Muscle Fatigue from the Perspective of a Single Crossbridge

Debold, Edward P.; Fitts, Robert H.; Sundberg, Christopher W.; Nosek, Thomas M.

doi:10.1249/mss.0000000000001047

Cited by 77 publications

(86 citation statements)

References 95 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…; Debold et al . ). However, investigations employing non‐invasive stimulations to the nervous system indicated that the age‐related increase in fatigability of the knee extensors during dynamic exercise is not a result of suboptimal neural drive or an inability of the action potential to propagate from the neuromuscular junction across the sarcolemma (Dalton et al .…”

Section: Discussionmentioning

confidence: 97%

“…; Debold et al . ). Thus, it is plausible that age‐related changes within the muscle result in the increased production of metabolites and/or an increased sensitivity of the muscle fibres to a given concentration of metabolite accumulation in old compared to young adults.…”

Section: Introductionmentioning

confidence: 97%

“…), which is characterized by an acute reduction in power that occurs in response to contractile activity (Debold et al . ; Hunter, ). This is particularly true for the old adult population because the age‐related decline in the ability to generate power is exacerbated by the increased fatigability that occurs when old adults perform moderate‐ to high‐velocity exercise (McNeil & Rice, ; Dalton et al .…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Bioenergetic basis for the increased fatigability with ageing

Sundberg

Prost

Fitts

et al. 2019

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

Key points The mechanisms for the age‐related increase in fatigability during dynamic exercise remain elusive. We tested whether age‐related impairments in muscle oxidative capacity would result in a greater accumulation of fatigue causing metabolites, inorganic phosphate (Pi), hydrogen (H+) and diprotonated phosphate (H2PO4−), in the muscle of old compared to young adults during a dynamic knee extension exercise. The age‐related increase in fatigability (reduction in mechanical power) of the knee extensors was closely associated with a greater accumulation of metabolites within the working muscle but could not be explained by age‐related differences in muscle oxidative capacity. These data suggest that the increased fatigability in old adults during dynamic exercise is primarily determined by age‐related impairments in skeletal muscle bioenergetics that result in a greater accumulation of metabolites. Abstract The present study aimed to determine whether the increased fatigability in old adults during dynamic exercise is associated with age‐related differences in skeletal muscle bioenergetics. Phosphorus nuclear magnetic resonance spectroscopy was used to quantify concentrations of high‐energy phosphates and pH in the knee extensors of seven young (22.7 ± 1.2 years; six women) and eight old adults (76.4 ± 6.0 years; seven women). Muscle oxidative capacity was measured from the phosphocreatine (PCr) recovery kinetics following a 24 s maximal voluntary isometric contraction. The fatiguing exercise consisted of 120 maximal velocity contractions (one contraction per 2 s) against a load equivalent to 20% of the maximal voluntary isometric contraction. The PCr recovery kinetics did not differ between young and old adults (0.023 ± 0.007 s−1 vs. 0.019 ± 0.004 s−1, respectively). Fatigability (reductions in mechanical power) of the knee extensors was ∼1.8‐fold greater with age and was accompanied by a greater decrease in pH (young = 6.73 ± 0.09, old = 6.61 ± 0.04) and increases in concentrations of inorganic phosphate, [Pi], (young = 22.7 ± 4.8 mm, old = 32.3 ± 3.6 mm) and diprotonated phosphate, [H2PO4−], (young = 11.7 ± 3.6 mm, old = 18.6 ± 2.1 mm) at the end of the exercise in old compared to young adults. The age‐related increase in power loss during the fatiguing exercise was strongly associated with intracellular pH (r = –0.837), [Pi] (r = 0.917) and [H2PO4−] (r = 0.930) at the end of the exercise. These data suggest that the age‐related increase in fatigability during dynamic exercise has a bioenergetic basis and is explained by an increased accumulation of metabolites within the muscle.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Bioenergetic basis for the increased fatigability with ageing

Sundberg

Prost

Fitts

et al. 2019

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…It is therefore possible that the eventual failure of subjects to maintain the requisite power output was caused by attainment of sufficiently low values of [PCr] and, perhaps, [ATP], and/or sufficiently high values of muscle metabolites ([P i ], [ADP], [H + ], and their sequelae) within some of the recruited muscle fibers [(51); see also (3, 23, 24)]. Clearly, subjects either could not, or would not, tolerate this “critical combination” of substrate and metabolite concentrations, but it is not possible to ascertain whether this was related to direct effects of the muscle metabolic milieu on contractile function (17) or to the attainment of some individual sensory “critical fatigue threshold” that might constrain central motor drive and muscle activation via feedback from type III/IV neural afferents (4). The appreciable metabolic perturbation we observed during severe-intensity exercise was associated with a concomitant decrease in M-wave amplitude in both VL and VM muscles.…”

Section: Discussionmentioning

confidence: 99%

“…It is therefore likely that the initial reduction in M-wave amplitude was a result of plasma [K + ] accumulation, which reduced the release of Ca 2+ from the sarcoplasmic reticulum, thus impairing excitation-contraction coupling (36, 71). As heavy-intensity exercise continued, it is possible that the combined metabolic and ionic perturbation, coupled with the ~60% decrease in muscle [glycogen], may have further impaired Ca 2+ release and cross-bridge formation (2, 3, 23, 24, 36, 40, 41) and/or the sensitivity of the myofilaments to Ca 2+ (17). Although fatigue development during heavy-intensity exercise appears to be more complicated than it is for severe-intensity exercise, it is related to the combined influence of ionic changes in muscle membrane excitability, muscle metabolite accumulation, and the decrease in energy substrate, which act collectively to impair excitation-contraction coupling.…”

Section: Discussionmentioning

confidence: 99%

Muscle metabolic and neuromuscular determinants of fatigue during cycling in different exercise intensity domains

Black

Jones

Blackwell

et al. 2017

Journal of Applied Physiology

192

233

View full text Add to dashboard Cite

The gas exchange threshold and the critical power demarcate discrete exercise intensity domains. For the first time, we show that the limit of tolerance during whole body exercise within these domains is characterized by distinct metabolic and neuromuscular responses. Fatigue development during exercise greater than critical power is associated with the attainment of consistent “limiting” values of muscle metabolites, whereas substrate availability and limitations to muscle activation may constrain performance at lower intensities.

show abstract