Increased cardiovascular response to static contraction of larger muscle groups

1983 ◽  
Vol 54 (2) ◽  
pp. 434-437 ◽  
Author(s):  
D. R. Seals ◽  
R. A. Washburn ◽  
P. G. Hanson ◽  
P. L. Painter ◽  
F. J. Nagle

The purpose of this study was to investigate the influence of the size of the active muscle mass on the cardiovascular response to static contraction. Twelve male subjects performed one-arm handgrip (HG), two-leg extension (LE), and a “dead-lift” maneuver (DL) in a randomly assigned order for 3 min at 30% of maximal voluntary contraction. O2 uptake (VO2), heart rate (HR), and mean intra-arterial blood pressure (MABP) were measured at rest and, in addition to absolute tension exerted, throughout contraction. There was a direct relationship between the size of the active muscle mass and the magnitude of the increases in VO2, HR, and MABP, even though all contractions were performed at the same relative intensity. Tension, VO2, HR, and MABP increased progressively from HG to LE to DL. It was concluded that at the same percentage of maximal voluntary contraction, the magnitude of the cardiovascular response to isometric exercise is directly influenced by the size of the contracting muscle mass.

2007 ◽  
Vol 103 (4) ◽  
pp. 1402-1411 ◽  
Author(s):  
Savio W. Wong ◽  
Derek S. Kimmerly ◽  
Nicholas Massé ◽  
Ravi S. Menon ◽  
David F. Cechetto ◽  
...  

In general, cardiac regulation is dominated by the sympathetic and parasympathetic nervous systems in men and women, respectively. Our recent study had revealed sex differences in the forebrain network associated with sympathoexcitatory response to baroreceptor unloading. The present study further examined the sex differences in forebrain modulation of cardiovagal response at the onset of isometric exercise. Forebrain activity in healthy men ( n = 8) and women ( n = 9) was measured using functional magnetic resonance imaging during 5 and 35% maximal voluntary contraction handgrip exercise. Heart rate (HR), mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA) were collected in a separate recording session. During the exercise, HR and MAP increased progressively, while MSNA was suppressed ( P < 0.05). Relative to men, women demonstrated smaller HR (8 ± 2 vs. 18 ± 3 beats/min) and MAP (3 ± 2 vs. 11 ± 2 mmHg) responses to the 35% maximal voluntary contraction trials ( P < 0.05). Although a similar forebrain network was activated in both groups, the smaller cardiovascular response in women was reflected in a weaker insular cortex activation. Nevertheless, men did not show a stronger deactivation at the ventral medial prefrontal cortex, which has been associated with modulating cardiovagal activity. In contrast, the smaller cardiovascular response in women related to their stronger suppression of the dorsal anterior cingulate cortex activity, which has been associated with sympathetic control of the heart. Our findings revealed sex differences in both the physiological and forebrain responses to isometric exercise.


2002 ◽  
Vol 92 (4) ◽  
pp. 1585-1593 ◽  
Author(s):  
J. R. Fowles ◽  
H. J. Green ◽  
R. Tupling ◽  
S. O'Brien ◽  
B. D. Roy

The purpose of this study was to investigate the hypothesis that reductions in Na+-K+- ATPase activity are associated with neuromuscular fatigue following isometric exercise. In control (Con) and exercised (Ex) legs, force and electromyogram were measured in 14 volunteers [age, 23.4 ± 0.7 (SE) yr] before and immediately after (PST0), 1 h after (PST1), and 4 h after (PST4) isometric, single-leg extension exercise at ∼60% of maximal voluntary contraction for 30 min using a 0.5 duty cycle (5-s contraction, 5-s rest). Tissue was obtained from vastus lateralis muscle before exercise in Con and after exercise in both the Con (PST0) and Ex legs (PST0, PST1, PST4), for the measurements of Na+-K+-ATPase activity, as determined by the 3- O-methylfluorescein phosphatase (3- O-MFPase) assay. Voluntary (maximal voluntary contraction) and elicited (10, 20, 50, 100 Hz) force was reduced 30–55% ( P < 0.05) at PST0 and did not recover by PST4. Muscle action potential (M-wave) amplitude and area (measured in the vastus medialis) and 3- O-MFPase activity at PST0-Ex were less than that at PST0-Con ( P < 0.05) by 37, 25, and 38%, respectively. M-wave area at PST1-Ex was also less than that at PST1-Con ( P < 0.05). Changes in 3- O-MFPase activity correlated to changes in M-wave area across all time points ( r = 0.38, P < 0.05, n= 45). These results demonstrate that Na+-K+- ATPase activity is reduced by sustained isometric exercise in humans from that in a matched Con leg and that this reduction in Na+-K+-ATPase activity is associated with loss of excitability as indicated by M-wave alterations.


2002 ◽  
Vol 14 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Kenneth R. Turley ◽  
D. Eric Martin ◽  
Eric D. Marvin ◽  
Kelley S. Cowley

To determine the reliability of cardiovascular responses to isometric exercise of different intensities, and to compare adult versus child responses, 27 boys (7–9 years old) and 27 men (18–26 years old) performed static handgrip exercise at 10, 20, and 30% of previously determined maximal voluntary contraction (MVC) for three min each on different days, while heart rate (HR) and blood pressure (BP) were measured. HR reliability was moderately high at all intensities in both boys and men ranging from R = 0.52–0.87. BP reliability was moderate in men and boys at 30% MVC while at 10% and 20% MVC reliability was very low for boys and only moderate for men. HR response from pre- to 3-min of static exercise was not different between boys versus men at any intensity. At 30% MVC diastolic (20.2 vs. 29.3 mmHg), systolic (17.4 vs. 36.2 mmHg) and mean (19.2 vs. 31.6 mmHg) BP responses were lower in boys versus men, respectively. At 20% MVC SBP (6.8 vs. 14.3 mmHg) and MBP (8.4 vs. 12.6 mmHg) responses were lower in boys versus men, respectively. In conclusion, the reliability of cardiovascular response to isometric exercise is low at low contraction intensities and moderate at higher contraction intensities. Further, BP response in men at 30% MVC is higher than boys, while responses are similar at lower contraction intensities.


2006 ◽  
Vol 100 (3) ◽  
pp. 1043-1048 ◽  
Author(s):  
Thad E. Wilson ◽  
Damian J. Dyckman ◽  
Chester A. Ray

Exercise-induced increases in skin sympathetic nerve activity (SSNA) are similar between isometric handgrip (IHG) and leg extension (IKE) performed at 30% of maximal voluntary contraction (MVC). However, the precise effect of exercise intensity and level of fatigue on this relationship is unclear. This study tested the following hypotheses: 1) exercise intensity and fatigue level would not affect the magnitude of exercise-induced increase in SSNA between IHG and IKE, and 2) altering IHG muscle mass would also not affect the magnitude of exercise-induced increase in SSNA. In protocol 1, SSNA (peroneal microneurography) was measured during baseline and during the initial and last 30 s of isometric exercise to volitional fatigue in 12 subjects who randomly performed IHG and IKE bouts at 15, 30, and 45% MVC. In protocol 2, SSNA was measured in eight subjects who performed one-arm IHG at 30% MVC with the addition of IHG of the contralateral arm in 10-s intervals for 1 min. Exercise intensity significantly increased SSNA responses during the first 30 s of IHG (34 ± 13, 70 ± 11, and 92 ± 13% change from baseline) and IKE (30 ± 17, 69 ± 12, and 76 ± 13% change from baseline) for 15, 30, and 45% MVC. During the last 30 s of exercise to volitional fatigue, there were no significant differences in SSNA between exercise intensities or limb. SSNA did not significantly change between one-arm and two-arm IHG. Combined, these data indicate that exercise-induced increases in SSNA are intensity dependent in the initial portion of isometric exercise, but these differences are eliminated with the development of fatigue. Moreover, the magnitude of exercise-induced increase in SSNA responses is not dependent on either muscle mass involved or exercising limb.


2018 ◽  
Vol 43 (2) ◽  
pp. 174-179 ◽  
Author(s):  
Leonardo Henrique Perinotto Abdalla ◽  
Benedito Sérgio Denadai ◽  
Natália Menezes Bassan ◽  
Camila Coelho Greco

The objective of this study was to test the hypotheses that end-test torque (ET) (expressed as % maximal voluntary contraction; MVC) is higher for plantar flexors (PF) than knee extensors (KE) muscles, whereas impulse above ET (IET) is higher for KE than PF. Thus, we expected that exercise tolerance would be longer for KE than PF only during the exercise performed above ET. After the determination of MVC, 40 men performed two 5-min all-out tests to determine ET and IET. Eleven participants performed a further 4 intermittent isometric tests, to exhaustion, at ET + 5% and ET – 5%, and 1 test for KE at the exercise intensity (%MVC) corresponding to ET + 5% of PF. The IET (7243.2 ± 1942.9 vs. 3357.4 ± 1132.3 N·m·s) and ET (84.4 ± 24.8 vs. 73.9 ± 19.5 N·m) were significantly lower in PF compared with KE. The exercise tolerance was significantly longer for PF (300.7 ± 156.7 s) than KE (156.7 ± 104.3 s) at similar %MVC (∼60%), and significantly shorter for PF (300.7 ± 156.7 s) than KE (697.0 ± 243.7 s) at ET + 5% condition. However, no significant difference was observed for ET – 5% condition (KE = 1030.2 ± 495.4 s vs. PF = 1028.3 ± 514.4 s). Thus, the limit of tolerance during submaximal isometric contractions is influenced by absolute MVC only during exercise performed above ET, which seems to be explained by differences on both ET (expressed as %MVC) and IET values.


1998 ◽  
Vol 274 (6) ◽  
pp. H2116-H2122 ◽  
Author(s):  
Charles L. Stebbins ◽  
Stefani Bonigut ◽  
Lea R. Liviakis ◽  
Paul A. Munch

Circulating arginine vasopressin (AVP) can enhance baroreflex function via its action in the area postrema (AP). We tested the hypothesis that AVP acts in the AP to enhance baroreflex function during static contraction and, in turn, attenuates the exercise pressor reflex. Thus mean arterial blood pressure ( n = 9) and heart rate (HR) ( n = 9) during 30 s of electrically stimulated hindlimb contraction were compared before and after bilateral microinjections of 200 nl of the AVP V1-receptor antagonist d(CH2)5Tyr(Me)-AVP (V1x) (1 ng/nl) into the AP of the anesthetized cat. This protocol was repeated in three other cats in which sinoaortic denervation (SAD) was performed before any intervention. Injection of V1xinto the AP had no effect on baseline blood pressure or HR. However, pressor and HR responses to static contraction were augmented by 44 ± 10 and 29 ± 9%, respectively. Static contraction also increased plasma AVP from 15.9 ± 2.0 to 25.5 ± 3.4 pg/ml. In the SAD cats, microinjection of V1x had no effect on contraction-induced increases in blood pressure or HR. These results suggest that baroreflex opposition of the reflex cardiovascular response to static contraction is enhanced by the action of AVP in the AP.


1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.


2011 ◽  
Vol 111 (6) ◽  
pp. 1694-1702 ◽  
Author(s):  
Matthew D. Muller ◽  
Zhaohui Gao ◽  
Rachel C. Drew ◽  
Michael D. Herr ◽  
Urs A. Leuenberger ◽  
...  

The effects of cold air inhalation and isometric exercise on coronary blood flow are currently unknown, despite the fact that both cold air and acute exertion trigger angina in clinical populations. In this study, we used transthoracic Doppler echocardiography to measure coronary blood flow velocity (CBV; left anterior descending coronary artery) and myocardial function during cold air inhalation and handgrip exercise. Ten young healthy subjects underwent the following protocols: 5 min of inhaling cold air (cold air protocol), 5 min of inhaling thermoneutral air (sham protocol), 2 min of isometric handgrip at 30% of maximal voluntary contraction (grip protocol), and 5 min of isometric handgrip at 30% maximal voluntary contraction while breathing cold air (cold + grip protocol). Heart rate, blood pressure, inspired air temperature, CBV, myocardial function (tissue Doppler imaging), O2 saturation, and pulmonary function were measured. The rate-pressure product (RPP) was used as an index of myocardial O2 demand, whereas CBV was used as an index of myocardial O2 supply. Compared with the sham protocol, the cold air protocol caused a significantly higher RPP, but there was a significant reduction in CBV. The cold + grip protocol caused a significantly greater increase in RPP compared with the grip protocol ( P = 0.045), but the increase in CBV was significantly less ( P = 0.039). However, myocardial function was not impaired during the cold + grip protocol relative to the grip protocol alone. Collectively, these data indicate that there is a supply-demand mismatch in the coronary vascular bed when cold ambient air is breathed during acute exertion but myocardial function is preserved, suggesting an adequate redistribution of blood flow.


2004 ◽  
Vol 97 (3) ◽  
pp. 1143-1151 ◽  
Author(s):  
Natasha R. Saunders ◽  
Michael E. Tschakovsky

Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the present study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition, where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction), rhythmic, dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% maximal voluntary contraction) in each of arm above ( condition A) or below ( condition B) heart level. Beat-by-beat measures of brachial arterial blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions ( condition A: E-E, 52.8 ± 10.7 vs. R-E, 60.3 ± 11.7 ml·min−1·100 mmHg−1, P = 0.66; condition B: E-E, 43.2 ± 12.8 vs. R-E, 33.9 ± 8.2 ml·min−1·100 mmHg−1, P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first nine contraction-relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in R-E and E-E transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.


1989 ◽  
Vol 67 (5) ◽  
pp. 1801-1806 ◽  
Author(s):  
D. R. Seals

The primary purpose of this study was to determine whether the sympathetic neural activation induced by isometric exercise is influenced by the size of the contracting muscle mass. To address this, in nine healthy subjects (aged 19-27 yr) we measured heart rate, systolic arterial blood pressure, and muscle sympathetic nerve activity in the leg (MSNA; peroneal nerve) before (control) and during 2.5 min of isometric handgrip exercise (30% of maximal voluntary force). Exercise was performed with the right and left arms separately and with both arms simultaneously (random order). During exercise, heart rate, systolic pressure, and MSNA increased above control under all conditions (P less than 0.05). For each variable, the magnitudes of the increases from control to the end of exercise were significantly greater when exercise was performed with two arms compared with either arm alone (P less than 0.05). In general, the increases in heart rate, systolic pressure, and MSNA elicited during two-arm exercise were significantly less than the simple sums of the responses evoked during exercise of each arm separately. These findings indicate that the magnitude of the sympathetic neural activation evoked during isometric exercise in humans is determined in part by the size of the active muscle mass. In addition, our results suggest that the sympathetic cardiovascular adjustments elicited during exercise of separate limbs are not simply additive but instead exhibit an inhibitory interaction (i.e., neural occlusion).


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