An Innovative Ergometer to Measure Neuromuscular Fatigue Immediately after Cycling.

PURPOSE: When assessing neuromuscular fatigue (NMF) from dynamic exercise using large muscle mass (e.g., cycling), most studies have delayed measurement for 1 to 3 min after task failure. This study aimed to determine the reliability of an innovative cycling ergometer permitting the start of fatigue measurement within 1 s after cycling. METHODS: Twelve subjects participated in two experimental sessions. Knee-extensor NMF was assessed by electrical nerve and transcranial magnetic stimulation with both a traditional chair setup (PRE- and POST-Chair, 2 min postexercise) and the new cycling ergometer (PRE, every 3 min during incremental exercise and POST-Bike, at task failure). RESULTS: The reduction in maximal voluntary contraction force POST-Bike (63% ± 12% PRE; P < 0.001) was not different between sessions and there was excellent reliability at PRE-Bike (intraclass correlation coefficient [ICC], 0.97; coefficients of variation [CV], 3.2%) and POST-Bike. Twitch (Tw) and high-frequency paired-pulse (Db100) forces decreased to 53% ± 14% and 62% ± 9% PRE, respectively (P < 0.001). Both were reliable at PRE-Bike (Tw: ICC, 0.97; CV, 5.2%; Db100: ICC, 0.90; CV, 7.3%) and POST-Bike (Tw: ICC, 0.88; CV, 11.9; Db100: ICC, 0.62; CV, 9.0%). Voluntary activation did not change during the cycling protocol (P > 0.05). Vastus lateralis and rectus femoris M-wave and motor-evoked potential areas showed fair to excellent reliability (ICC, 0.45-0.88). The reduction in maximal voluntary contraction and Db100 was greater on the cycling ergometer than the isometric chair. CONCLUSIONS: The innovative cycling ergometer is a reliable tool to assess NMF during and immediately postexercise. This will allow fatigue etiology during dynamic exercise with large muscle mass to be revisited in various populations and environmental conditions.

Skeletal muscle fatigue--regulation of excitation-contraction coupling to avoid metabolic catastrophe.

ATP provides the energy in our muscles to generate force, through its use by myosin ATPases, and helps to terminate contraction by pumping Ca(2+) back into the sarcoplasmic reticulum, achieved by Ca(2+) ATPase. The capacity to use ATP through these mechanisms is sufficiently high enough so that muscles could quickly deplete ATP. However, this potentially catastrophic depletion is avoided. It has been proposed that ATP is preserved not only by the control of metabolic pathways providing ATP but also by the regulation of the processes that use ATP. Considering that contraction (i.e. myosin ATPase activity) is triggered by release of Ca(2+), the use of ATP can be attenuated by decreasing Ca(2+) release within each cell. A lower level of Ca(2+) release can be accomplished by control of membrane potential and by direct regulation of the ryanodine receptor (RyR, the Ca(2+) release channel in the terminal cisternae). These highly redundant control mechanisms provide an effective means by which ATP can be preserved at the cellular level, avoiding metabolic catastrophe. This Commentary will review some of the known mechanisms by which this regulation of Ca(2+) release and contractile response is achieved, demonstrating that skeletal muscle fatigue is a consequence of attenuation of contractile activation; a process that allows avoidance of metabolic catastrophe.