Effect of exhaustive ultra-endurance exercise in muscular glycogen and both Alpha1 and Alpha2 Ampk protein expression in trained rats

Abstract

Glycogen is the main store of readily energy in skeletal muscle and plays a key role in muscle function, demonstrated by the inability to sustain prolonged high-intensity exercise upon depletion of these glycogen stores. With prolonged exercise, glycogen depletion occurs and 5'-AMP-activated protein kinase (AMPK), a potent regulator of muscle metabolism and gene expression, is activated promoting molecular signalling that increases glucose uptake by muscular skeletal cells. The aim of this study was primarily to determine the effect of ultra-endurance exercise on muscle glycogen reserves and secondly to verify the influence of this type of exercise on AMPK protein expression. Twenty-four male Wistar rats, 60 days old, were divided into four experimental groups: sedentary, sedentary exhausted (SE), endurance trained (T) and endurance trained exhausted (TE). The animals ran for 10 to 90 min/day, 5 days/week, for 12 weeks to attain trained status. Rats were killed immediately after the exhaustion protocol, which consisted of running on a treadmill (at approximately 60% Vmax until exhaustion). Optical density of periodic acid-Schiff was detected and glycogen depletion observed predominantly in type I muscle fibres of the TE group and in both type I and II muscle fibres in the SE group. Plasma glucose decreased only in the TE group. Hepatic glycogen was increased in T group and significantly depleted in TE group. AMPK protein expression was significantly elevated in TE and T groups. In conclusion, acute exhaustive ultra-endurance exercise promoted muscle glycogen depletion. It seems that total AMPK protein and gene expression is more influenced by status training.

Gradual strenuous running regimen predisposes to osteoarthritis due to cartilage cell death and altered levels of glycosaminoglycans

“…The novel protocol of ultra-endurance training in rats developed in this work was intended to evaluate the effects of excessive exercise in healthy joint cartilage 17 ; most rat models of osteoarthritis induction employ a surgical procedure that alters the articular harmony 29e31 . A previous model of strenuous running developed by PAP et al 29 involved intracranial stimulation of the rats, whereas TANG et al 32 and SEKIYA et al 33 introduced a modified protocol that motivated the animals by external electrical stimulation of the tail.…”

“…Ultra-endurance exercise is defined as running a distance of at least 50 km or for more than 4 h 15,16 . To induce this condition in experimental studies, a novel protocol was devised according to the Animal Research: Reporting In Vivo Experiments (ARRIVE) guidelines 17,18 . A motorized treadmill (AVS Projetos, São Paulo, SP, Brazil) with six individual lanes and no inclination was used.…”

“…The top speed was designated as that recorded 3 min prior to the point of exhaustion. Since the need to correct and control intensity training, each rat ran at 60% its top speed; this intensity was used throughout the study 17 .…”

Increased physical activity severely induces osteoarthritic changes in knee joints with papain induced sulfate-glycosaminoglycan depleted cartilage

“…The following 5 weeks, rats were forced to run for 5 days per week, the first 5 minutes at 20 cm/sec to warm-up, and the following 25 minutes at 35 cm/sec. The pace and duration of this protocol are equal to about 25% of a total exhaustion protocol for rats [27]. In total, running rats covered a total distance of 15 km over the total 6-week period, which is a protocol known to protect from cartilage degradation in both MIA and surgical models for OA [7,9].…”

Hsp90 Inhibition Protects Against Biomechanically Induced Osteoarthritis in Rats

“…This was followed by 50 minutes of running at 33.3 cm/second (1.20 km/hour). The pace and duration of this protocol are equal to ∼50% of a total exhaustion protocol (). At the end of the 6‐week protocol, the rats had completed 30 km of strenuous running, which leads to the development of moderate OA in their knee joints that does not heal spontaneously ().…”