Cardiac work remains high after strength exercise in elderly.

Moderate- to high-intensity strength training is recommended for healthy adults. In young subjects, a single session of strength training decreases blood pressure, while heart rate and cardiac work remain elevated afterwards. However, these effects have not been clearly demonstrated in elderly subjects. To investigate this issue, 16 elderly subjects each underwent a Control and an Exercise (3 sets, 8 RM, 9 exercises) session conducted in random order. Haemodynamic variables and heart rate variability were measured before and after the interventions. Systolic blood pressure did not change after the exercise session but did increase after the control session (+8.1±1.6 mm Hg, P≤0.05). Diastolic blood pressure, as well as systemic vascular resistance increased similarly after both sessions. Cardiac output and stroke volume decreased, while heart rate, rate-pressure product and the low- to high-frequency ratio of heart rate variability increased only after the exercise session ( - 0.5±0.1 L/min, - 9.3±2.0 ml,+3.8±1.6 bpm, +579.3±164.1 mmHg.bpm and +0.71±0.34, P≤0.05). Ambulatory blood pressure was similar after both sessions, while heart rate and rate pressure product remained higher after the exercise session for up to 4.5 h. After a single session of strength training, cardiac sympathetic modulation and heart rate remain elevated in elderly subjects, keeping cardiac work elevated for a long period of time.

Low dose of propranolol down-modulates bone resorption by inhibiting inflammation and osteoclast differentiation.

BACKGROUND AND PURPOSE: Bones are widely innervated, suggesting an important role for the sympathetic regulation of bone metabolism, although there are controversial studies. We investigated the effects of propranolol in a model of experimental periodontal disease. EXPERIMENTAL APPROACH: Rats were assigned as follows: animals without ligature; ligated animals receiving vehicle and ligated animals receiving 0.1, 5 or 20 mg·kg(-1) propranolol. After 30 days, haemodynamic parameters were measured by cardiac catheterization. Gingival tissues were removed and assessed for IL-1ß, TNF-α and cross-linked carboxyterminal telopeptides of type I collagen (CTX) by elisa, or intercellular adhesion molecule 1 (ICAM-1), receptor activator of NF-κ B ligand (RANKL) and osteoprotegerin (OPG) by Western blot analysis. Sections from the mandibles were evaluated for bone resorption. Also, we analysed the ability of propranolol to inhibit osteoclastogenesis in vitro. RESULTS: Propranolol at 0.1 and 5 mg·kg(-1) reduced the bone resorption as well as ICAM-1 and RANKL expression. However, only 0.1 mg·kg(-1) reduced IL-1ß, TNF-α and CTX levels as well as increased the expression of OPG, but did not alter any of the haemodynamic parameters. Propranolol also suppressed in vitro osteoclast differentiation and resorptive activity by inhibiting the nuclear factor of activated T cells (NFATc)1 pathway and the expression of tartrate-resistant acid phosphatase (TRAP), cathepsin K and MMP-9. CONCLUSIONS AND IMPLICATIONS: Low doses of propranolol suppress bone resorption by inhibiting RANKL-mediated osteoclastogenesis as well as inflammatory markers without affecting haemodynamic parameters.

Acute effect of amiodarone on cardiovascular reflexes of normotensive and renal hypertensive rats.

The aim of the present study was to evaluate the effect of amiodarone on mean arterial pressure (MAP), heart rate (HR), baroreflex, Bezold-Jarisch, and peripheral chemoreflex in normotensive and chronic one-kidney, one-clip (1K1C) hypertensive rats (N = 9 to 11 rats in each group). Amiodarone (50 mg/kg, iv) elicited hypotension and bradycardia in normotensive (-10 +/- 1 mmHg, -57 +/- 6 bpm) and hypertensive rats (-37 +/- 7 mmHg, -39 +/- 19 bpm). The baroreflex index (deltaHR/deltaMAP) was significantly attenuated by amiodarone in both normotensive (-0.61 +/- 0.12 vs -1.47 +/- 0.14 bpm/mmHg for reflex bradycardia and -1.15 +/- 0.19 vs -2.63 +/- 0.26 bpm/mmHg for reflex tachycardia) and hypertensive rats (-0.26 +/- 0.05 vs -0.72 +/- 0.16 bpm/mmHg for reflex bradycardia and -0.92 +/- 0.19 vs -1.51 +/- 0.19 bpm/mmHg for reflex tachycardia). The slope of linear regression from delta pulse interval/deltaMAP was attenuated for both reflex bradycardia and tachycardia in normotensive rats (-0.47 +/- 0.13 vs -0.94 +/- 0.19 ms/mmHg and -0.80 +/- 0.13 vs -1.11 +/- 0.13 ms/mmHg), but only for reflex bradycardia in hypertensive rats (-0.15 +/- 0.02 vs -0.23 +/- 0.3 ms/mmHg). In addition, the MAP and HR responses to the Bezold-Jarisch reflex were 20-30% smaller in amiodarone-treated normotensive or hypertensive rats. The bradycardic response to peripheral chemoreflex activation with intravenous potassium cyanide was also attenuated by amiodarone in both normotensive (-30 +/- 6 vs -49 +/- 8 bpm) and hypertensive rats (-34 +/- 13 vs -42 +/- 10 bpm). On the basis of the well-known electrophysiological effects of amiodarone, the sinus node might be the responsible for the attenuation of the cardiovascular reflexes found in the present study.

Acute effect of amiodarone on cardiovascular reflexes of normotensive and renal hypertensive rats

The aim of the present study was to evaluate the effect of amiodarone on mean arterial pressure (MAP), heart rate (HR), baroreflex, Bezold-Jarisch, and peripheral chemoreflex in normotensive and chronic one-kidney, one-clip (1K1C) hypertensive rats (N = 9 to 11 rats in each group). Amiodarone (50 mg/kg, iv) elicited hypotension and bradycardia in normotensive (-10 ± 1 mmHg, -57 ± 6 bpm) and hypertensive rats (-37 ± 7 mmHg, -39 ± 19 bpm). The baroreflex index (deltaHR/deltaMAP) was significantly attenuated by amiodarone in both normotensive (-0.61 ± 0.12 vs -1.47 ± 0.14 bpm/mmHg for reflex bradycardia and -1.15 ± 0.19 vs -2.63 ± 0.26 bpm/mmHg for reflex tachycardia) and hypertensive rats (-0.26 ± 0.05 vs -0.72 ± 0.16 bpm/mmHg for reflex bradycardia and -0.92 ± 0.19 vs -1.51 ± 0.19 bpm/mmHg for reflex tachycardia). The slope of linear regression from deltapulse interval/deltaMAP was attenuated for both reflex bradycardia and tachycardia in normotensive rats (-0.47 ± 0.13 vs -0.94 ± 0.19 ms/mmHg and -0.80 ± 0.13 vs -1.11 ± 0.13 ms/mmHg), but only for reflex bradycardia in hypertensive rats (-0.15 ± 0.02 vs -0.23 ± 0.3 ms/mmHg). In addition, the MAP and HR responses to the Bezold-Jarisch reflex were 20-30 percent smaller in amiodarone-treated normotensive or hypertensive rats. The bradycardic response to peripheral chemoreflex activation with intravenous potassium cyanide was also attenuated by amiodarone in both normotensive (-30 ± 6 vs -49 ± 8 bpm) and hypertensive rats (-34 ± 13 vs -42 ± 10 bpm). On the basis of the well-known electrophysiological effects of amiodarone, the sinus node might be the responsible for the attenuation of the cardiovascular reflexes found in the present study.

Chronic converting enzyme inhibition normalizes QT interval in aging rats.

The aim of the present study was to investigate the effects of converting enzyme inhibition by captopril on ECG parameters in aged rats. Four-month-old male rats received captopril dissolved in tap water (0.5 mg/l) or tap water for 2 or 20 months. At the end of treatment, under anesthesia, RR and PR interval, P wave and QRS duration, QT and corrected QT interval were measured in all animals. On the following day, chronic ECG (lead II) recordings were performed to quantify supraventricular (SVPB) or ventricular premature beats (VPB). After sacrifice, the hearts were removed and weighed. RR interval was similar in young and untreated aged rats, but significantly larger in aged rats treated with captopril. P wave and QRS length did not differ among groups. PR interval was significantly larger in old than in young rats and was not affected by captopril. Corrected QT interval was larger in aged than in young rats (117 +/- 4 vs 64 +/- 6 ms, P<0.05) and was reduced by captopril (71 +/- 6 ms, P<0.05). VPB were absent in young rats and highly frequent in untreated old animals (8.4 +/- 3.0/30 min). Captopril significantly reduced VPB in old rats (0.3 +/- 0.1/30 min, P<0.05). The cardiac hypertrophy found in untreated aged rats was prevented by captopril (3.44 +/- 0.14 vs 3.07 +/- 0.10 mg/g, P<0.05). The beneficial effects of angiotensin converting enzyme inhibition on the rat heart during the aging process are remarkable.

Antihypertensive action of amiodarone in spontaneously hypertensive rats.

The antihypertensive effect of amiodarone was investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The SHR and WKY were treated with amiodarone (1 mg/mL PO) or tap water (control) for 20 weeks. The indirect arterial pressure (AP) was monitored weekly using the tail-cuff method. At the end of the 20th week, the direct AP was measured, and the systolic AP and pulse interval time series were submitted to autoregressive spectral analysis. In addition, cardiac baroreflex sensitivity and left ventricular weight were evaluated as well. The indirect AP was reduced 1 week after the beginning of amiodarone treatment. The direct mean AP and pulse interval were, respectively, 135+/-8 mm Hg and 191+/-3 ms in SHR treated with amiodarone (187+/-8 mm Hg and 156+/-7 ms in control SHR, P<0.05) and 87+/-3 mm Hg and 207+/-8 ms in WKY treated with amiodarone (105+/-8 mm Hg and 174+/-4 ms in control WKY, P<0.05). In SHR treated with amiodarone, the low-frequency oscillations of AP were lower (8.5+/-1.2 mm Hg(2) versus 14.4+/-2.9 mm Hg(2) in control SHR, P<0.05), whereas the reflex bradycardia was higher (0.84+/-0.12 ms/mm Hg versus 0.32+/-0.22 ms/mm Hg in control SHR, P<0.05). The left ventricle weight was also smaller in SHR treated with amiodarone (2.94+/-0.12 mg/g versus 3.45+/-0.24 mg/g in control SHR, P<0.05). In WKY, amiodarone induced similar changes as in SHR, except for a lack of effect in the left ventricle weight. These data indicate that amiodarone has an antihypertensive action in SHR that is associated with a reduction in vasomotor sympathetic modulation, an increase in vagal cardiac baroreflex sensitivity, and a decrease in cardiac hypertrophy.

Sympathetic rhythms and cardiovascular oscillations.

Spectral analysis of heart rate and arterial pressure variabilities is a powerful noninvasive tool, which is increasingly used to infer alterations of cardiovascular autonomic regulation in a variety of physiological and pathophysiological conditions, such as hypertension, myocardial infarction and congestive heart failure. A most important methodological issue to properly interpret the results obtained by the spectral analysis of cardiovascular variability signals is represented by the attribution of neurophysiological correlates to these spectral components. In this regard, recent applications of spectral techniques to the evaluation of the oscillatory properties of sympathetic efferent activity in animals, as well as in humans, offer a new approach to a better understanding of the relationship between cardiovascular oscillations and autonomic regulation.

Power spectra of arterial pressure and heart rate in streptozotocin-induced diabetes in rats.

BACKGROUND: Chronic diabetes is associated with alterations in autonomic modulation of the cardiovascular system. Although the rat has been used extensively in studies of experimental diabetes, there have been no reports on the changes in autonomic modulation of the cardiovascular function in chronic diabetic rats. OBJECTIVE: To examine chronic diabetic rats to determine the autonomic modulation of arterial pressure and heart rate variabilities in the time and frequency domain. MATERIALS AND METHODS: Diabetes was induced in rats by a single injection of streptozotocin, and 30 min of pulsatile arterial pressure was recorded in conscious rats, 5, 10-20 days and 12-18 weeks after the streptozotocin injection. Control rats were injected with vehicle. Beat-by-beat systolic arterial pressure and heart rate were obtained from pulsatile pressure. The spectral density powers of systolic arterial pressure and heart rate were calculated using fast Fourier transformation, and integrated in low-(0.015-0.25 Hz), mid- (0.25-0.75 Hz) and high- (0.75-3.0 Hz) frequency bands. The standard deviations of systolic arterial pressure and heart rate were also calculated. RESULTS: Basal systolic arterial pressure and heart rate were reduced in diabetic animals studied 10-20 days and 12-18 weeks after the streptozotocin injection. The standard deviations of systolic arterial pressure and heart rate were also reduced in the chronically diabetic animals. Diabetes reduced low- and mid-frequency variability but not the high-frequency variability of systolic arterial pressure. The low-frequency variability, but not the mid-frequency variability, of the heart rate was also reduced, while the high-frequency variability of the heart rate was reduced in the more chronically diabetic rats. CONCLUSION: Our findings that the mid-frequency band variability of arterial pressure was reduced in diabetic patients suggest that sympathetic modulation of the cardiovascular system is impaired, corroborating other studies in such patients using this and other approaches.