scholarly journals PO-076 High and moderate intensity strength exercises to exhaustion activate different signaling cascades regulating protein metabolism in trained skeletal muscle

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Evgeny Lysenko ◽  
Daniil Popov ◽  
Tatiana Vepkhvadze ◽  
Olga Vinogradova

Objective The aim of the study was to evaluate the activation of signaling cascades regulating protein synthesis and degradation after strength exercise sessions of high and moderate intensity in the muscles of athletes adapted to strength training. Methods Eight strength-trained men were recruited for the experiment. The volunteers performed 4 sets of leg press to volitional fatigue with moderate intensity (65% 1RM) for one leg and 4 sets of leg press to volitional fatigue with high intensity (85% of 1RM) for contralateral leg. The sets for both legs were performed in turn with rest intervals of 2 min. Biopsy from m. vastus lateralis was performed before, 1, 5 and 10 hours after cessation of exercise. Content of signaling proteins was evaluated using Western blot. Results Total work performed by the leg during moderate intensity strength exercise was 32% (P˂0,001) higher in comparison with contralateral leg performing high intensity exercise. The phosphorylation levels of p70S6kThr389 and 4E-BP1Thr37 / 46 increased only after the exercise of moderate intensity (P˂0.05). On the contrary, the phosphorylation level of ERK1 / 2Thr202 / Tyr204 increased only after the exercise of high intensity (P˂0.05). The level of phosphorylation of eEF2Thr56 significantly decreased after 1 (P˂0.001), 5 (P˂0.01) and 10 (P˂0.01) hours after the exercise of high intensity. The phosphorylation level of ACCSer79, an AMPK activation marker, was significantly increased 1 hour after the exercise of moderate intensity (P˂0.01). The phosphorylation level of FOXO1Ser256 significantly decreased after the exercises of both intensities (5 hours after the exercise of moderate intensity, P˂0.001; 1 hour after the exercise of high intensity, P˂0.05). Conclusions Strength exercises of high and moderate intensity, performed to volitional fatigue, may cause activation of different signaling cascades. Herewith, activation of mTORC1 after strength exercise is more dependent on the total work, whereas the ERK1 / 2 and eEF2 activation on the exercise intensity. The work was supported by RFBR grant №17-04-00878.

2020 ◽  
Vol 15 (8) ◽  
pp. 1181-1188
Author(s):  
Evgeny B. Myakinchenko ◽  
Andrey S. Kriuchkov ◽  
Nikita V. Adodin ◽  
Victor Feofilaktov

Purpose: To compare the training-volume (TrV) distribution of Russian international-level male biathletes, female biathletes, and cross-country skiers (XC) during an annual cycle. Methods: Day-to-day TrVs were recorded and averaged for a 5-year period for male biathletes (n = 6), female biathletes (n = 8), and XC (n = 14) with VO2max values of 77.7 (3.8), 64.6 (1.9), and 79.4 (3.5) mL·min−1·kg−1, respectively. Results: The volumes of low- and moderate-intensity endurance training and all types of nonspecific endurance and strength training gradually decreased toward the competition period. However, the volumes and proportions of high-intensity endurance training and specific exercises (roller skiing, skiing, and shooting during high-intensity endurance training) increased by the time of the competition period. The total volume of training, volumes of low- and moderate-intensity endurance training, moderate- and high-load strength training (70%–95% 1RM), and power/speed loads did not increase gradually but reached their maximum immediately after a short stage of initial training. All teams employed the “pyramid” model of intensity distribution. Compared with the biathletes, XC demonstrated a larger (P < .01) annual volume of endurance training (~190 h), low-intensity endurance training (~183 h), and strength training (~818 sets). They also engaged in more upper-body and core-strength exercises (~769 sets), and they reached their maximum aerobic TrVs in June, while the biathletes reached theirs in July. Conclusions: In recent decades, the traditional model of periodization has been altered. The Russian XC and biathletes had significant differences in TrVs.


2018 ◽  
Vol 40 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Marta Gormicho Boavida Marques Esgalhado ◽  
Milena Barcza Stockler-Pinto ◽  
Ludmila Ferreira Medeiros de França Cardozo ◽  
Jorge Eduardo Barboza ◽  
Denise Mafra

ABSTRACT Background: Irisin is a recently identified exercise-induced hormone that stimulates the "browning" of the white adipose tissue, at least in mice. In chronic kidney disease (CKD) patients, irisin regulation is not fully understood, and little attention has been given to the effects of exercise on irisin levels in these patients. The purpose of this study was to assess the effects of high intensity exercise on irisin plasma levels in CKD patients under hemodialysis (HD). Methods: Fifteen HD patients (5 men, 44.4 ± 15.1 years old) were studied and served as their own controls. High intensity (single session) intradialytic strength exercises consisted of three sets of ten repetitions with four different movements in both lower limbs during 30 minutes. Blood samples were collected on different days (exercise and non-exercise day) at exactly the same time (30 and 60 minutes after the start of dialysis session). Plasma irisin levels were measured by ELISA assay and anthropometric and biochemical parameters were evaluated. Results: Irisin plasma levels were significantly reduced in both exercise day (125.0 ± 18.5 to 117.4 ± 15.0 ng/mL, p=0.02) and non-exercise day (121.5 ± 13.7 to 115.4 ± 17.2 ng/mL, p=0.02) after 60 minutes of dialysis. Conclusion: These data suggest that intense intradialytic strength exercise was unable to increase the circulating concentration of irisin in HD patients. Moreover, our data show that after one hour of dialysis session, irisin plasma levels may be reduced.


2005 ◽  
Vol 99 (4) ◽  
pp. 1372-1377 ◽  
Author(s):  
A. Marcuello ◽  
J. González-Alonso ◽  
J. A. L. Calbet ◽  
R. Damsgaard ◽  
M. J. López-Pérez ◽  
...  

Several weeks of intense endurance training enhances mitochondrial biogenesis in humans. Whether a single bout of exercise alters skeletal muscle mitochondrial DNA (mtDNA) content remains unexplored. Double-stranded mtDNA, estimated by slot-blot hybridization and real time PCR and expressed as mtDNA-to-nuclear DNA ratio (mtDNA/nDNA) was obtained from the vastus lateralis muscle of healthy human subjects to investigate whether skeletal muscle mtDNA changes during fatiguing and nonfatiguing prolonged moderate intensity [2.0–2.5 h; ∼60% maximal oxygen consumption (V̇o2 max)] and short repeated high-intensity exercise (5–8 min; ∼110% V̇o2 max). In control resting and light exercise (2 h; ∼25% V̇o2 max) studies, mtDNA/nDNA did not change. Conversely, mtDNA/nDNA declined after prolonged fatiguing exercise (0.863 ± 0.061 vs. 1.101 ± 0.067 at baseline; n = 14; P = 0.005), remained lower after 24 h of recovery, and was restored after 1 wk. After nonfatiguing prolonged exercise, mtDNA/nDNA tended to decline ( n = 10; P = 0.083) but was reduced after three repeated high-intensity exercise bouts (0.900 ± 0.049 vs. 1.067 ± 0.071 at baseline; n = 7; P = 0.013). Our findings indicate that prolonged and short repeated intense exercise can lead to significant reductions in human skeletal muscle mtDNA content, which might function as a signal stimulating mitochondrial biogenesis with exercise training.


2016 ◽  
Vol 310 (11) ◽  
pp. R1297-R1311 ◽  
Author(s):  
Jackson J. Fyfe ◽  
David J. Bishop ◽  
Evelyn Zacharewicz ◽  
Aaron P. Russell ◽  
Nigel K. Stepto

We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean ± SD: age, 27 ± 4 yr; V̇o2 peak, 45.7 ± 9 ml·kg−1·min−1) performed three experimental trials in a randomized order: 1) RE (8 × 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 × 2 min at 120% lactate threshold (LT); HIT + RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT + RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and +1 h (RE + 1 h) and +3 h (RE + 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACCSer79 and p70S6KThr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTORSer2448 and rps6Ser235/236 phosphorylation at POST. RE-induced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE + 1 h for MICT + RE vs. both HIT + RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE + 1 h for HIT + RE vs. both MICT + RE and RE. Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE.


1997 ◽  
Vol 77 (05) ◽  
pp. 0839-0844 ◽  
Author(s):  
Vittorio Pengo ◽  
Fabio Barbero ◽  
Alberto Banzato ◽  
Elisabetta Garelli ◽  
Franco Noventa ◽  
...  

SummaryBackground. The long-term administration of oral anticoagulants to patients with mechanical heart valve prostheses is generally accepted. However, the appropriate intensity of oral anticoagulant treatment in these patients is still controversial.Methods and Results. From March 1991 to March 1994, patients referred to the Padova Thrombosis Center who had undergone mechanical heart valve substitution at least 6 months earlier were randomly assigned to receive oral anticoagulants at moderate intensity (target INR = 3) or moderate-high intensity (target INR = 4). Principal end points were major bleeding, thromboembolism and vascular death. Minor bleeding was a secondary end-point.A total of 104 patients were assigned to the target 3 group and 101 to the target 4 group; they were followed for from 1.5 years to up 4.5 years (mean, 3 years). Principal end-points occurred in 13 patients in the target 3 group (4 per 100 patient-years) and in 20 patients in the target 4 group (6.9 per 100 patient-years). Major hemorrhagic events occurred in 15 patients, 4 in the target 3 group (1.2 per 100 patient-years) and 11 in the target 4 group (3.8 per 100 patient-years) (p = 0.019). The 12 recorded episodes of thromboembolism, 4 of which consisted of a visual deficit, were all transient ischemic attacks, 6 in the target 3 group (1.8 per 100 patient-years) and 6 in the target 4 group (2.1 per 100 patient- years). There were 3 vascular deaths in each group (0.9 and 1 per 100 patient-years for target 3 and target 4 groups, respectively). Minor bleeding episodes occurred 85 times (26 per 100 patient-years) in the target 3 group and 123 times (43 per 100 patient-years) in the target 4 group (p = 0.001).Conclusions. Mechanical heart valve patients on anticoagulant treatment who had been operated on at least 6 months earlier experienced fewer bleeding complications when maintained on a moderate intensity regimen (target INR = 3) than those on a moderate-high intensity regimen (target INR = 4). The number of thromboembolic events and vascular deaths did not differ between the two groups.


2018 ◽  
Vol 24 (4) ◽  
pp. 427-441 ◽  
Author(s):  
Marija Vavlukis ◽  
Sasko Kedev

Background: Diabetic dyslipidemia has specifics that differ from dyslipidemia in patients without diabetes, which contributes to accelerated atherosclerosis equally as dysglycemia. The aim of this study was to deduce the interdependence of diabetic dyslipidemia and cardiovascular diseases (CVD), therapeutic strategies and the risk of diabetes development with statin therapy. Method: We conducted a literature review of English articles through PubMed, PubMed Central and Cochrane, on the role of diabetic dyslipidemia in atherosclerosis, the antilipemic treatment with statins, and the role of statin therapy in newly developed diabetes, by using key words: atherosclerosis, diabetes mellitus, diabetic dyslipidemia, CVD, statins, nicotinic acid, fibrates, PCSK9 inhibitors. Results: hyperglycemia and dyslipidemia cannot be treated separately in patients with diabetes. It seems that dyslipidemia plays one of the key roles in the development of atherosclerosis. High levels of TG, decreased levels of HDL-C and increased levels of small dense LDL- C particles in the systemic circulation are the most specific attributes of diabetic dyslipidemia, all of which originate from an inflated flux of free fatty acids occurring due to the preceding resistance to insulin, and exacerbated by elevated levels of inflammatory adipokines. Statins are a fundamental treatment for diabetic dyslipidemia, both for dyslipidemia and for CVD prevention. The use of statin treatment with high intensity is endorsed for all diabetes-and-CVD patients, while a moderate - intensity treatment can be applied to patients with diabetes, having additional risk factors for CVD. Statins alone are thought to possess a small, although of statistical significance, risk of incident diabetes, outweighed by their benefits. Conclusion: As important as hyperglycemia and glycoregulation are in CVD development in patients with diabetes, diabetic dyslipidemia plays an even more important role. Statins remain the cornerstone of antilipemic treatment in diabetic dyslipidemia, and their protective effects in CVD progression overcome the risk of statin- associated incident diabetes.


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