Decline In Stroke Volume Research Articles

Blood pressure regulation in women – differences emerge when challenged by orthostasis

Blood pressure regulation in women – differences emerge when challenged by orthostasis

Continuous Cardiac Stroke Volume Monitoring Leads to Early Detection of Cardiac Tamponade in the Percutaneous intracardiac Intervention

Background: Cardiac tamponade is one of the major complications which can result from catheter-based cardiac management, and if its detection or treatment is delayed, it can be fatal. Detecting cardiac tamponade in the earliest possible stages is crucial for preventing its development into a life threatening condition. Methods and results: In this study, an internal blood pressure reading was conducted as part of catheter ablation, cardiac electro physiologic study, and bi-ventricular pacing treatments, and this blood pressure wave form was used along with a FloTrac system to produce a continuous estimate of cardiac output. These data were then retrospectively analyzed to determine whether the FloTrac cardiac output showed changes prior to the onset of declining blood pressure, which is the typical indicator used to diagnose cardiac tamponade. The study was conducted on 213 subjects who were undergoing catheter ablation, cardiac electrophysiologic study, and bi-ventricular pacing treatments. Out of this group, 4 (1.9%) were diagnosed with cardiac tamponade. The FloTrac data for all of these cardiac tamponade subjects showed a decline in stroke volume and cardiac output, with the onset of these changes coming an average of 15.5 ± 6.2 minutes and 8.7 ± 1.0 minutes respectively in advance of the onset of declining blood pressure measurements from the internal blood pressure readings. Conclusion: Continuous cardiac output measurements can be used to detect cardiac tamponade at an earlier stage than continuous internal blood pressure readings, and this could enable accelerated treatment of these complications.

Cardiovascular drift and cerebral and muscle tissue oxygenation during prolonged cycling at different pedalling cadences

We hypothesized that a faster cycling cadence could exaggerate cardiovascular drift and affect muscle and cerebral blood volume and oxygenation. Twelve healthy males (mean age, 23.4 ± 3.8 years) performed cycle ergometry for 90 min on 2 separate occasions, with pedalling frequencies of 40 and 80 r·min(-1), at individual workloads corresponding to 60% of their peak oxygen consumption. The main measured variables were heart rate, ventilation, cardiac output, electromyographic activity of the vastus lateralis, and regional muscle and cerebral blood volume and oxygenation. Cardiovascular drift developed at both cadences, but it was more pronounced at the faster than at the slower cadence, as indicated by the drop in cardiac output by 1.0 ± 0.2 L·min(-1), the decline in stroke volume by 9 ± 3 mL·beat(-1), and the increase in heart rate by 9 ± 1 beats·min(-1) at 80 r·min(-1). At the faster cadence, minute ventilation was higher by 5.0 ± 0.5 L·min(-1), and end-tidal CO(2) pressure was lower by 2.0 ± 0.1 torr. Although higher electromyographic activity in the vastus lateralis was recorded at 80 r·min(-1), muscle blood volume did not increase at this cadence, as it did at 40 r·min(-1). In addition, muscle oxygenation was no different between cadences. In contrast, cerebral regional blood volume and oxygenation at 80 r·min(-1) were not as high as at 40 r·min(-1) (p < 0.05). Faster cycling cadence exaggerates cardiovascular drift and seems to influence muscle and cerebral blood volume and cerebral oxygenation, without muscle oxygenation being radically affected.

Predictors of orthostatic intolerance in healthy young women

Orthostatic intolerance is more prevalent in women. The purpose of this investigation was to evaluate the physiological responses of orthostatic tolerant and intolerant females to progressive lower body negative pressure (LBNP) and to identify predictors of orthostatic tolerance. Following baseline measurements, eleven healthy, moderately active women (mean age 24 ± 3 yr) underwent an orthostatic challenge involving four 12-minute stages of progressive LBNP at -15, -30, -45 and -60 mmHg. Traditional haemodynamic characteristics, as well as baroreceptor sensitivity, were analyzed across all stages. Five women became presyncopal during the test and were classified as low tolerant (LT) while the remaining six were classified as high tolerant (HT). LBNP by group (tolerance) interactions were significantly different for stroke volume (P=0.008) and the rate of decline (slope) of stroke volume (P=0.03). During the early stages of LBNP, the LT group displayed a higher stroke volume than the HT group (76.4 ± 8.6 vs. 60.0 ± 13.3 mL/beat; P=0.02) yet by the final stage, stroke volumes were similar (22.5 ± 11.9 vs. 22.7 ± 4.5 mL/beat, P = 0.99). Baroreceptor sensitivity, heart rate variability and blood pressure variability were not significantly different between the groups. The results of this investigation suggest that orthostatic intolerance in women can be identified during the initial stages of an LBNP challenge, as evidenced by a more rapid decline in stroke volume.

Pressure-Volume Relationships in Patients With Transthyretin (ATTR) Cardiac Amyloidosis Secondary to V122I Mutations and Wild-Type Transthyretin

Background— ATTR cardiac amyloidosis can result from a mutated variant of transthyretin (eg, V122I) or wild-type variant (ATTRwt). We evaluated pressure-volume (PV) indices at baseline and over time to further characterize abnormal pump function in these subjects. Methods and Results— Twenty-nine subjects (18 with ATTRwt and 11 with ATTRm (V122I) had 2-dimensional echocardiograms with complete Doppler measures at baseline and every 6 months for up to 2 years. PV indices were derived from echocardiographic measures of ventricular volume coupled with sphygmomanometer-measured pressure and Doppler estimates of filling pressure. The end-systolic and end-diastolic PV relations and the area between them as a function of end-diastolic pressure, the isovolumic PV area (PVA iso ), were calculated. Clinical, demographic, and PV indices were compared between V122I and ATTRwt subjects and between survivors and nonsurvivors at baseline and over time. Cox proportional hazards model identified correlates for mortality. Stroke volume decline was associated with alterations in ventricular-vascular coupling and a decrease in ventricular capacitance with significant decrement in ejection fraction (56±12% to 48±14%, P =0.0001) over 18 months. PVA iso was lower in V122I subjects compared with wild-type at baseline and declined over time. Twelve (41%) subjects died or underwent a cardiac transplant after a mean follow-up of 478 days (range, 31 to 807). Multivariable survival analysis demonstrated that initial ejection fraction (a measure of ventricular-vascular coupling) &lt;50% was associated with increased mortality (hazard ratio, 6.6; 95% confidence interval, 1.1 to 40.3). Conclusions— In ATTR cardiac amyloidosis secondary to a V122I mutation and wild-type transthyretin, PV analysis reveals alterations that are associated with reductions in the ability of the ventricle to perform work and, ultimately, with reduced survival in these subjects.

Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction?

The mechanisms of heart failure are ill understood with multiple, heterogeneous hypotheses proposed to describe the condition. This study examines the individual effects of left ventricular hypertrophy, long-axis shortening and the effect of left ventricular remodeling on ejection fraction, end-diastolic volume and stroke volume using a mathematical model of left ventricular contraction. Reducing long-axis shortening caused a decline in stroke volume independently of hypertrophy. Increasing concentric left ventricular hypertrophy resulted in an increase in ejection fraction secondary to augmented wall thickening. A decline in stroke volume occurred despite a preserved ejection fraction when concentric hypertrophy was present. Normalization of stroke volume by remodeling resulted in a marked increase in end-diastolic volume in the absence of hypertrophy and an end-diastolic volume similar to normal in the presence of concentric hypertrophy. The model predicts that the dominant compensatory mechanism in chronic heart failure is remodeling with normalization of stroke volume. Observational data cited supports this conclusion.

Last Word on Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individuals

POINT-COUNTERPOINTLast Word on Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individualsJosé González-AlonsoJosé González-AlonsoPublished Online:01 Jan 2008https://doi.org/10.1152/japplphysiol.01116.2007MoreSectionsPDF (25 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: This pro-and-con debate expects the presenters to advance polarized views on whether stroke volume declines during exercise at maximal effort in healthy individuals not to provide a balanced assessment of the literature, as Drs. Warburton and Gledhill appear to contend (3). In this context, Drs. Vella and Robergs' (2) remark that “Scientists must refrain from concluding absolute interpretations, resulting in oversimplified explanations and understanding” is perplexing and shows that the aims of the debate remain unclear. It is reassuring, however, that there is an overwhelming consensus in regards to the paucity of data describing the stroke volume (and related cardiovascular variables) behavior in the few seconds prior to exhaustion and thus a dire need for further investigation (by many different laboratories) of the integrative cardiovascular response to maximal as well as supramaximal exercise in different human populations. Knowing that there are indeed absolute, highly predictable cardiovascular responses to exercise in healthy humans and higher animals, it is tempting to hypothesize that the decline in stroke volume seen in our limited number of studies (1) is a universal phenomenon encompassing the cascade of events leading to fatigue during exercise of true maximal effort.REFERENCES1 González-Alonso J. Point: Stroke volume does decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/japplphysiol.00595.2007.Google Scholar2 Lucia A, Foster C, Lepretre P-M, Henriksen E, Sundsted M, Hedberg P, Vella CA, Robergs RA, Coyle EF, Trinity JD, Billat VL. Comments on Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/japplphysiol.01073.2007.Google Scholar3 Warbuton DER, Gledhill N. Counterpoint: Stroke volume does not decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/japplphysiol.00595.2007a.Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: J. González-Alonso, Centre for Sports Medicine and Human Performance, Brunel Univ., Uxbridge, UK (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 104Issue 1January 2008Pages 284-284 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01116.2007History Published online 1 January 2008 Published in print 1 January 2008 Metrics

Cardiovascular changes under normoxic and hypoxic conditions in the air-breathing teleostSynbranchus marmoratus: importance of the venous system

Synbranchus marmoratus is a facultative air-breathing fish, which uses its buccal cavity as well as its gills for air-breathing. S. marmoratus shows a very pronounced tachycardia when it surfaces to air-breathe. An elevation of heart rate decreases cardiac filling time and therefore may cause a decline in stroke volume (V(S)), but this can be compensated for by an increase in venous tone to maintain stroke volume. Thus, the study on S. marmoratus was undertaken to investigate how stroke volume and venous function are affected during air-breathing. To this end we measured cardiac output (Q), heart rate (f(H)), central venous blood pressure (P(CV)), mean circulatory filling pressure (MCFP), and dorsal aortic blood pressures (P(DA)) in S. marmoratus. Measurements were performed in aerated water (P(O2)>130 mmHg), when the fish alternated between gill ventilation and prolonged periods of apnoeas, as well as during hypoxia (P(O2)<or=50 mmHg), when the fish changed from gill ventilation to air-breathing. Q increased significantly during gill ventilation compared to apnoea in aerated water through a significant increase in both f(H) and V(S). P(CV) and MCFP also increased significantly. During hypoxia, when the animals surface to ventilate air, we found a marked rise in f(H), P(CV), MCFP, Q and V(S), whereas P(DA) decreased significantly. Simultaneous increases in P(CV) and MCFP in aerated, as well as in hypoxic water, suggests that the venous system plays an important regulatory role for cardiac filling and V(S) in this species. In addition, we investigated adrenergic regulation of the venous system through bolus infusions of adrenergic agonists (adrenaline, phenylephrine and isoproterenol; 2 microg kg(-1)). Adrenaline and phenylephrine caused a marked rise in P(CV) and MCFP, whereas isoproterenol led to a marked decrease in P(CV), and tended to decrease MCFP. Thus, it is evident that stimulation of both alpha- and beta-adrenoreceptors affects venous tone in S. marmoratus.

Fluid Ingestion Attenuates the Decline in V̇O2peak Associated with Cardiovascular Drift

This study investigated whether manipulation of cardiovascular drift (CV drift) by changing exercise duration or by fluid ingestion is associated with altered peak oxygen uptake VO(2peak).VO(2peak) was measured in 11 trained men immediately after they cycled at 60% control VO(2max) in 30 degrees C, 40% relative humidity for 15, 60, and 120 min with no fluid (15 NF, 60 NF, 120 NF) or 120 min with fluid (120 F). Stroke volume (SV), heart rate (HR), and related measures were measured in 120 NF and 120 F at 15, 60, and 120 min.Body mass decreased 0.7, 2.3, and 3.7% in 120 F, 60 NF, and 120 NF. SV at the end of submaximal exercise and VO(2peak) measured immediately thereafter were reduced significantly (P < 0.05) from 15-min values in 120 NF (13.8 and 8.7%) but not in 60 NF (4.6 and 1.2%) or 120 F (2.1 and 1.9%).The progressive decline in SV during prolonged, constant-rate submaximal exercise in a warm environment, reflective of increased cardiovascular strain associated with hyperthermia, dehydration, and other changes that occur over time, reduces VO(2peak). Fluid ingestion improves performance in prolonged exercise, in part, by mitigating the decline in SV and its determinants, and preserving VO(2peak).

Limitations to systemic and locomotor limb muscle oxygen delivery and uptake during maximal exercise in humans

Reductions in systemic and locomotor limb muscle blood flow and O2 delivery limit aerobic capacity in humans. To examine whether O2 delivery limits both aerobic power and capacity, we first measured systemic haemodynamics, O2 transport and O2 uptake during incremental and constant (372 +/- 11 W; 85% of peak power; mean +/- S.E.M.) cycling exercise to exhaustion (n = 8) and then measured systemic and leg haemodynamics and during incremental cycling and knee-extensor exercise in male subjects (n = 10). During incremental cycling, cardiac output and systemic O2 delivery increased linearly to 80% of peak power (r2 = 0.998, P < 0.001) and then plateaued in parallel to a decline in stroke volume (SV) and an increase in central venous and mean arterial pressures (P < 0.05). In contrast, heart rate and increased linearly until exhaustion (r2 = 0.993; P < 0.001) accompanying a rise in systemic O2 extraction to 84 +/- 2%. In the exercising legs, blood flow and O2 delivery levelled off at 73-88% of peak power, blunting leg per unit of work despite increasing O2 extraction. When blood flow increased linearly during one-legged knee-extensor exercise, per unit of work was unaltered on fatigue. During constant cycling, , SV, systemic O2 delivery and reached maximal values within approximately 5 min, but dropped before exhaustion (P < 0.05) despite increasing or stable central venous and mean arterial pressures. In both types of maximal cycling, the impaired systemic O2 delivery was due to the decline or plateau in because arterial O2 content continued to increase. These results indicate that an inability of the circulatory system to sustain a linear increase in O2 delivery to the locomotor muscles restrains aerobic power. The similar impairment in SV and O2 delivery during incremental and constant load cycling provides evidence for a central limitation to aerobic power and capacity in humans.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure (LBNP). Ten older fit (OF) [73.9 +/- 2 years; 39.0 +/- 2 ml.kg(-1).min(-1) (age and estimated VO(2)peak, respectively)], 10 older unfit (OU) (70.9 +/- 1 years; 27.1 +/- 2 ml.kg(-1).min(-1)), 10 young fit (YF) (22.6 +/- 0.5 years; 57.1 +/- 2 ml.kg(-1).min(-1)), and 10 young unfit (YU) (23.1 +/- 1 years; 41.1 +/- 2 ml.kg(-1).min(-1)) participants underwent graded LBNP of -10 mmHg every 4 minutes to either presyncope or -100 mmHg. Compared to the other groups, YF had an earlier increase in heart rate (-40 mmHg vs the last stage; YF vs OF, OU, and YU, respectively) and decline in stroke volume (-20 mmHg vs -40 mmHg; YF vs OF, OU, and YU, respectively). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage. OF had an earlier decline in total peripheral conductance than the other groups (-20 mmHg vs -40 mmHg). Tolerance to maximal LBNP did not differ among the groups. Despite differences in the responses to submaximal LBNP, neither age nor cardiovascular fitness affect tolerance to maximal LBNP.

Fluid Ingestion Attenuates The Decline In Vo2max Associated With Cardiovascular Drift

Cardiovascular drift (CV drift), characterized by the progressive rise in heart rate (HR) and fall in stroke volume (SV) during prolonged moderate-intensity exercise, is a well established phenomenon, but its effects on maximal oxygen uptake (VO2max) are not clear. PURPOSE To determine whether manipulation of CV drift by altering duration of exercise and fluid ingestion is associated with corresponding changes in VO2max. METHODS CV drift was measured in 11 moderately-trained men (age=26±5 yr, VO2max=57.8±6.7 ml/kg/min) as they cycled for either 60 min with no fluid (60NF), 120 min with no fluid (120NF), or 120 min while ingesting a 7% carbohydrate-electrolyte drink to replace sweat losses (120F). A control trial of 15 min with no fluid (15NF) also was conducted in order to assess VO2max before CV drift occurred. All exercise was performed at 60% VO2max in 30°C, 40% relative humidity, and wind speed ∼2.5 m/s. After submaximal exercise, without cessation of cycling, subjects began a continuous incremental-test to exhaustion to measure VO2max. RESULTS Subjects became 2.3%, 3.7%, and 0.7% dehydrated in 60NF, 120NF and 120F, respectively. Compared to 15NF, SV decline was not significant in 60NF (6 ml, 4.6%) but was in 120NF (16 ml, 13.8%, p < 0.05). Fluid ingestion (120F) significantly reduced the decline in SV to 3 ml (2.1%) compared to 120NF (p < 0.05). Compared to 15NF, VO2max was not decreased in 60NF (−1.2%), but was lower in 120NF by 5.1 ml/min/kg (−8.7%, p < 0.05). Fluid ingestion (120F) significantly reduced the decline in VO2max 1.3 ml/min/kg (−1.9%) compared to 120NF (p < 0.05). Changes in VO2max were significantly correlated with changes in SV and HR after 15 min during submaximal exercise (r=.62 and .47, SEE=5.8 and 6.6, respectively, p < 0.05). CONCLUSION Manipulation of CV drift by altering exercise duration and fluid ingestion is associated with proportional changes in VO2max. The results provide support for the hypothesis that, under these conditions, CV drift causes reduced VO2max.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

0177 Orthostatic hypotension has and has not been reported among the elderly and endurance athletes may or may not have reduced tolerance to orthostatic stress. One of the limitations of many of the aging studies is in the use of submaximal rather than maximal orthostatic stress and a focus on either aging or fitness, not both. Purpose: The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure. Methods: Ten older fit (OF; 73.9 + 2 yo; 39.0 + 2 ml·kg-1·min-1), ten older unfit (OU; 70.9 + 1 yo; 27.1 + 2 ml·kg-1·min-1), ten young fit (YF; 22.6 + 0.5 yo; 57.1 + 2 ml·kg-1·min-1) and ten young unfit (YU; 23.1 + 1 yo; 41.1 + 2 ml·kg-1·min-1) participants underwent graded LBNP to either presyncope or −100 mmHg. Results: Compared to the other groups, YF had an earlier increase in HR (−40 mmHg vs the last stage, p<0.05) and decline in stroke volume (−20 mmHg vs −40 mmHg, p<0.05). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage (p<0.05). OF had an earlier decline in total peripheral conductance than the other groups (−20 mmHg vs −40 mmHg, p<0.05). Tolerance to maximal LBNP did not differ between the groups. Conclusion: Despite differences in the responses to submaximal LBNP, which suggest that mechanisms to maintain blood pressure are different, neither age nor cardiovascular fitness affect tolerance to LBNP.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

0177 Orthostatic hypotension has and has not been reported among the elderly and endurance athletes may or may not have reduced tolerance to orthostatic stress. One of the limitations of many of the aging studies is in the use of submaximal rather than maximal orthostatic stress and a focus on either aging or fitness, not both. Purpose: The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure. Methods: Ten older fit (OF; 73.9 + 2 yo; 39.0 + 2 ml·kg-1·min-1), ten older unfit (OU; 70.9 + 1 yo; 27.1 + 2 ml·kg-1·min-1), ten young fit (YF; 22.6 + 0.5 yo; 57.1 + 2 ml·kg-1·min-1) and ten young unfit (YU; 23.1 + 1 yo; 41.1 + 2 ml·kg-1·min-1) participants underwent graded LBNP to either presyncope or −100 mmHg. Results: Compared to the other groups, YF had an earlier increase in HR (−40 mmHg vs the last stage, p<0.05) and decline in stroke volume (−20 mmHg vs −40 mmHg, p<0.05). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage (p<0.05). OF had an earlier decline in total peripheral conductance than the other groups (−20 mmHg vs −40 mmHg, p<0.05). Tolerance to maximal LBNP did not differ between the groups. Conclusion: Despite differences in the responses to submaximal LBNP, which suggest that mechanisms to maintain blood pressure are different, neither age nor cardiovascular fitness affect tolerance to LBNP.

Cardiovascular Drift During Prolonged Exercise: New Perspectives

COYLE, E. F., and J. GONZÁLEZ-ALONSO. Cardiovascular drift during prolonged exercise: New perspectives. Exerc. Sports Sci. Rev. Vol. 29, No. 2, pp. 88–92, 2001. We propose that cardiovascular drift, characterized by a progressive decline in stroke volume after 10–20 min of exercise, is primarily due to increased heart rate rather than a progressive increase in cutaneous blood flow as body temperature rises.

Cardiovascular drift during prolonged exercise: new perspectives.

We propose that cardiovascular drift, characterized by a progressive decline in stroke volume after 10-20 min of exercise, is primarily due to increased heart rate rather tahn a progressive increase in cutaneous blood flow as body temperature rises.

The influence of recovery posture on post-exercise hypotension in normotensive men.

Postexercise hypotension may be the result of an impaired vasoconstrictor response. This hypothesis was investigated by examining the central and peripheral hemodynamic responses during supine and seated recovery after maximal upright exercise. After supine or seated baseline measurements, seven normotensive male volunteers completed a graded upright cycling protocol to volitional exhaustion. This was immediately followed by either supine or seated recovery. Measurements of pulsatile arterial blood pressure and central and peripheral hemodynamic variables recorded 30 min before exercise were compared with those taken throughout 60 min of recovery. Compared with baseline, mean arterial pressure (MAP) was reduced after exercise (P < 0.05) although the degree of change was not different between the supine (-9 +/- 4 mm Hg) and seated positions (-6 +/- 2 mm Hg). This change in MAP was associated with a reduction in diastolic blood pressure (DBP) (P < 0.05) and arterial pulse pressure (APP) (P < 0.01) for the supine and seated positions, respectively. The reduction in APP during seated recovery was accompanied by a decline in stroke volume (SV) (P < 0.05), not seen in the supine position, that limited the contribution of cardiac output (CO) to the maintenance of MAP. This effect of seated recovery was compensated by greater systemic (SVR) and regional vascular resistances in the forearm (FVR) and the forearm skin (SkVRA). There was also evidence of an augmented return of FVR and SkVRA to resting levels in the seated position after exercise. The lower peripheral resistance in the supine compared with seated recovery position suggests there is potential for greater vasoconstriction, although this is not evoked to increase blood pressure. This further suggests that the arterial baroreceptor reflex is reset to a lower operating pressure after exercise.

Stroke volume decline during prolonged exercise is influenced by the increase in heart rate.

This study determined whether the decline in stroke volume (SV) during prolonged exercise is related to an increase in heart rate (HR) and/or an increase in cutaneous blood flow (CBF). Seven active men cycled for 60 min at approximately 57% peak O2 uptake in a neutral environment (i.e., 27 degrees C, <40% relative humidity). They received a placebo control (CON) or a small oral dose (i.e., approximately 7 mg) of the beta1-adrenoceptor blocker atenolol (BB) at the onset of exercise. At 15 min, HR and SV were similar during CON and BB. From 15 to 55 min during CON, a 13% decline in SV was associated with an 11% increase in HR and not with an increase in CBF. CBF increased mainly from 5 to 15 min and remained stable from 20 to 60 min of exercise in both treatments. However, from 15 to 55 min during BB, when the increase in HR was prevented by atenolol, the decline in SV was also prevented, despite a normal CBF response (i.e., similar to CON). Cardiac output was similar in both treatments and stable throughout the exercise bouts. We conclude that during prolonged exercise in a neutral environment the decline in SV is related to the increase in HR and is not affected by CBF.

Influence of cycle frequency, muscle strain and muscle length on work and power production of rainbow trout (Oncorhynchus mykiss) ventricular muscle

This study investigates the effects of cycle frequency, strain and length on work and power output of isolated rainbow trout (Oncorhynchus mykiss) ventricular preparations using the work loop technique. These effects are discussed in the context of the whole heart using analogies with heart rate, stroke volume and end-diastolic volume. Power output was dependent on cycle frequency, increasing threefold beween 0.3 and 1.1 Hz. The frequency for maximum power output was approximately 1.1 Hz, corresponding to the frequency for maximum power in perfused heart experiments. The length for maximum work production (Lopt) was found to be the same as the length for maximum isometric force production (Lmax). The decline in net work at lengths greater than Lopt/Lmax was attributed to an increase in passive work (the work done on an unstimulated muscle) or to hysteresis and to a large increase in lengthening work. The strain yielding maximum work decreased with increasing frequency. This is discussed in the context of the decline in stroke volume observed at increased heart rates in vivo. Muscle strain in intact hearts paced at 0.3 Hz was +/-11.9 % (23.8 % peak to peak), a value similar to the optimum strain at 0.3 Hz in vitro (+/-12 %).

Involvement of interleukin-1 receptor mechanisms in development of arterial hypotension in rat heatstroke.

Rats, under urethan anesthesia, were exposed to a high ambient temperature (42 degrees C) to induce heatstroke and to assess the hemodynamic changes associated with heatstroke. Compared with normothermic controls, rats with heatstroke showed higher values of colonic temperature, heart rate, and plasma levels of interleukin (IL)-1 but lower values of R wave amplitude, P-R and Q-T intervals, systolic wave amplitude, diastolic and dicrotic wave duration, mean arterial pressure, stroke volume, and cardiac output. Animals injected intravenously with an IL-1-receptor antagonist at the time of heatstroke induction were protected from some of the cardiovascular effects of heatstroke, such as depressed ventricular depolarization, decreased stroke volume, decreased cardiac output, and arterial hypotension. The hemodynamic changes associated with heatstroke could be mimicked by IL-1beta administration. Other cardiovascular parameters such as total peripheral vascular resistance were unaffected by heatstroke induction or IL-1beta treatment. The results indicate that a selective decline in stroke volume or ventricular depolarization resulting from increased plasma levels of IL-1 may be an important mechanism signaling arterial hypotension or circulatory failure in rat heatstroke.