I've always been interested as to why a muscle fatigues? Is there something going at the muscle level its self, or is it modified via the brain as a way for the body to protect itself? Most likely a combination of both, but here are some new studies that may help us untangle this mystery
MECHANISMS OF FATIGUE INDUCED BY ISOMETRIC CONTRACTIONS IN EXERCISING HUMANS AND IN MOUSE ISOLATED SINGLE MUSCLE FIBRES.
Place N, Bruton JD, Westerblad H. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Muscle fatigue (i.e. the decrease in muscle performance during exercise) has been studied extensively using a variety of experimental paradigms, from mouse to human, from single cell to whole-body exercise. Given the disparity of models used to characterize muscle fatigue, it can be difficult to establish whether the results of basic in vitro studies are applicable to exercise in humans.
In the present brief review, our attempt is to relate neuromuscular alterations caused by repeated or sustained isometric contraction in humans to changes in excitation-contraction (E-C) coupling observed in intact single muscle fibres, where force and the free myoplasmic [Ca(2+)] can be measured.
Accumulated data indicate that impairment of E-C coupling, most likely located within muscle fibres, accounts for the fatigue-induced decrease in maximal force in humans, whereas central (neural) fatigue is of greater importance for the inability to continue a sustained low-intensity contraction. Based on data from intact single muscle fibres, the fatigue-induced impairment in E-C coupling involves: (i) a reduced number of active cross-bridges owing to a decreased release of Ca(2+); (ii) a decreased sensitivity of the myofilaments to Ca(2+); and/or (iii) a reduced force produced by each active cross-bridge.
Conclusion: Data from single muscle fibre studies can be used to increase our understanding of fatigue mechanisms in some, but not all, types of human exercise. To further increase the understanding of fatigue mechanisms in humans, we propose future studies using in vitro stimulation patterns that are closer to the in vivo situation.
Acute norepinephrine reuptake inhibition decreases performance in normal and high ambient temperature.
Roelands B, Goekint M, Heyman E, Piacentini MF, Watson P, Hasegawa H, Buyse L, Pauwels F, De Schutter G, Meeusen R. Department of Human Physiology and Sports Medicine, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium.
Combined inhibition of dopamine (DA)/norepinephrine (NE) reuptake improves exercise performance and increases core temperature in the heat. A recent study demonstrated that this effect may primarily be related to increased DA activity. NE reuptake inhibition (NERI), however, has received little attention in humans, certainly in the heat, where central fatigue appears to be a main factor influencing performance. Therefore the present study examines the effect of NERI (reboxetine) on exercise capacity, thermoregulation, and hormonal response in normal and high temperature.
Nine healthy well-trained male cyclists participated in this study. Subjects ingested either placebo (Pla; 2 x 8 mg) or reboxetine (Rebox; 2 x 8 mg). Subjects exercised in temperate (18 degrees C) or warm (30 degrees C) conditions and cycled for 60 min at 55% W(max) immediately followed by a time trial (TT; Pla18/Rebox18; Pla30/Rebox30) to measure exercise performance. Acute NERI decreased power output and consequently exercise performance in temperate (P = 0.018) and warm (P = 0.007) conditions. Resting heart rate was significantly elevated by NERI (18 degrees C: P = 0.02; 30 degrees C: P = 0.018). In Rebox18, heart rate was significantly higher than in the Pla18, while in the heat no effect of the drug treatment was reported during exercise. In Rebox30, all hormone concentrations increased during exercise, except for growth hormone (GH), which was significantly lower during exercise. In Rebox18, prolactin (PRL) concentrations were significantly elevated; GH was significantly higher at rest, but significantly lower during exercise.
Conclusion: Manipulation of the NE system decreases performance and modifies hormone concentrations, thereby indicating a central NE effect of the drug. These findings confirm results from previous studies that predominantly increased DA activity is important in improving performance.
Neuromuscular fatigue following constant versus variable-intensity endurance cycling in triathletes.
Lepers R, Theurel J, Hausswirth C, Bernard T. University of Burgundy, Faculty of Sport Sciences, France. firstname.lastname@example.org
The aim of this study was to determine whether or not variable power cycling produced greater neuromuscular fatigue of knee extensor muscles than constant power cycling at the same mean power output. Eight male triathletes (age: 33+/-5 years, mass: 74+/-4 kg, VO2max: 62+/-5 mL kg(-1) min(-1), maximal aerobic power: 392+/-17 W) performed two 30 min trials on a cycle ergometer in a random order. Cycling exercise was performed either at a constant power output (CP) corresponding to 75% of the maximal aerobic power (MAP) or a variable power output (VP) with alternating +/-15%, +/-5%, and +/-10% of 75% MAP approximately every 5 min. Maximal voluntary contraction (MVC) torque, maximal voluntary activation level and excitation-contraction coupling process of knee extensor muscles were evaluated before and immediately after the exercise using the technique of electrically evoked contractions (single and paired stimulations). Oxygen uptake, ventilation and heart rate were also measured at regular intervals during the exercise. Averaged metabolic variables were not significantly different between the two conditions. Similarly, reductions in MVC torque (approximately -11%, P<0.05)>0.05) between CP and VP trials. The magnitude of central and peripheral fatigue was also similar at the end of the two cycling exercises.
Conclusion: Following 30 min of endurance cycling, semi-elite triathletes experienced no additional neuromuscular fatigue by varying power (from +/-5% to 15%) compared with a protocol that involved a constant power.
Differential effects of endurance and resistance training on central fatigue.
Triscott S, Gordon J, Kuppuswamy A, King N, Davey N, Ellaway P. Department of Clinical Neuroscience, Imperial College London, London, UK.
The effect of long-term endurance and resistance training on central fatigue has been studied using transcranial magnetic stimulation by exercising the biceps brachii to exhaustion and recording motor-evoked potentials from the non-exercised homologous biceps. Three groups of eight healthy individuals took part: two groups of individuals who had more than 8 years of athletic training in either an endurance or resistance sport, and a group of controls. The size of a motor-evoked potential (area of averaged rectified response) was significantly depressed in all three groups in the non-exercised arm after exhaustive exercise of the opposite arm. Recovery of motor-evoked potentials occurred earlier in endurance athletes (20 min) than in control participants (30 min) and resistance athletes (>30 min). Dexterity and maximum voluntary contraction of the biceps for the non-exercised arm were not depressed in any group.
In a separate session, the limit of endurance time for the biceps was reduced significantly following exhaustive exercise of the biceps of the other arm for resistance athletes and control participants, whereas there was no change in the endurance athletes.
Conclusion: Athletic training has an effect on the mechanism of central fatigue that may be specific to the nature of training.
My Notes: The SAID principle once again!