title: Rats bred for low aerobic capacity become promptly fatigued and have slow metabolic recovery after stimulated, maximal muscle contractions.
abstract: OBJECTIVE
  Muscular fatigue is a complex phenomenon affected by muscle fiber type and several metabolic and ionic changes within myocytes. Mitochondria are the main determinants of muscle oxidative capacity which is also one determinant of muscle fatigability. By measuring the concentrations of intracellular stores of high-energy phosphates it is possible to estimate the energy production efficiency and metabolic recovery of the muscle. Low intrinsic aerobic capacity is known to be associated with reduced mitochondrial function. Whether low intrinsic aerobic capacity also results in slower metabolic recovery of skeletal muscle is not known. Here we studied the influence of intrinsic aerobic capacity on in vivo muscle metabolism during maximal, fatiguing electrical stimulation.
  
  
  METHODS
  Animal subjects were genetically heterogeneous rats selectively bred to differ for non-trained treadmill running endurance, low capacity runners (LCRs) and high capacity runners (HCRs) (n = 15-19). We measured the concentrations of major phosphorus compounds and force parameters in a contracting triceps surae muscle complex using (31)P-Magnetic resonance spectroscopy ((31)P-MRS) combined with muscle force measurement from repeated isometric twitches.
  
  
  RESULTS
  Our results demonstrated that phosphocreatine re-synthesis after maximal muscle stimulation was significantly slower in LCRs (p<0.05). LCR rats also became promptly fatigued and maintained the intramuscular pH poorly compared to HCRs. Half relaxation time (HRT) of the triceps surae was significantly longer in LCRs throughout the stimulation protocol (p≤0.05) and maximal rate of torque development (MRTD) was significantly lower in LCRs compared to HCRs from 2 min 30 s onwards (p≤0.05).
  
  
  CONCLUSIONS
  We observed that LCRs are more sensitive to fatigue and have slower metabolic recovery compared to HCRs after maximal muscle contractions. These new findings are associated with reduced running capacity and with previously found lower mitochondrial content, increased body mass and higher complex disease risk of LCRs.
authors.affiliation: Department of Biology of Physical Activity, Neuromuscular Research Center, University of Jyväskylä, Jyväskylä, Finland.
authors.forename: Sira
authors.initials: S
authors.lastname: Torvinen
authors.forename: Mika
authors.initials: M
authors.lastname: Silvennoinen
authors.forename: Harri
authors.initials: H
authors.lastname: Piitulainen
authors.forename: Johanna
authors.initials: J
authors.lastname: Närväinen
authors.forename: Pasi
authors.initials: P
authors.lastname: Tuunanen
authors.forename: Olli
authors.initials: O
authors.lastname: Gröhn
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.forename: Heikki
authors.initials: H
authors.lastname: Kainulainen
mesh_terms: D000818:Animals; D001947:Breeding; D004558:Electric Stimulation; D004734:Energy Metabolism / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D009119:Muscle Contraction / Q000502:physiology*; D018763:Muscle Fatigue / Q000502:physiology*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats
chemical_list: D010710:Phosphates; D010725:Phosphocreatine