To evaluate whether captopril (3×50 mg/day) potentiates post-resistance exercise hypotension (PREH) in hypertensives (HT), 12 HT men received captopril and placebo for 4 weeks each in a double-blinded, randomized-crossover design. On each therapy, subjects underwent 2 sessions: Control (C - rest) and Resistance Exercise (RE - 7 exercises, 3 sets to moderate fatigue, 50% of 1 RM -repetition maximum). Measurements were taken before and after 30-60 min (Post1) and 7 h (Post2), and ambulatory blood pressure (BP) was monitored for 24 h. There were no differences in PREH characteristics and mechanisms between the placebo and captopril periods. At Post1, systolic/diastolic BP decreased significantly and similarly after RE with both therapies (Placebo=-13±2/-9±1 mmHg vs. Captopril=-12±2/-10±1 mmHg, P<0.05). RE reduced cardiac output in some subjects and systemic vascular resistance in others. Heart rate and cardiac sympathetic modulation increased, while stroke volume and baroreflex sensitivity decreased after RE (Placebo: +13±2 bpm, +21±5 nu, -11±5 ml, -4±2 ms/mmHg; Captopril: +13±2 bpm, +35±4 nu, 17±5 ml, -3±1 ms/mmHg, P<0.05). At Post2, all variables returned to pre-intervention values. Ambulatory BP was similar between the sessions. Thus, captopril did not potentiate the magnitude and duration of PREH in HT men, and it did not influence PREH mechanisms.
This study tested the hypotheses that activation of central command and muscle mechanoreflex during post-exercise recovery delays fast-phase heart rate recovery with little influence on the slow phase. Twenty-five healthy men underwent three submaximal cycling bouts, each followed by a different 5-min recovery protocol: active (cycling generated by the own subject), passive (cycling generated by external force) and inactive (no-cycling). Heart rate recovery was assessed by the heart rate decay from peak exercise to 30 s and 60 s of recovery (HRR30s, HRR60s fast phase) and from 60 s-to-300 s of recovery (HRR60−300s slow phase). The effect of central command was examined by comparing active and passive recoveries (with and without central command activation) and the effect of mechanoreflex was assessed by comparing passive and inactive recoveries (with and without mechanoreflex activation). Heart rate recovery was similar between active and passive recoveries, regardless of the phase. Heart rate recovery was slower in the passive than inactive recovery in the fast phase (HRR60s=20±8vs.27 ±10 bpm, p<0.01), but not in the slow phase (HRR60−300s=13±8vs.10±8 bpm, p=0.11). In conclusion, activation of mechanoreflex, but not central command, during recovery delays fast-phase heart rate recovery. These results elucidate important neural mechanisms behind heart rate recovery regulation.
The purpose of this study is investigate the role of microRNA‐126 on cardiac angiogenesis induced by swimming training. Two groups of adult female Wistar rats (n=7/group) received either a sedentary (control), endurance training protocol 1 (T1), or training protocol 2 (T2). GroupT1: TF 60min/day swimming, 5x/week/10week with 5% overload, GroupT2: T1 to same protocol without the 8th week, 9th week trained 2x/day, 10th trained 3x/day. After the training period, hearts were harvested and total RNA isolated. MicroRNA‐126 gene expression analysis was performed by real‐time PCR. We assessed: markers of training, the cardiac capillary/fiber ratio, protein expression of VEGF, Spred‐1, Raf‐1/ERK1/2, PI3K/Akt/eNOS. The cardiac capillary/fiber ratio increased in Trained Groups. VEGF protein expression was increased 42% in T1 and 108 % in T2. Cardiac miRNA‐126 expression increased 26% (T1) and 42% (T2) compared with S. Spred‐1 protein level decreased 41% (T1) and 39% (T2), which consequently increase in angiogenic signaling pathway Raf‐1/ERK1/2. The gene expression of PI3KR2 was reduced 39% (T1) and 78% (T2), which consequently increase in angiogenic signaling pathway PI3K/Akt/eNOS. This study showed the involvement of miRNA‐126 in the regulation of exercise‐induced cardiac angiogenesis, by regulation of its targets that converged in an increase in the VEGF signaling and hence in angiogenic pathways.
Experimental groups (n=56): Control (C), Anabolic Steroid (AS), AS+Losartan (AS+L), AS+Spironolactone (AS+S), Trained (T), Trained AS (TAS), Trained AS+Losartan (TAS+L) and Trained AS+Spironolactone (TAS+S). The AS was administered twice a week (10mg/kg/wk). The swimming training (ST) was performed for 10 weeks (5x/wk). The Losartan and Spironolactone were administered in drink water. AS induced cardiac hypertrophy (CH) in AS group compared to C group and it was increased in TAS group. AS treatment increased collagen volumetric fraction and collagen type III expression. The Losartan treatment inhibited the CH, but not Spironolactone. However, both treatments prevented cardiac collagen formation. AS groups increased the angiotensin converting enzyme (ACE) activity, AT1 and AT2 receptors expression. Treatment with Losartan or Spironolactone prevented the increase in ACE activity, but not AT1 and AT2 receptors expression. CYP11B2 expression was increased in TAS group and 11 βHSD2, TGFβ and osteopontin expression were increased in AS and TAS group. Both antagonists inhibited the AS effects and its association with ST. The results show the important participation of RAAS on CH induced by the association of AS and ST. For the first time we are showing the aldosterone (aldosterone synthase and 11β‐HSD2 expression) participation in these association.
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