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vascular screening system (Fukuda Denshi) in supine position after 15 min of rest. A short questionnaire about PAs of the last 7 days was administered within SAPALDIA 2 to classify the subjects’ PA level at baseline (inactive: 150 min getting out of breath and 2-3 hrs sweating per week due to PA; moderate: either ≥150 min out of breath or ≥2-3 hrs sweating; vigorous: both ≥150 min out of breath and ≥2-3 hrs sweating). The analyses involved ANOVA and multivariable regression models and included 1776 persons aged 49-81 yrs (868 males, 908 females, 63.4±7.9 yrs) with a normal ankle brachial index (0.9≤ABI≤1.3). Results: The PA groups did not significantly differ regarding the cardiovascular risk factors adjusted for in the final regression model: age, sex, BMI and systolic BP (of SAPALDIA 2 and 3) and baseline HDL cholesterol. The PA level at baseline was significantly associated with CAVI in SAPALDIA 3 with 8.56 (SD 1.1) in those with vigorous activity versus 8.68 (SD 1.09) among the inactive (p=0.005). CAVI did not differentiate between the PA levels “moderate” and “inactive” (p=0.388). Discussion: A physically active lifestyle may slow down or reduce arterial stiffening in an ageing population in the long-term if performed with a vigorous intensity. Future analyses will focus on changes of PA over time in association with CAVI and the promotion of cardiovascular health.

18:00 - 19:30 Oral presentations OP-PM32 Physiology [PH] 9


Beaven, C.M., Kilduff, L.P., Cook, C.J.

Mid Sweden University Purpose: To examine the effects of moderate load resistance exercise with and without intermittent blood flow restriction (BFR) on strength, power and repeated sprint ability, along with acute and chronic levels of salivary hormones. Methods: In a cross-over design, twenty male semi-professional rugby union athletes were randomly assigned to a lower-body BFR intervention (an occlusion cuff inflated to 180 mmHg worn on the proximal thighs during all exercise sets) or a control intervention that trained without BFR. Experimental sessions were performed three times a week at the same time of day for three weeks with 5 sets of 5 repetitions of bench press, leg squat and pull-ups performed at 70% of 1-repetition maximum. Saliva was collected before and after the first experimental training session of each week. Strength and power, as well as repeated sprint performance was assessed prior to, and at the conclusion of the experimental period. Results: Significantly greater improvements in bench press (5.4 vs 3.3 kg), squat (7.8 vs 4.3 kg), leg power (168 vs 68 W), maximum sprint time (0.03 vs 0.01 s) and repeated sprint performance maintenance (1.01 vs 0.28%) were observed following the BFR intervention. Salivary testosterone (Effect Size: 0.84 to 0.61) and cortisol concentrations (ES: 0.65 to 0.20) were acutely elevated following the BFR intervention sessions compared to the controls; however the cortisol increase was attenuated across the training block (p=

1.12x10-5). Baseline salivary testosterone was also significantly elevated across the 3 week training blocks with BFR training compared to the controls (p= 0.0284). Exercise-induced elevations in testosterone were correlated to performance improvements for leg squat strength (r= 0.68; p= 0.0005), bench press strength (r= 0.45; p= 0.0233), and countermovement jump power production gains (r= 0.46; p= 0.0201). Conclusions: BFR training was shown to improve the rate of strength training gains and fatigue resistance in trained athletes, possibly allowing greater gains from lower loading which could be of benefit during high training loads or in competitive seasons. The clear improvement in bench press strength resulting from lower-body occlusion suggests a systemic effect of BFR training. It is of interest to note that there was an association between adaptation and alterations in acute and chronic salivary testosterone levels that could speculatively provide a simple correlative marker of the adaptive response.


Durand, F., Guezennec, C.Y.

Performance Health and Altitude Laboratory Introduction Many athletes show significant exercise-induced arterial hypoxemia (EIAH) at maximal exercise. EIAH was primarily associated with an excessively widened alveolar to arterial PO2 difference, which was not sufficiently compensated by hyperventilation (Hopkins 2006). Ventilatory response was insufficient to compensate for the underlying excessive alveolar to arterial O2 difference (Durand et al. 1998). Elsewhere hypoxia increases sympathetic system activity via hypoxia-induced stimulation of the carotid chemoreceptor. This enhanced catecholamine response participate to hypoxia induced hyperventilation during physical exercise. It could be hypothesized that a reduced catecholamine response to intensive exercise could be involved in the mechanism of EIAH. Methods Twenty males endurance-trained subjects (mean age 26± 1.2yr) divided in two group, one group (n=10) of athletes without exercise induced hypoxemia (HTN), one group (n=10) of athletes with a previously identified exercise-induced hypoxemia (HTH) performed an incremental exercise on ergocycle until exhaustion (30 w.min-1). Blood samples were drawn from brachial artery before the test and at the end of last load. The training volume was of 12.7±0.6 h. weeks-1 in HTN and 16.3 ± 1.1h.weeks-1 in HTH. Results The athletes reached same maximal oxygen consumption (62.2 ± 1.9 vs 63.8 ± 1.6 ml.min-1.kg-1) and same maximal ventilation ( 161 ± 4.5 vs 156.4 ± 1.6 L.min-1) with slightly lesser maximal power in HTH without statistical significance (360 ± 12 vs 343 ± 10 W). Blood gases analysis evidence a significant fall (p≤0.05) in PaO2 of 16 ± 1.5 mmHg from rest to maximal exercise in HTH and higher PaCo2 (p≤ 0.05) at the end of exercise (32.5 ± 1.2 vs 36 ± 1.6 mmHg). Plasma catecholamine assays evidences lesser increase at the end of exercise in HTH compared to HTN (Epinephrine 1203 ± 214 vs 1863 ± 355; Norepinephrine 5132 ± 708 vs 7565 ± 785.09 pg.ml-1). The difference remain after 5 min of recovery. Discussion These data evidence that EIAH is associated with a reduced sympathetic response to exercise. This could be responsible for an impaired ventilation/perfusion ratio at pulmonary level (Barman 1998) by the ways of an action on pulmonary circulation which need more investigations. The lesser catecholamine response observed here could be due to a possible overreaching in HTH athletes which is sustained by the lesser maximal power in spite of same aerobic capacity and greater training volume in HTH. References Barman SA. (1995). J Appl

Physiol, 78(4) :1452-8. Durand F, Mucci P. Préfaut C. (1998). Med Sci Sports Exerc, 32(5):926-32. Hopkins SR. (2006). Adv Exp Med Biol, 588:


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Christensen, A., Nielsen, J., Nellemann, B., Vestergaard, P.F., Stødkilde-Jørgensen, H., Jørgensen, J.O.L., Christensen, B.

University of Southerne Denmark Introduction It is well known that aerobic training increases the content of mitochondria and intramyocellular lipid (IMCL) within skeletal muscle (Hoppeler 1986). Recent studies indicate that recombinant human erythropoietin (EPO) may activate mitochondrial biogenesis (Carraway et al. 2010) and increase fat oxidation (Hojman et al. 2009). In the present study, we aimed to investigate the effect of EPO and endurance training on IMCL content of untrained individuals. We hypothesized that EPO and training would lead to increased IMCL content and that there would be an additive effect of the two interventions on IMCL content. Methods Young (range: 18-35 years), nonsmoking, untrained men were randomly assigned to 1 of 4 groups: 1) placebo (PL) (n=8), 2) EPO (E) (n=8), 3) placebo and training (PLT) (n=8), and 4) EPO and training (ET) (n=7). Training consisted of supervised ergometer cycling for 40 min at 65% of maximal watt 3 times pr.

week for 10 weeks. The EPO groups were given 40 μg rHuEPO (Darbepoietin alpha) for the first 3 weeks and 20 μg the last 7 weeks. IMCL of the anterior tibial muscle was assessed by 1H magnetic resonance spectroscopy (Madsen et al. 2012). Data was log-transformed before analysis and values are presented as % of baseline (geometric means) and 95% confidence interval for the means. Results EPO treatment increased hematocrit by 12% in E and 13% in ET. There were no additive effect of EPO and endurance training (P = 0.32) or main effect of EPO (P = 0.80) on IMCL content (PL: 87% (60-127); E: 101% (59-170) ; PLT: 151% (90-256) ; ET: 116% (64-209)). However, endurance training tended to increase IMCL (PL and E: 93% (70-124); PLT and ET: 134% (94-189); P = 0.09). Discussion Our findings suggest that prolonged EPO exposure has no major effect on IMCL content in sedentary controls or any additive effect on endurance training-mediated increase in IMCL content as assessed by 1H magnetic resonance spectroscopy. Thus, any effect of EPO on IMCL is less pronounced or different compared to the effect of endurance training. However, considerations of fiber phenotypes and subcellular localization of IMCL should be considered for a complete evaluation of the effect of EPO on IMCL content. References Carraway et al. (2010). Circ Res, 106(11),1722–1730 Hoppeler H. (1986). Int. J Sports Med., 7,187-204. Hojman P et al. (2009). Plos One, 4,6,e5894 Madsen et al. (2012). J Clin Endocrinol Metab, 97(4),1227–1235



Hanson, E.D., Betik, A.C., O'Connor, M., Truong, J., Hayes, A.

Victoria University Introduction The loss of testosterone with aging or as a consequence of prostate cancer treatment has adverse effects on muscle mass and function. Protein supplementation and resistance training both have been used to mitigate these declines. However, studies are lacking that combine these complementary therapies in hypogonadal populations and that examine the mechanism(s) responsible for hypertrophy in the absence of testosterone. Using immobilization and subsequent reloading as a model of resistance exercise, this study examined the effects of testosterone and protein supplementation on muscle mass and function as a means of reducing the side effects of androgen deficiency. Methods Fischer 344 male rats underwent castration or sham surgery and were allowed to recover prior to unilateral hind limb immobilization (Childs 2003). With immobilization and throughout the study, animals were randomized to receive a high protein diet (50%) with branched chain amino acids (150mg/kg/d) added to their drinking water or standard chow (20% protein).

Following 10d of immobilization, casts were removed and the animals underwent limb reloading for 0, 6, or 14d before muscles were stimulated ex vivo to assess force production. Results Body mass was significantly lower in castrated animals following surgery. Immobilized muscle mass was significantly lower in extensor digitorum longus (EDL, -7.8%), gastrocnemius (-20.8%), plantaris (-17.2%), and soleus (-27.7%). Castration also decreased muscle mass (-5%) but there was no effect of diet. Immobilized muscle mass increased with reloading but was not completely restored. Force production (stimulated at 10-100 Hz) was reduced in both EDL (-21.4 to -26.0%) and soleus (-45.4 to -74.7%) with immobilization but only soleus force recovery was influenced by castration over the time course of the study with no influence of diet. Discussion Recent work in humans suggests that load-mediated muscle hypertrophy may be independent of testosterone (West 2010, Hanson 2012), which contradicts previous findings (Galvao 2006, Kvorning 2006). The group differences in total body and muscle mass and greater force declines with immobilization in castrated animals support the hypothesis that testosterone is important for maintaining skeletal muscle but similar mass and force measurements in sham and castrated rats after 14d of reloading suggests testosterone-independent hypertrophy. The lack of dietary influence on muscle mass is contradictory to previous findings (Baptista 2010, Yamamoto 2010), although this may be related to differences in dose and models of atrophy. References Childs, TE, Spangenburg EE, et al. (2003) Am J Physiol Cell Physiol. Hanson, ED, Sheaff AK, et al., (2012). J Gerontol A Biol Sci Med Sci. Galvao, DA, Nosaka, K, et al., (2006). Med Sci Sport Exerc. Kvorning T, Andersen, M, et al (2006). Am J Physiol Endocrinol Metab. West, DW, Burd, NA, et al. (2010). J Appl Physiol. Baptista, IL, Leal, ML, et al. (2010) Muscle Nerve. Yamamoto, D, Taki T, et al. (2010) Muscle Nerve.



Kwak, H.B.

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