Respiratory and cardiovascular responses to static handgrip exercise in humans

1993 ◽  
Vol 75 (6) ◽  
pp. 2789-2796 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
R. Manconi ◽  
...  

We studied the time course of respiratory and cardiovascular responses by evaluating changes in the breathing pattern, mean blood pressure (MBP), and heart rate elicited by 3 min of static handgrip at 15, 25, and 30% of the maximum voluntary contraction (MVC) in 15 healthy volunteers. Muscle tension and integrated electromyographic activity remained fairly constant during each trial. During 15% MVC bouts, initially only mean inspiratory flow increased; then, tidal volume and minute ventilation (VI) also rose progressively. No significant changes in MBP and heart rate were observed. During 25 and 30% MVC bouts, not only did mean inspiratory flow, VT, and VI increase but MBP and heart rate increased as well. A slight and delayed rise in respiratory rate was also observed. Unlike 15 and 25% MVC handgrip, 30% MVC handgrip caused a small decrease in end-tidal PCO2. Changes in the pattern of breathing occurred more promptly than those in cardiovascular variables in the majority of subjects. Furthermore, we found a positive correlation between changes in VI and those in cardiovascular variables at the end of 25 and 30% MVC trials. This study indicates that respiratory and cardiovascular responses to static handgrip exercise are controlled independently.

1995 ◽  
Vol 78 (2) ◽  
pp. 449-457 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
F. Lavorini ◽  
...  

We investigated the effects of prostaglandin synthesis blockade on the changes in breathing pattern, mean blood pressure (MBP), and heart rate (HR) elicited by 3 min of static handgrip at 30% of the maximum voluntary contraction in 12 healthy volunteers. Before each handgrip trial, subjects were treated with intravenous administration of either saline placebo (control) or 1 mg/kg of ketoprofen. Muscle tension and integrated electromyographic activity of exercising muscles remained fairly constant during each trial. In agreement with our earlier findings, during control handgrip minute ventilation progressively increased (P < 0.01) due to a rise in tidal volume and, to a lesser extent, in respiratory frequency. Mean inspiratory flow, MBP, and HR also increased (P < 0.01). End-tidal PCO2 decreased (P < 0.05) during the late phases of control handgrip bouts. Ketoprofen administration reduced serum thromboxane B2 levels (from 57.5 +/- 7.0 to 1.6 +/- 0.4 pg/ml; P < 0.01) and significantly attenuated mean increases in minute ventilation (40.25 +/- 0.60%), tidal volume (37.78 +/- 7.48%), respiratory frequency (55.94 +/- 17.92%), inspiratory flow (42.66 +/- 5.11%), MBP (22.33 +/- 6.82%), and HR (11.04 +/- 2.75%) during the 3rd min of handgrip. End-tidal PCO2 remained close to normocapnic levels. In agreement with previous animal investigations, the present results show that arachidonic acid metabolites are involved in the regulation of the cardiovascular responses to static efforts in humans, possibly through a stimulatory action on muscle receptors. Furthermore, they provide the first experimental evidence that products of the cyclooxygenase metabolic pathway play a role in the mediation of the respiratory adjustments elicited by this form of exercise.


1995 ◽  
Vol 78 (5) ◽  
pp. 1688-1698 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35–75 mmHg consistently reduced ventilation 15–40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40–80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.


1974 ◽  
Vol 46 (3) ◽  
pp. 295-306 ◽  
Author(s):  
D. J. Ewing ◽  
J. B. Irving ◽  
F. Kerr ◽  
J. A. W. Wildsmith ◽  
B. F. Clarke

1. The blood pressure and heart rate responses to static muscular exercise were measured in sixty normal subjects and 124 patients with diabetes mellitus, aged 25–54 years, during a standardized sustained handgrip test at 30% maximum voluntary contraction (MVC). 2. The normal range of the response was established. Females had a smaller blood pressure rise than males, and their MVC was lower. In the normal subjects there was a significant correlation between the size of the MVC and the height of the blood pressure response. The absolute muscle tension exerted should be taken into account in addition to the percentage MVC, when comparing responses to sustained exercise in different disease states. 3. The diabetic subjects showed a similar sex difference in their response. The mean diastolic blood pressure rises were smaller than in the control groups, both in males and females, but this was related to a smaller mean MVC. 4. Twenty-two of the diabetic subjects had an abnormally low response to sustained handgrip, which was not related to age, duration of diabetes, treatment or control of the disease. These diabetic subjects probably had damage of the autonomic fibres mediating the response. The findings would suggest that sustained handgrip is a useful and simple method of detecting involvement of the autonomic nervous system in diabetes.


1998 ◽  
Vol 274 (5) ◽  
pp. H1472-H1480 ◽  
Author(s):  
A. Chlorakos ◽  
B. L. Langille ◽  
S. L. Adamson

The cardiovascular effects of repeated administration of the nitric oxide (NO) synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) were assessed daily for 3 days in fetal sheep near term (124–126 days gestation) beginning 4 days after surgery ( n = 7). In the first hour on day 1, fetal infusion ofl-NAME (30 mg bolus, 6 mg/min infusion iv for 3 h) significantly increased fetal arterial pressure from 41 ± 2 to 58 ± 3 mmHg, decreased heart rate from 173 ± 5 to 134 ± 3 beats/min, increased umbilicoplacental resistance from 0.16 ± 0.02 to 0.28 ± 0.07 mmHg ⋅ ml−1 ⋅ min, and inhibited the hypotensive response to acetylcholine (ACh; 2 μg iv bolus). All changes were sustained except for arterial pressure, which decreased significantly to 50 ± 3 mmHg in the third hour. Within 17 h, all cardiovascular variables returned to control.l-NAME readministered on days 2 and 3 had no effect on cardiovascular variables. l-NAME did not potentiate the pressor response to angiotensin II on day 2 and caused a surprising attenuation of the pressor response to endothelin-1 on day 3. We conclude that, whereas NO normally contributes to low arterial pressure, high heart rate, and low umbilicoplacental vascular resistance in fetal sheep near term, the role of NO in these functions is replaced by an alternate mechanism within 17 h after NO synthesis inhibition withl-NAME.


1983 ◽  
Vol 54 (6) ◽  
pp. 1457-1462 ◽  
Author(s):  
S. R. Muza ◽  
L. Y. Lee ◽  
R. L. Wiley ◽  
S. McDonald ◽  
F. W. Zechman

Previous research indicates that fatiguing static exercise causes hyperventilation and a decrease of end-tidal CO2 partial pressure PETCO2. The objectives of this study were 1) to examine the changes in pattern of breathing during static exercise, and 2) to define the isocapnic ventilatory response. Six healthy males were studied once a week at one of three levels of static handgrip exercise: 15, 25, or 30% maximum voluntary contraction (MVC) was sustained for 5 min while holding PETCO2 constant or allowing it to run free. During 25 and 30% MVC, we observed 1) progressive increases in mean tidal volume (VT), inspiratory ventilation (VI), VT/TI, heart rate (HR), and arterial BP, 2) increased breath-to-breath variability of VT, 3) no significant changes in respiratory frequency (f), and 4) progressive decreases in PETCO2. Keeping PETCO2 constant at preexercise levels did not change the pattern or magnitude of the ventilatory response to exercise. The time course and magnitude of the subjects' perceived effort resembled the time course and magnitude of the ventilatory response. The variability of VT during the response to static exercise suggests an element of control instability. The identical ventilatory responses during hypocapnic and isocapnic conditions may result from the slow response of the central chemoreceptors; an overriding influence of muscle afferents; and/or increased central command arising with fatigue.


2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Hamid Arazi ◽  
Abbas Asadi ◽  
Morteza Purabed

The purpose of this study was to assess the effects of listening to music during warm-up and resistance exercise on physiological (heart rate and blood pressure) and psychophysical (rating of perceived exertion) responses in trained athletes. Twelve strength trained male participants performed warm-up and resistance exercise without music (WU+RE without M), warm-up and resistance exercise with music (WU+RE with M), WU with M and RE without M, and WU without M and RE with M, with 48 hours space between sessions. After completing each session, the rating of perceived exertion (RPE) was measured. Also, heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP), mean arterial pressure (MAP), and rate pressure product (RPP) were assessed before, after, and 15, 30, 45, and 60 min after exercise. Results indicated that RPE was higher for WU+RE without M condition in comparison with other conditions. All conditions showed increases in cardiovascular variables after exercise. The responses of HR, SBP, and RPP were higher for WU+RE without M condition. Thus, using music during warm-up and resistance exercise is a legal method for decreasing RPE and cardiovascular responses due to resistance exercise.


1977 ◽  
Vol 71 (1) ◽  
pp. 7-26 ◽  
Author(s):  
P. J. BUTLER ◽  
N. H. WEST ◽  
D. R. JONES

1. Five pigeons were trained to fly in a boundary-layer wind-tunnel at a velocity of 10 m s−1 for at least 10 min, and a number of respiratory and cardiovascular variables were recorded. For comparison, heart rate, respiratory frequency and E.M.G. from the pectoralis major muscles were also recorded, using radio-telemetry, from free-flying pigeons. 2. For the flights in the wind tunnel there were immediate increases in respiratory frequency and heart rate upon take-off; these variables continued to increase during the flight, eventually becoming on average 411 breaths min−1 (20 × resting) and 670 beats min−1 (6 × resting) respectively. There was a 1:1 relationship between ventilation and wing beat. Oxygen uptake and carbon dioxide production reached their highest values of 12.5 × and 14.4 × resting respectively within 1 min of take-off and then declined to steady levels of 200 ml kg−1 min S.T.P.D. (10 × resting) and 184 ml kg−1 min S.T.P.D. (10.7 × resting) 4 min after take-off. If allowances are made for the weightand drag of the VOO2 mask and tubes, these stable values are at least 12% higher than would occur in an unloaded bird. Body temperature rose steadily after take-off, reaching a stable value of 43.3°C, which was 2°C above resting, after 6 min of flight. There was a 1.8 × rise in a -vOO2 content difference and little change in cardiac stroke volume during flight, so that the rise in heart rate was the major factor in transporting the extra O2 to the active muscles. Respiratory quotient rose from 0.85 at rest to 0.99, 30 s after take off, and then fell to 0.92 after 7 min of flight. Blood lactate rose to 59.8 mg% (6.5 × its resting value). 3. Comparisons with the free-flying birds indicated that the pattern of flight in the wind tunnel was somewhat abnormal, especially at the beginning of a flight, and this may account for the value of VOO2 being higher at the start of a flight and then declining to a steady value as the flight progressed. 4. Upon landing, heart rate, V·O1V·CO2 and body temperature began to fall immediately, and within 2 min, heart rate, V·O2 and V·CO2 had returned to the ‘tunnel on’ resting values. Respiratory frequency increased upon landing and its decline closely matched the fall in body temperature. R.Q. rose above unity immediately upon landing as CO2 was removed in excess of its metabolic production, and then fell below the resting value as CO2 was retained, presumably to maintain acid/base balance during the metabolism of lactic acid.


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.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Damir Zubac ◽  
Nandu Goswami ◽  
Vladimir Ivančev ◽  
Zoran Valić ◽  
Boštjan Šimunič

AbstractThe present study examined whether differences in the heart rate recovery following flywheel exercise cessation were associated with differences in maximal oxygen uptake ($${\dot{\text{V}}}$$ V ˙ O2 max.), age and sex in trained adults. Eleven men (age range 22–49 years, $${\dot{\text{V}}}$$ V ˙ O2 max. = 43.6 ± 7.6 mL kg min−1) and ten women (age range 20—53 years, $${\dot{\text{V}}}$$ V ˙ O2 max. = 38.0 ± 5.7 mL kg min−1) were randomly assigned to complete a squat-exercise on the flywheel ergometer set at three different moments of inertia, while their cardiovascular responses were continuously monitored. During the flywheel exercise the mean arterial pressure rose by ~ 35 to 40% (p = .001), and the increment was more robust in men than women. The cardiac index was two-fold greater across both sexes compared to the baseline (p = .001), while the rise in heart rate (~ 144 bpm) was more pronounced in women to compensate for their load-dependent stroke index decline (p = .001). The load-independent time-course changes in heart rate recovery markers were comparable between the sexes. When these indicators were pooled, a stepwise regression revealed age as the only relevant predictor of both fast and slow components of the heart rate recovery (~ 30% of the shared variance explained, p = .014). The present data suggest that the heart rate recovery declines with age, irrespective of sex, or well-preserved cardiorespiratory fitness in moderately-trained adults.


2000 ◽  
pp. 523-533 ◽  
Author(s):  
K Yamaguchi ◽  
K Watanabe ◽  
K Yamaya

OBJECTIVE: To examine local actions of nitric oxide (NO) on the neural mechanisms controlling the release of vasopressin (AVP) and the cardiovascular system in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic functions, and to pursue the problem of whether it may have any role in the AVP and cardiovascular responses evoked by plasma hypertonicity or by increased prostaglandin E(2) (PGE(2)) in the AV3V - one possible factor implicated in osmotic responses. METHODS: We infused NO-related agents into the AV3V, its adjacent area, the nucleus of the vertical limb of the diagonal band (VDB), or into the lateral cerebral ventricle of conscious rats, monitoring effects on plasma AVP, osmolality, sodium, potassium and chloride, arterial pressure and heart rate in the presence or absence of an osmotic or PGE(2) stimulus. The infusion sites were determined histologically. RESULTS: Infusion of L-arginine, the substrate of NO synthase (NOS), into the AV3V structures such as the median preoptic nucleus and periventricular nucleus produced dose-related increases in plasma AVP, arterial pressure and heart rate 5 or 15 min later, whereas infusion of D-arginine (which is not a substrate for NO synthesis) was without significant effect on these variables. Plasma osmolality or electrolytes were not changed by these treatments. The AV3V infusion of sodium nitroprusside (SNP), a spontaneous releaser of NO, also induced dose-dependent augmentations of plasma AVP, without evoking remarkable alteration in the cardiovascular parameters. The infusion of L- or D-arginine into the VDB affected none of the variables significantly. When applied intracerebroventricularly, L-arginine caused only increases in plasma AVP, whereas SNP caused only reductions in arterial pressure, leaving other variables at stable values. The effects of AV3V L-arginine on plasma AVP and the cardiovascular variables were abolished by N(G)-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NOS, applied 15 min before. In contrast, infusion of L-NAME to the AV3V did not exert a significant effect on the responses of plasma AVP or cardiovascular variables to AV3V application of PGE(2) or i.v. infusion of hypertonic NaCl. The infusion of L-NAME alone did not affect plasma variables including AVP, although it tended to increase basal arterial pressure and heart rate. CONCLUSION: These results suggest that NO generated in or near the AV3V may act to enhance AVP release, arterial pressure and heart rate, but it may not play an essential role in eliciting the responses of these variables to osmotic or PGE(2) stimuli.


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