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Authors: M. Michalis, K.J. Finn, R. Podstawski, S. Gabnai, Á. Koller, A. Cziráki, M. Szántó, Z. Alföldi and F. Ihász

Abstract

Within recent years the popularity of sportive activities amongst older people, particularly competitive activities within certain age groups has increased. The purpose of this study was to assess the differences in the cardiorespiratory output at anaerobic threshold and at maximal power, output during an incremental exercise, among senior and young athletes. Ten elderly male subjects [mean (SD) age: 68.45 ± 9.32 years] and eight young male subjects [mean (SD) age: 25.87 ± 5.87 years] performed an incremental exercise test on a treadmill ergometer. No significant differences in body size were evident; however, the differences between the groups for peak power (451.62 ± 49 vs. 172.4 ± 32.2 W), aerobic capacity (57.97 ± 7.5 vs. 40.36 ± 8.6 mL kg−1 min−1), maximal heart rate (190.87 ± 9.2 vs. 158.5 ± 9.1 beats min−1), peak blood lactate (11 ± 1.7 vs. 7.3 ± 1.4 mmol L−1), and % VO2max at ventilatory thresholds (93.18 ± 4.3 vs. 79.29 ± 9.9%) were significantly lower in the senior athletes. The power output at anaerobic threshold was also higher (392 ± 48 vs. 151 ± 23 W) in the young athletes, explaining the significant difference in terms of performance between these groups. We have observed an evident deterioration in some of the cardiovascular parameters; however, the submaximal exercise economy seems to be preserved with aging. Exercise economy (i.e. metabolic cost of sustained submaximal exercise) was not different considerably with age in endurance-trained adults.

Open access

Abstract

Objective

Prior research has evaluated the effects of acute exercise on episodic memory function. These studies have, on occasion, demonstrated that acute exercise may enhance both short- and long-term memory. It is uncertain as to whether the acute exercise improvements in long-term memory are a result of acute exercise attenuating declines in long-term memory, or rather, are driven by the enhancement effects of acute exercise on short-term memory. The present empirical study evaluates whether the decline from short- to long-term is influenced by acute exercise. This relationship is plausible as exercise has been shown to activate neurophysiological pathways (e.g., RAC1) that are involved in the mechanisms of forgetting.

Methods

To evaluate the effects of acute exercise on forgetting, we used data from 12 of our laboratory's prior experiments (N = 538). Across these 12 experiments, acute exercise ranged from 10 to 15 mins in duration (moderate-to-vigorous intensity). Episodic memory was assessed from word-list or paragraph-based assessments. Short-term memory was assessed immediately after encoding, with long-term memory assessed approximately 20-min later. Forgetting was calculated as the difference in short- and long-term memory performance.

Results

Acute exercise (vs. seated control) was not associated with an attenuated forgetting effect (d = 0.10; 95% CI: −0.04, 0.25, P = 0.17). We observed no evidence of a significant moderation effect (Q = 6.16, df = 17, P = 0.17, I 2 = 0.00) for any of the evaluated parameters, including study design, exercise intensity and delay period.

Conclusion

Across our 12 experimental studies, acute exercise was not associated with an attenuated forgetting effect. We discuss these implications for future research that evaluates the effects of acute exercise on long-term memory function.

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Abstract

Background and aims

Compulsive sexual behavior disorder (CSBD) has been a long debated issue. While formerly the discussion was about whether to regard CSBD as a distinctive disorder, the current debate is dealing with the classification of this phenomenon. One of the prominent voices in this field considers CSBD as a behavioral addiction and proposes CSBD to be called and diagnosed as sexual addiction (SA). This present debate paper will review the existing evidence supporting this view and it will argue against it.

Results

We have found that a great deal of the current literature is anecdotal while empirical evidence is insufficient. First, the reports about the prevalence of CSBD are contradictory. Additionally, the field mainly suffers from inconsistent defining criteria of CSBD and a consensus which symptoms should be included. As a result, the empirical evidence that does exist is mostly about some symptoms individually and not on the disorder as a whole construct.

Conclusions

We conclude that currently, there is not enough data supporting CSBD as a behavioral addiction. Further research has to be done, examining CSBD phenomenology as a whole construct and based on a homogeneous criterion.

Open access
Authors: M. Nakamura, N. Satoh, H. Tsukada, T. Mizuno, W. Fujii, A. Suzuki, S. Horita, M. Nangaku and M. Suzuki

Abstract

Purpose

Acid-base transport in renal proximal tubules (PTs) is mainly sodium-dependent and conducted in coordination by the apical Na+/H+ exchanger (NHE3), vacuolar H+-adenosine triphosphatase (V-ATPase), and the basolateral Na+/HCO3 - cotransporter. V-ATPase on PTs is well-known to play an important role in proton excretion. Recently we reported a stimulatory effect of insulin on these transporters. However, it is unclear whether insulin is involved in acid-base balance in PTs. Thus, we assessed the role of insulin in acid-base balance in PTs.

Methods

V-ATPase activity was evaluated using freshly isolated PTs obtained from mice, and specific inhibitors were then used to assess the signaling pathways involved in the observed effects.

Results

V-ATPase activity in PTs was markedly enhanced by insulin, and its activation was completely inhibited by bafilomycin (a V-ATPase-specific inhibitor), Akt inhibitor VIII, and PP242 (an mTORC1/2 inhibitor), but not by rapamycin (an mTORC1 inhibitor). V-ATPase activity was stimulated by 1 nm insulin by approximately 20% above baseline, which was completely suppressed by Akt1/2 inhibitor VIII. PP242 completely suppressed the insulin-mediated V-ATPase stimulation in mouse PTs, whereas rapamycin failed to influence the effect of insulin. Insulin-induced Akt phosphorylation in the mouse renal cortex was completely suppressed by Akt1/2 inhibitor VIII and PP242, but not by rapamycin.

Conclusion

Our results indicate that stimulation of V-ATPase activity by insulin in PTs is mediated via the Akt2/mTORC2 pathway. These results reveal the mechanism underlying the complex signaling in PT acid-base balance, providing treatment targets for renal disease.

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Beköszöntő

111 éves az Üllői úti Semmelweis Egyetem I. sz. Sebészeti Klinikájának épülete

Author: Attila Szijártó
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Authors: János Horányi, Rezső Szlávik, Krisztina Fekete and Attila Szijártó
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