Regulatory, Integrative and Comparative Physiology

Hemodynamic responses to static and dynamic muscle contractions at equivalent workloads

Jason W. Daniels, Charles L. Stebbins, John C. Longhurst


We tested the hypothesis that static contraction causes greater reflex cardiovascular responses than dynamic contraction at equivalent workloads [i.e., same tension-time index (TTI), holding either contraction time or peak tension constant] in chloralose-anesthetized cats. When time was held constant and tension was allowed to vary, dynamic contraction of the hindlimb muscles evoked greater increases (means ± SE) in mean arterial pressure (MAP; 50 ± 7 vs. 30 ± 5 mmHg), popliteal blood velocity (15 ± 3 vs. 5 ± 1 cm/s), popliteal venous Pco 2 (15 ± 3 vs. 3 ± 1 mmHg), and a greater decrease in popliteal venous pH (0.07 ± 0.01 vs. 0.03 ± 0.01), suggesting greater metabolic stimulation during dynamic contraction. Similarly, when peak tension was held constant and time was allowed to vary, dynamic contraction evoked a greater increase in blood velocity (13 ± 1 vs. −1 ± 1 cm/s) without causing any differences in other variables. To investigate the reflex contribution of mechanoreceptors, we stretched the hindlimb dynamically and statically at the same TTI. A larger reflex increase in MAP during dynamic stretch (32 ± 8 vs. 24 ± 6 mmHg) was observed when time was held constant, indicating greater mechanoreceptor stimulation. However, when peak tension was held constant, there were no differences in the reflex cardiovascular response to static and dynamic stretch. In conclusion, at comparable TTI, when peak tension is variable, dynamic muscle contraction causes larger cardiovascular responses than static contraction because of greater chemical and mechanical stimulation. However, when peak tensions are equivalent, static and dynamic contraction or stretch produce similar cardiovascular responses.

  • static and dynamic muscle stretch
  • skeletal muscle blood flow
  • exercise
  • kao stimulator

individuals with cardiovascular disease often are directed away from exercise involving static contraction, because it is thought that there is a greater reflex autonomic response associated with a larger afterload placed on the heart compared with dynamic contraction. Several attempts have been made to compare the cardiovascular response to both static and dynamic contraction (1-3); however, comparisons between static and dynamic contraction have not been adequately investigated with the same muscle group performing equivalent amounts of work.

Both static and rhythmic contraction of hindlimb muscles in anesthetized animals induce reflex increases in cardiac output, blood pressure, and heart rate (HR) (5, 6, 10, 12, 13). The magnitude of this reflex response is dependent on the amount of muscle mass and/or tension development, such that the greater the muscle mass involved or tension developed, the greater the pressor reflex (3, 5, 12).

Previous studies suggest that static contraction causes greater pressor responses than those caused by dynamic contraction (9, 15,19). This difference is reportedly due to continuous restriction of muscle blood flow during static contraction that results in greater accumulation of local metabolites and greater activation of chemosensitive muscle afferents (9, 15). However, differences in the energy of activation between these two types of contraction may play an important role because they can lead to differences in muscle metabolism and in the production and accumulation of local metabolites (4, 7, 17).

Differential stimulation of muscle mechanoreceptors (intermittent vs. continuous) also may contribute to differences in the pressor response to dynamic contraction. Unfortunately, separating the effects of mechanoreceptors from those of metaboreceptors on the exercise pressor reflex can be difficult. Nevertheless, comparing the reflex cardiovascular response to passive dynamic and static muscle stretch provides a viable alternative because stretch is not associated with any metabolic changes (18).

Although previous attempts have been made to compare cardiovascular responses with dynamic and static contractions (9, 15,19), such comparisons have not been performed at equivalent workloads. Because the magnitude of the reflex cardiovascular response is directly related to the force production (15), adequate comparison of the response patterns during dynamic and static exercise cannot be made accurately unless force production is similar.

The integration of force over time, termed tension-time index (TTI), appears to be a reasonable quantitative technique for equating force produced during static and dynamic contraction. This approach provides an accurate means to compare the cardiovascular response during these two disparate types of contraction within the same groups of muscle (1, 15). Therefore, we tested the following hypotheses:1) when developed tension over time (TTI) is similar, static contraction induces a greater reflex-pressor response than dynamic contraction; 2) the smaller response to dynamic contraction is due, in part, to greater skeletal muscle blood flow, which tends to “wash out” local metabolites that induce the exercise pressor reflex.


This study was approved by the Animal Use and Care Administrative Advisory Committee at the University of California, Davis.

Surgical Preparation

Adult cats of either sex (2.3–5.0 kg) were anesthetized with ketamine (25–30 mg/kg im) followed by α-chloralose (60–80 mg/kg iv). Additional doses of α-chloralose (10 mg/kg) were administered as needed throughout the experiment. The trachea was intubated, and respiration was maintained by a mechanical ventilator. A catheter was placed in the left femoral vein for administration of drugs or fluids and in the left femoral artery for sampling arterial blood gases and for measurement of systemic arterial blood pressure. Arterial blood pressure was measured with a pressure transducer (Statham P23ID) attached to the arterial catheter. HR was assessed with a cardiotachometer (Gould 13–4515–65) that was triggered by the arterial blood pressure signal.

Arterial blood gases and pH were maintained within the following ranges: Pco 2 25–35 Torr, Po 2 >90 Torr, pH 7.35–7.45. If necessary, 100% oxygen was supplemented to maintain arterial Po 2 >90 Torr, whereas arterial pH was maintained by administering intravenous sodium bicarbonate (8.4%) as needed. In six cats, the saphenous vein was cannulated, and a catheter was directed in a retrograde fashion into the popliteal vein so that its tip was positioned just proximal to the triceps surae muscle group. This allowed blood samples (0.4 ml/sample) to be withdrawn from the venous effluent of the triceps surae muscle group. A total of four blood samples (1.6 ml/cat) was obtained in each protocol. Samples were taken immediately before and after contraction or muscle stretch. In some animals, the popliteal artery was dissected free of the surrounding tissue, and a Doppler flow transducer was placed around the artery for assessment of blood velocity to the triceps surae. Blood velocity was measured by a Doppler flow velocity meter (Triton Instruments, model 100) and was expressed in centimeters per second.

Each animal was placed in a spinal unit (David Kopf), and the right sciatic nerve was dissected free of surrounding tissue and placed on a shielded electrode. The nerve was kept moist with mineral oil, and an electrode was attached to either a stimulus-isolation unit (Grass PSIU6) and a square-wave stimulator (Grass S88) for static contraction or a Kao, sinusoidal wave stimulator for dynamic contractions.

Tension produced by the contraction of the triceps surae was recorded as an index of overall hindlimb contraction. The right hindlimb was clamped in a fixed position, and the Achilles tendon was detached at the calcaneus bone and attached to an isometric force transducer (Grass FT-10). Mean tension was displayed simultaneously through a low-pass filter (0.35 Hz). Tension was expressed as average developed tension or TTI, which was determined by integrating the area under the mean tension curves during the 30-s contraction period.


Static versus dynamic contraction (TTI matched with time constant and variable peak tension).

In seven cats, the triceps surae was contracted statically for 30 s by electrically stimulating the sciatic nerve at a frequency of 40 Hz (pulse duration = 0.025 ms). The triceps surae was also contracted dynamically for 30 s by electrically stimulating the sciatic nerve with the modified Kao stimulator (60-Hz carrier frequency, modulated sinusoidally at 1 Hz). Static and dynamic contractions were evoked with voltages that varied between 1.5 and 2.5 times the motor threshold. To ensure that group III and IV muscle afferents were not stimulated, the cats were paralyzed with vecuronium (3–5 mg/kg iv) at the end of the experiment, and the stimulus was repeated to demonstrate a lack of change in blood pressure or HR. The order of contractions was randomized.

Static versus dynamic stretch (TTI matched with time constant and variable peak tension).

To determine the role of mechanoreceptors in the reflex cardiovascular responses to both static and dynamic contraction, we stretched the hindlimb dynamically (1 Hz) and statically for 30 s to equivalent TTI (n = 5 cats). Average developed tension was equivalent to that produced by electrically induced contractions using the same stimulation parameters as described previously.

Static versus dynamic contraction/stretch (TTI matched with variable time and constant peak tension).

We conducted both static (30 s) and dynamic (60 s) contractions (n = 6 cats) in addition to static (30 s) and dynamic stretch (60 s; n = 5 cats) during which peak tension and TTI were matched. On the basis of data from a previous study (18), the triceps surae muscle was stretched to ∼90–110% of its maximal in vivo muscle length (i.e., the length attained at full dorsiflexion). This set of experiments was carried out to determine whether our observed differences in reflex responses were the result of differences in peak tension.

Statistical analysis.

Two sets of comparisons were made: one between the baseline values, and the other between the peak changes in response to dynamic and static contraction or static and dynamic stretch using the Student's pairedt-test. All values are expressed as means ± SE. Statistical significance was accepted at P≤0.05.


Static Versus Dynamic Contraction

TTI matched with time constant and variable peak tension.

To match TTI between these two contractions over the same time interval (30 s), in seven cats, dynamic contractions were evoked to generate greater peak tension (5 ± 1 vs. 2 ± 1 kg; Fig.1). Dynamic contraction evoked a greater increase in mean arterial pressure (MAP) compared with static contraction (Fig. 2). Dynamic contraction also induced significantly greater changes in venous effluent Pco 2 and pH (Table1), even though popliteal blood velocity was significantly greater for dynamic than for static contraction. No significant differences were observed in venous lactate concentration ([lactate]) or Po 2.

Fig. 1.

Original record of the cardiovascular response to static and dynamic contraction at matched tension-time index with peak tension held constant (A) and with time held constant (B). Variables shown are mean arterial pressure (MAP), heart rate, absolute tension, and mean tension. bpm, Beats/min.

Fig. 2.

Peak changes (Δ; means ± SE) in MAP, heart rate, and mean blood velocity during static and dynamic contraction (n = 7) at equivalent tension-time indexes, constant time (30 s), and variable peak tension. Numbers below histograms represent baseline values. *P < 0.05, static vs. dynamic.

View this table:
Table 1.

Metabolic responses to dynamic and static contraction at equivalent tension-time index

TTI matched with variable time and constant peak tension.

In this protocol (n = 6), peak developed tension was matched during static (2.0 ± 0.5 kg) and dynamic (2.0 ± 0.5 kg) contraction, but the time of contraction was varied (30 s static vs. 60 s dynamic) to equate TTI (Fig. 1). Dynamic contraction evoked increases in MAP that were similar to those caused by static contraction (Fig. 3), despite greater increases in popliteal blood velocity during dynamic contraction. In addition, there were no differences in HR, Po 2, Pco 2, pH, or [lactate] (Table 1).

Fig. 3.

Peak changes (means ± SE) in MAP, heart rate, and mean blood velocity during static and dynamic contraction (n = 6) at equivalent tension-time indexes, constant peak tension, and variable time (30 s static vs. 60 s dynamic). Numbers below histograms represent baseline values. *P< 0.05, static vs. dynamic.

Static Versus Dynamic Stretch

TTI matched with time constant and variable peak tension.

During 30 s of passive stretch (n = 5), greater reflex increases in MAP and HR were observed during dynamic compared with during static stretch (Fig. 4). No significant change in popliteal artery blood velocity was observed (Fig. 4).

Fig. 4.

Peak changes (means ± SE) in MAP, heart rate, and mean blood velocity during static and dynamic stretch (n = 5) at equivalent tension-time indexes, constant time (30 s), and variable peak tension. Numbers below histograms represent baseline values. *P < 0.05, static vs. dynamic.

TTI matched with variable time and constant peak tension.

There were no significant differences in the reflex cardiovascular response to static and dynamic stretch during these conditions (Fig.5).

Fig. 5.

Peak changes (means ± SE) in MAP, heart rate, and mean blood velocity during static and dynamic stretch (n = 5) at equivalent tension-time indexes, constant peak tension, and variable time (30 s static vs. 60 s dynamic). Numbers below histograms represent baseline values.


The results of our study did not confirm our hypothesis. We had proposed that static contraction would elicit a greater reflex-pressor response than dynamic contraction at comparable workloads. Instead, we found that the pressor response to dynamic contraction was not reduced compared with static contraction under these conditions. Moreover, by holding contraction time constant and by increasing peak tension during dynamic contraction to equate TTI, the pressor response to dynamic contraction was greater than that caused by static contraction. This difference in the cardiovascular response occurred despite the fact that active muscle blood velocity was significantly higher during dynamic contraction. We expected that the greater blood flow during dynamic contraction would result in less activation of the exercise-pressor reflex both because of a greater supply of oxygen and because of greater “metabolite washout” in the active muscle. However, venous Pco 2 and H+ levels during dynamic contraction were actually higher than during static contraction.

Short duration, intermittent contractions have previously been shown to cause greater increases in energy metabolism and muscle metabolite production than static contraction (4, 7, 17, 18). These differences appear to be related to greater ATP requirements for the initial activation of the muscle during intermittent contraction (7). Thus the greater cost of muscle activation and higher peak tensions during dynamic contraction probably augmented the production of muscle metabolites. However, the higher muscle blood flow associated with the greater peak tension likely limited accumulation of these local metabolites. Overall, greater stimulation of metaboreceptors most likely contributed to the larger reflex-pressor response to dynamic contraction.

When TTI was matched by maintaining similar peak tensions and increasing contraction time during dynamic contraction, we observed similar increases in blood pressure and venous metabolite concentrations during both types of contraction. However, blood velocity was still considerably greater during dynamic contraction. These findings support the premise that when peak tension is equal, there are both a greater production and removal of metabolites during dynamic contraction that result in no net accumulation compared with static contraction. Greater metabolite production during dynamic contraction presumably was due to the greater metabolic cost of repetitive muscle activation. However, increased accumulation of these substances appears to have been offset by higher blood flows.

These findings also provide support for the contention that dynamic contraction causes a greater pressor response than static contraction (when TTI is equated by holding time constant), because there is greater activation of metaboreceptors. Nevertheless, differential activation of mechanoreceptors could also be involved. We examined this possibility by comparing dynamic and static stretch using the same protocols in which dynamic and static contractions were compared. Because passive stretch of skeletal muscle reflexly increases blood pressure, myocardial contractility, and HR, without changing muscle metabolite concentrations (18), this technique allowed us to isolate the effects of mechanoreceptor activation from those caused by metaboreceptor activation. In all likelihood, this technique primarily stimulated group III muscle afferent nerve endings, because these afferents are believed to be primarily mechanically sensitive, whereas group IV muscle afferents are considered to be predominately chemically sensitive (10).

Comparison of the pressor responses induced by static and dynamic stretch at the same TTI, when peak tension was matched, revealed no differences between the two modes of stretch. However, at comparable TTI, when a greater peak tension was produced so that time could be held constant during dynamic and static stretch, a greater pressor response occurred during dynamic stretch. These patterns of response were consistent with those observed during static and dynamic contraction under similar conditions. Although discharge activity of mechanoreceptors can be altered by the frequency of muscle contraction in that continuous activation may lead to adaptation or decreased firing (9), our data suggest that the smaller pressor response to static contraction when time was held constant was not due to adaptation, because there was no difference between the cardiovascular response to static and dynamic contraction when peak tension was held constant. However, when peak tension was varied, greater mechanoreceptor stimulation may have occurred due to higher peak tension development during dynamic contraction such that a greater reflex sympathetic nerve activation and a greater pressor response occurred.

This potential contribution of mechanoreceptors is in agreement with Victor et al. (20), who showed that intermittent tetanic contraction evokes synchronized renal nerve discharge, supporting a role for mechanoreceptor afferents in the reflex cardiovascular response to dynamic contraction. Therefore, we believe that our findings indicate that greater activation of both metabo- and mechanoreceptors contribute to the larger reflex-pressor response during dynamic contraction at comparable workloads when peak tension is allowed to vary.

Previous studies in humans have reported comparable pressor responses to static and dynamic contraction (2, 3). In these studies, oxygen uptake was used to assess work intensity; therefore, workloads were equated by matching oxygen uptake. The problem with this approach is that whole body metabolism, as indicated by oxygen uptake, may not accurately reflect the level of activation of the sympathetic nervous system (16). For example, a level of static exercise (isometric leg extension) that requires less oxygen consumption than dynamic exercise (cycle ergometery) can induce greater increases in muscle sympathetic nerve activity compared with dynamic contraction (16). Most likely, whole body metabolism (oxygen uptake) does not correlate closely with sympathetic nerve activity during exercise, because these changes in autonomic activity are more dependent on local metabolic changes in exercising muscle rather than whole body metabolism. Therefore, comparison of the cardiovascular responses during these two forms of exercise at the same level of oxygen consumption could lead to inaccurate conclusions, especially if there are large differences in the amount of active muscle mass involved.

To evoke dynamic contraction in this study, we used a modified Kao stimulator (see methods) to evoke dynamic contractions, because it allowed us to more closely simulate rhythmic contractions as they occur naturally (8). The Kao stimulator produces a sinusoidal stimulus that increases slowly from low to peak intensity and then gradually decreases in a similar fashion (8). This pattern of activation is similar to that present during voluntary contraction and causes a pattern of mechanoreceptor activation that is different from that induced with a standard square-wave stimulator, because the stimulus intensity increases and decreases gradually. Thus sequential activation of muscle mechanoreceptors by the Kao stimulator may influence the magnitude of the corresponding pressor response compared with contraction evoked by unmodified stimulation in which peak intensity is reached instantaneously. Additional studies employing afferent unit recording will be required to confirm this potential differential activation of muscle mechanosensitive receptors during dynamic muscular contraction.

It also should be noted that cardiovascular response to electrically induced muscle contraction does reach a true steady state, because muscle tension usually begins to decline within ∼15–20 s. This outcome is particularly true for static contraction (see Fig. 1). We have found that even when the decline in tension is small, the pressor response to contraction usually peaks within 20–45 s and does not achieve a plateau for >5–10 s. That is why a contraction period of only 30 s was selected.


Our findings have clinical implications. Individuals with cardiovascular disease are directed away from exercise involving static contractions or resistance-type training. This sentiment appears to be related to reports of large pressor responses to heavy-resistance activity (11). Our results indicate that the magnitude of the pressor response to contraction of a given muscle mass is not dependent on the mode of contraction (static vs. dynamic) as long as peak-tension production is similar. Thus, with peak tensions matched at low to moderate work intensities in similar muscle groups, static and dynamic contraction should result in a similar afterload on the heart.

In conclusion, the greater pressor response to dynamic contraction, compared with static contraction at the same TTI when time was held constant, was likely the result of enhanced muscle metabo- and mechanoreceptor activation. Enhanced stimulation of mechanically sensitive muscle afferents was induced by higher peak-tension development during the rhythmic contraction. Augmented activation of metaboreceptors during dynamic contraction was probably due to a larger accumulation of metabolites caused by the greater initial energy cost of muscle activation associated with dynamic contractions. However, when both TTI and peak tension were equivalent, static and dynamic contractions produced similar cardiovascular responses.


Work described in this paper was supported in part by National Heart, Lung, and Blood Institute Grants HL-48373, HL-36527, and PPG P01 HL-52165 and by the Rosenfeld Heart Fund.


  • The results of this study were presented in part at the Annual Experimental Biology meetings, Washington, D.C., April 1999.

  • Address for reprint requests and other correspondence: C. L. Stebbins, Div. of Cardiovascular Medicine, TB 172, Univ. of California, Davis, Davis, CA 95616–8634 (E-mail:clstebbins{at}

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


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