DOI: 10.1556/2060.2020.00033

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 5 538). 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 paragraphbased 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 5 0.10; 95% CI: -0.04, 0.25, P 5 0.17). We observed no evidence of a significant moderation effect (Q 5 6.16, df 5 17, P 5 0.17, I2 5 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.

Keywords: cognition, memory encoding, memory consolidation, physical activity

DOI: 10.1556/2060.2020.00030

Abstract: Purpose: Acid-base transport in renal proximal tubules (PTs) is mainly sodium-dependent and conducted in coordination by the apical Naþ/Hþ exchanger (NHE3), vacuolar Hþ-adenosine triphosphatase (VATPase), and the basolateral Naþ/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.

Keywords: V-ATPase, insulin, proximal tubules, mTOR, mTORC2

DOI: 10.1556/2060.2020.00036

Abstract: Objective: Parkinson’s disease (PD) is a progressive neurodegenerative disorder. In order to explore a noninvasive treatment of PD, in the current study the authors evaluated the neuroprotective efficacy of caloric vestibular stimulation (CVS) using the rotenone-induced rat model of PD. The rotenone models of PD are gaining attention due to high reproducibility. It is also considered to be an improved model to exhibit the pathogenesis of PD and test the neuroprotective effect of various therapeutic interventions. Materials and methods: Rotenone was i.p. injected (3 mg/kg body weight) to male Wistar albino rats for 21 days to induce PD. As PD is chronic and progressive in nature, the efficacy of chronic CVS intervention was evaluated for 30 days after inducing PD in rats. Motor symptoms were evaluated by assessing locomotor activity in actophotometer, whereas movement analysis was done using Ludolph test and motor coordination was evaluated using rotarod apparatus. The neurochemical and neuropathological changes were also observed in the corpus striatum of rats. Results: Rotenone administration showed decreased locomotor activity, motor coordination and general movement associated with significant (P < 0.05) reduction in dopamine content in the corpus striatum. The immunohistochemical analysis revealed a marked decrease in tyrosine hydroxylase (TH) immunoreactivity in striatal neurons indicating the significant loss of dopaminergic neurons in substantia nigra (SN) following rotenone injection. However, chronic treatment with CVS restored the nerve terminals in the striatum from rotenone damage. CVS treatment improved the dopaminergic system function by restoring dopamine content in the striatum. CVS also improved the motor deformities clearly suggesting the neuroprotective function. Conclusion: The results of the present study suggested CVS to be a safe and simple neuroprotective measure against neurodegenerative changes in PD and a promising noninvasive technique to overcome the motor symptoms associated with it. The findings could be useful for further investigations and clinical applications of CVS in the treatment of PD.

Keywords: parkinson’s disease, rotenone, rotarod, actophotometer, dopamine, tyrosine hydroxylase, caloric vestibular stimulation

DOI: 10.1556/2060.2020.00034

Abstract: Purpose: Progesterone has been reported to inhibit the proliferation of breast cancer and osteosarcoma cells; however, its inhibitory mechanism has not yet been clarified. The aim of the present study was to clarify the effects of progesterone on apoptosis in breast cancer (MCF-7) and human osteosarcoma (MG-63) cells. Materials and methods: In this experimental study the cytotoxic effect of progesterone was measured in MCF-7 and MG-63 cells exposed to different concentrations of progesterone using MTT assay, and effective concentrations were identified. The expression levels of the Bax, P53 and Bcl-2 genes were evaluated by real-time PCR, and caspase-3, 8 and 9 activity levels were determined using a colorimetric method. Hoechst staining and flow cytometry were used to confirm apoptosis. The data were statistically analyzed using one-way analysis of variance (ANOVA) and independent- samples t-test. Results: Compared to the control group, we observed a significant increase in the expression levels of the Bax and P53 genes and the activity levels of caspase-3 and 9, and a significant decrease in the expression level of the Bcl-2 gene in MCF-7 and MG-63 treated with effective concentration of progesterone. The caspase-8 activity level did not change significantly in treated MG-63 but increased in treated MCF-7 cells. Hoechst staining and flow cytometry results confirmed apoptosis in the cells exposed to effective concentration of progesterone. Conclusions: The cytotoxic effect of progesterone on breast cancer and osteosarcoma cells was mediated by apoptotic pathways. In this context, progesterone triggers the extrinsic and intrinsic apoptotic pathways in MCF-7 cells and induces the intrinsic apoptotic pathway in MG-63 cells.

Keywords: apoptosis, progesterone, MCF-7, MG-63, caspase

DOI: 10.1556/2060.2020.00035

Abstract: In recent years, free fatty acid binding proteins (FABPs) are implicated in spermatogenesis and sperm morphology. FABPs are members of the intracellular lipid-binding protein family; they exhibit tissue specific expression like the FABP9/PERF15 (Perforated15) male germ cell-specific fatty acid linkage-protein. The aim of the study was to assess the levels of seminal FABP-9 in normozoospermic and oligozoospermic men, and the possible relations between seminal FABP-9 levels and semen parameters. Research was carried out on 60 male volunteers who were admitted to Selcuk University Faculty of Medicine of Andrology Laboratory. Normozoospermic individuals (n 5 30) were identified as Group 1, and Oligozoospermic individuals (n 5 30) were identified as Group 2. The semen samples were collected in sterile plastic containers. Sperm parameters were assessed according to Kruger’s criteria. Seminal plasma FABP-9 levels were analyzed by ELISA method. Outcomes were statistically evaluated at 0.05 significance level with SPSS (22.0). The Receiver Operating Characteristic (ROC) curve was used to evaluate the performance of FABP-9 levels as compared to that of the concentration and motility data of the sperm. FABP-9 levels were significantly higher in normozoospermic individuals (3.41 ± 1.64 ng/mL) than in oligozoospermic individuals (1.99 ± 0.78 ng/mL). There were significant correlations between FABP-9 levels and sperm concentration, total sperm count, motility, progressive motility, immobility, Total Progressive Motil Sperm Count (TPMSC), head anomaly, and teratozoospermia index. We suggest that FABP-9 level is an important biomarker, and low levels of semen FABP-9 may impact the fertility status based on the ROC findings.

Keywords: infertile male, semen, fatty acid binding protein-9, spermyogram, fertility

DOI: 10.1556/2060.2020.00031

Abstract: Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42-87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject’s hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ΔE calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE-VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

Keywords: altitude acclimatization, hypobaric hypoxia, incremental exercise, mechanical efficiency, normobaric hypoxia, work of breathing

DOI: 10.1556/2060.2020.00032

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.

Keywords: senior athletes, running economy, “exceptionally successful aging” metabolic cost