The purpose of this study was to examine blood pressure (BP), heart rate (HR), and cardiac vagal reactivation (VR) after an aerobic training session (ATS), a strength training session (STS), and a combined aerobic and strength training session (ASTS) in normotensive men. Eleven healthy men (age 26.8 ± 2.9 years, body mass index 24.3 ± 1.6 kg·m) with at least 6 months of strength and aerobic training experience performed an STS, an ATS, and an ASTS in a counterbalanced crossover design. Blood pressure and HR were measured at rest and at 15-minute intervals post-training for 1 hour. Vagal reactivation was measured during the first minute immediately post-exercise. After STS and ASTS, systolic BP (SBP) and mean arterial BP (MAP) remained significantly lower than at rest at all time intervals (p < 0.05). After ATS, SBP was significantly lower than at rest at 30 minutes and beyond (p < 0.01); however, no significant differences were observed for MAP. Post-training HR remained high after STS and ASTS at all intervals (p < 0.01). However, after ATS, the HR remained high only at the 15-minute post-exercise interval (p < 0.01). Vagal reactivation was significantly less pronounced after the first 30 seconds post-exercise (p < 0.01) in ASTS (531.3 ± 329.6 seconds) than in ATS (220.7 ± 88.5 seconds) and in STS (317.6 ± 158.5 seconds). The delta of the HR decrease at 60 seconds post-exercise was greater (p < 0.00) in ATS (33.4 ± 12.7 b·min) than in STS (14.1 ± 7.2 b·min) and in ASTS (11.4 ± 7.1 b·min). In conclusion, post-exercise BP reduction was independent of the type of exercise; however, HR remained significantly greater after combination of strength and aerobic exercise, implying a reduction in cardiac VR after this type of training. Therefore, strength and conditioning professionals may prescribe aerobic, strength, or a combination of aerobic and strength exercise to assist individuals concerned with BP control, thus allowing for variety in training while similarly impacting post-exercise SBP regardless of desired exercise modality.
We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger (P < 0.05) in trained vs. untrained animals: R-R interval (365 +/- 49 vs. 286 +/- 60 ms), WCL (177 +/- 20 vs. 146 +/- 32 ms), and functional refractory period of the left ventricle (172 +/- 27 vs. 141 +/- 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.
Caffeine can affect muscle cell physiology and the inflammatory response during exercise. The purpose of this study was to analyse muscle damage markers and inflammatory cell infiltration into the soleus muscle of sedentary and exercised animals submitted to chronic caffeine intake. Thirty-two male Wistar rats were divided into the following four groups (n = 8 per group): sedentary control (SCO); sedentary + caffeine (SCAF); trained control (TCO); and trained + caffeine (TCAF). The animals were housed in individual cages and received tap water or caffeine (1 mg ml −1 ); they were maintained at rest or submitted to swimming for up to 40 min day −1 with a 4% load, five times per week for 30 days. Blood samples were collected for analysis of serum lactate, creatine kinase and calcium. The right soleus muscle and the epididymal fat depot were weighed, and the muscle was submitted to histological analysis. Training and caffeine did not change body or muscle weight, food and liquid intake or serum calcium levels among groups. Decreased fat tissue (P < 0.05) was observed in the SCAF (4.05 ± 1.03 g), TCO (4.14 ± 0.78 g) and TCAF groups (4.02 ± 1.02 g) compared with the SCO group (5.31 ± 1.06 g). Serum creatine kinase activity was significantly reduced in the SCAF (787.3 ± 230.3 U l −1 ), TCO (775.3 ± 232.3 U l −1 ) and TCAF groups (379.5 ± 110.5 U l −1 ) compared with the SCO group (1610.2 ± 276.5 U l −1 ). Few damaged muscle fibres (P < 0.05) were found in SCAF (16.7 ± 12.8%) and TCAF groups (17.3 ± 11.7%) compared with the SCO group (53.6 ± 13.9%). The SCAF group presented fewer fields with inflammatory cells (7.6 ± 8.7 fields) compared with the SCO group (123 ± 146 fields). The results suggest that the chronic intake of caffeine, as well as chronic low-intensity exercise, decreased muscle damage and inflammatory infiltration into skeletal muscle.
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