Caffeine Ingestion Attenuates Fatigue-induced Loss of Muscle Torque Complexity

The temporal structure, or complexity, of muscle torque output decreases with neuromuscular fatigue. The role of central fatigue in this process is unclear. PURPOSEWe tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. METHODSEleven healt...

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Veröffentlicht in:Medicine and science in sports and exercise 2018-02, Vol.50 (2), p.236-245
Hauptverfasser: PETHICK, JAMIE, WINTER, SAMANTHA L, BURNLEY, MARK
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WINTER, SAMANTHA L
BURNLEY, MARK
description The temporal structure, or complexity, of muscle torque output decreases with neuromuscular fatigue. The role of central fatigue in this process is unclear. PURPOSEWe tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. METHODSEleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction, with a 60% duty factor (6-s contraction, 4-s rest), 60 min after ingesting 6 mg·kg caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central, and peripheral fatigue was quantified using maximal voluntary contractions with femoral nerve stimulation. RESULTSCaffeine ingestion increased endurance by 30% ± 16% (mean ± SD; P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P < 0.01), as global, central, and peripheral fatigue developed (all P < 0.01). Complexity decreased significantly more slowly after caffeine ingestion (ApEn, −0.04 ± 0.02 vs –0.06 ± 0.01 (P = 0.004); DFA α, 0.03 ± 0.02 vs 0.04 ± 0.03 (P = 0.024)), as did the rates of global (−18.2 ± 14.1 vs –23.0 ± 17.4 N·m·min, P = 0.004) and central (−3.5 ± 3.4 vs –5.7 ± 3.9 %·min, P = 0.02) but not peripheral (−6.1 ± 4.1 vs –7.9 ± 6.3 N·m·min, P = 0.06) fatigue. CONCLUSIONSCaffeine ingestion slowed the fatigue-induced loss of torque complexity and increased the time to task failure during intermittent isometric contractions, most likely through central mechanisms.
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The role of central fatigue in this process is unclear. PURPOSEWe tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. METHODSEleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction, with a 60% duty factor (6-s contraction, 4-s rest), 60 min after ingesting 6 mg·kg caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central, and peripheral fatigue was quantified using maximal voluntary contractions with femoral nerve stimulation. RESULTSCaffeine ingestion increased endurance by 30% ± 16% (mean ± SD; P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P &lt; 0.01), as global, central, and peripheral fatigue developed (all P &lt; 0.01). Complexity decreased significantly more slowly after caffeine ingestion (ApEn, −0.04 ± 0.02 vs –0.06 ± 0.01 (P = 0.004); DFA α, 0.03 ± 0.02 vs 0.04 ± 0.03 (P = 0.024)), as did the rates of global (−18.2 ± 14.1 vs –23.0 ± 17.4 N·m·min, P = 0.004) and central (−3.5 ± 3.4 vs –5.7 ± 3.9 %·min, P = 0.02) but not peripheral (−6.1 ± 4.1 vs –7.9 ± 6.3 N·m·min, P = 0.06) fatigue. 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The role of central fatigue in this process is unclear. PURPOSEWe tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. METHODSEleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction, with a 60% duty factor (6-s contraction, 4-s rest), 60 min after ingesting 6 mg·kg caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central, and peripheral fatigue was quantified using maximal voluntary contractions with femoral nerve stimulation. RESULTSCaffeine ingestion increased endurance by 30% ± 16% (mean ± SD; P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P &lt; 0.01), as global, central, and peripheral fatigue developed (all P &lt; 0.01). Complexity decreased significantly more slowly after caffeine ingestion (ApEn, −0.04 ± 0.02 vs –0.06 ± 0.01 (P = 0.004); DFA α, 0.03 ± 0.02 vs 0.04 ± 0.03 (P = 0.024)), as did the rates of global (−18.2 ± 14.1 vs –23.0 ± 17.4 N·m·min, P = 0.004) and central (−3.5 ± 3.4 vs –5.7 ± 3.9 %·min, P = 0.02) but not peripheral (−6.1 ± 4.1 vs –7.9 ± 6.3 N·m·min, P = 0.06) fatigue. 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The role of central fatigue in this process is unclear. PURPOSEWe tested the hypothesis that caffeine administration would attenuate the fatigue-induced loss of torque complexity. METHODSEleven healthy participants performed intermittent isometric contractions of the knee extensors to task failure at a target torque of 50% maximal voluntary contraction, with a 60% duty factor (6-s contraction, 4-s rest), 60 min after ingesting 6 mg·kg caffeine or a placebo. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Global, central, and peripheral fatigue was quantified using maximal voluntary contractions with femoral nerve stimulation. RESULTSCaffeine ingestion increased endurance by 30% ± 16% (mean ± SD; P = 0.019). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P &lt; 0.01), as global, central, and peripheral fatigue developed (all P &lt; 0.01). Complexity decreased significantly more slowly after caffeine ingestion (ApEn, −0.04 ± 0.02 vs –0.06 ± 0.01 (P = 0.004); DFA α, 0.03 ± 0.02 vs 0.04 ± 0.03 (P = 0.024)), as did the rates of global (−18.2 ± 14.1 vs –23.0 ± 17.4 N·m·min, P = 0.004) and central (−3.5 ± 3.4 vs –5.7 ± 3.9 %·min, P = 0.02) but not peripheral (−6.1 ± 4.1 vs –7.9 ± 6.3 N·m·min, P = 0.06) fatigue. CONCLUSIONSCaffeine ingestion slowed the fatigue-induced loss of torque complexity and increased the time to task failure during intermittent isometric contractions, most likely through central mechanisms.</abstract><cop>United States</cop><pub>American College of Sports Medicine</pub><pmid>28991045</pmid><doi>10.1249/MSS.0000000000001441</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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title Caffeine Ingestion Attenuates Fatigue-induced Loss of Muscle Torque Complexity
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