scholarly journals Maximal oxygen uptake is not limited by a central nervous system governor

2007 ◽  
Vol 102 (2) ◽  
pp. 781-786 ◽  
Author(s):  
T. Brink-Elfegoun ◽  
L. Kaijser ◽  
T. Gustafsson ◽  
B. Ekblom
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Work Rate ◽  
Rate Pressure Product ◽  
Limiting Factor ◽  
Time To Exhaustion ◽  
The Central Nervous System

We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (V̇o2 max). We measured cardiac output (Q̇) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting V̇o2 max. Eight well-trained men (age 24.4 ± 2.8 yr, weight 81.3 ± 7.8 kg, and V̇o2 max 59.1 ± 2.0 ml·min−1·kg−1) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured V̇o2 max, maximal Q̇, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q̇ times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently V̇o2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.

scholarly journals Fractal fluctuations in the cardiovascular dynamical system : from the autonomic control to the central nervous system influence

2021 ◽  
Author(s):  
Asif Hasan Sharif
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Dynamic Feature ◽  
Scale Free ◽  
Autonomic Nervous ◽  
Factorization Technique ◽  
The Central Nervous System

The fractal component in the complex fluctuations of the human heart rate represents a dynamic feature that is widely observed in diverse fields of natural and artificial systems. It is also of clinical significance as the diminishing of the fractal dynamics appears to correlate with heart disease processes and adverse cardiac events in old age. While the autonomic nervous system directly controls the pacemaker cells of the heart, it does not provide an immediate characterization of the complex heart rate variability (HRV). The central nervous system (CNS) is known to be an important modulator for various cardiac functions. However, its role in the fractal HRV is largely unclear. In this research, human experiments were conducted to study the influence of the central nervous system on fractal dynamics of healthy human HRV. The head up tilt (HUT) maneuver is used to provide a perturbation to the autonomic nervous system. The subsequent fractal effect in the simultaneously recorded electroencephalography and beat-to-beat heart rate data was examined. Using the recently developed multifractal factorization technique, the common multifractality in the data fluctuation was analyzed. An empirical relationship was uncovered which shows the increase (decrease) in HRV multifractality is associated with the increase (decrease) in multifractal correlation between scale-free HRV and the cortical expression of the brain dynamics in 8 out of 11 healthy subjects. This observation is further supported using surrogate analysis. The present findings imply that there is an integrated central-autonomic component underlying the cortical expression of the HRV fractal dynamics. It is proposed that the central element should be incorporated in the fractal HRV analysis to gain a more comprehensive and better characterization of the scale-free HRV dynamics. This study provides the first contribution to the HRV multifractal dynamics analysis in HUT. The multivariate fractal analysis using factorization technique is also new and can be applied in the more general context in complex dynamics research.

Hypophysectomy alters cardiorespiratory variables: central effects of pituitary endorphins in shock

1981 ◽  
Vol 241 (4) ◽  
pp. H479-H485 ◽  
Author(s):  
J. W. Holaday ◽  
M. O'Hara ◽  
A. I. Faden
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Hypovolemic Shock ◽  
Cardiovascular Effects ◽  
Central Effects ◽  
Hypophysectomized Rats ◽  
The Central Nervous System

The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.

Stereoselective actions of S-nitrosocysteine in central nervous system of conscious rats

1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Intracerebroventricular Injection ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Recognition Sites ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Intracerebroventricular Injections

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.

Central nervous system cardiovascular effects of bombesin in conscious rats

1985 ◽  
Vol 248 (4) ◽  
pp. H425-H431 ◽  
Author(s):  
L. A. Fisher ◽  
C. R. Cave ◽  
M. R. Brown
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Circulation ◽  
Alpha Adrenergic Receptors ◽  
The Central Nervous System ◽  
Atropine Methyl Nitrate

The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.

Nitrict Oxide Synthase Inhibitors, 7-Nitro Indazole and Nitro sup G -L-Arginine Methyl Ester, Dose Dependently Reduce the Threshold for Isoflurane Anesthesia

1996 ◽  
Vol 85 (5) ◽  
pp. 1111-1119 ◽  
Author(s):  
Thomas N. Pajewski ◽  
Cosmo A. DiFazio ◽  
Jeffrey C. Moscicki ◽  
Roger A. Johns
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
No Synthase ◽  
Maximal Effect ◽  
Neuronal No Synthase ◽  
No Synthase Inhibitor ◽  
The Central Nervous System ◽  
Synthase Inhibitor

Background Nitric oxide (NO), a recognized cell messenger for activating soluble guanylate cyclase, is produced by the enzyme NO synthase in a wide variety of tissues, including vascular endothelium and the central nervous system. The authors previously reported the possible involvement of the NO pathway in the anesthetic state by showing that a specific NO synthase inhibitor, nitroG-L-arginine methyl ester (L-NAME), dose dependently and reversibly decreases the minimum alveolar concentration (MAC) for halothane anesthesia. The availability of a structurally distinct inhibitor selective for the neuronal isoform of NO synthase, 7-nitro indazole (7-NI), allowed for the possibility of dissociating the central nervous system effects of neuronal NO synthase inhibition from the cardiovascular effects of endothelial NO synthase inhibition. Methods The effect of two structurally distinct inhibitors of NO synthase, L-NAME and 7-NI, on the MAC of isoflurane was investigated in Sprague-Dawley rats while concurrently monitoring the animals' arterial blood pressure and heart rate. L-NAME (1 to 30 mg/kg given intravenously, dissolved in 0.9% saline) and 7-NI (20 to 1,000 mg/kg given intraperitoneally, dissolved in arachis oil) were administered after determining control MAC and 30 min before determining MAC in the presence of NO synthase inhibitor. Results L-NAME and 7-NI caused a dose-dependent decrease from isoflurane control MAC (maximal effect: 35.5 +/- 2.5% and 43.0 +/- 1.7%, respectively) with a ceiling effect observed for both NO synthase inhibitors (above 10 mg/kg and 120 mg/kg, respectively). L-NAME administration significantly increased systolic and diastolic blood pressures (maximal effect: 39.9 +/- 2.2% and 64.3 +/- 4.0%, respectively), which were not accompanied by any changes in heart rate. 7-NI administration resulted in no changes in blood pressure and a small but clinically insignificant decrease in heart rate. Conclusions Inhibition of the NO synthase pathway decreased the MAC for isoflurane, which suggests that inhibition of the NO pathway decreases the level of consciousness and augments sedation, analgesia, and anesthesia. The MAC reduction by two structurally distinct NO synthase inhibitors supports that this is a specific effect on NO synthase. Furthermore, the action of the neuronal NO synthase inhibitor 7-NI supports an effect selective for neuronal NO synthase and also avoids the hypertensive response of generalized NO synthase inhibitors.

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