Muscle Strength Science Abstracts

1. Neuromuscul Disord. 2003 Aug;13(6):479-84.

Modification of the functional capacity of sarcoplasmic reticulum membranes in patients suffering from chronic fatigue syndrome.

Fulle S, Belia S, Vecchiet J, Morabito C, Vecchiet L, Fanò G.
Laboratorio Interuniversitario di Miologia, Università ‘G. d’Annunzio’, Nuovo Polo Didattico, 66013 Chieti Scalo, Italy. s.fulle@unich.it
In chronic fatigue syndrome, several reported alterations may be related to specific oxidative modifications in muscle. Since sarcoplasmic reticulum membranes are the basic structures involved in excitation-contraction coupling and the thiol groups of Ca(2+) channels of SR terminal cisternae are specific targets for reactive oxygen species, it is possible that excitation-contraction coupling is involved in this pathology. We investigated the possibility that abnormalities in this compartment are involved in the pathogenesis of chronic fatigue syndrome and consequently responsible for characteristic fatigue. The data presented here support this hypothesis and indicate that the sarcolemmal conduction system and some aspects of Ca(2+) transport are negatively influenced in chronic fatigue syndrome. In fact, both deregulation of pump activities (Na(+)/K(+) and Ca(2+)-ATPase) and alteration in the opening status of ryanodine channels may result from increased membrane fluidity involving sarcoplasmic reticulum membranes.
2. Acta Physiol Scand. 2002 Nov;176(3):227-32.

Altered sarcoplasmic reticulum function in rat diaphragm after high-intensity exercise.

Matsunaga S, Inashima S, Tsuchimochi H, Yamada T, Hazama T, Wada M.
Institute of Health Sciences and Physical Education, Osaka City University, Osaka-shi, Osaka, Japan.
The present study examined the effects of acute high-intensity exercise on Ca(2+) uptake and release rates and Ca(2+)-adenosine triphosphatase (ATPase) activity of the sarcoplasmic reticulum (SR) from the costal diaphragm. The rats were run on a treadmill at an estimated requirement of 100% of maximal O2 consumption until fatigued (average time to exhaustion: 4.79 min). Muscle lactate and inorganic phosphate after exercise were increased by 65% (P < 0.05) and 35% (P < 0.05), respectively. With exercise, Ca(2+) uptake and release, which were detected in homogenates using the Ca(2+) fluorescent dye indo-1, were decreased by 24% (P < 0.05) and 22% (P < 0.05), respectively. The reduction in Ca(2+) uptake was paralleled by decreased activity of SR Ca(2+)-ATPase in both the absence and presence of Ca(2+) ionophore. These findings demonstrate that, in the diaphragm as well as in the locomotor muscles that have been explored in previous studies, the attenuations of the SR function is brought about by acute high-intensity exercise. These changes in the SR of the diaphragm may contribute, at least in part, to deteriorations in exercise tolerance and work productivity resulting from repetitive physical activities.
3. J Appl Physiol. 2002 Mar;92(3):912-22. 

Effects of fatigue and training on sarcoplasmic reticulum Ca(2+) regulation in human skeletal muscle.

Li JL, Wang XN, Fraser SF, Carey MF, Wrigley TV, McKenna MJ.
School of Human Movement, Recreation and Performance, Victoria University of Technology, Melbourne, 8001 Victoria, Australia.
Little is known about fatigue and training effects on sarcoplasmic reticulum (SR) function in human muscle, and we therefore investigated this in eight untrained controls (UT), eight endurance-trained (ET), and eight resistance-trained athletes (RT). Muscle biopsies (vastus lateralis) taken at rest and after 50 maximal quadriceps contractions (180 degrees/s, 0.5 Hz) were analyzed for fiber composition, metabolites and maximal SR Ca(2+) release, Ca(2+) uptake, and Ca(2+)-ATPase activity. Fatigue reduced (P < 0.05) Ca(2+) release (42.1 +/- 3.8%, 43.4 +/- 3.9%, 31.3 +/- 6.1%), Ca(2+) uptake (43.0 +/- 5.2%, 34.1 +/- 4.6%, 28.4 +/- 2.8%), and Ca(2+)-ATPase activity (38.6 +/- 4.2%, 48.5 +/- 5.7%, 29.6 +/- 5.0%), in UT, RT, and ET, respectively. These decreases were correlated with fatigability and with type II fiber proportion (P < 0.05). Resting SR measures were correlated with type II proportion (r > or = 0.51, P < 0.05). ET had lower resting Ca(2+) release, Ca(2+) uptake, and Ca(2+)-ATPase (P < 0.05) than UT and RT (P < 0.05), probably because of their lower type II proportion; only minor effects were found in RT. Thus SR function is markedly depressed with fatigue in controls and in athletes, is dependent on fiber type, and appears to be minimally affected by chronic training status.
4. Acta Physiol Scand. 2004 Feb;180(2):195-208. 

Effects of prolonged exercise and recovery on sarcoplasmic reticulum Ca2+ cycling properties in rat muscle homogenates.

Schertzer JD, Green HJ, Fowles JR, Duhamel TA, Tupling AR.
Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada.
To examine the effects of exercise and exercise plus active and passive recovery on sarcoplasmic reticulum (SR) Ca2+-handling properties.
Crude muscle homogenates were prepared from adult rat gastrocnemius muscle from two experiments. In one experiment, the muscle was extracted immediately after prolonged treadmill running (RUN), after a 45 min period of reduced exercise intensity (RUN+) following RUN and compared with controls (CON). In the second experiment, muscle was extracted during passive recovery following the same run protocol at 10 min (REC10), 25 min (REC25) and 45 min (REC45) and compared with CON.
Sarcoplasmic reticulum Ca2+-uptake was 31% higher (P < 0.05) in RUN+ compared with CON and RUN. Higher values (P < 0.05) were also found in REC25 (48%) and REC45 (50%) compared with CON. Maximal Ca2+-ATPase was increased by 23% (P < 0.05) in RUN+ compared with CON and RUN and by 65-68% (P < 0.05) in REC25 and REC45 compared with CON. A higher (P < 0.05) Hill coefficient for Ca2+-ATPase activity was observed in RUN+ (2.3 +/- 0.2) compared with CON (1.7 +/- 0.2) or RUN (1.6 +/- 0.2), but not for any REC conditions. In addition, the coupling ratio (Ca2+-uptake/Ca2+-ATPase activity) was higher (P < 0.05) in RUN+ (2.2 +/- 0.10) compared with CON (1.9 +/- 0.05) and RUN (1.9 +/- 0.08). CONCLUSIONS: It is concluded that in crude homogenates, SR Ca2+-uptake and Ca2+-ATPase activity are elevated in recovery following prolonged running and that the elevation in these properties is more pronounced during passive compared with active recovery.
5. Can J Appl Physiol. 2004 Jun;29(3):308-29. 

The sarcoplasmic reticulum in muscle fatigue and disease: role of the sarco(endo)plasmic reticulum Ca2+-ATPase.

Tupling AR.
Department of Kinesiology, University of Waterloo, Waterloo, Ontario.
Skeletal muscles induced to contract repeatedly respond with a progressive loss in their ability to generate a target force or power. This condition is known simply as fatigue. Commonly, fatigue may persist for prolonged periods of time, particularly at low activation frequencies, which is called low-frequency fatigue. Failure to activate the contractile apparatus with the appropriate intracellular free calcium ([Ca2+]f) signal contributes to fatigue but the precise mechanisms involved are unknown. The sarcoplasmic reticulum (SR) is the major organelle in muscle that is responsible for the regulation of [Ca2+]f, and numerous studies have shown that SR function, both Ca2+ release and Ca2+ uptake, is impaired following fatiguing contractile activity. The major aim of this review is to provide insight into the various cellular mechanisms underlying the alterations in SR Ca2+ cycling and cytosolic [Ca2+]f that are associated both with the development of fatigue during repeated muscle contraction and with low-frequency or long-lasting fatigue. The primary focus will be on the role of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) in normal muscle function, fatigue, and disease.