High efficiency in human muscle: an anomaly and an opportunity?

Nelson, Frank E.; Ortega, Justus D.; Jubrias, Sharon A.; Conley, Kevin E.; Kushmerick, Martin J.

doi:10.1242/jeb.052985

Cited by 19 publications

(18 citation statements)

References 39 publications

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“…3 as elevations in ATP max of the quadriceps (ΔATP max , 32%) and the power output by the legs at VȮ 2,max (ΔP max , 17%). The smaller rise in P max versus ATP max (Δ17%/Δ32%=0.53) is exactly what is expected from the 50% contraction efficiency of converting ATP into muscle work in humans (Nelson et al, 2011).…”

Section: Elevating Etc Flux In Old Mitochondriasupporting

confidence: 57%

Mitochondria to motion: optimizing oxidative phosphorylation to improve exercise performance

Conley

2016

Journal of Experimental Biology

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Mitochondria oxidize substrates to generate the ATP that fuels muscle contraction and locomotion. This review focuses on three steps in oxidative phosphorylation that have independent roles in setting the overall mitochondrial ATP flux and thereby have direct impact on locomotion. The first is the electron transport chain, which sets the pace for oxidation. New studies indicate that the electron transport chain capacity per mitochondria declines with age and disease, but can be revived by both acute and chronic treatments. The resulting higher ATP production is reflected in improved muscle power output and locomotory performance. The second step is the coupling of ATP supply from O 2 uptake (mitochondrial coupling efficiency). Treatments that elevate mitochondrial coupling raise both exercise efficiency and the capacity for sustained exercise in both young and old muscle. The final step is ATP synthesis itself, which is under dynamic control at multiple sites to provide the 50-fold range of ATP flux between resting muscle and exercise at the mitochondrial capacity. Thus, malleability at sites in these subsystems of oxidative phosphorylation has an impact on ATP flux, with direct effects on exercise performance. Interventions are emerging that target these three independent subsystems to provide many paths to improve ATP flux and elevate the muscle performance lost to inactivity, age or disease.

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Section: Elevating Etc Flux In Old Mitochondriasupporting

confidence: 57%

Mitochondria to motion: optimizing oxidative phosphorylation to improve exercise performance

Conley

2016

Journal of Experimental Biology

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“…), assuming an ATP change of standard Gibbs free energy (Δ G °) of 52 kJ mol −1 (Nelson et al . ). Using the submaximal

{\dot{V}}_{{normalO}_{2}}

–power relationship, the power output eliciting an O 2 demand equal to the measured

{\dot{V}}_{O_{2} \max}

was 258 ± 30 W. These two estimations (213 and 258 W) of the maximal aerobically sustainable load were significantly lower than the W mean reached during the sprints.…”

Section: Resultsmentioning

confidence: 97%

What limits performance during whole‐body incremental exercise to exhaustion in humans?

Morales-Álamo

Losa‐Reyna

Torres‐Peralta

et al. 2015

The Journal of Physiology

169

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Key pointsr At the end of an incremental exercise to exhaustion a large functional reserve remains in the muscles to generate power, even at levels far above the power output at which task failure occurs, regardless of the inspiratory O 2 pressure during the incremental exercise.r Exhaustion (task failure) is not due to lactate accumulation and the associated muscle acidification; neither the aerobic energy pathways nor the glycolysis are blocked at exhaustion.r Muscle lactate accumulation may actually facilitate early recovery after exhaustive exercise even under ischaemic conditions. r Although the maximal rate of ATP provision is markedly reduced at task failure, the resynthesis capacity remaining exceeds the rate of ATP consumption, indicating that task failure during an incremental exercise to exhaustion depends more on central than peripheral mechanisms.Abstract To determine the mechanisms causing task failure during incremental exercise to exhaustion (IE), sprint performance (10 s all-out isokinetic) and muscle metabolites were measured before (control) and immediately after IE in normoxia (P IO 2 : 143 mmHg) and hypoxia (P IO 2 : 73 mmHg) in 22 men (22 ± 3 years). After IE, subjects recovered for either 10 or 60 s, with open circulation or bilateral leg occlusion (300 mmHg) in random order. This was followed by a 10 s sprint with open circulation. Post-IE peak power output (W peak ) was higher than the power output reached at exhaustion during IE (P < 0.05). After 10 and 60 s recovery in normoxia, W peak was reduced by 38 ± 9 and 22 ± 10% without occlusion, and 61 ± 8 and 47 ± 10% with occlusion (P < 0.05). Following 10 s occlusion, W peak was 20% higher in hypoxia than normoxia (P < 0.05), despite similar muscle lactate accumulation ([La]) and phosphocreatine and ATP reduction. Sprint performance and anaerobic ATP resynthesis were greater after 60 s compared with 10 s occlusions, despite the higher [La] and [H + ] after 60 s compared with 10 s occlusion recovery (P < 0.05). The mean rate of ATP turnover during the 60 s occlusion was 0.180 ± 0.133 mmol (kg wet wt) −1 s −1 , i.e. equivalent to 32% of leg peak O 2 uptake (the energy expended by the ion pumps). A greater degree of recovery is achieved, however, without occlusion. In conclusion, during incremental exercise task failure is not due to metabolite accumulation or lack of energy resources. Anaerobic metabolism, despite the accumulation of lactate and H + , facilitates early Abbreviations Cr, creatine; d.w., dry weight; F IO2 , inspired oxygen fraction; HR, heart rate; HR peak , peak heart rate; Hyp, hypoxia; IE, incremental exercise to exhaustion; La, lactate; Mb, myoglobin; Nx, normoxia; PCr, phosphocreatine; P ETCO2 , end-tidal CO 2 pressure; P ETO2 , end-tidal O 2 pressure; P IO2 , partial pressure of inspired O 2 ; RER, respiratory exchange ratio; S pO2 , haemoglobin oxygen saturation measured by pulse-oximetry; TOI, tissue oxygenation index;V CO2 , CO 2 production;V CO2peak , peak CO 2 production;V E , minute ventilation;V O2 , O 2 consumpt...

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“…S2). The power output that is possible from ΔATP max can be estimated from the free energy of ATP hydrolysis (55 J mmol −1 for the phosphocreatine and pH levels during exercise; Conley et al 2012), the increase in muscle volume (Δ V Q ) and the efficiency of converting ATP into work (ɛ c = 0.5 or 50% for human muscle; Whipp & Wasserman, 1969; Nelson et al 2011). This calculation yields an increase of 12 W (=ΔATP max ×Δ V Q ×ɛ c ), which indicates that the quadriceps was responsible for a significant fraction of the measured increase in P max of 17 W. This result suggests that the majority of the adaptation in leg power output came from the quadriceps, with a smaller contribution from other thigh muscles.…”

Section: Discussionmentioning

confidence: 99%

Elevated energy coupling and aerobic capacity improves exercise performance in endurance‐trained elderly subjects

Conley

Jubrias²,

Cress³

et al. 2013

Experimental Physiology

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Increased maximal oxygen uptake (V(O(2)max)), mitochondrial capacity and energy coupling efficiency are reported after endurance training (ET) in adult subjects. Here we test whether leg exercise performance (power output of the legs, P(max), at V(O(2)max)) reflects these improvements with ET in the elderly. Fifteen male and female subjects were endurance trained for a 6 month programme, with 13 subjects (69.5 ± 1.2 years old, range 65-80 years old; n = 7 males; n = 6 females) completing the study. This training significantly improved P(max) (Δ17%; P = 0.003), V(O(2)max) (Δ5.4%; P = 0.021) and the increment in oxygen uptake (V(O(2))) above resting (ΔV(O(2)m-r) = V(O(2)max) - V(O(2)rest; Δ9%; P < 0.02). In addition, evidence of improved energy coupling came from elevated leg power output per unit V(O(2))at the aerobic capacity [Δ(P(max)/ΔV(O(2)m-r)); P = 0.02] and during submaximal exercise in the ramp test as measured by delta efficiency (ΔP(ex)/ΔV(O(2)); P = 0.04). No change was found in blood lactate, muscle glycolysis or fibre type. The rise in P(max) paralleled the improvement in muscle oxidative phosphorylation capacity (ATP(max)) in these subjects. In addition, the greater exercise energy coupling [Δ(P(max)/ΔV(O(2)m-r)) and delta efficiency] was accompanied by increased mitochondrial energy coupling as measured by elevated ATP production per unit mitochondrial content in these subjects. These results suggest that leg exercise performance benefits from elevations in energy coupling and oxidative phosphorylation capacity at both the whole-body and muscle levels that accompany endurance training in the elderly.

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High efficiency in human muscle: an anomaly and an opportunity?

Cited by 19 publications

References 39 publications

Mitochondria to motion: optimizing oxidative phosphorylation to improve exercise performance

Mitochondria to motion: optimizing oxidative phosphorylation to improve exercise performance

What limits performance during whole‐body incremental exercise to exhaustion in humans?

Elevated energy coupling and aerobic capacity improves exercise performance in endurance‐trained elderly subjects

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