Regularly swimming exercise modifies opioidergic neuromodulation in rostral ventrolateral medulla in hypertensive rats.

Moderate exercise reduces arterial pressure (AP) and heart rate (HR) in spontaneously hypertensive rats (SHR) and changes neurotransmission in medullary areas involved in cardiovascular regulation. We investigated if regularly swimming exercise (SW) affects the cardiovascular adjustments mediated by opioidergic neuromodulation in the RVLM in SHR and Wistar-Kyoto (WKY) rats. Rats were submitted to 6 wks of SW. The day after the last exercise bout, α-chloralose-anesthetized rats underwent a cannulation of the femoral artery for AP and HR recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Bilateral injection of endomorphin-2 (EM-2, 0.4 mmol/L, 60 nL) into the RVLM increased MAP in SW-SHR (20 ± 4 mmHg, N = 6), which was lower than in sedentary (SED)-SHR (35 ± 4 mmHg, N = 6). The increase in MAP in SW-SHR induced by EM-2 into the RVLM was similar in SED- and SW-WKY. Naloxone (0.5 mmol/L, 60 nL) injected into the RVLM evoked an enhanced hypotension in SW-SHR (-66 ± 8 mmHg, N = 6) compared to SED-SHR (-25 ± 3 mmHg, N = 6), which was similar in SED- and SW-WKY. No significant changes were observed in HR after EM-2 or naloxone injections into the RVLM. Changes in hindquarter and mesenteric conductances evoked by EM-2 or naloxone injections into the RVLM in SW- or SED-SHR were not different. Mu Opioid Receptor expression by Western blotting was reduced in SW-SHR than in SED-SHR and SW-WKY. Therefore, regularly SW alters the opioidergic neuromodulation in the RVLM in SHR and modifies the mu opioid receptor expression in this medullary area.

Acute effects of different static stretching exercises orders on cardiovascular and autonomic responses.

The present study examined the acute effects of static stretching (SS) exercise order on cardiac responses. Seventeen individuals were submitted to two experimental SS session: Order "A" (larger to small muscles groups) and Order "B" (small to larger muscles groups). Heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP), rate-pressure product (RPP) oxygen saturation (SpO2), and heart rate variability (HRV) were measured at rest, midpoint of the session, immediately after the session, and in 5, 10, and 20 minutes after. SS increased HR and RPP in both orders, while reducing the rMSSD index and SpO2. In the order "A", the SBP and DBP increased at the midpoint of the session. In the order "B", the SBP and DBP increased only immediately after the end of the session. DBP and RPP significantly higher in order "A" compared to order "B" in the midpoint of the session. It was also demonstrated higher values of DBP and minor mean R-R intervals in order "B" at 10 min-post session. SS increased cardiac overload in both performed orders. The overload generated by the SS of the larger muscles groups was greater when compared to the smaller muscles groups, suggesting that the exercise order interferes in cardiac overload.

Does the combination of resistance training and stretching increase cardiac overload?

OBJECTIVES: To compare the effects of combinations of resistance training (RT) and static stretching (SS) on heart rate (HR), systolic pressure (SBP), diastolic pressure (DBP), rate pressure product (RPP), oxygen saturation (SpO2), rating of perceived effort (RPE), and heart rate variability (HRV) in men. METHODS: Twelve normotensive healthy men participated in four protocols: a) SS+RT, b) RT+SS, c) RT, and d) SS. Variables were measured before, immediately after, and 15, 30, and 45 min after the sessions. RESULTS: The combination of SS and RT increased (p<0.001) HR when compared to the effects of the noncombined protocols (from 2.38 to 11.02%), and this result indicated metabolic compensation. Regarding DBP, there were differences (p<0.001) between the RT and SS groups (53.93±8.59 vs. 67.00±7.01 mmHg). SS has been shown to be able to reduce (p<0.001) SpO2 (4.67%) due to the occlusion caused by a reduction in the caliber of the blood vessels during SS compared to during rest. The increase in RPP (6.88% between RT and SS+RT) along with the HR results indicated higher metabolic stress than that reflected by the RPE (combined protocols increased RPE from 21.63 to 43.25%). The HRV analysis confirmed these results, showing increases (p<0.01) in the LF index between the combined and noncombined protocols. Compared to the effect of RT, the combination of SS and RT promoted a vagal suppression root mean square of the successive differences (RMSSD) index (from 9.51 to 21.52%) between the RT and SS+RT groups (p<0.01) and between the RT and RT+SS groups (p<0.001). CONCLUSION: Static stretching increases cardiac overload and RPE, reducing oxygen supply, especially when performed in combination with RT.

Does the combination of resistance training and stretching increase cardiac overload?

OBJECTIVES: To compare the effects of combinations of resistance training (RT) and static stretching (SS) on heart rate (HR), systolic pressure (SBP), diastolic pressure (DBP), rate pressure product (RPP), oxygen saturation (SpO2), rating of perceived effort (RPE), and heart rate variability (HRV) in men. METHODS: Twelve normotensive healthy men participated in four protocols: a) SS+RT, b) RT+SS, c) RT, and d) SS. Variables were measured before, immediately after, and 15, 30, and 45 min after the sessions. RESULTS: The combination of SS and RT increased (p<0.001) HR when compared to the effects of the noncombined protocols (from 2.38 to 11.02%), and this result indicated metabolic compensation. Regarding DBP, there were differences (p<0.001) between the RT and SS groups (53.93±8.59 vs. 67.00±7.01 mmHg). SS has been shown to be able to reduce (p<0.001) SpO2 (4.67%) due to the occlusion caused by a reduction in the caliber of the blood vessels during SS compared to during rest. The increase in RPP (6.88% between RT and SS+RT) along with the HR results indicated higher metabolic stress than that reflected by the RPE (combined protocols increased RPE from 21.63 to 43.25%). The HRV analysis confirmed these results, showing increases (p<0.01) in the LF index between the combined and noncombined protocols. Compared to the effect of RT, the combination of SS and RT promoted a vagal suppression root mean square of the successive differences (RMSSD) index (from 9.51 to 21.52%) between the RT and SS+RT groups (p<0.01) and between the RT and RT+SS groups (p<0.001). CONCLUSION: Static stretching increases cardiac overload and RPE, reducing oxygen supply, especially when performed in combination with RT.

Cholinergic activation of neurons in the medulla oblongata changes urinary bladder activity by plasma vasopressin release in female rats.

The central control of the micturition is dependent on cortical areas and other ascending and descending pathways in the brain stem. The descendent pathways from the pons to the urinary bladder (UB) can be direct or indirect through medullary neurons (MN). Chemical stimulation with l-glutamate of MN known for their involvement in cardiovascular regulation evokes changes in pelvic nerves activities, which innervate the urinary bladder. Different neurotransmitters have been found in medullary areas; nevertheless, their involvement in UB control is few understood. We focused to investigate if cholinergic activation of neurons in the medulla oblongata changes the urinary bladder activity. Carbachol (cholinergic agonist) or atropine (cholinergic antagonist) was injected into the 4thV in anesthetized female Wistar rats and the intravesical pressure (IP), mean arterial pressure (MAP), heart rate (HR) and renal conductance (RC) were recorded for 30 min. Carbachol injection into the 4thV increased IP with peak response at 30 min after carbachol and yielded no changes in MAP, HR and RC. Atropine injection into the 4thV decreased IP and elicited no changes in MAP, HR and RC. Plasma vasopressin levels evaluated by ELISA kit assay increased after carbachol into the 4th V. Intravenous blockade of V1 receptors prior to carbachol into the 4thV abolished the increase in IP evoked by carbachol. Therefore, our findings suggest that cholinergic activation of neurons in the medulla oblongata by carbachol injections into the 4thV increases IP due to plasma vasopressin release, which acts in V1 receptors in the UB.

Participation of α2 -adrenoceptors in sodium appetite inhibition during sickness behaviour following administration of lipopolysaccharide.

Sickness behaviour, a syndrome characterized by a general reduction in animal activity, is part of the active-phase response to fight infection. Lipopolysaccharide (LPS), an effective endotoxin to model sickness behaviour, reduces thirst and sodium excretion, and increases neurohypophysial secretion. Here we review the effects of LPS on thirst and sodium appetite. Altered renal function and hydromineral fluid intake in response to LPS occur in the context of behavioural reorganization, which manifests itself as part of the syndrome. Recent data show that, in addition to its classical effect on thirst, non-septic doses of LPS injected intraperitoneally produce a preferential inhibition of intracellular thirst versus extracellular thirst. Moreover, LPS also reduced hypertonic NaCl intake in sodium-depleted rats that entered a sodium appetite test. Antagonism of α2 -adrenoceptors abolished the effect of LPS on sodium appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and α2 -adrenoceptors to control sodium appetite and sickness behaviour.

Lipopolysaccharide reduces sodium intake and sodium excretion in dehydrated rats.

The objective of this study was to find out if lipopolysaccharide (LPS) administered intraperitoneally affects sodium and water intake and renal excretion in dehydrated rats. LPS (0.3-5 mg/kg b.w.) inhibited 0.3M NaCl intake induced by subcutaneous injection of the diuretic furosemide (FURO, 10 mg/kg b.w.) combined with the angiotensin converting enzyme inhibitor, captopril (CAP, 5 mg/kg b.w.). Only the highest doses of LPS (2.5 and 5 mg/kg) inhibited water intake induced by FURO/CAP. LPS (0.6 mg/kg) reduced urinary volume and sodium excretion, but had no effect on mean arterial pressure or heart rate of rats treated with FURO/CAP. LPS (0.3-5.0 mg/kg) abolished intracellular thirst and reduced by 50% the urine sodium concentration of rats that received 2 ml of 2M NaCl by gavage. LPS (0.3-5.0 mg/kg) also reduced thirst in rats treated with FURO alone (10 mg/rat sc). The results suggest that LPS has a preferential, but not exclusive, inhibitory effect on sodium intake and on intracellular thirst. The inhibition of hydro-mineral intake and the antinatriuresis caused by LPS in dehydrated rats may contribute to the multiple effects of the endotoxin on fluid and electrolyte balance and be part of the strategy to cope with infections.