Effect of vibration during fatiguing resistance exercise on subsequent muscle activity during maximal voluntary isometric contractions

This investigation was designed to determine if vibration during fatiguing resistance exercise would alter associated patterns of muscle activity. A cross-over design was employed with 8 subjects completing a resistance exercise bout once with a vibrating dumbbell (V) (44 Hz, 3 mm displacement) and once without vibration (NV). For both exercise bouts, 10 sets were performed with a load that induced concentric muscle failure during the 10th repetition. The appropriate load for each set was determined during a pretest. Each testing session was separated by 1 week. Electromyography (EMG) was obtained from the biceps brachii muscle at 12 different time points during a maximum voluntary contraction (MVC) at a 170 degrees elbow angle after each set of the dumbbell exercise. The time points were as follows: pre (5 minutes before the resistance exercise bout), T1-T10 (immediately following each set of resistance exercise), and post (15 minutes after the resistance exercise bout). EMG was analyzed for median power frequency (MPF) and maximum (mEMG). NV resulted in a significant decrease in MPF at T1-T4 (p < or 0.05) and a significant increase in mEMG at T2 during the MVC. V had an overall trend of lower mEMG in comparison to NV. The mEMG and MPF values associated with NV were similar to previously reported investigations. The lower mEMG values and the higher MPF of V in comparison to NV are undocumented. The EMG patterns observed with vibration may indicate a more efficient and effective recruitment of high threshold motor units during fatiguing contractions. This may indicate the usage of vibration with resistance exercise as an effective tool for strength training athletes.     

The effect of six weeks endurance training on dynamic muscular control of the knee following fatiguing exercise

The aim of the study was to examine whether six weeks of endurance training minimizes the effects of fatigue on postural control during dynamic postural perturbations. Eighteen healthy volunteers were assigned to either a 6-week progressive endurance training program on a cycle ergometer or a control group. At week 0 and 7, dynamic exercise was performed on an ergometer until exhaustion and immediately after, the anterior–posterior centre of pressure (COP) sway was analyzed during full body perturbations. Maximal voluntary contractions (MVC) of the knee flexors and extensors, muscle fiber conduction velocity (MFCV) of the vastus lateralis and medialis during sustained isometric knee extension contractions, and power output were measured. Following the training protocol, maximum knee extensor and flexor force and power output increased significantly for the training group with no changes observed for the control group. Moreover, the reduction of MFCV due to fatigue changed for the training group only (from 8.6% to 3.4%). At baseline, the fatiguing exercise induced an increase in the centre of pressure sway during the perturbations in both groups (>10%). The fatiguing protocol also impaired postural control in the control group when measured at week 7. However, for the training group, sway was not altered after the fatiguing exercise when assessed at week 7. In summary, six weeks of endurance training delayed the onset of muscle fatigue and improved the ability to control balance in response to postural perturbations in the presence of muscle fatigue. Results implicate that endurance training should be included in any injury prevention program.     

Limiting mechanisms of force production after repetitive dynamic contractions in human triceps surae.

The influence of repetitive dynamic fatiguing contractions on the neuromuscular characteristics of the human triceps surae was investigated in 10 subjects. The load was 50% of the torque produced during a maximal voluntary contraction, and the exercise ended when the ankle range of motion declined to 50% of control. The maximal torque of the triceps surae and the electromyographic (EMG) activities of the soleus and medial gastrocnemius were studied in response to voluntary and electrically induced contractions before and after the fatiguing task and after 5 min of recovery. Reflex activities were also tested by recording the Hoffmann reflex (H reflex) and tendon reflex (T reflex) in the soleus muscle. The results indicated that whereas the maximal voluntary contraction torque, tested in isometric conditions, was reduced to a greater extent (P < 0.05) at 20 degrees of plantar flexion (-33%) compared with the neutral position (-23%) of the ankle joint, the EMG activity of both muscles was not significantly reduced after fatigue. Muscle activation, tested by the interpolated-twitch method or the ratio of the voluntary EMG to the amplitude of the muscle action potential (M-wave), as well as the neuromuscular transmission and sarcolemmal excitation, tested by the M-wave amplitude, did not change significantly after the fatiguing exercise. Although the H and T reflexes declined slightly (10-13%; P < 0.05) after fatigue, these adjustments did not appear to have a direct deleterious effect on muscle activation. In contrast, alterations in the mechanical twitch time course and postactivation potentiation indicated that intracellular Ca(2+)-controlled excitation-contraction coupling processes most likely played a major role in the force decrease after dynamic fatiguing contractions performed for short duration.     

Jogging gait kinetics following fatiguing lumbar paraspinal exercise

A relationship exists between lumbar paraspinal muscle fatigue and quadriceps muscle activation. The objective of this study was to determine whether hip and knee joint moments during jogging changed following paraspinal fatiguing exercise. Fifty total subjects (25 with self-reported history of low back pain) performed fatiguing, isometric lumbar extension exercise until a shift in EMG median frequency corresponding to a mild level of muscle fatigue was observed. We compared 3-dimensional external joint moments of the hip and knee during jogging before and after lumbar paraspinal fatigue using a 10-camera motion analysis system. Reduced external knee flexion, knee adduction, knee internal rotation and hip external rotation moments and increased external knee extension moments resulted from repetitive lumbar paraspinal fatiguing exercise. Persons with a self-reported history of LBP had larger knee flexion moments than controls during jogging. Neuromuscular changes in the lower extremity occur while resisting knee and hip joint moments following isolated lumbar paraspinal exercise. Persons with a history of LBP seem to rely more heavily on quadriceps activity while jogging.     

Effects of fatiguing unilateral plantar flexions on corticospinal and transcallosal inhibition in the primary motor hand area

Background

Corticospinal excitability of the primary motor cortex (M1) representing the hand muscle is depressed by bilateral lower limb muscle fatigue. The effects of fatiguing unilateral lower limb contraction on corticospinal excitability and transcallosal inhibition in the M1 hand areas remain unclear. The purpose of this study was to determine the effects of fatiguing unilateral plantar flexions on corticospinal excitability in the M1 hand areas and transcallosal inhibition originated from the M1 hand area contralateral to the fatigued ankle.

Methods

Ten healthy volunteers (26.2 ± 3.8 years) participated in the study. Using transcranial magnetic stimulation, we examined motor evoked potentials (MEPs) and interhemispheric inhibition (IHI) recorded from resting first dorsal interosseous (FDI) muscles before, immediately after, and 10 min after fatiguing unilateral lower limb muscle contraction, which was consisted of 40 unilateral maximal isometric plantar flexions intermittently with a 2-s contraction followed by 1 s of rest.

Results

We demonstrated no significant changes in MEPs in the FDI muscle ipsilateral to the fatigued ankle and decrease in IHI from the M1 hand area contralateral to the fatigued ankle to the ipsilateral M1 hand area after the fatiguing contraction. MEPs in the FDI muscle contralateral to the fatigued ankle were increased after the fatiguing contraction.

Conclusions

These results suggest that fatiguing unilateral lower limb muscle contraction differently influences corticospinal excitability of the contralateral M1 hand area and IHI from the contralateral M1 hand area to the ipsilateral M1 hand area. Although fatiguing unilateral lower limb muscle contraction increases corticospinal excitability of the ipsilateral M1 hand area, the increased corticospinal excitability is not associated with the decreased IHI.     

Quantifying the history dependency of muscle recovery from a fatiguing intermittent task

Muscle fatigue and recovery are complex processes influencing muscle force generation capacity. While fatigue reduces this capacity, recovery acts to restore the unfatigued muscle state. Many factors can potentially affect muscle recovery, and among these may be a task dependency of recovery following an exercise. However, little has been reported regarding the history dependency of recovery after fatiguing contractions. We examined the dependency of muscle recovery subsequent to four different histories of fatiguing muscle contractions, imposed using two cycle times (30 and 60 s) during low to moderate levels (15% and 25% of maximum voluntary contraction (MVC)) of intermittent static exertions involving index finger abduction. MVC and low-frequency electrical stimulation (LFES) measures (i.e., magnitude, rise and relaxation rates) of muscle capacity were used, all of which indicated a dependency of muscle recovery on the muscle capacity state existing immediately after fatiguing exercise. This dependency did not appear to be modified by either the cycle time or exertion level leading to that state. These results imply that the post-exercise rate of recovery is primarily influenced by the immediate post-exercise muscle contractile status (estimated by MVC and LFES measures). Such results may help improve existing models of muscle recovery, facilitating more accurate predictions of localized muscle fatigue development and thereby helping to enhance muscle performance and reduce the risk of injury.     

Skeletal muscle plasma membrane glucose transport and glucose transporters after exercise

Recent reports have shown that immediately after an acute bout of exercise the glucose transport system of rat skeletal muscle plasma membranes is characterized by an increase in both glucose transporter number and intrinsic activity. To determine the duration of the exercise response we examined the time course of these changes after completion of a single bout of exercise. Male rats were exercised on a treadmill for 1 h (20 m/min, 10% grade) or allowed to remain sedentary. Rats were killed either immediately or 0.5 or 2 h after exercise, and red gastrocnemius muscle was used for the preparation of plasma membranes. Plasma membrane glucose transporter number was elevated 1.8- and 1.6-fold immediately and 30 min after exercise, although facilitated D-glucose transport in plasma membrane vesicles was elevated 4- and 1.8-fold immediately and 30 min after exercise, respectively. By 2 h after exercise both glucose transporter number and transport activity had returned to nonexercised control values. Additional experiments measuring glucose uptake in perfused hindquarter muscle produced similar results. We conclude that the reversal of the increase in glucose uptake by hindquarter skeletal muscle after exercise is correlated with a reversal of the increase in the glucose transporter number and activity in the plasma membrane. The time course of the transport-to-transporter ratio suggests that the intrinsic activity response reverses more rapidly than that involving transporter number.     

Effect of local and general fatiguing exercises on disturbed and static postural control

This study compared the effect of local and general fatiguing exercise on disturbed and static postural control performances. Surface electromyography and center of pressure signals were respectively recorded during self-initiated perturbation test and static postural stability test from 7 young male subjects. Local fatiguing exercise was performed using intermittent isometric knee extensions at the level of 40% of maximal voluntary torques. General fatiguing exercise was implemented with rowing ergometer at a speed of 200 ± 5 m/min. Results of disturbed postural tests showed no significant change of anticipatory postural adjustment (APAs) organizations in individual muscles following both fatiguing exercises, but observed larger APAs coactivations in trunk and dorsal muscle pairs following local than general fatiguing exercise, and larger compensatory postural adjustments (CPAs) coactivation in dorsal muscle pair after both fatiguing exercises. In addition, the results of static postural tests indicated efficient static postural stability accompanying the down-weighting of visual input and the up-weighting of vestibular/somatosensory component following both fatiguing exercises. These findings evidenced a general compensation in the central nervous system in response to the neuromuscular deficiencies induced by local fatiguing exercise and put forward the function of sensory recalibration in maintaining postural stability under fatigue conditions.     

Effects of muscle metabolites on responses of muscle sympathetic nerve activity to mechanoreceptor(s) stimulation in healthy humans

Based on animal studies, it has been speculated that muscle metabolites sensitize muscle mechanoreceptors and increase mechanoreceptor-mediated muscle sympathetic nerve activity (MSNA). However, this hypothesis has not been directly tested in humans. In this study, we tested the hypothesis that in healthy individuals passive stretch of forearm muscles would evoke significant increases in mean MSNA when muscle metabolite concentrations were increased. In 12 young healthy subjects, MSNA, ECG, and blood pressure were recorded. Subjects performed static fatiguing isometric handgrip at 30% maximum voluntary contraction followed by 4 min of postexercise muscle ischemia (PEMI). After 2 min of PEMI, wrist extension (i.e., wrist dorsiflexion) was performed. The static stretch protocol was also performed during 1) a freely perfused condition, 2) ischemia alone, and 3) PEMI after nonfatiguing exercise. Finally, repetitive short bouts of wrist extension were also performed under freely perfused conditions. This last paradigm evoked transient increases in MSNA but had no significant effect on mean MSNA over the whole protocol. During the PEMI after fatiguing handgrip, static stretch induced significant increases in MSNA (552 +/- 74 to 673 +/- 90 U/min, P < 0.01) and mean blood pressure (102 +/- 2 to 106 +/- 2 mmHg, P < 0.001). Static stretch performed under the other three conditions had no significant effects on mean MSNA and blood pressure. The present data verified that in healthy humans mechanoreceptor(s) stimulation evokes significant increases in mean MSNA and blood pressure when muscle metabolite concentrations are increased above a certain threshold.     

Sirtuin 1 (SIRT1) deacetylase activity is not required for mitochondrial biogenesis or peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) deacetylation following endurance exercise

The protein deacetylase, sirtuin 1 (SIRT1), is a proposed master regulator of exercise-induced mitochondrial biogenesis in skeletal muscle, primarily via its ability to deacetylate and activate peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). To investigate regulation of mitochondrial biogenesis by SIRT1 in vivo, we generated mice lacking SIRT1 deacetylase activity in skeletal muscle (mKO). We hypothesized that deacetylation of PGC-1α and mitochondrial biogenesis in sedentary mice and after endurance exercise would be impaired in mKO mice. Skeletal muscle contractile characteristics were determined in extensor digitorum longus muscle ex vivo. Mitochondrial biogenesis was assessed after 20 days of voluntary wheel running by measuring electron transport chain protein content, enzyme activity, and mitochondrial DNA expression. PGC-1α expression, nuclear localization, acetylation, and interacting protein association were determined following an acute bout of treadmill exercise (AEX) using co-immunoprecipitation and immunoblotting. Contrary to our hypothesis, skeletal muscle endurance, electron transport chain activity, and voluntary wheel running-induced mitochondrial biogenesis were not impaired in mKO versus wild-type (WT) mice. Moreover, PGC-1α expression, nuclear translocation, activity, and deacetylation after AEX were similar in mKO versus WT mice. Alternatively, we made the novel observation that deacetylation of PGC-1α after AEX occurs in parallel with reduced nuclear abundance of the acetyltransferase, general control of amino-acid synthesis 5 (GCN5), as well as reduced association between GCN5 and nuclear PGC-1α. These findings demonstrate that SIRT1 deacetylase activity is not required for exercise-induced deacetylation of PGC-1α or mitochondrial biogenesis in skeletal muscle and suggest that changes in GCN5 acetyltransferase activity may be an important regulator of PGC-1α activity after exercise.     

Acute changes in motor unit discharge property after concentric versus eccentric contraction exercise in knee extensor

This study aimed to investigate the motor unit firing property immediately after concentric or eccentric contraction exercise. Eighteen healthy men performed repetitive maximal isokinetic knee extension exercises with only concentric or eccentric contraction until they exerted less than 80% of the baseline strength. Before and after the fatiguing exercise, high-density surface electromyography of the vastus lateralis was recorded during submaximal ramp-up isometric contraction and individual motor units were identified. Only motor units that could be tracked before and after exercise were analyzed. Muscle cross-sectional area of the vastus lateralis was measured using ultrasound, and electrically evoked torque was recorded before and after the exercise. Sixty-five and fifty-three motor units were analyzed before and after the concentric and eccentric contractions, respectively. The results showed that motor units with moderate to high recruitment thresholds significantly decreased recruitment thresholds under both conditions, and the motor unit discharge rates significantly increased after concentric contraction compared to eccentric contraction. A greater muscle cross-sectional area was observed with concentric contraction. The evoked torque was significantly decreased under both conditions, but no difference between the conditions. These results suggest that fatiguing exercise with concentric contraction contributes to greater neural input to muscles and metabolic responses than eccentric contraction.     

Electromyography of selected lower-limb muscles fatigued by exercise at the intensity of soccer match-play.

Surface electromyography has been useful in comparing muscular activity among different sports movements and it is a valuable technique for evaluating muscle activation, co-ordination and fatigue. Since these important variables have not been investigated during the full game in soccer, the present study aimed to investigate the activity of major muscles of the lower extremity during a soccer-simulation fatiguing protocol. Ten amateur soccer players (age 21.40+/-3.13 years; height 1.77+/-0.06 m; mass 74.55+/-8.5 kg) were tested. The exercise protocol, performed on a programmable motorised treadmill, consisted of the different intensities observed during soccer match-play (walking, jogging, running, sprinting). Electromyographic activity was recorded from the rectus femoris (RF), biceps femoris (BF), tibialis anterior (TA) and gastrocnemius (GC) muscles before exercise, at half-time and immediately after the 90-min exercise protocol. The EMG data were analysed using custom-written software to compute the root mean square (RMS) value over ten gait cycles. With regard to RF, BF and TA, a significant main effect (P< 0.05) was found for condition (pre-game, half-time and post-game), speed (6, 12, 15 and 21 km h(-1)) (P<0.05) and interaction between condition and speed (P< 0.05). For GC, a significant effect was not found for condition or interaction between condition and speed, but a significant main effect (P< 0.001) was found for speed, with the RMS value increasing continually with increasing speed from 6 to 2 1km h(-1). The results indicated that after a simulation of the exercise intensity of soccer-play the EMG activity in major lower-limb muscles was less than before. This decrease indicated that prolonged intermittent exercise had an effect on muscle activity even when work-rate was sustained.     

An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.     

Chronic intermittent hypoxia and incremental cycling exercise independently depress muscle in vitro maximal Na+-K+-ATPase activity in well-trained athletes.

Athletes commonly attempt to enhance performance by training in normoxia but sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia reduces muscle Na(+)-K(+)-ATPase content, whereas fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair performance. We examined whether LHTL and intense exercise would decrease muscle Na(+)-K(+)-ATPase activity and whether these effects would be additive and sufficient to impair performance or plasma K(+) regulation. Thirteen subjects were randomly assigned to two fitness-matched groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate altitude (3,000 m, inspired O(2) fraction = 15.48%) for 23 nights and lived and trained by day under normoxic conditions in Canberra (altitude approximately 600 m). Con lived, trained, and slept in normoxia. A standardized incremental exercise test was conducted before and after LHTL. A vastus lateralis muscle biopsy was taken at rest and after exercise, before and after LHTL or Con, and analyzed for maximal Na(+)-K(+)-ATPase activity [K(+)-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase)] and Na(+)-K(+)-ATPase content ([(3)H]ouabain binding sites). 3-O-MFPase activity was decreased by -2.9 +/- 2.6% in LHTL (P < 0.05) and was depressed immediately after exercise (P < 0.05) similarly in Con and LHTL (-13.0 +/- 3.2 and -11.8 +/- 1.5%, respectively). Plasma K(+) concentration during exercise was unchanged by LHTL; [(3)H]ouabain binding was unchanged with LHTL or exercise. Peak oxygen consumption was reduced in LHTL (P < 0.05) but not in Con, whereas exercise work was unchanged in either group. Thus LHTL had a minor effect on, and incremental exercise reduced, Na(+)-K(+)-ATPase activity. However, the small LHTL-induced depression of 3-O-MFPase activity was insufficient to adversely affect either K(+) regulation or total work performed.     

Evidence of long term muscle fatigue following prolonged intermittent contractions based on mechano- and electromyograms.

The focus of the present study is the long term element of muscle fatigue provoked by prolonged intermittent contractions at submaximal force levels and analysed by force, surface electromyography (EMG) and mechanomyogram (MMG). It was hypothesized that fatigue related changes in mechanical performance of the biceps muscle are more strongly reflected in low than in high force test contractions, more prominent in the MMG than in the EMG signal and less pronounced following contractions controlled by visual compared to proprioceptive feedback. Further, it was investigated if fatigue induced by 30 min intermittent contractions at 30% as well as 10% of maximal voluntary contraction (MVC) lasted more than 30 min recovery. In six male subjects the EMG and MMG were recorded from the biceps brachii muscle during three sessions with fatiguing exercise at 10% with visual feedback and at 30% MVC with visual and proprioceptive feedback. EMG, MMG, and force were evaluated during isometric test contractions at 5% and 80% MVC before prolonged contraction and after 10 and 30 min of recovery. MVC decreased significantly after the fatiguing exercise in all three sessions and was still decreased even after 30 min of recovery. In the time domain significant increases after the fatiguing exercise were found only in the 5% MVC tests and most pronounced for the MMG. No consistent changes were found for neither EMG nor MMG in the frequency domain and feedback mode did not modify the results. It is concluded that long term fatigue after intermittent contractions at low force levels can be detected even after 30 min of recovery in a low force test contraction. Since the response was most pronounced in the MMG this may be a valuable variable for detection of impairments in the excitation-contraction coupling.     

The role of the cyclooxygenase products in evoking sympathetic activation in exercise

Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment (n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to approximately 33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Delta502 +/- 111; post ketorolac: Delta348 +/- 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block (P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.     

Sympathetic activation is associated with increases in EMG during fatiguing exercise

The purpose of this study was to test the hypothesis that efferent sympathetic neural discharge is coupled with the development of muscle fatigue during voluntary exercise in humans. In 12 healthy subjects (aged 20-34 yr) we measured heart rate (HR), arterial blood pressure (AP), and noncontracting, skeletal muscle sympathetic nerve activity (MSNA) in the leg (peroneal nerve) before (control) and during each of three trials of submaximal (30% of maximum) isometric handgrip exercise performed to exhaustion. In six of the subjects of eletromyographic (EMG) activity of the exercising forearm was also measured. HR and AP increased significantly (P less than 0.05) in the 1st min of exercise in all trials. In contrast, neither MSNA nor EMG activity increased significantly above control during the 1st min of exercise, but both parameters subsequently increased in a progressive and parallel manner (P less than 0.05). The overall correlation coefficient between MSNA and EMG activity (144 observations) was 0.85 (P less than 0.001). With successive trials the magnitudes of the increases in HR, AP, MSNA, and EMG activity were greater at any absolute point in time during exercise. These results indicate that sympathetic activation to noncontracting skeletal muscle is directly related to the development of muscle fatigue (as assessed by the change in EMG) during prolonged isometric exercise in humans. Furthermore, our findings demonstrate that previous fatiguing contractions alter the time course of the sympathetic neural adjustments to exercise.     

Bed rest reduces metabolic protein content and abolishes exercise-induced mRNA responses in human skeletal muscle

The aim was to test the hypothesis that 7 days of bed rest reduces mitochondrial number and expression and activity of oxidative proteins in human skeletal muscle but that exercise-induced intracellular signaling as well as mRNA and microRNA (miR) responses are maintained after bed rest. Twelve young, healthy male subjects completed 7 days of bed rest with vastus lateralis muscle biopsies taken before and after bed rest. In addition, muscle biopsies were obtained from six of the subjects prior to, immediately after, and 3 h after 45 min of one-legged knee extensor exercise performed before and after bed rest. Maximal oxygen uptake decreased by 4%, and exercise endurance decreased nonsignificantly, by 11%, by bed rest. Bed rest reduced skeletal muscle mitochondrial DNA/nuclear DNA content 15%, hexokinase II and sirtuin 1 protein content ～45%, 3-hydroxyacyl-CoA dehydrogenase and citrate synthase activity ～8%, and miR-1 and miR-133a content ～10%. However, cytochrome c and vascular endothelial growth factor (VEGF) protein content as well as capillarization did not change significantly with bed rest. Acute exercise increased AMP-activated protein kinase phosphorylation, peroxisome proliferator activated receptor-γ coactivator-1α, and VEGF mRNA content in skeletal muscle before bed rest, but the responses were abolished after bed rest. The present findings indicate that only 7 days of physical inactivity reduces skeletal muscle metabolic capacity as well as abolishes exercise-induced adaptive gene responses, likely reflecting an interference with the ability of skeletal muscle to adapt to exercise.     

Unilateral lower limb muscle fatigue induces bilateral effects on undisturbed stance and muscle EMG activities

The study investigated the effects of an unilateral ankle muscle fatigue onto independent postural control parameters including the trajectories of the estimated resultant CoP (CoPres) and his components: the centre of gravity (CG) and CoP–CG trajectories.Nine healthy men realized series of 10 toe-lift immediately followed by 10 knee flexions until exhaustion with one (Ex) leg. Maximal isometric voluntary contractions, postural sway measures of each leg, and muscular activities of the ankle muscles were recorded before and immediately after the fatiguing exercise.As expected, the latter induced a decrease in maximal voluntary peak force associated with a greater variability of the relative contribution of each leg on the CoPres, enhanced all postural parameters of the non-exercised leg. A significant decreased of the tibialis anterior EMG activity for the Ex leg and an increased one for the NoEx leg. Finally, following unilateral fatigue, the body sway destabilisation seemed to occur only along the medio-lateral (ML) axis.The enhanced and greater variability of the variance along ML axis might be explained by the recourse at the loading–unloading strategy choice and suggests a central attempt to compensate for pain sensation.