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After all me and Vincent′s debates on ′to fatigue or not to fatigue′ I put some info. together. I am more convinced that heavy weights AND fatigue are good. (note the calcium info., it′s related to temporaty ATP depletion)
*** Recuitment
Zytnicki et al., 1990 found a reduction in the inhibitory effect of Group Ib feedback on motor neurons, also Hutton & Nelson, 1986, found that tendon organs repsonses drop with fatigue. Overall, fatigue enhances the reflex EMG and motor neuron responses to brief pertubations (Darling & Hayes, 1983; Windhorst et al., 1986)
Kirsch & Rymer, 1987 found that the neural drive was increased after a fatiguing contraction. A rapid stretch was applied to the elbow flexors before and after a fatiguing task. Torque was equal at both times, although the muscles were fatigued and had a lowered force output. EMG was also higher post fatigue.
"The sense of effort" is directly related to the corollary discharge. This applies also to longer fatiguing contractions. (Cafarelli, 1988; Jones & Hunter, 1983)
"Post-tetanic potentiation" is also a contender. During intermitant stimulation, the potentiation of twitch force rose from 29% to 150% after 20 to 40 seconds.
***Calcium influx needed for hypertrophy (fatigue increases calcium accumulation see below)
Skeletal muscle fibers adapt to higher contractile loads by increasing their size and by expressing slower isoforms of muscle contractile proteins (Dunn and Michel 1997 ). Calcineurin, a Ca2+/calmodulin(CaM)1-dependent phosphatase, appears crucial in the signaling of this adaptive response, since functional overload-induced fiber hypertrophy and fiber type transformations are prevented in vivo by administration of the specific calcineurin inhibitors cyclosporin A (CsA) and FK506 (Dunn et al. 1999 ). Calcineurin is likely activated in overloaded muscles via the chronic increases in intracellular calcium that occur under these conditions (Panchenko et al. 1974 ) as a result of a doubling of nerve-mediated muscle fiber activation (Gardiner et al. 1986 ) and load-related increases in insulin-like growth factor (Adams and Haddad 1996 ; Musaro et al. 1999 ; Semsarian et al. 1999 ). Once activated, calcineurin may signal downstream to genes involved in regulating muscle fiber size and myofibrillar protein phenotype via dephosphorylation of its substrate transcription factors, nuclear factor of activated T cells (NFAT) and myocyte enhancer factor 2 (MEF2) (Chin et al. 1998 ; Musaro et al. 1999 ; Semsarian et al. 1999 ; Wu et al. 2000 ).
***Calcium related to fatigue
Metabolic factors contributing to altered Ca2+ regulation in skeletal muscle fatigue.
Steele DS, Duke AM.
School of Biomedical Sciences, University of Leeds, Leeds, UK.
AIM: Skeletal muscle fatigue is characterized by a failure to maintain force production or power output during intense exercise. Many recent studies on isolated fibres have used brief repetitive tetanic contractions to mimic fatigue resulting from intensive exercise and to investigate the underlying cellular mechanisms. Such studies have shown that characteristic changes in Ca2+ regulation occur during fatiguing stimulation. This includes prolongation of the ′Ca2+-tails′ which follow each period of tetanic stimulation and a progressive rise in resting [Ca2+]. More importantly, the final stage of fatigue is associated with a rapid decrease in tetanic [Ca2+]i and force. These fatigue-induced changes in sarcoplasmic reticulum (SR) Ca2+ regulation are temporally associated with alterations in the intracellular levels of phosphate metabolites and a causal relationship has often been proposed. The aim of this review is to evaluate the evidence linking changes in the levels of phosphate metabolites and altered Ca2+ regulation during fatigue. RESULTS: The following current hypotheses will be discussed: (1) the early changes in Ca2+ regulation reflect alterations in the intracellular levels of phosphate metabolites, (2) inhibition of the SR Ca2+ release mechanism (e.g. caused by ATP depletion and increased [Mg2+]) contributes to the decrease in tetanic [Ca2+]i during the final stages of fatigue and (iii) delayed entry of inorganic phosphate ions (Pi) into the SR, followed by precipitation of calcium phosphate (Ca-Pi), can explain the fatigue-induced decrease in tetanic [Ca2+]i. CONCLUSION: There is strong evidence that changes in phosphate metabolite levels contribute to early changes in SR Ca2+ regulation during fatigue and that inhibition of the SR Ca2+ release mechanism can partially explain the rapid decrease in tetanic [Ca2+]i during the final stages of fatigue. While precipitation of Ca-Pi may occur within the SR during fatigue, there is currently insufficient evidence to establish whether this contributes to the late decline in tetanic [Ca2+]i.
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