Enzymes musculaires et exercice physique [Muscle enzyme activity and exercise]

Exercise is classically associated with muscular soreness, presenting one to two days later, delayed onset muscular soreness. Blood muscle enzymes and protein elevations are characteristic, and may cause renal failure. Creatin phosphokinase peak appears on the fourth day and depends on exercise type and individual parameters. This effect is attenuated with repeated bouts, by habituation. Metabolic complications are rare. The knowledge of this reaction, even with common exercises, allows to postpone investigations for a complex metabolic disorder, or to avoid stopping a medication for fear of a side effect, as with statins. Indeed, it is necessary to wait for seven days without any exercise before interpreting an elevated CK result.

Power spectral changes of the superimposed M wave during isometric voluntary contractions of increasing strength.

INTRODUCTION: We examined the power spectral changes of the compound muscle action potential (M wave) evoked during isometric contractions of increasing strength. METHODS: Surface electromyography (sEMG) of the vastus lateralis and medialis was recorded from 20 volunteers who performed 4-s step-wise isometric contractions of different intensities. A maximal M wave was elicited by a single stimulus to the femoral nerve and superimposed on the voluntary contractions. The spectral characteristics (Fmean and Fmedian) of sEMG and M-wave signals were calculated. RESULTS: M-wave spectral indicators increased systematically with contraction intensity up to 60% MVC and then leveled off at higher forces. Over the 10-60% MVC range, the increase in spectral indicators was 3 times higher for M waves (36%) than for sEMG (12%). CONCLUSIONS: The consistent increase in M-wave spectral characteristics with force is due to the fact that the number of motor units recruited by the superimposed supramaximal stimulus is approximately stable.

β-Adrenergic modulation of skeletal muscle contraction: key role of excitation-contraction coupling.

Our aim is to describe the acute effects of catecholamines/β-adrenergic agonists on contraction of non-fatigued skeletal muscle in animals and humans, and explain the mechanisms involved. Adrenaline/β-agonists (0.1-30 μm) generally augment peak force across animal species (positive inotropic effect) and abbreviate relaxation of slow-twitch muscles (positive lusitropic effect). A peak force reduction also occurs in slow-twitch muscles in some conditions. β2 -Adrenoceptor stimulation activates distinct cyclic AMP-dependent protein kinases to phosphorylate multiple target proteins. β-Agonists modulate sarcolemmal processes (increased resting membrane potential and action potential amplitude) via enhanced Na(+) -K(+) pump and Na(+) -K(+) -2Cl(-) cotransporter function, but this does not increase force. Myofibrillar Ca(2+) sensitivity and maximum Ca(2+) -activated force are unchanged. All force potentiation involves amplified myoplasmic Ca(2+) transients consequent to increased Ca(2+) release from sarcoplasmic reticulum (SR). This unequivocally requires phosphorylation of SR Ca(2+) release channels/ryanodine receptors (RyR1) which sensitize the Ca(2+) -induced Ca(2+) release mechanism. Enhanced trans-sarcolemmal Ca(2+) influx through phosphorylated voltage-activated Ca(2+) channels contributes to force potentiation in diaphragm and amphibian muscle, but not mammalian limb muscle. Phosphorylation of phospholamban increases SR Ca(2+) pump activity in slow-twitch fibres but does not augment force; this process accelerates relaxation and may depress force. Greater Ca(2+) loading of SR may assist force potentiation in fast-twitch muscle. Some human studies show no significant force potentiation which appears to be related to the β-agonist concentration used. Indeed high-dose β-agonists (∼0.1 μm) enhance SR Ca(2+) -release rates, maximum voluntary contraction strength and peak Wingate power in trained humans. The combined findings can explain how adrenaline/β-agonists influence muscle performance during exercise/stress in humans.

Influence on Strength and Flexibility of a Swing Phase-Specific Hamstring Eccentric Program in Sprinters' General Preparation

Guex, KJ, Lugrin, V, Borloz, S, and Millet, GP. Influence on strength and flexibility of a swing phase-specific hamstring eccentric program in sprinters' general preparation. J Strength Cond Res 30(2): 525-532, 2016-Hamstring injuries are common in sprinters and mainly occur during the terminal swing phase. Eccentric training has been shown to reduce hamstring injury rate by improving several risk factors. The aim of this study was to test the hypothesis that an additional swing phase-specific hamstring eccentric training in well-trained sprinters performed at the commencement of the winter preparation is more efficient to improve strength, ratio, optimum angle, and flexibility than a similar program without hamstring eccentric exercises. Twenty sprinters were randomly allocated to an eccentric (n = 10) or a control group (n = 10). Both groups performed their usual track and field training throughout the study period. Sprinters in the eccentric group performed an additional 6-week hamstring eccentric program, which was specific to the swing phase of the running cycle (eccentric high-load open-chain kinetic movements covering the whole hamstring length-tension relationship preformed at slow to moderate velocity). Isokinetic and flexibility measurements were performed before and after the intervention. The eccentric group increased hamstring peak torques in concentric at 60 degrees .s by 16% (p < 0.001) and at 240 degrees .s by 10% (p < 0.01), in eccentric at 30 degrees .s by 20% (p < 0.001) and at 120 degrees .s by 22% (p < 0.001), conventional and functional ratios by 12% (p < 0.001), and flexibility by 4 degrees (p < 0.01), whereas the control group increased hamstring peak torques only in eccentric at 30 degrees .s by 6% (p </= 0.05) and at 120 degrees .s by 6% (p < 0.01). It was concluded that an additional swing phase-specific hamstring eccentric training in sprinters seems to be crucial to address different risk factors for hamstring strain injuries, such as eccentric and concentric strength, hamstring-to-quadriceps ratio ratio, and flexibility.

Walking-induced muscle fatigue impairs postural control in adolescents with unilateral spastic cerebral palsy.

BACKGROUND: Fatigue is likely to be an important limiting factor in adolescents with spastic cerebral palsy (CP). AIMS: To determine the effects of walking-induced fatigue on postural control adjustments in adolescents with unilateral CP and their typically developing (TD) peers. METHODS: Ten adolescents with CP (14.2±1.7yr) and 10 age-, weight- and height-matched TD adolescents (14.1±1.9yr) walked for 15min on a treadmill at their preferred walking speed. Before and after this task, voluntary strength capacity of knee extensors (MVC) and postural control were evaluated in 3 conditions: eyes open (EO), eyes closed (EC) and with dual cognitive task (EODT). RESULTS: After walking, MVC decreased significantly in CP (-11%, P<0.05) but not in TD. The CoP area was only significantly increased in CP (90%, 34% and 60% for EO, EC and EODT conditions, respectively). The CoP length was significantly increased in the EO condition in CP and TD (20% and 21%) and was significantly increased in the EODT condition by 18% in CP only. CONCLUSIONS: Unlike TD adolescents, treadmill walking for 15min at their preferred speed lead to significant knee extensor strength losses and impairments in postural control in adolescents with unilateral spastic CP.