Andy
Senior Member (Voting rights)
Abstract
The cellular mechanisms for the age-related loss in skeletal muscle contractile function and increased fatigability are unresolved. We previously observed that the depressive effects of fatiguing levels of hydrogen (H+)(pH6.8-6.6-6.2) and inorganic phosphate (Pi)(12-20-30mM) did not differ in myofibers from young compared with older adults. However, these studies used saturating Ca2+, when fatigue during high-intensity contractions in vivo also likely involves a decrease in myoplasmic free Ca2+.Thus, we compared the Ca2+ sensitivity of myofibers from 10 young (22.1±3.6; 5women) and 13 older (71.7±5.5; 7women) adults in conditions mimicking quiescent (pH7+4mM Pi) and fatigued (pH6.2+30mM Pi) muscle. Fast fiber cross-sectional area was ~35% smaller in older (4,859±2,116μm2) compared with young (7,446±2,399μm2, P=0.002), which corresponded with lower maximal absolute force (Po) in both quiescent (old=0.75±0.30mN; young=1.13±0.32 mN, P=0.002) and fatigue conditions (old=0.35±0.14mN; young=0.52±0.16mN, P=0.002).
There were no differences in fast fiber size-specific Po, indicating the age-related decline in force was due to differences in fiber size. Elevated H+ and Pi shifted the force-pCa relationship to the right, confirming non-human studies that these metabolites contribute to fatigue by depressing the sensitivity of the myofilaments to Ca2+. However, Ca2+ sensitivity was not different with age or sex in either condition, and the metabolite-induced shift in the force-pCa relationship did not differ with age in either the slow (P=0.507) or fast (P=0.115) fibers.
These data suggest the age-related increase in fatigability of limb muscles cannot be explained by an increased sensitivity of the myofibers to elevated H+ and Pi in maximal or submaximal Ca2+.
Open access