Effects of Long-Term Exercise on Human Muscle Mitochondria

Morgan, TE; Cobb, L. A.; Short, F. A.; Ross, Russell; Gunn, D. R.

doi:10.1007/978-1-4613-4609-8_8

Cited by 114 publications

(66 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Associated with these changes, the authors also observed a significant improvement in running time to exhaustion when compared with an untrained control group (186±18 min vs. 29±3 min). Similar findings have subsequently been observed by other groups using guinea pigs (Barnard et al, 1970), rats (Gollnick & Ianuzzo, 1972) and later humans (Morgan et al, 1971). Using a single-leg cycling design, Morgan et al (1971) observed that an increase in mitochondrial protein content was largely due to increases in mitochondrial size (i.e.…”

Section: Exercise-induced Mitochondrial Biogenesissupporting

confidence: 81%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

View full text Add to dashboard Cite

PGC-1α is regarded as a key regulator of mitochondrial biogenesis due to its central role in regulating the activity of key transcription factors associated with encoding mitochondrial components. Additionally, PGC-1α has shown to mediate adaptations that increase fat metabolism and angiogenesis, contributing to the overall oxidative phenotype of the muscle. While it is well established that exercise is a potent stimulator of PGC-1α, recent evidence indicates that heat and cold exposures may also influence mitochondrial biogenesis through the up-regulation of PGC-1α. This highlights the potential use of these modalities in conjunction with exercise to enhance training adaptations. As such, the purpose of this review is to describe the possible mechanisms and pathways by which exercise, as well as hot and cold exposures may influence mitochondrial biogenesis. It is clear that changes in intracellular calcium, oxidative stress and phosphorylation potential are major up-regulators of PGC-1α during exercise. Moreover, there is evidence implicating calcium signalling, in addition to β-adrenergic activation in cold-induced mitochondrial biogenesis, while PGC-1α during heat exposure is likely triggered by changes in phosphorylation potential and nitric oxide signalling. However, these mechanisms appear to change considerably when cold/heat is administered following exercise, and seem to be dependent on the experimental models used (i.e. in vitro vs. in vivo, rodent vs. human). Understanding the effects heat/cold exposure and its interaction with exercise may lead to the optimisation and development of temperature-related interventions to enhance training adaptations, or aid in the treatment of mitochondrial related diseases.

show abstract

Section: Exercise-induced Mitochondrial Biogenesissupporting

confidence: 81%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

View full text Add to dashboard Cite

show abstract

“…[18,58] Within skeletal muscle there is an increased mitochondrial volume as well as oxidative enzyme activity. [4,[58][59][60][61][62] As a result, trained muscles are able to oxidise more substrate [18] which is also expressed in an increased oxygen consumption at maximal exercise intensities. [59,61] Trained muscles store more intracellular fat and also express a higher LPL activity, which will favour the maximising of FA flux to the mitochondria.…”

Section: Endurance Trainingmentioning

confidence: 99%

“…[4,[58][59][60][61][62] As a result, trained muscles are able to oxidise more substrate [18] which is also expressed in an increased oxygen consumption at maximal exercise intensities. [59,61] Trained muscles store more intracellular fat and also express a higher LPL activity, which will favour the maximising of FA flux to the mitochondria. [8,9,58,[63][64][65] This may enhance the capacity to utilise intramuscular TG as fuel [3,35,36,60,61,63] while using less blood-borne FA.…”

Section: Endurance Trainingmentioning

confidence: 99%

“…[59,61] Trained muscles store more intracellular fat and also express a higher LPL activity, which will favour the maximising of FA flux to the mitochondria. [8,9,58,[63][64][65] This may enhance the capacity to utilise intramuscular TG as fuel [3,35,36,60,61,63] while using less blood-borne FA. The advantage of a shift from extracellular to intracellular stores of FA [66,67] is that potential barriers in overall FA utilisation, such as the endothelium and the sarcolemma, are irrelevant when intracellular TG is utilised.…”

Section: Endurance Trainingmentioning

confidence: 99%

See 1 more Smart Citation

Strategies to Enhance Fat Utilisation During Exercise

Hawley

Brouns²,

Jeukendrup³

1998

Sports Medicine

101

View full text Add to dashboard Cite

“…Adaptações como o aumento do volume sistólico (Negrão, Forjaz, Rondon & Brum, .1996), o aumento do débito cardíaco máximo (Blomqvist & Saltin, 1983;Brandão, Wanjngarten, Rondon, Giogi, Hironaka & Negrão, 1993), o aumento do metabolismo oxidativo do músculo esquelético (Henriksson & Reitman, 1977;Morgan, Cobb, Short, Ross & Gunn, 1971) e o aumento do consumo máximo de oxigênio (Blomqvist & Saltin, 1983;Rowell, 1986) possibilitam um melhor fornecimento e utilização de oxigênio e de substratos energéticos durante o exercício físico (Negrão et alii, 1996), aumentando a capacidade do atleta em resistir ao esforço físico por uma intensidade e duração maiores (Maughan, 1990).…”

Section: Introductionunclassified

Effects of physical detraining on athlete performance: a review about skeletal muscle and cardiovascular changes

Evangelista¹,

Brum²

1999

Rev. paul. educ. fís.

View full text Add to dashboard Cite

As adaptações cardiovasculares e metabólicas adquiridas com o treinamento físico de "endurance" podem ser revertidas quando o atleta é submetido a um período de inatividade física, devido ao reajuste dos sistemas corporais às alterações dos estímulos fisiológicos induzidos pelo treinamento físico. Reduções significantes do consumo máximo de oxigênio (V02max) parecem ocorrer dentro de duas a quatro semanas de destreinamento físico, provocando um grande declínio da "performance" do atleta em esportes de "endurance"! A queda inicial do V02max está associada à redução do débito cardíaco conseqüente da redução do volume sistólico, haja visto que a freqüência cardíaca permanece praticamente inalterada. O destreinamento físico também provoca alterações das adaptações do músculo esquelético que resultam em uma redução significante da diferença artério-venosa máxima de oxigênio contribuindo também para a redução do V02max Se a condição física elevada de um atleta pode ser obtida após alguns anos seguidos de treinamento físico efetivo, preparadores físicos e técnicos devem estar atentos para que possíveis eventualidades que impeçam a continuidade da preparação física do atleta não resultem em prejuízos na sua "performance" Sendo assim, esta revisão tem como objetivo descrever o curso temporal e a magnitude de perda das adaptações fisiológicas adquiridas com o treinamento físico, bem como os mecanismos envolvidos nas mesmas. UNITERMOS: Destreinamento físico; Adaptações cardiovasculares e músculo-esqueléticas; Consumo máximo de oxigênio; Fisiologia do exercício. INTRODUÇÃO

show abstract

Effects of Long-Term Exercise on Human Muscle Mitochondria

Cited by 114 publications

References 6 publications

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Strategies to Enhance Fat Utilisation During Exercise

Effects of physical detraining on athlete performance: a review about skeletal muscle and cardiovascular changes

Contact Info

Product

Resources

About