Incomplete recovery of [ATP] in vivo following muscular fatigue in young and older adults
Authors: Smith Zoe , Hayes Kate , Fitzgerald Liam , Shah Amir , Kent Jane 
Published: May 2023

Muscular fatigue (i.e., acute fall in peak power) may result in ATP loss, which is slow to recover in vivo due to the formation of inosine monophosphate (IMP). Slow recovery of ATP may alter the muscle’s ability to resist fatigue during subsequent work; this effect could be more problematic in older muscle. Based on the lower metabolic economy (ME; W·cm-3·mM ATP-1) and greater fatigue reported in older muscle during dynamic contractions, our objective was to use 31-phosphorus magnetic resonance (MR) spectroscopy to noninvasively quantify changes in intracellular energy metabolites and pH in vivo during and after maximal isotonic knee extensions, to test the hypotheses that fatigue would be greater, and [ATP] would decline more and be slower to recover in older compared with younger muscle. Nineteen young (10 female, 31±5 yr, mean+SD) and 17 older (9F, 72±4 yr) healthy adults completed 120 contractions (0.5 Hz, torque=20% of voluntary maximum) while positioned supine in a 3T MR system. Muscle fatigue: peak power for final 3 contractions/peak power for highest 3 contractions x 100. Muscle fat-free contractile volume, determined by MRI, was used to normalize peak power, yielding specific power (W·cm-3). MR spectra from the vastus lateralis muscle were recorded during rest, contractions, and 10 min of recovery. Phosphocreatine (PCr), inorganic phosphate (Pi), phosphomonoesters (PME) and ATP peaks were fit in jMRUI and relative concentrations determined assuming resting [ATP]=8.2 mM. Intracellular [IMP], pH, ATP production (ATPTOT, mM) and ME (specific power/ATPTOT) were calculated. Statistics: t-test and rmANOVA. Specific power was ~61% greater in young than older (p<0.001), but fatigue did not differ by age (young: 55±13% vs. older: 51±17% initial peak power; p=0.48). As expected, PCr and pH decreased and Pi increased during contractions (p<0.001). [ATP] declined to 6.5±0.9 mM in young and 6.7±0.7 mM in older and [IMP] increased to 1.6±0.8 mM in young and 1.3±0.7 mM in older (p<0.001, both). There were no effects of age on changes in any metabolite or ATPTOT (p≥ 0.23). In contrast, ME was greater in young than older (p<0.001). Neither [ATP] nor [IMP] returned to resting values following 10 min of recovery in either group (p<0.001; age effect: p≥ 0.36). Our results suggest that the net breakdown of ATP during fatiguing dynamic contractions is not exacerbated in older age, despite a lower ME in the older group. The potential impact of lower specific power on the ability to keep pace with energy demands in the older remains to be determined. Regardless, the incomplete recovery of [ATP] following fatigue may place both young and older adults at a disadvantage for subsequent bouts of muscular work. As older adults are generally weaker and thus closer to the minimum threshold for power needed in daily tasks, even without fatigue, the slow recovery of [ATP] may be more detrimental to this population.

This research was supported by NIH R01-AG058607 (JAK) and an ACSM Foundation Doctoral Student Research Grant from the American College of Sports Medicine Foundation awarded to LFF.

This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.