Gymnastik- och idrottshögskolan, GIH

Aim

In adults, prolonged periods of sitting have been linked to acute negative effects on vascular structure and function. The aim of this study was to evaluate the acute effects of physical activity (PA) breaks during prolonged sitting on arterial stiffness, cortisol and psychological factors in adolescents.

Methods

Adolescents underwent different short (3-min) breaks starting every 20 min, during 80 min of sitting on three separate days. Breaks were (A) social seated breaks (SOC), (B) low-intensity simple resistance activity PA breaks (SRA) and (C) moderate-intensity step-up PA breaks (STEP). The arterial stiffness measures were augmentation index (AIx), AIx@75 and pulse wave velocity (PWV). Cortisol was measured from saliva. Psychological factors were self-reported.

Results

Eleven girls and six boys (average age 13.6 ± 0.7 years) participated, with average baseline heart rates of 72 ± 11 bpm, systolic/diastolic blood pressure 111 ± 7/64 ± 6 mmHg and cortisol 10.9 ± 5.8 nmoL/L. PWV, cortisol and psychological factors did not change after any of the conditions. AIx@75 increased significantly (4.9 ± 8.7–9.2 ± 13.2) after the STEP intervention compared with SOC and SRA (time × condition p < 0.05).

Conclusion

Arterial stiffness increased after prolonged sitting with frequent, short step-up activity breaks. The results indicate potential important intensity-dependent effects of physical activity on vascular regulation in youth.

There is a debate on whether lipid-mediated insulin resistance derives from an increased or decreased capacity of muscle to oxidize fats. Here we examine the involvement of muscle fiber composition in the metabolic responses to a 3-day fast (starvation, which results in increases in plasma lipids and insulin resistance) in two groups of healthy young subjects: 1, area occupied by type I fibers = 61.0 ± 11.8%; 2, type I area = 36.0 ± 4.9% (P<0.001). Muscle biopsies and intravenous glucose tolerance tests were performed after an overnight fast and after starvation. Biopsies were analyzed for muscle fiber composition and mitochondrial respiration. Indices of glucose tolerance and insulin sensitivity were determined. Glucose tolerance was similar in both groups after an overnight fast and deteriorated to a similar degree in both groups after starvation. In contrast, whole-body insulin sensitivity decreased markedly after starvation in group 1 (P<0.01), whereas the decrease in group 2 was substantially smaller (P=0.06). Non-esterified fatty acids and β-hydroxybutyrate levels in plasma after an overnight fast were similar between groups and increased markedly and comparably in both groups after starvation, demonstrating similar degrees of lipid load. The capacity of permeabilized muscle fibers to oxidize lipids was significantly higher in group 1 vs. 2, whereas there was no significant difference in pyruvate oxidation between groups. The data demonstrate that loss of whole-body insulin sensitivity after short-term starvation is a function of muscle fiber composition and is associated with an elevated rather than a diminished capacity of muscle to oxidize lipids.

Brain-derived neurotrophic factor (BDNF) and cortisol are both capable of modulating synaptic plasticity, but it is unknown how physical activity-induced changes in their plasma levels relate to corticospinal plasticity in humans. Sixteen inactive middle-aged men and women participated in three separate interventions consisting of 3hours prolonged sitting (SIT); 3hours sitting interrupted every 30minutes with frequent short physical activity breaks (FPA); and 2.5hours prolonged sitting followed by 25minutes of moderate intensity exercise (EXE). These 3hour sessions were each followed by a 30min period of paired associative stimulation over the primary motor cortex (PAS). Blood samples were taken and corticospinal excitability measured at baseline, pre PAS, 5min and 30min post PAS. Here we report levels of plasma BDNF and cortisol over three activity conditions and relate these levels to previously published changes in corticospinal excitability of a non-activated thumb muscle. There was no interaction between time and condition in BDNF, but cortisol levels were significantly higher after EXE compared to after SIT and FPA. Higher cortisol levels at pre PAS predicted larger increases in corticospinal excitability from baseline to all subsequent time points in the FPA condition only, while levels of BDNF at pre PAS did not predict such changes in any of the conditions. Neither BDNF nor cortisol modified changes from pre PAS to the subsequent time points, suggesting that the increased corticospinal excitability was not mediated though an augmented effect of the PAS protocol. The relationship between cortisol and plasticity has been suggested to be U-shaped. This is possibly why the moderately high levels of cortisol seen in the FPA condition were positively associated with changes AURC, while the higher cortisol levels seen after EXE were not. A better understanding of the mechanisms for how feasible physical activity breaks affect neuroplasticity can inform the theoretical framework for how work environments and schedules should be designed. DATA AVAILABILITY: Data are available from the corresponding author upon reasonable request.

CONTEXT: Muscle fiber composition is associated with peripheral insulin action.

OBJECTIVE: We investigated whether extreme differences in muscle fiber composition are associated with alterations in peripheral insulin action and secretion in young, healthy subjects who exhibit normal fasting glycemia and insulinemia.

METHODS: Relaxation time following a tetanic contraction was used to identify subjects with a high or low expression of type I muscle fibers: group I (n=11), area occupied by type I muscle fibers = 61.0 ± 11.8%; group II (n=8), type I area = 36.0 ± 4.9% (P<0.001). Biopsies were obtained from the vastus lateralis muscle and analyzed for mitochondrial respiration on permeabilized fibers, muscle fiber composition and capillary density. An intravenous glucose tolerance test was performed and indices of glucose tolerance, insulin sensitivity and secretion were determined.

RESULTS: Glucose tolerance was similar between groups, whereas whole-body insulin sensitivity was decreased by ~50% in group II vs group I (P=0.019). First phase insulin release (area under the insulin curve during 10 min after glucose infusion) was increased by almost 4-fold in group II vs I (P=0.01). Whole-body insulin sensitivity was correlated with % area occupied by type I fibers (r=0.54; P=0.018) and capillary density in muscle (r=0.61; P=0.005), but not with mitochondrial respiration. Insulin release was strongly related to % area occupied by type II fibers (r=0.93; P<0.001).

CONCLUSIONS: Assessment of muscle contractile function in young healthy subjects may prove useful in identifying individuals with insulin resistance and enhanced glucose stimulated insulin secretion prior to onset of clinical manifestations.

BACKGROUND: Reliable physical activity measurements in community-dwelling older adults are important to determine effects of targeted health promotion interventions. Many exercise interventions aim to improve time spent sedentary (SED), in light-intensity-physical-activity (LPA) and moderate-to-vigorous-intensity-physical-activity (MVPA), since these parameters have independently proposed associations with health and longevity. However, many previous studies rely on self-reports which have lower validity compared to accelerometer measured physical activity patterns. In addition, separating intervention-effects from reactivity measurements requires sufficient test-retest reliability for accelerometer assessments, which is lacking in older adults.

OBJECTIVES: The study objective was to investigate the reliability of sensor-based PA-patterns in community-dwelling older adults. Furthermore, to investigate change over time of physical activity patterns and examine any compensatory-effect from the eight-week supervised exercise-intervention.

METHODS: An exercise-group (n = 78, age-range:65-91yrs) performed two 1h-exercise sessions/week during eight-weeks. PA-pattern was assessed (using hip-worn accelerometers), twice before and once during the last-week of the intervention. A control-group (n = 43, age-range:65-88yrs) performed one pre-test and the end-test with no exercise-intervention. A dependent-t-test, mean-difference (95%-CI), limits-of-agreement and intraclass-correlation-coefficient-ICC were used between the two pre-tests. Repeated-measures-ANOVA were used to analyze any intervention-effects.

RESULTS: The exercise-groups´ two pre-tests showed generally no systematic change in any PA- or SED-parameter (ICC ranged 0.75-0.90). Compared to the control group, the exercise intervention significantly (time x group-interaction, p<0.05) increased total-PA-cpm (exercise-group/control-group +17%/+7%) and MVPA-min/week (+41/-2min) and decreased %-of-wear-time for SED-total (-4.7%/-2.7%) and SED-bouts (-5.7%/-1.8%), and SED-bouts min/d (-46/-16min). At baseline level, no significant differences were found between the two groups for any parameter.

CONCLUSIONS: The current study presents a good test-retest-reliability of sensor-based-one-week-assessed-PA-pattern in older-adults. Participating in an 8-week supervised exercise intervention improved some physical activity and sedentary parameters compared to the control group. No compensatory-effect was noted in the intervention-group i.e., no decrease in any PA-parameter or increase in SED at End-test (in %-of-wear-time, min/day or total-PA).

This protocol describes the simultaneous use of a broad span of methods to examine muscle aerobic capacity, glucose tolerance, strength, and power in elderly people performing short-term resistance training (RET). Supervised progressive resistance training for 1 h three times a week over 8 weeks was performed by RET participants (71±1 years, range 65-80). Compared to a control group without training, the RET showed improvements on the measures used to indicate strength, power, glucose tolerance, and several parameters of muscle aerobic capacity. Strength training was performed in a gym with only robust fitness equipment. An isokinetic dynamometer for knee extensor strength permitted the measurement of concentric, eccentric, and static strength, which increased for the RET group (8-12% post- versus pre-test). The power (rate of force development, RFD) at the initial 0-30 ms also showed an increase for the RET group (52%). A glucose tolerance test with frequent blood glucose measurements showed improvements only for the RET group in terms of blood glucose values after 2 h (14%) and the area under the curve (21%). The blood lipid profile also improved (8%). From muscle biopsy samples prepared using histochemistry, the amount of fiber type IIa increased, and a trend towards a decrease in IIx in the RET group reflected a change to a more oxidative profile in terms of fiber composition. Western blot (to determine the protein content related to the signaling for muscle protein synthesis) showed a rise of 69% in both Akt and mTOR in the RET group; this also showed an increase in mitochondrial proteins for OXPHOS complex II and citrate synthase (both ~30%) and for complex IV (90%), in only the RET group. We demonstrate that this type of progressive resistance training offers various improvements (e.g., strength, power, aerobic capacity, glucose tolerance, and plasma lipid profile).

Little is known about the molecular regulation of skeletal muscle protein turnover during exercise in field conditions where energy is intake inadequate. Here, 17 male and 7 female soldiers performed an 8 day long field based military operation. Vastus lateralis muscle biopsies, in which autophagy, the ubiquitin-proteasome system and the mTORC1 signaling pathway where studied, were collected before and after the operation. The 187 h long operation resulted in a 15% and 29% negative energy balance as well as a 4.1% and 4.6% loss of body mass in women and men respectively. After the operation protein levels of ULK1 as well as the phosphorylation of ULK1^Ser317 and ULK1^Ser555 had increased by 11%, 39% and 13%, respectively, and this was supported by a 17% increased phosphorylation of AMPK^Thr172 (P<0.05). The LC3b-I/II ratio was 3-fold higher after compared to before the operation (P<0.05), whereas protein levels of p62/SQSTM1 were unchanged. The β1, β2, and β5 activity of the proteasome and protein levels of MAFbx did not change, while levels of MuRF-1 were slightly reduced (6%, P<0.05). Protein levels and phosphorylation status of key components in the mTORC1 signaling pathway remained at basal levels after the operation. Muscle levels of glycogen decreased from 269±12 to 181±9 mmol ∙ kg dry muscle^-1 after the exercise period (P<0.05). In conclusion, the 8 days of field based exercise resulted in induction of autophagy without any increase in proteasome activity or protein ubiquitination. Simultaneously, the regulation of protein synthesis through the mTORC1 signaling pathway was maintained.

The primary aim of this study was to investigate the effect of short-term resistance training (RET) on mitochondrial protein content and glucose tolerance in elderly. Elderly women and men (age 71 ± 1, mean ± SEM) were assigned to a group performing 8 weeks of resistance training (RET, n = 12) or no training (CON, n = 9). The RET group increased in (i) knee extensor strength (concentric +11 ± 3%, eccentric +8 ± 3% and static +12 ± 3%), (ii) initial (0-30 ms) rate of force development (+52 ± 26%) and (iii) contents of proteins related to signaling of muscle protein synthesis (Akt +69 ± 20 and mammalian target of rapamycin +69 ± 32%). Muscle fiber type composition changed to a more oxidative profile in RET with increased amount of type IIa fibers (+26.9 ± 6.8%) and a trend for decreased amount of type IIx fibers (-16.4 ± 18.2%, P = 0.068). Mitochondrial proteins (OXPHOS complex II, IV, and citrate synthase) increased in RET by +30 ± 11%, +99 ± 31% and +29 ± 8%, respectively. RET resulted in improved oral glucose tolerance measured as reduced area under curve for glucose (-21 ± 26%) and reduced plasma glucose 2 h post-glucose intake (-14 ± 5%). In CON parameters were unchanged or impaired. In conclusion, short-term resistance training in elderly not only improves muscular strength, but results in robust increases in several parameters related to muscle aerobic capacity.

Introduction

It is well known that ultra-endurance exercise, such as Adventure racing and military operations, often induce substantial energy deficits. This suggests a catabolic state, but the exact effects on protein turnover have not yet been sufficiently investigated. The aim of this study was to examine several markers involved in muscle protein turnover before and after a multi-day physically demanding military training operation.

Methods

Seven female (age 21 ± 5 years, weight 71.2 ± 6.6 kg) and seventeen male (age 20 ± 1 years, weight 76.6 ± 6.2 kg) performed a 185 hours military training operation. Energy intake was estimated from food supply and energy expenditure was calculated from continuous heart rate and accelerometer recordings. Muscle biopsies were taken from M Vastus Lateralis before and after the operation.

Results

A negative energy balance of 1,500-2,000 kcal/24 hours was estimated. Body weight declined 3.4 (95% CI 3.0-3.8) kg and muscle explosive strength, evaluated from squad and counter movement jumps, was reduced 5 and 6 %, respectively, after the operation with no difference between genders. Muscle glycogen content was reduced from 269 ± 58 to 181 ± 44 mmol/kg dry muscle (p<0.05) with no difference between genders. Muscle content of mTOR and p70 as well as MAFbx were unchanged while the protein content of MuRF-1 was significantly down regulated in both genders.

Discussion

The study indicated that prolonged low intensity exercise with substantial energy deficit reduces muscle function and muscle glycogen content. Proteins for muscle synthesis mTOR and p70 were unchanged while the down regulation of MuRF-1 indicates a protection against muscle break down during the energy deficit situation, preserving the muscle mass.

The purpose of the study was to investigate the specific effect of leucine on mTORC1 signalling and amino acid metabolism in connection with resistance exercise. Comparisons were made between ingestion of supplements with and without leucine. Eight young women performed leg press exercise on 2 occasions. In randomized order they received either an aqueous solution of essential amino acids with leucine (EAA) or without leucine (EAA-Leu), given as small boluses throughout the experiment. Muscle biopsies were taken after an overnight fast before exercise and 1 and 3 h postexercise and samples of blood were taken repeatedly during the experiment. Plasma and muscle concentrations of leucine rose 60%-140% (p < 0.05) with EAA and fell 35%-45% (p < 0.05) with the EAA-Leu supplement. In the EAA-trial, plasma and muscle levels of tyrosine (not present in the supplement) and the sum of the EAA were 15%-25% (p < 0.05) lower during recovery. Phosphorylation of mTOR and p70S6k was elevated to a larger extent following 1 h of recovery with leucine in the supplement (120% vs. 49% (p < 0.05) and 59- vs. 8-fold (p < 0.05) for EAA and EAA-Leu, respectively). The levels of MAFbx and MuRF-1 mRNA and of the corresponding proteins were not significantly altered after 3 h recovery from exercise. In conclusion, the presence of leucine in the supplement enhances the stimulatory effect on mTORC1 signalling and reduces the level of tyrosine and the sum of the EAA in muscle and plasma, suggesting a stimulation of protein synthesis and (or) inhibition of breakdown, leading to improvement in net protein balance.

Energistatus, muskelfysiologiska data och fysiskt stridsvärde studerades före och efter en 8 dygn långa grundmilitär slutövning (GMU) vid AMF-1 Berga Örlogsskolor i månadsskiftet oktober november 2013.

Totalt deltog 105 soldater i övningen, fördelat på 3 plutoner om vardera 35 soldater. En subgrupp på 24 soldater (8 kvinnor) bestående av 8 soldater från vardera pluton studerades mer ingående.

Medelhjärtfrekvensen för de 6 soldater (2 kvinnor) som hade i stort sett kompletta mätningar från den 187 timmar långa övningen, inklusive viloperioder, var 88 ± 7 slag/minut. Utifrån hjärtfrekvensdata beräknades den totala energiomsättningen till i genomsnitt 44 000 ± 6 600 kcal, vilket motsvarar 5 600 ± 840 kcal per dygn och 235 ± 35 kcal/tim. Total energiförbrukning var i genomsnitt 39 000 kcal för kvinnorna och 46 500 kcal för männen. I övrigt noterades inte några betydande skillnader mellan kvinnor och män. Däremot var det stora individuella variationer i energiutgift, vilka till ca hälften berodde på skillnader i kroppsvikt. Med hänsyn till kroppsvikt och buren vikt var energiförbrukningen ca 3,1 ± 0,23 kcal per timme per kg totalvikt. Den individuella variationen beror på skillnad i buren vikt, på olika uppgifter och på individuella fysiologiska skillnader.

Utifrån beräknat energiintag blev det totala energiunderskottet under övningen 12 000-15 000 kcal, vilket är ca 1 500-2 000 kcal per dygn. Viktminskningen under övningen var 2,9 kg för kvinnor och 3,7 kg för män. Denna viktminskning på >4 % leder troligen till försämrad uthållighetsförmåga.

Den maximala muskelstyrkan i armar och ben var i stort sett oförändrade efter övningen, liksom den beräknade maximala syreupptagningsförmågan. Däremot upplevdes ett lågintensivt cykelarbete som betydligt tyngre efter övningen. Muskeluthållighet mättes inte i denna studie.

Ett skjutprov om 5 skott i liggande på 100 m mot en tredjedelsfigur visade 64 deltagande soldater på en försämrad träffprocent från 90,5% före till 79,4 % efter övningen. Alla soldater hade minst en träff före medan 6 soldater hade alla bom efter övningen.

Slutsatsen från studien är att GMU-övningen resulterade i ett stort energiunderskott. Stridsvärdet, bedömt från skjutprovet var klart försämrat. Maximala fysiologiska parametrar var i stort sett oförändrade, medan skattad ansträngning och därmed uthållighetsförmåga, försämrades.

The current dogma is that the muscle adaptation to resistance exercise is blunted when combined with endurance exercise. The suggested mechanism (based on rodent experiments) is that activation of adenosine monophosphate-activated protein kinase (AMPK) during endurance exercise impairs muscle growth through inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). The purpose of this study was to investigate potential interference of endurance training on the signaling pathway of resistance training [mTORC1 phosphorylation of ribosomal protein S6 kinase 1 (S6K1)] in human muscle. Ten healthy and moderately trained male subjects performed on two separate occasions either acute high-intensity and high-volume resistance exercise (leg press, R) or R followed by 30 min of cycling (RE). Muscle biopsies were collected before and 1 and 3 h post resistance exercise. Phosphorylation of mTOR (Ser(2448)) increased 2-fold (P < 0.05) and that of S6K1 (Thr(389)) 14-fold (P < 0.05), with no difference between R and RE. Phosphorylation of eukaryotic elongation factor 2 (eEF2, Thr(56)) was reduced ∼70% during recovery in both trials (P < 0.05). An interesting finding was that phosphorylation of AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC, Ser(79)) decreased ∼30% and ∼50%, respectively, 3 h postexercise (P < 0.05). Proliferator-activated receptor-γ coactivator-1 (PGC-1α) mRNA increased more after RE (6.5-fold) than after R (4-fold) (RE vs. R: P < 0.01) and was the only gene expressed differently between trials. These data show that the signaling of muscle growth through the mTORC1-S6K1 axis after heavy resistance exercise is not inhibited by subsequent endurance exercise. It is also suggested that prior activation of mTORC1 signaling may repress subsequent phosphorylation of AMPK.

Resistance exercise is known to stimulate muscle hypertrophy and this effect is mainly mediated by the mammalian target of rapamycin (mTOR) pathway. In contrast, endurance exercise results in a divergent phenotypic response which to a large extent is mediated by adenosine monophosphate-activated protein kinase (AMPK). Research indicates that molecular interference may exist, possibly through an inhibitory effect on mTOR signalling by AMPK, when these two modes of exercise are combined.

PURPOSE: To investigate the impact of subsequent endurance exercise on resistance exercise induced mTOR signalling.

METHODS: In a randomized and cross-over fashion, ten male subjects performed either heavy resistance exercise (R) or heavy resistance exercise followed by endurance exercise (RE) on two separate occasions. The R protocol consisted of thirteen sets of leg press exercise with 3 minutes of recovery allowed between each set. In the RE session, resistance exercise was followed by 15 minutes recovery after which 30 min of cycling was initiated at an intensity equal to 70 % of the subjects' maximal oxygen consumption. Muscle biopsies were collected before, 1 and 3 hours after resistance exercise in both trials. Samples were analyzed for several signalling proteins in the mTOR pathway using western blot technique.

RESULTS: Phosphorylation of mTOR increased approx. twofold at 1 h post resistance exercise and remained elevated at the 3 h time point (p< 0.01) with no difference between the two trials. Phosphorylation of p70S6k, a downstream target of mTOR, was increased about 6-and18-fold at 1 h and 3 h post resistance exercise (p< 0.01). There was no difference in p70S6k phosphorylation at any time point between the two trials. Phosphorylation of the eukaryotic elongation factor eEF2 was decreased 3- to 4-fold at both time points post resistance exercise (p< 0.01) with no difference between trials. Phosphorylation of AMPK was unchanged at the 1 h time point but decreased approximately 30 % from pre-exercise values in both trials at 3 h post resistance exercise (p< 0.01).

CONCLUSIONS: The signalling response following heavy resistance exercise is not blunted by subsequent endurance exercise. Supported by the Swedish National Centre for Research in Sports.