Knee extensor and plantar flexor muscle size and function following 90 days of bed rest with or without resistance exercise

Alkner, Björn; Tesch, Per A.

doi:10.1007/s00421-004-1172-8

Cited by 250 publications

(313 citation statements)

References 42 publications

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“…In response to decreased mechanical stress, skeletal muscle tissue undergoes rapid atrophy characterized by the loss of mass and size. 204,205 On the other hand, mechanical stimulation of the tissue leads to increased mitochondrial content, 206 improved insulin sensitivity, 207 enhanced muscle strength, and increased size. 208 During catabolic conditions, muscle proteins are catabolized to maintain gluconeogenesis in the liver, 209 but excessive degradation of the muscle tissue may be extremely damaging for the organism, leading to muscle wasting and even death.…”

Section: Exercise As a Modelmentioning

confidence: 99%

Heat shock response and autophagy—cooperation and control

2015

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Abbreviations: AKT, v-akt murine thymoma viral oncogene homolog 1; AMPK, adenosine monophosphate-activated protein kinase; ATG, autophagy-related; BECN1, Beclin 1, autophagy related; EIF4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; FOXO, forkhead box O; HSF1, heat shock transcription factor 1; HSP, heat shock protein; HSPA8/ HSC70, heat shock 70kDa protein 8; IL, interleukin; LC3, MAP1LC3, microtubule-associated protein 1 light chain 3; MTMR14/ hJumpy, myotubularin related protein 14; MTOR, mechanistic target of rapamycin; NR1D1/Rev-Erb-a, nuclear receptor subfamily 1, group D, member 1; PBMC, peripheral blood mononuclear cell; PPARGC1A/PGC-1a, peroxisome proliferator-activated receptor, gamma, coactivator 1 a; RHEB, Ras homolog enriched in brain; SOD, superoxide dismutase; SQSTM1/p62, sequestosome 1; TPR, translocated promoter region, nuclear basket protein; TSC, tuberous sclerosis complex; ULK1, unc-51 like autophagy activating kinase 1.Protein quality control (proteostasis) depends on constant protein degradation and resynthesis, and is essential for proper homeostasis in systems from single cells to whole organisms. Cells possess several mechanisms and processes to maintain proteostasis. At one end of the spectrum, the heat shock proteins modulate protein folding and repair. At the other end, the proteasome and autophagy as well as other lysosome-dependent systems, function in the degradation of dysfunctional proteins. In this review, we examine how these systems interact to maintain proteostasis. Both the direct cellular data on heat shock control over autophagy and the time course of exercise-associated changes in humans support the model that heat shock response and autophagy are tightly linked. Studying the links between exercise stress and molecular control of proteostasis provides evidence that the heat shock response and autophagy coordinate and undergo sequential activation and downregulation, and that this is essential for proper proteostasis in eukaryotic systems.

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Section: Exercise As a Modelmentioning

confidence: 99%

Heat shock response and autophagy—cooperation and control

2015

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“…(2) Resistive exercise Subjects trained the back, thigh and calf muscle groups using supine squat (SS) and calf press (CP) exercises using a gravity independent inertial ergometer (Alkner and Tesch 2004). A total of 19 sessions were scheduled for each subject approximately every third day (2-3 days/week) beginning on day 2 of HDBR.…”

Section: Groupsmentioning

confidence: 99%

“…The SS exercise consisted of 4 sets of 7 maximal concentric and eccentric repetitions, while the CP exercise consisted of 4 sets of 14 maximal concentric and eccentric repetitions. This resistive exercise protocol was identical to a previous 90-day HDBR study conducted in males (Alkner and Tesch 2004).…”

Section: Groupsmentioning

confidence: 99%

“…This paper reports the results from a part of an extensive WISE study (for Women International Space Simulation for Exploration) which was conducted to evaluate whether the combination of an aerobic treadmill exercise within LBNP and resistive exercise performed on a Xywheel ergometer prevents physiological deconditioning in women during 60 days of HDBR. Association of a resistive Xywheel exercise to the LBNP/Ex countermeasure was justiWed by the positive eVects obtained on bone and muscle with resistive exercise after a 90-day bed rest study in men (Rittweger et al 2005;Alkner and Tesch 2004). EVects on bone, muscle and other aspects of this study (e.g., eVects on female endocrine responses, aerobic capacity…) will be reported elsewhere.…”

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confidence: 91%

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WISE-2005: effect of aerobic and resistive exercises on orthostatic tolerance during 60 days bed rest in women

et al. 2009

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Cardiovascular deconditioning after long duration spaceXight is especially challenging in women who have a lower orthostatic tolerance (OT) compared with men. We hypothesized that an exercise prescription, combining supine aerobic treadmill exercise in a lower body negative pressure (LBNP) chamber followed by 10 min of resting LBNP, three to four times a week, and Xywheel resistive training every third day would maintain orthostatic tolerance (OT) in women during a 60-day head-down-tilt bed rest (HDBR). Sixteen women were assigned to two groups (exercise, control). Pre and post HDBR OT was assessed with a tilt/LBNP test until presyncope. OT time (mean § SE) decreased from 17.5 § 1.0 min to 9.1 § 1.5 min (¡50 § 6%) in control group (P < 0.001) and from 19.3 § 1.3 min to 13.0 § 1.9 min (¡35 § 7%) in exercise group (P < 0.001), with no signiWcant diVerence in OT time between the two groups after HDBR (P = 0.13). Nevertheless, compared with controls post HDBR, exercisers had a lower heart rate during supine rest (mean § SE, 71 § 3 vs. 85 § 4, P < 0.01), a slower increase in heart rate and a slower decrease in stroke volume over the course of tilt/ LBNP test (P < 0.05). Blood volume (mean § SE) decreased in controls (¡9 § 2%, P < 0.01) but was maintained in exercisers (¡4 § 3%, P = 0.17).Our results suggest that the combined exercise countermeasure did not signiWcantly improve OT but protected blood volume and cardiovascular response to sub tolerance levels of orthostatic stress.

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“…travelers as well as in immobilized subjects, are associated with alterations in protein turnover (1,2,11,15,41,44,66). Specific disuse-induced changes include a negative nitrogen balance, a decrease in whole body protein synthesis, and an increase in lower-limb proteolysis leading to decreased amounts of contractile protein in skeletal muscle (11,20,44,57,67).…”

mentioning

confidence: 99%