section: Discussionmentioning

confidence: 99%

Muscle blood flow response to contraction: influence of venous pressure

Valić

Buckwalter²,

Clifford³

2005

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…The rationale for this study was that the primary evidence for a muscle pump effect in exercise hyperemia comes from results of experiments which have demonstrated that limb position influences the blood flow response to muscle contraction (12,22,25,31,36). We reasoned that a critical control experiment has been lacking, i.e., testing whether the response to vascular challenges other than contraction elicit positional differences in blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Because of technical limitations, it has not been feasible to perform experiments to directly test this hypothesis, yet the idea has persisted despite the lack of direct confirmation. Data from studies showing a greater blood flow response to muscle contractions when the limb is in the dependent position (12,22,25,31,36) have been the primary evidence for a skeletal muscle pump contribution to exercise hyperemia. We have argued previously that the magnitude of contraction-elicited changes in blood flow is far greater than can be accounted for by putative changes in intravascular pressure (38) and that the time course of changes in blood flow does not correlate with that predicted from the muscle pump (4).…”

Section: Discussionmentioning

confidence: 99%

“…The best evidence supporting the muscle pump is the greater blood flow response to muscle contractions when the limb is below the heart, when veins should be full due to gravity, compared with the above heart position when veins are empty (e.g., Refs. 12,22,25,31,36).On the other hand, a number of studies over the last decade have provided evidence that muscle contraction causes rapid vasodilation. Experiments performed using the hamster cremaster (2, 24) or retractor muscles (39) demonstrate that muscle contraction causes vasodilation of arterioles within 2-3 s of the onset of muscle contraction.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Jasperse

Shoemaker

Gray

et al. 2015

Journal of Applied Physiology

View full text Add to dashboard Cite

Jasperse JL, Shoemaker JK, Gray EJ, Clifford PS. Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia. J Appl Physiol 119: 569 -575, 2015. First published July 2, 2015; doi:10.1152/japplphysiol.01253.2013.-Studies have reported a greater blood flow response to muscle contractions when the limb is below the heart compared with above the heart, and these results have been interpreted as evidence for a skeletal muscle pump contribution to exercise hyperemia. If limb position affects the blood flow response to other vascular challenges such as reactive hyperemia, this interpretation may not be correct. We hypothesized that the magnitude of reactive hyperemia would be greater with the limb below the heart. Brachial artery blood flow (Doppler ultrasound) and blood pressure (finger-cuff plethysmography) were measured in 10 healthy volunteers. Subjects lay supine with one arm supported in two different positions: above or below the heart. Reactive hyperemia was produced by occlusion of arterial inflow for varying durations: 0.5 min, 1 min, 2 min, or 5 min in randomized order. Peak increases in blood flow were 77 Ϯ 11, 178 Ϯ 24, 291 Ϯ 25, and 398 Ϯ 33 ml/min above the heart and 96 Ϯ 19, 279 Ϯ 62, 550 Ϯ 60, and 711 Ϯ 69 ml/min below the heart (P Ͻ 0.05). Thus a standard stimulus (vascular occlusion) elicited different responses depending on limb position. To determine whether these differences were due to mechanisms intrinsic to the arterial wall, a second set of experiments was performed in which acute intraluminal pressure reduction for 0.5 min, 1 min, 2 min, or 5 min was performed in isolated rat soleus feed arteries (n ϭ 12). The magnitude of dilation upon pressure restoration was greater when acute pressure reduction occurred from 85 mmHg (mimicking pressure in the arm below the heart; 28.3 Ϯ 7.9, 37.5 Ϯ 5.9, 55.1 Ϯ 9.9, and 68.9 Ϯ 8.6% dilation) than from 48 mmHg (mimicking pressure in the arm above the heart; 20.8 Ϯ 4.8, 22.6 Ϯ 4.4, 31.2 Ϯ 5.8, and 49.2 Ϯ 7.1% dilation). These data support the hypothesis that arm position differences in reactive hyperemia are at least partially mediated by mechanisms intrinsic to the arterial wall. Overall, these results suggest the need to reevaluate studies employing positional changes to examine muscle pump influences on exercise hyperemia. muscle blood flow; muscle contraction; skeletal muscle pump; functional hyperemia AT THE ONSET OF DYNAMIC EXERCISE, there is a rapid increase in blood flow [30,31,41, and see Fig. 2 in Clifford and Hellsten (5)]. In fact, even a single muscle contraction produces a prompt increase in blood flow (1,7,14,26,36,39). There has been a debate over the last few decades about whether this rapid hyperemia is due to the muscle pump mechanism or to rapid vasodilation (5, 35).The muscle pump, as described by Laughlin (20), depends on an increased pressure gradient across the skeletal muscle vascular bed. Muscle contraction compresses the veins within the contracting muscle, expelling blood from the veins. ...

show abstract

Exercise Hyperpnea

Ward

2006

Wiley Encyclopedia of Biomedical Engineering

View full text Add to dashboard Cite

Control schemes of ventilation during moderate exercise [i.e., below the lactate threshold ( θ L )] have classically incorporated both proportional humoral feedback (carotid and central chemoreflex) and neurogenic feed forward (central command, muscle, cardiocirculatory) to provide stability of arterial PCO 2 (PaCO 2 ) pH (pHa), and PO 2 (PaO 2 ). In response to a step work‐rate (WR) forcing from prior rest in the upright posture, increases abruptly for some 15–20 s, this being followed by a subsequent more‐prominent exponential component (consistent with first‐order kinetics). The lack of any sustained error signals in the mean levels of PaCO 2 , pHa, or PaO 2 , coupled with the dynamic matching of with pulmonary CO 2 output but not O 2 uptake or WR, suggests that the controller operates as if it incorporates an errorless humoral feedback element proportional to (or some close proxy). In addition, the controller seems to evidence considerable redundancy, with particular sensory deficits having little effect on the steady‐state response to exercise or the stability of PaCO 2 between rest and exercise. Above θ L , kinetics become markedly nonlinear, with steady states being either delayed or not attained, which reflects the influence of the developing metabolic acidemia (1) indirectly, via bicarbonate‐mediated body CO 2 stores washout, which augments ; and (2) directly, to effect respiratory compensation for the falling pHa (this being constrained by the falling PaCO 2 that results from increasing out of proportion to ). The carotid bodies are important in mediating this respiratory compensation, although with surprisingly slow kinetics, In conclusion, despite there now being general agreement regarding the overall characteristics of the response to exercise, the precise details of the control process(es) remain unresolved.

show abstract

Early Leg Blood Flow Adjustment During Dynamic Foot Plantarflexions in Upright and Supine Body Position

Cited by 45 publications

References 19 publications

Muscle blood flow response to contraction: influence of venous pressure

Muscle blood flow response to contraction: influence of venous pressure

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Exercise Hyperpnea

Contact Info

Product

Resources

About