The effects of hypoxia and fatigue on skeletal muscle electromechanical delay

Mark Jacunski, Gerrard Rafferty

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Acute hypoxia impairs muscle endurance and accelerates fatigue, but the underlying mechanisms, including any effects on muscle electrical activation, are incompletely understood. Electromyographic, mechanomyographic and force signals, elicited by common fibular nerve stimulation, were used to determine electromechanical delay (EMDTOT) of the tibialis anterior muscle in normoxia and hypoxia (FiO2 0.125) at rest and following fatiguing ankle dorsiflexor exercise (60% maximum voluntary contraction, 5 seconds on, 3 seconds off) in 12 healthy participants (mean (SD) age 27.4 (9.0) years). EMDTOT was determined from electromyographic to force signal onset, electrical activation latency from electromyographic to mechanomyographic (EMDE-M) and mechanical latency from mechanomyographic to force (EMDM-F). Twitch force fell significantly following fatiguing exercise in normoxia (46.8 (14.7) vs 20.6 (14.3) N, p=0.0002) and hypoxia (52.9 (15.4) vs 28.8 (15.2) N, p=0.0006). No effect of hypoxia on twitch force at rest was observed. Fatiguing exercise resulted in significant increases in mean (SD) EMDTOT in normoxia (Δ 4.7 (4.57) ms P=0.0152) and hypoxia (Δ 3.7 (4.06) ms p=0.0384) resulting from increased mean (SD) EMDM-F only (normoxia Δ 4.1 (4.1) ms p=0.0391, hypoxia Δ 3.4 (3.6) ms p=0.0303). Mean (SD) EMDE-M remained unchanged during normoxic (Δ 0.6 (1.08) ms) and hypoxic (Δ 0.25 (0.75) ms) fatiguing exercise. No differences in percentage change from baseline for twitch force, EMDTOT, EMDE-M and EMDM-F between normoxic and hypoxic fatigue conditions were observed. Hypoxia in isolation or in combination with fatigue had no effect on the electrochemical latency associated with electrically evoked muscle contraction
Original languageEnglish
JournalExperimental Physiology
Publication statusAccepted/In press - 3 Mar 2020


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