Exercise reduces LV contractile deterioration in post-infarction heart failure and alleviates the extent of mitochondrial dysfunction, which is paralleled with preserved complex I activity.

In several conditions associated with adrenergic stimulation, an increase in peripheral count of larger platelets has been observed, but the mechanism remained elusive. Larger platelets have greater prothrombotic potential and increase the risk of acute thrombotic events. The human spleen retains one-third of total body platelets, with mean volume (MPV) about 20% greater than that of circulating platelets. We aimed to answer whether low-dose epinephrine infusion results in spleen contraction and MPV increase. We undertook the continuous ultrasonic measurements of spleen volume, hepatic and central circulation with concurrent blood sampling in response to intravenous infusion of epinephrine (6 min of 0·06 µg kg(-1) per min, followed by 3 min of 0·12 µg kg(-1) per min) in nine healthy young subjects. The spleen volume started to decrease immediately after the onset of infusion, in the presence of substantial decreases in peripheral resistance and mean blood pressure and increases in heart rate and cardiac output. The majority of spleen emptying, approximately 25%, (95% CI 71·3-299·7) was observed 1 min after infusion onset, the hepatic vein flow peaked at the end of infusion for 28·4% (95% CI 1074·6-407·9), while increases in platelet count for approximately 31% (95% CI 187·8-314·8) and MPV for 4·4% (95% CI 7·3-10·9) lagged until 1 min after infusion cessation. We suggest that spleen is a dynamic reservoir of large platelets, which are mobilized even by low-dose epinephrine infusion in conditions of decreased blood pressure.

Limited information exists concerning arterial blood pressure (BP) changes in underwater breath-hold diving. Simulated chamber dives to 50 m of freshwater (mfw) reported very high levels of invasive BP in two divers during static apnea (SA), whereas a recent study using a noninvasive subaquatic sphygmomanometer reported unchanged or mildly increased values at 10 m SA dive. In this study we investigated underwater BP changes during not only SA but, for the first time, dynamic apnea (DA) and shortened (SHT) DA in 16 trained breath-hold divers. Measurements included BP (subaquatic sphygmomanometer), ECG, and pulse oxymetry (arterial oxygen saturation, SpO₂, and heart rate). BP was measured during dry conditions, at surface fully immersed (SA), and at 2 mfw (DA and SHT DA), whereas ECG and pulse oxymetry were measured continuously. We have found significantly higher mean arterial pressure (MAP) values in SA (∼40%) vs. SHT DA (∼30%). Postapneic recovery of BP was slightly slower after SHT DA. Significantly higher BP gain (mmHg/duration of apnea in s) was found in SHT DA vs. SA. Furthermore, DA attempts resulted in faster desaturation vs. SA. In conclusion, we have found moderate increases in BP during SA, DA, and SHT DA. These cardiovascular changes during immersed SA and DA are in agreement with those reported for dry SA and DA.

No abstract

Marked bradycardia occurs at the end of breath‐hold dives. However, vagal modulation of heart rate (HR) during maximal static (SA) and dynamic (DA) underwater apneas is not well‐known. HR, HR variability (SD1) and arterial oxygen saturation (SpO2) were analyzed at the immersed baseline and at initial‐, mid‐ and end‐apnea (each 30 s) of maximal underwater SA and DA in nine breath‐hold divers. DA lasted 78±8 s and SA 225±20 s (mean±SEM) and resulted in similar decreases in SpO2 (78±3 and 75±3 %, p=0.352, respectively). Initially, DA increased HR from 80±5 to 122±5 bpm (p<0.001), followed by decrease in HR at mid‐apnea and end‐apnea (101±6 and 80±8 bpm). During SA, HR decreased at mid‐apnea (from 78±4 to 66±3 bpm, p=0.004) but did not decrease further at end‐apnea phase. SD1 decreased at the initial phase of DA (from 28±5 to 10±4 ms, p=0.005) being lower compared with SA (24±4 ms, p=0.005). At the end of DA and SA, SD1 tended to increase above the baseline (67±16 and 66±10 ms, p=0.088 and p=0.093, respectively) and did not differ from each other (p=0.804). We concluded that apnea blunts the effects of exercise on HR variability at the end of DA when despite the higher HR. This indicates complex interplay between vagal and sympathetic responses to apnea and exercise. Supported by TEKES, Finland, Paavo Nurmi Foundation, Finland and Croatian Ministry of Science.