Search

Overreaching (OVR) is defined as the initial phase of overtraining syndrome and is known as a metabolic imbalance leading to short-term fatigue. Exercise increases reactive oxygen species production, which can oxidize intracellular structures impairing cell function and thus leads to OVR process. The aim of this work is to study the behavior of oxidative stress markers in subjects submitted to an OVR protocol. Thirty rats were divided in exercise and control group, and submitted to an 8-week-endurance training (ET) and a 3-week-OVR protocol. Thiobarbituric acid reactive substances (TBARs), reactive carbonylated derivatives (RCD), glutathione reductase (GR), catalase (CAT) and citrate synthase (CS) activities and stress protein HSP72 were measured in soleus (SO), extensor digital longus (EDL) and semitendinuous (ST) muscles. ET induced significant enhancement ( P<0.05) in CS, GR, CAT, TBARs, RCD and HSP72 in SO, EDL and ST. OVR induced higher levels ( P<0.05) of TBARs, RCD and HSP72 compared with ET only in SO, while in EDL and ST all measured parameters ranged at same levels reached during ET. We concluded that stress-induced OVR protocol is fiber type dependent, the SO muscle fiber type I being the most affected by this treatment. [ABSTRACT FROM AUTHOR]

Exercise can alter gene transcriptional and protein translational rates leading to changes in protein abundance toward adaptation to exercise. We investigated the alterations in protein abundance in skeletal muscle after one bout of an exhaustive exercise through proteomic analysis. Gastrocnemius muscles were sampled from non-exercised control rats and from rats exercised on a treadmill with incremental increases in speed until exhaustion (approximately 30 min). Rats were sacrificed 3 and 24 h after exercise cessation. Two-dimensional gel electrophoresis was performed and spots with a significant alteration in relative volume were identified by mass spectrometry. Six spots presented statistically significant altered abundances after exercise. The spots identified as the metabolic related proteins triosephosphate isomerase 1, glyceraldehyde-3-phosphate dehydrogenase, the β subunit of pyruvate dehydrogenase E1 and carnitine palmitoyltransferase 2 were all more abundant after exercise. One spot identified as heat shock cognate 70 was also more abundant after exercise. One spot demonstrated a decreased abundance after exercise and was identified as α-actin. These results suggest that a single session of exhaustive incremental exercise in untrained muscle can alter thin filaments synthesis/degradation rate and enhance cytosolic and mitochondrial proteins synthesis. The identified proteins may be important to a general preconditioning of skeletal muscle for subsequent exercise sessions. [ABSTRACT FROM AUTHOR]

A novel method to measure oxidative stress resulting from exhaustive exercise in rats is presented. In this new procedure we evaluated the erythrocyte antioxidant enzymes, catalase (CAT) and glutathione reductase (GR), the plasma oxidative attack markers, reactive carbonyl derivatives (RCD) and thiobarbituric reactive substances (TBARS). Muscular tissue damage was evaluated by monitoring plasma creatine kinase (CK) and plasma taurine (Tau) concentrations. Also, we monitored total sulphydryl groups (TSG) and uric acid (UA), and the level of the 70 kDa heat shock protein (HSP70) in leukocytes as a marker of oxidative stress. In the study we found a correspondence between erythrocyte CAT and GR activities and leukocyte HSP70 levels, principally 3 h after the acute exercise, and this suggested an integrated mechanism of antioxidant defense. The increase in levels of plasma Tau was coincident with the increasing plasma levels of CK and TBARS, principally after two hours of exercise. Thus tissue damage occurred before the expression of any anti-oxidant system markers and the monitoring of Tau, CK or TBARS may be important for the estimation of oxidative stress during exhaustive exercise. Furthermore, the integrated analyses could be of value in a clinical setting to quantify the extent of oxidative stress risk and reduce the need to perform muscle biopsies as a tool of clinical evaluation. [ABSTRACT FROM AUTHOR]