Reactive oxygen species mediated diaphragm fatigue in a rat model of chronic intermittent hypoxia.

Respiratory muscle dysfunction documented in sleep apnoea patients is perhaps due to oxidative stress secondary to chronic intermittent hypoxia (CIH). We sought to explore the effects of different CIH protocols on respiratory muscle form and function in a rodent model. Adult male Wistar rats were exposed to CIH (n = 32) consisting of 90 s normoxia-90 s hypoxia (either 10 or 5% oxygen at the nadir; arterial O2 saturation ∼ 90 or 80%, respectively] for 8 h per day or to sham treatment (air-air, n = 32) for 1 or 2 weeks.

Diaphragm muscle remodeling in a rat model of chronic intermittent hypoxia.

Respiratory muscle remodeling occurs in human sleep apnea--a common respiratory disorder characterized by chronic intermittent hypoxia (CIH) due to recurrent apnea during sleep. We sought to determine if CIH causes remodeling in rat sternohyoid (upper airway dilator) and diaphragm muscles. Adult male Wistar rats were exposed to CIH (n=8), consisting of 90 sec of hypoxia (5% at the nadir; SaO₂ ~80%)/90 sec of normoxia, 8 hr per day, for 7 consecutive days.

Effects of step exercise on muscle damage and muscle Ca2+ content in men and women.

Eccentric exercise often produces severe muscle damage, whereas concentric exercise of a similar load elicits a minor degree of muscle damage. The cellular events initiating muscle damage are thought to include an increase in cytosolic Ca. It was hypothesized that eccentric muscle activity in humans would lead to a larger degree of cell damage and increased intracellular Ca accumulation in skeletal muscle than concentric activity would.

Effects of concentric and repeated eccentric exercise on muscle damage and calpain-calpastatin gene expression in human skeletal muscle.

The purpose of this study was to compare the responsiveness of changes in Ca(2+)-content and calpain-calpastatin gene expression to concentric and eccentric single-bout and repeated exercise. An exercise group (n = 14) performed two bouts of bench-stepping exercise with 8 weeks between exercise bouts, and was compared to a control-group (n = 6). Muscle strength and soreness and plasma creatine kinase and myoglobin were measured before and during 7 days following exercise bouts.

Causes of excitation-induced muscle cell damage in isometric contractions: mechanical stress or calcium overload?

Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca2+, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl-p-toluene sulfonamide (BTS), which specifically blocks muscle contraction.

Excitation-induced cell damage and beta2-adrenoceptor agonist stimulated force recovery in rat skeletal muscle.

Intensive exercise leads to a loss of force, which may be long lasting and associated with muscle cell damage. To simulate this impairment and to develop means of compensating the loss of force, extensor digitorum longus muscles from 4-wk-old rats were fatigued using intermittent 40-Hz stimulation (10 s on, 30 s off). After stimulation, force recovery, cell membrane leakage, and membrane potential were followed for 240 min.

Anoxia induces Ca2+ influx and loss of cell membrane integrity in rat extensor digitorum longus muscle.

Anoxia can lead to skeletal muscle damage. In this study we have investigated whether an increased influx of Ca2+, which is known to cause damage during electrical stimulation, is a causative factor in anoxia-induced muscle damage. Isolated extensor digitorum longus (EDL) muscles from 4-week-old Wistar rats were mounted at resting length and were either resting or stimulated (30 min, 40 Hz, 10 s on, 30 s off) in the presence of standard oxygenation (95% O2, 5% CO2), anoxia (95% N2, 5% CO2) or varying degrees of reduced oxygenation.

Excitation-induced Ca2+ influx and muscle damage in the rat: loss of membrane integrity and impaired force recovery.

Prolonged or unaccustomed exercise leads to loss of contractility and muscle cell damage. The possible role of an increased uptake of Ca(2+) in this was explored by examining how graded fatiguing stimulation, leading to a graded uptake of Ca(2+), results in progressive loss of force, impairment of force recovery, and loss of cellular integrity. The latter is indicated by increased [(14)C]sucrose space and lactic acid dehydrogenase (LDH) release.

Effects of running distance and training on Ca2+ content and damage in human muscle.

Purpose: Muscle damage and soreness are well-known adverse effects of running, especially when covering distances in excess of habitual running activity. Loss of Ca homeostasis is hypothesized to initiate the development of exercise-induced muscle damage. We tested the hypothesis that the Ca content of vastus lateralis muscle increases after a 10- or 20-km run and studied the relations between Ca accumulation and running distance, endurance training, and fiber type distribution.

Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans.

The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10 degrees C) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion.