Sarcoplasmic reticulum Ca<sup>2+</sup>release and muscle fatigue

Favero, Terence G.

doi:10.1152/jappl.1999.87.2.471

Cited by 107 publications

(100 citation statements)

References 144 publications

(169 reference statements)

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“…[27][28][29] It has been shown that increased fatigue is associated with an increase in half-relaxation time of torque in the QF of humans with SCI. 30 This suggests that sarcoplasmic reticulum (SR) Ca 2 þ -ATPases are not functioning optimally and/or they are reduced in SCI.…”

Section: Discussionmentioning

confidence: 99%

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

et al. 2005

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Study design: Longitudinal. Objectives: The purpose of this study was to evaluate the effect of lower extremity resistance training on quadriceps fatigability, femoral artery diameter, and femoral artery blood flow. Setting: Academic Institution. Methods: Five male chronic spinal cord injury (SCI) individuals (American Spinal Injury Association (ASIA): A complete; C5-T10; 3675 years old) completed 18 weeks of home-based neuromuscular electrical stimulation (NMES) resistance training. Subjects trained the quadriceps muscle group twice a week with four sets of 10 dynamic knee extensions against resistance while in a seated position. All measurements were made before training and after 8, 12, and 18 weeks of training. Ultrasound was used to measure femoral artery diameter and blood flow. Blood flow was measured before and after 5 and 10 min of distal cuff occlusion, and during a 4-min isometric electrical stimulation fatigue protocol. Results: Training resulted in significant increases in weight lifted and muscle mass, as well as a 60% reduction in muscle fatigue (P ¼ 0.001). However, femoral arterial diameter did not increase. The range was 0.4470.03 to 0.4670.05 cm over the four time points (P ¼ 0.70). Resting, reactive hyperemic, and exercise blood flow did not appear to change with training. Conclusion: NMES resistance training improved muscle size and fatigue despite an absence of response in the supplying vasculature. These results suggest that the decreases in arterial caliber and blood flow seen with SCI are not tightly linked to muscle mass and fatigue resistance. In addition, muscle fatigue in SCI patients can be improved without increases in arterial diameter or blood flow capacity.

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Section: Discussionmentioning

confidence: 99%

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

et al. 2005

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“…There is evidence that hypoxemia impairs Ca 2ϩ release and, particularly, Ca 2ϩ uptake by the sarcoplasmic reticulum (10), probably via a decrease in the number of functional Ca 2ϩ release channels (12). The effect of hypoxemia on Ca 2ϩ cycling may occur via several mechanisms, including a more rapid accumulation of hydrogen ions (1), inorganic phosphate (21), and/or free radicals (35).…”

Section: Characteristics and Causes Of Muscle Fatiguementioning

confidence: 99%

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

Romer

Haverkamp²,

Lovering³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

113

126

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-The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O 2 uptake (V O2 peak) ϭ 56.4 Ϯ 2.8 ml⅐kg Ϫ1 ⅐min Ϫ1 ; mean Ϯ SE]. Subjects exercised on a cycle ergometer at Ն90% V O2 peak to exhaustion (13.2 Ϯ 0.8 min), during which time arterial O 2 saturation (SaO 2 ) fell from 97.7 Ϯ 0.1% at rest to 91.9 Ϯ 0.9% (range 84 -94%) at end exercise, primarily because of changes in blood pH (7.183 Ϯ 0.017) and body temperature (38.9 Ϯ 0.2°C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (FIO 2 ) ϭ 0.25-0.31] that prevented EIAH (Sa O 2 ϭ 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at FI O 2 0.21, the mean force response across 1-100 Hz decreased 33 Ϯ 5% compared with only 15 Ϯ 5% when EIAH was prevented (P Ͻ 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at FIO 2 0.21 (SaO 2 ϭ 95.3 Ϯ 0.7%), the decrease in evoked force was exacerbated by 35% (P Ͻ 0.05) in response to further desaturation induced via FI O 2 0.17 (SaO 2 ϭ 87.8 Ϯ 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O 2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (Ϫ6 Ϯ 1% ⌬Sa O 2 from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism. magnetic stimulation; low-and high-frequency fatigue; quadriceps twitch force; voluntary activation; peripheral fatigue; central fatigue EXERCISE-INDUCED ARTERIAL HYPOXEMIA (EIAH), defined as a reduced arterial HbO 2 saturation below preexercise levels, occurs during sustained, heavy-intensity exercise to exhaustion in a significant number of healthy subjects (9). The desaturation is attributable primarily to a reduced arterial O 2 partial pressure (Pa O 2 ) in some highly fit subjects (17, 22, 52) or, more universally, to a rightward shift of the O 2 dissociation curve because of a time-and intensity-dependent metabolic acidosis and an increase in body temperature (42,50). EIAH has a detrimental effect on maximal O 2 uptake (V O 2 max ) (16, 41) and endurance exercise performance (36, 37).Multiple "peripheral" and "central" mechanisms have been proposed to explain how arterial hypoxemia limits endurance exercise performance. There is potential for reduced O 2 transport to cause limb muscle fatigue during heavy exercise via an effect of hypoxia on Ca 2ϩ uptake and Ca 2ϩ release by the sarcoplasmic reticulum (10). Changes in the intracellular environment may impair Ca 2ϩ cycling and other excitation/ contraction processes. Alternatively, an inability of the sarcolemma and T tubule to conduct repetitive action potentials may indirectly reduce Ca 2ϩ cycling. The possibility that such peripheral processes are involved in exercise limitation during hypoxemia is suggested by the finding that...

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“…10 Another common theory of muscle fatigue involves the impaired control of calcium (Ca 2 þ ) release into the sarcoplasmic reticulum. 15 Alterations in the function and concentration of Ca 2 þ ATPase have been suggested after SCI to explain the slowing of relaxation time 12 and changes in sarcoplasmic reticulum Ca 2 þ ATPase isoform expression. 11 The phenomenon of enhanced force after a brief maximal summated contraction is known as post-activation potentiation or post-tetanic potentiation, depending on whether the stimulus is voluntary (post-activation potentiation) or electrically stimulated (post-tetanic potentiation).…”

Section: Discussionmentioning

confidence: 99%

Muscle fatigue characteristics in paralyzed muscle after spinal cord injury

Pelletier

Hicks

2010

Spinal Cord

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Study design: The study design used is cross-sectional. Objectives: The aim of this study is to examine muscle contractile and excitability characteristics during fatigue of the tibialis anterior in six individuals with chronic spinal cord injury (SCI) and matched able-bodied (AB) controls. Setting: McMaster University, Hamilton, ON, Canada. Methods: Muscle compound action potential (M-wave) characteristics, muscle twitch properties, and summated force were examined during a 2 min fatigue protocol of intermittent bursts at 30 Hz (4 s tetanus, 2 s rest) or maximal voluntary contraction (MVC). Evoked twitch responses were followed during a recovery period. Results: M-wave amplitude was smaller in SCI (2.5±1.6 mV in SCI, 5.7±3.2 mV in AB) at baseline, but there was no change in M-wave amplitude or area during fatigue in either group. There was an increase in M-wave duration toward the end of recovery in the SCI group. Peak torque (PT) was not different between groups at baseline (3.8 ± 1.8 Nm in SCI, 3.7 ± 0.6 Nm in AB); PT potentiated significantly during fatigue in the AB, but not SCI group. There was significantly greater fatigue of both PT (43% decline) and summated force (57% decline) in the SCI group compared with the AB group (13% increase and 22% decline for PT and MVC, respectively). Conclusion: The dorsiflexor muscles in people with SCI are significantly more fatiguable than those in AB controls, but decreases in muscle excitability do not seem to be an important contributor to the increased fatiguability. The mechanisms behind the increased fatigue must lie distal to the muscle membrane.

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Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Cited by 107 publications

References 144 publications

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

Muscle fatigue characteristics in paralyzed muscle after spinal cord injury

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Sarcoplasmic reticulum Ca2+release and muscle fatigue

Cited by 107 publications

References 144 publications

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

Muscle fatigue characteristics in paralyzed muscle after spinal cord injury

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Resources

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Sarcoplasmic reticulum Ca²⁺release and muscle fatigue