Measurement of human capacity for aerobic muscular work

1960 ◽  
Vol 15 (6) ◽  
pp. 1001-1006 ◽  
Author(s):  
Charles E. Billings ◽  
Joseph F. Tomashefski ◽  
Earl T. Carter ◽  
William F. Ashe
Keyword(s):  
Heart Rate ◽  
Cardiovascular Response ◽  
Constant Speed ◽  
Strong Positive Correlation ◽  
Scoring Method ◽  
End Point ◽  
Precise Measure ◽  
Temporal Measurement ◽  
Response To Exercise ◽  
Work Done

In an effort to define a simple, precise measure of cardiovascular response to exercise, a test devised by Bruno Balke was studied. The test involves walking at constant speed on a treadmill, the slope of which is periodically increased, while heart rate is measured accurately each minute. Balke had noted that physiologic alterations indicative of impending exhaustion occurred at or near the time the heart rate reached 180/min.; he used the time at which the rate was attained as an end point. Our studies suggested that a single temporal measurement was insufficiently sensitive as an estimate of cardiovascular response to the procedure. Another scoring method was derived, involving the integration of heart rates with respect to time. A strong positive correlation was found between the described score and the work done during each of 133 test runs. Additionally, evidence was obtained which suggests that it may not be necessary to force subjects to an end point near exhaustion in order to estimate their ability to tolerate exercise of this type. Submitted on March 14, 1960

scholarly journals The Chronic Effects of Narghile Use on Males’ Cardiovascular Response During Exercise: A Systematic Review

2021 ◽  
Vol 15 (2) ◽  
pp. 155798832199770
Author(s):  
Faten Chaieb ◽  
Helmi Ben Saad
Keyword(s):  
Systematic Review ◽  
Heart Rate ◽  
Cardiovascular Response ◽  
Recovery Period ◽  
Cardiopulmonary Exercise Test ◽  
Negative Effects ◽  
Chronic Effects ◽  
Blood Pressures ◽  
Response To Exercise ◽  
Harmful Effects

Narghile use has regained popularity throughout the world. Public opinion misjudges its chronic harmful effects on health, especially on the cardiovascular system. This systematic review aimed to evaluate the chronic effects of narghile use on cardiovascular response during exercise. It followed the preferred reporting items for systematic reviews guidelines. Original articles from PubMed and Scopus published until January 31, 2020, written in English, and tackling the chronic effects of narghile use on human cardiovascular response during exercise were considered. Five studies met the inclusion criteria. Only males were included in these studies. They were published between 2014 and 2017 by teams from Tunisia ( n = 4) and Jordan ( n = 1). One study applied the 6-min walk test, and four studies opted for the cardiopulmonary exercise test. Narghile use was associated with reduced submaximal (e.g., lower 6-min walk distance) and maximal aerobic capacities (e.g., lower maximal oxygen uptake) with abnormal cardiovascular status at rest (e.g., increase in heart rate and blood pressures), at the end of the exercise (e.g., lower heart rate, tendency to chronotropic insufficiency) and during the recovery period (e.g., lower recovery index). To conclude, chronic narghile use has negative effects on cardiovascular response to exercise with reduced submaximal and maximal exercise capacities.

Cardiovascular response to cycle exercise during and after pregnancy

1989 ◽  
Vol 66 (1) ◽  
pp. 336-341 ◽  
Author(s):  
S. P. Sady ◽  
M. W. Carpenter ◽  
P. D. Thompson ◽  
M. A. Sady ◽  
B. Haydon ◽  
...  
Keyword(s):  
Heart Rate ◽  
Maximal Exercise ◽  
Cardiovascular Response ◽  
Work Load ◽  
Cycle Ergometry ◽  
Maximal Heart Rate ◽  
O2 Uptake ◽  
Cycle Exercise ◽  
Vascular Beds ◽  
Response To Exercise

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Cardiovascular response to exercise in pacemaker implanted patients with fixed heart rate.

1989 ◽  
Vol 30 (6) ◽  
pp. 809-816 ◽  
Author(s):  
Kozui MIYAZAWA ◽  
Ichiro YAMAGUCHI ◽  
Eiichi KOMATSU ◽  
Shigeru KAGAYA ◽  
Junshi ODA
Keyword(s):  
Heart Rate ◽  
Cardiovascular Response ◽  
Response To Exercise

scholarly journals Abnormal cardiovascular response to exercise in hypertension: contribution of neural factors

2017 ◽  
Vol 312 (6) ◽  
pp. R851-R863 ◽  
Author(s):  
Jere H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiovascular Response ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Functional Sympatholysis ◽  
Neural Factors ◽  
Response To Exercise

During both dynamic (e.g., endurance) and static (e.g., strength) exercise there are exaggerated cardiovascular responses in hypertension. This includes greater increases in blood pressure, heart rate, and efferent sympathetic nerve activity than in normal controls. Two of the known neural factors that contribute to this abnormal cardiovascular response are the exercise pressor reflex (EPR) and functional sympatholysis. The EPR originates in contracting skeletal muscle and reflexly increases sympathetic efferent nerve activity to the heart and blood vessels as well as decreases parasympathetic efferent nerve activity to the heart. These changes in autonomic nerve activity cause an increase in blood pressure, heart rate, left ventricular contractility, and vasoconstriction in the arterial tree. However, arterial vessels in the contracting skeletal muscle have a markedly diminished vasoconstrictor response. The markedly diminished vasoconstriction in contracting skeletal muscle has been termed functional sympatholysis. It has been shown in hypertension that there is an enhanced EPR, including both its mechanoreflex and metaboreflex components, and an impaired functional sympatholysis. These conditions set up a positive feedback or vicious cycle situation that causes a progressively greater decrease in the blood flow to the exercising muscle. Thus these two neural mechanisms contribute significantly to the abnormal cardiovascular response to exercise in hypertension. In addition, exercise training in hypertension decreases the enhanced EPR, including both mechanoreflex and metaboreflex function, and improves the impaired functional sympatholysis. These two changes, caused by exercise training, improve the muscle blood flow to exercising muscle and cause a more normal cardiovascular response to exercise in hypertension.

Role of arterial baroreceptors in mediating cardiovascular response to exercise

1976 ◽  
Vol 230 (1) ◽  
pp. 85-89 ◽  
Author(s):  
RJ McRitchie ◽  
SF Vatner ◽  
D Boettcher ◽  
GR Heyndrickx ◽  
TA Patrick ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Severe Exercise ◽  
Response To Exercise ◽  
Arterial Baroreceptor

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.

Intersubject variability in cardiac output-O2 uptake relation of men during exercise

1986 ◽  
Vol 61 (6) ◽  
pp. 2168-2174 ◽  
Author(s):  
I. Yamaguchi ◽  
E. Komatsu ◽  
K. Miyazawa
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Regression Line ◽  
Maximum Level ◽  
Intersubject Variability ◽  
O2 Uptake ◽  
Vascular Conductance ◽  
Individual Variations ◽  
Response To Exercise

Intersubject variability in the relation between cardiac output (Q) and O2 uptake (VO2) was examined during supine cycling up to the maximum level in 40 normal untrained men age 27 +/- 4 (SD) yr. In individual subjects, Q increased linearly against VO2 in the submaximum exercise range. The SD of Q on VO2 was so small (0.47 +/- 0.25 l/min) that Q could be given by a linear function of VO2 as Q = K(VO2 - VO2 r) + Qr, where K, VO2 r, and Qr are the slope of the regression line, the resting VO2, and resting Q, respectively. K varied widely among the subjects studied, ranging from 5.5 to 10.3 and was independent of both physical characteristics and Qr, which ranged from 3.7 to 8.3 l/min. However, K correlated significantly with changes in heart rate, stroke volume, mean arterial pressure, and systemic vascular conductance. From these results, we concluded that the intersubject variability in the Q-VO2 relation was caused independently by individual variations in resting hemodynamics and in cardiovascular response to exercise.

Cardiovascular response to submaximal exercise in sustained microgravity

1996 ◽  
Vol 81 (1) ◽  
pp. 26-32 ◽  
Author(s):  
B. E. Shykoff ◽  
L. E. Farhi ◽  
A. J. Olszowka ◽  
D. R. Pendergast ◽  
M. A. Rokitka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Life Sciences ◽  
Submaximal Exercise ◽  
Arterial Blood ◽  
Response To Exercise

Cardiac output (Q), heart rate (HR), blood pressure, and oxygen consumption (VO2) were measured repeatedly both at rest and at two levels of exercise in six subjects during microgravity exposure. Exercise was at 30 and 60% of the workload producing the individual's maximal VO2 in 1 G. Three of the subjects were on a 9-day flight, Spacelab Life Sciences-1, and three were on a 15-day flight, Spacelab Life Sciences-2. We found no temporal differences during the flights. Thus we have combined all microgravity measurements to compare in-flight values with erect or supine control values. At rest, Q in flight was 126% of Q erect (P < 0.01) but was not different from Q supine, and HR in flight was 81% of HR erect (P < 0.01) and 91% of HR supine (P < 0.05). Thus resting stroke volume (SV) in flight was 155% of SV erect (P < 0.01) and 109% SV supine (P < 0.05). Resting mean arterial blood pressure and diastolic pressure were lower in flight than erect (P < 0.05). Exercise values were considered as functions of VO2. The increase in Q with VO2 in flight was less than that at 1 G (slope 3.5 vs. 6.1 x min-1.l-1.min-1). SV in flight fell with increasing VO2, whereas SV erect rose and SV supine remained constant. The blood pressure response to exercise was not different in flight from erect or supine. We conclude that true microgravity causes a cardiovascular response different from that seen during any of its putative simulations.

A Comparison of the Bronchodilator and Vasopressor Effects of Exercise Levels of Adrenaline in Man

1983 ◽  
Vol 64 (5) ◽  
pp. 475-479 ◽  
Author(s):  
J. B. Warren ◽  
N. Dalton
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Glucose ◽  
Exercise Test ◽  
Cardiovascular Response ◽  
Normal Subjects ◽  
Significant Rise ◽  
Cardiovascular Physiology ◽  
Plasma Adrenaline ◽  
Response To Exercise

1. Plasma adrenaline was measured at rest and on exercise in six normal, non-atopic subjects. The exercise test produced a minimum tachycardia of 158 beats/min and a mean plasma adrenaline level of 1.89 nmol/l. 2. On a separate occasion, two doses of l-adrenaline (0.025 μg min−1 kg−1 and 0.05 μg min−1 kg−1) were infused in the same subjects at rest to produce two mean plasma levels similar to those found on exercise. 3. Significant bronchodilation and elevation of plasma glucose occurred with both infusion doses when compared with placebo. 4. Neither infusion caused a significant change in heart rate and only the higher dose caused a small but significant rise in systolic and fall in diastolic blood pressure. 5. Our results suggest that adrenaline as a hormone, at the levels found on exercise, is capable of causing bronchodilation and glycogenolysis in normal subjects. Its contribution to the cardiovascular response to exercise appears to be slight and suggests that its role in cardiovascular physiology may also be marginal.

Effects of Physical Training on Stuttering

1968 ◽  
Vol 11 (4) ◽  
pp. 767-776 ◽  
Author(s):  
B. Don Franks ◽  
Elizabeth B. Franks
Keyword(s):  
College Students ◽  
Group Therapy ◽  
Physical Training ◽  
Cardiovascular Response ◽  
Training Group ◽  
Physical Stress ◽  
Submaximal Exercise ◽  
Endurance Running ◽  
Response To Exercise

Eight college students enrolled in group therapy for stuttering were divided into two equal groups for 20 weeks. The training group supplemented therapy with endurance running and calisthenics three days per week. The subjects were tested prior to and at the conclusion of the training on a battery of stuttering tests and cardiovascular measures taken at rest, after stuttering, and after submaximal exercise. There were no significant differences (0.05 level) prior to training. At the conclusion of training, the training group was significandy better in cardiovascular response to exercise and stuttering. Although physical training did not significantly aid the reduction of stuttering as measured in this study, training did cause an increased ability to adapt physiologically to physical stress and to the stress of stuttering.

Heart rate as a marker of relapse during withdrawal of heart failure therapy in patients with recovered dilated cardiomyopathy: an analysis from TRED-HF

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
B Halliday ◽  
A Vazir ◽  
R Owen ◽  
J Gregson ◽  
R Wassall ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Function ◽  
Dilated Cardiomyopathy ◽  
Funding Source ◽  
End Point ◽  
Therapy Withdrawal ◽  
The Mean ◽  
Withdrawal Of Therapy ◽  
Continue Therapy

Abstract Introduction In TRED-HF, 40% of patients with recovered dilated cardiomyopathy (DCM) relapsed in the short-term during phased withdrawal of drug therapy. Non-invasive markers of relapse may be used to monitor patients who wish a trial of therapy withdrawal and provide insights into the pathophysiological drivers of relapse. Purpose To investigate the relationship between changes in heart rate (HR) and relapse amongst patients with recovered DCM undergoing therapy withdrawal in TRED-HF. Methods Patients with recovered DCM were randomised to phased withdrawal of therapy or to continue therapy for 6 months. After 6 months of continued therapy, those in the control arm underwent withdrawal of therapy in a single arm crossover phase. HR was measured at each study visit. Mean HR and 95% confidence intervals (CI) were calculated at baseline, 45 days after baseline, 45 days prior to the end of the study or relapse and at the end of the study or relapse. Patients were stratified by treatment arm and the occurrence of the primary relapse end-point. Heart rate at follow-up was compared amongst patients who had therapy withdrawn and relapsed versus those who had therapy withdrawn and did not. ANCOVA was used to adjust for differences in HR at baseline between the two groups. Results Of 51 patients randomised, 26 were assigned to continue therapy and 25 to withdraw therapy. In the randomised and cross-over phases, 20 patients met the primary relapse end-point; one patient withdrew from the study and one patient completed follow-up in the control arm but did not enter the cross-over phase. Mean HR (standard deviation) at baseline and follow-up for (i) patients in the control arm was 69.9 (9.8) & 65.9 (9.1) respectively; (ii) for those who had therapy withdrawn and did not relapse was 64.6 (10.7) & 74.7 (10.4) respectively; and (iii) for those who had therapy withdrawn and relapsed was 68.3 (11.3) & 86.1 (11.8) respectively [all beats per minute]. The mean change in HR between the penultimate visit and the final visit for those who had therapy withdrawn and did not relapse was −2.4 (9.7) compared to 3.1 (15.5) for those who relapsed. After adjusting for differences in HR at baseline, the mean difference in HR measured at follow-up between patients who underwent therapy withdrawal and did, and did not relapse was 10.4bpm (95% CI 4.0–16.8; p=0.002) (Figure 1 & Table 1). Conclusion(s) A larger increase in HR may be a simple and effective marker of relapse for patients with recovered DCM who have insisted on a trial of therapy withdrawal. Whether HR control is crucial to the maintenance of remission amongst patients with improved cardiac function, or is simply a marker of deteriorating cardiac function, warrants further investigation. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): British Heart Foundation

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