The O₂cost of the tension-time integral in isolated single myocytes during fatigue

Abstract

One proposed explanation for the Vo(2) slow component is that lower-threshold motor units may fatigue and develop little or no tension but continue to use O(2), thereby resulting in a dissociation of cellular respiration from force generation. The present study used intact isolated single myocytes with differing fatigue resistance profiles to investigate the relationship between fatigue, tension development, and aerobic metabolism. Single Xenopus skeletal muscle myofibers were allocated to a fast-fatiguing (FF) or a slow-fatiguing (SF) group, based on the contraction frequency required to elicit a fall in tension to 60% of peak. Phosphorescence quenching of a porphyrin compound was used to determine Delta intracellular Po(2) (Pi(O(2)); a proxy for Vo(2)), and developed isometric tension was monitored to allow calculation of the time-integrated tension (TxT). Although peak DeltaPi(O(2)) was not different between groups (P = 0.36), peak tension was lower (P < 0.05) in SF vs. FF (1.97 +/- 0. 17 V vs. 2. 73 +/- 0.30 V, respectively) and time to 60% of peak tension was significantly longer in SF vs. FF (242 +/- 10 s vs. 203 +/- 10 s, respectively). Before fatigue, both DeltaPi(O(2)) and TxT rose proportionally with contraction frequency in SF and FF, resulting in DeltaPi(O(2))/TxT being identical between groups. At fatigue, TxT fell dramatically in both groups, but DeltaPi(O(2)) decreased proportionately only in the FF group, resulting in an increase in DeltaPi(O(2))/TxT in the SF group relative to the prefatigue condition. These data show that more fatigue-resistant fibers maintain aerobic metabolism as they fatigue, resulting in an increased O(2) cost of contractions that could contribute to the Vo(2) slow component seen in whole body exercise.

Knee Extensor Fatigue Threshold Is Related to Whole-Body V˙O2max

“…Recent findings suggest that a reduction of mechanical efficiency of early recmited motor units may also contribute to the steady rise in VO2 (6). This is in line with data from isolated frog fibers showing reduced force production relative to oxygen consumption when slowly fatiguing fibers were fatigued (18). Clearly, this could also contribute to a rise in muscle deoxygenation above critical exercise intensity.…”

“…Although great care should be taken to interpret changes in rsEMG in terms of motor unit recmitment and rate coding (14) when rsEMG does increase, it is usually paralleled by additional motor unit recmitment and/ or increased rate coding (10,19). It is important to note that recent findings support the idea that reduced efficiency of early recmited motor units may also contribute to the rise in oxygen consumption during very heavy exercise (6,18). The concurrent decrease in mean power frequency during contractions above fatigue threshold may relate to decreases in muscle flber action potential conduction velocity, which, in tum, have been linked to fatigue-related metabolic changes such as accumulation of potassium and decreased pH (33).…”

Lower Extremity Motor Impairments in Ambulatory Chronic Hemiparetic Stroke: Evidence for Lower Extremity Weakness and Abnormal Muscle and Joint Torque Coupling Patterns

“…This was particularly the case during ankle plantar and dorsiflexion. Abnormal coactivation patterns with a bias in extension not only decrease specificity in motor control but also demand a higher energetic cost to achieve the required torques 45 .…”

Endurance training decreases the non‐linearity in the oxygen uptake–power output relationship in humans

“…However, the mechanism responsible for this effect remains unclear. There is a growing body of evidence to suggest that the increase in the oxygen cost of work during heavy‐intensity exercise is caused by fatigue of the active muscle fibres (Zoladz et al 2008; Hepple et al 2010; Cannon et al 2011) and, in particular, by a disturbance in the concentrations of muscle metabolites, i.e. a decrease in muscle phosphocreatine and a rise in free ADP, free AMP, free inosine monophosphate, creatine, inorganic phosphate and H + , potent to decrease muscle mechanical efficiency (Woledge, 1998; Zoladz et al 2006).…”