António Ascensão

Biochemical impact of a soccer match — analysis of oxidative stress and muscle damage markers throughout recovery

BACKGROUND Exercise is a prone condition to enhanced oxidative stress and damage and the specific activity pattern of a soccer match may favour additional pro-oxidant redox alterations. To date, no studies have reported the impact of a soccer match on oxidative stress and muscle damage markers. AIM To analyse the effect of a competitive soccer match on plasma levels of oxidative stress and muscle damage markers, and to relate these findings with lower limb functional data. METHODS Blood samples, leg muscle strength, sprint ability and delayed-onset muscle soreness (DOMS) were obtained in 16 soccer players before, at 30 min, 24, 48 and 72 h after a soccer match. Plasma creatine kinase (CK), myoglobin (Mb), malondialdehyde (MDA), sulfhydryl (-SH) groups, total antioxidant status (TAS), uric acid (UA) and blood leukocyte counts were determined. RESULTS A soccer match elevated plasma Mb following 30 min and CK levels throughout the 72 h-recovery period. MDA increased throughout the recovery period and -SH decreased until 48 h post-match. TAS increased at 30 min and UA increased throughout the 72 h recovery. Blood neutrophils increased at 30 min whereas lymphocytes decreased and returned to baseline from 24 to 72 h. DOMS was higher than baseline until 72 h. Lower limb strength and sprint ability were lower than baseline until 72 h recovery. CONCLUSION The present data suggest that a soccer match increases the levels of oxidative stress and muscle damage throughout the 72 h-recovery period. The extent to which the redox alterations are associated with the recovery of muscle function should be further analysed.

Effects of cold water immersion on the recovery of physical performance and muscle damage following a one-off soccer match

Abstract The aim of this study was to assess the effects of a single session of cold or thermoneutral water immersion after a one-off match on muscular dysfunction and damage in soccer players. Twenty-male soccer players completed one match and were randomly divided into cryotherapy (10 min cold water immersion, 10°C, n = 10) and thermoneutral (10 min thermoneutral water immersion, 35°C, n = 10) groups. Muscle damage (creatine kinase, myoglobin), inflammation (C-reactive protein), neuromuscular function (jump and sprint abilities and maximal isometric quadriceps strength), and delayed-onset muscle soreness were evaluated before, within 30 min of the end, and 24 and 48 h after the match. After the match, the players in both groups showed increased plasma creatine kinase activity (30 min, 24 h, 48 h), myoglobin (30 min) and C-reactive protein (30 min, 24 h) concentrations. Peak jump ability and maximal strength were decreased and delayed-onset muscle soreness increased in both groups. However, differential alterations were observed between thermoneutral water and cold water immersion groups in creatine kinase (30 min, 24 h, 48 h), myoglobin (30 min), C-reactive protein (30 min, 24 h, 48 h), quadriceps strength (24 h), and quadriceps (24 h), calf (24 h) and adductor (30 min) delayed-onset muscle soreness. The results suggest that cold water immersion immediately after a one-off soccer match reduces muscle damage and discomfort, possibly contributing to a faster recovery of neuromuscular function.

Physical and Physiological Demands of Elite Team Handball

Abstract Póvoas, SCA, Seabra, AFT, Ascensão, AAMR, Magalhães, J, Soares, JMC, and Rebelo, ANC. Physical and physiological demands of elite team handball. J Strength Cond Res 26(12): 3365–3375, 2012—This study aimed to analyze elite team handball physical and physiological demands during match play. Time-motion (N = 30) and heart rate (HR; N = 60) analyses were performed throughout 10 official matches. The defined locomotor categories were standing still, walking, jogging, fast running, sprinting, backwards movement, sideways medium-intensity movement, and sideways high-intensity movement, and playing actions studied were jumps, shots, stops when preceded by high-intensity activities, changes of direction and one-on-one situations. During matches, the mean distances covered were 4,370 ± 702.0 m. Around 80% of the total time was spent standing still (43.0 ± 9.27%) and walking (35.0 ± 6.94%) and only 0.4 ± 0.31% with sprinting. The most frequent high-intensity actions were stops, changes of direction, and one-on-one situations. Effective mean HR was 157 ± 18.0 b·min−1 (82 ± 9.3% of HRmax), and total HR was 139 ± 31.9 b·min−1 (72 ± 16.7% of HRmax). The HR, time spent in high-intensity activities, frequency of stops, changes of direction, one-on-one situations, and most intense periods of the game were higher during the first half than during the second half (p ⩽ 0.05). The opposite was observed for the number of time outs and the time between each change of activity (p = 0.00). Handball is an intermittent exercise that primarily uses aerobic metabolism, interspersed by high-intensity actions that greatly tax anaerobic metabolism. Additionally, exercise intensity decreases from the first to the second half of the match, suggesting that neuromuscular fatigue may occur during the game. The training of elite handball players should comprise exercises targeting the ability to perform specific high-intensity actions throughout the game and to rapidly recover during the less intense periods.

Physical exercise as a possible strategy for brain protection: Evidence from mitochondrial-mediated mechanisms

Aging and neurodegenerative conditions such as Alzheimer and Parkinson diseases are characterized by tissue and mitochondrial changes that compromise brain function. Alterations can include increased reactive oxygen species production and impaired antioxidant capacity with a consequent increase in oxidative damage, mitochondrial dysfunction that compromises brain ATP production, and ultimately increased apoptotic signaling and neuronal death. Among several non-pharmacological strategies to prevent brain degeneration, physical exercise is a surprisingly effective strategy, which antagonizes brain tissue and mitochondrial dysfunction. The present review aims to discuss the role of physical exercise in the modulation of the mechanisms involved in neuroprotection including the activation of signaling pathways underlying brain protection.

Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats

The use of DOX (doxorubicin), an antibiotic used in oncological treatments, is limited by a dose-related cardiotoxicity against which acute exercise is protective. However, the mitochondrial-related mechanisms of this protection remain unknown. Therefore the present study aimed to determine the effects of an acute endurance exercise bout performed 24 h before DOX treatment on heart and liver mitochondrial function. A total of 20 adult male Wistar rats were divided into groups as follows: non-exercised with saline (NE + SAL), non-exercised DOX-treated (NE + DOX), exercised with saline (EX + SAL) and exercised DOX-treated (EX + DOX). The animals performed a 60 min exercise bout on a treadmill or remained sedentary 24 h before receiving either a DOX bolus (20 mg/kg of body weight) or saline. Heart and liver mitochondrial function [oxygen consumption, membrane potential (DeltaPsi) and cyclosporin-A-sensitive calcium-induced MPTP (mitochondrial permeability transition pore) opening] were evaluated. The activities of the respiratory complex, Mn-SOD (superoxide dismutase), caspases 3 and 9, as well as the levels of ANT (adenine nucleotide translocase), VDAC (voltage-dependent anion channel), CypD (cyclophilin D), Bax and Bcl-2, were measured. Acute exercise prevented the decreased cardiac mitochondrial function (state 3, phosphorylative lagphase; maximal DeltaPsi generated both with complex I- and II-linked substrates and calcium-induced MPTP opening) induced by DOX treatment. Exercise also prevented the DOX-induced decreased activity of cardiac mitochondrial chain complexes I and V, and increased caspase 3 and 9 activities. DOX administration and exercise caused increased cardiac mitochondrial SOD activity. Exercise ameliorated liver mitochondrial complex activities. No alterations were observed in the measured MPTP and apoptosis-related proteins in heart and liver mitochondria. The results demonstrate that acute exercise protects against cardiac mitochondrial dysfunction, preserving mitochondrial phosphorylation capacity and attenuating DOX-induced decreased tolerance to MPTP opening.

Endurance training reverts heart mitochondrial dysfunction, permeability transition and apoptotic signaling in long-term severe hyperglycemia

The present study analyzed the effects of endurance training against cardiac mitochondrial dysfunction, particularly on the susceptibility to mitochondrial permeability transition pore (MPTP) induction in streptozotocin (STZ)-induced hyperglycemia. Twenty-four young male Wistar rats were randomly assigned into sedentary citrate (SED+CIT), sedentary type I diabetes (SED+STZ; 50mg/kg), T+CIT (14-week treadmill running, 60min/day) and T+STZ (injected 4weeks before training). After 18weeks, isolated heart mitochondria were used for in vitro oxygen consumption and transmembrane potential (∆Ψ) assessment. Cyclosporin-A (CyclA)-sensitive osmotic swelling and Ca(2+) fluxes were measured to study MPTP susceptibility. Voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), cyclophilin D (CypD), transcription factor A (Tfam), Bax, Bcl-2 contents, caspase-3 and -9 activities were determined. In the sedentary group, long-term severe hyperglycemia decreased state 3, CCCP-induced uncoupling and increased oligomycin-inhibited respiration, state 4 and lag phase with glutamate-malate. A decreased state 3 and state 4 with succinate were observed. Moreover, hyperglycemia decreased Ca(2+) uptake and increased CyclA-sensitive Ca(2+) release and Ca(2+)-induced mitochondrial swelling. The oxygen consumption and ∆Ψ parameters impaired by long-term severe hyperglycemia were reverted by endurance training (SED+STZ vs. T+STZ). Training increased mitochondrial Ca(2+) uptake and decreased Ca(2+) release in hyperglycemic groups. Additionally, endurance training reverted the hyperglycemia-induced CypD elevation, attenuating decrease of ANT, VDAC and Tfam. Moreover, training prevented the STZ-induced elevation in Bax, Bax-to-Bcl-2 ratio, caspase-3 and -9 and the increased Bcl-2. Endurance training reestablished heart mitochondrial respiratory dysfunction caused by long-term severe hyperglycemia and reduced the increased susceptibility to MPTP induction probably by modulation of MPTP regulatory proteins.

Beneficial effects of exercise on muscle mitochondrial function in diabetes mellitus.

The physiopathology of diabetes mellitus has been closely associated with a variety of alterations in mitochondrial histology, biochemistry and function. Generally, the alterations comprise increased mitochondrial reactive oxygen and nitrogen species (RONS) generation, resulting in oxidative stress and damage; decreased capacity to metabolize lipids, leading to intramyocyte lipid accumulation; and diminished mitochondrial density and reduced levels of uncoupling proteins (UCPs), with consequent impairment in mitochondrial function. Chronic physical exercise is a physiological stimulus able to induce mitochondrial adaptations that can counteract the adverse effects of diabetes on muscle mitochondria. However, the mechanisms responsible for mitochondrial adaptations in the muscles of diabetic patients are still unclear. The main mechanisms by which exercise may be considered an important non-pharmacological strategy for preventing and/or attenuating diabetes-induced mitochondrial impairments may involve (i) increased mitochondrial biogenesis, which is dependent on the increased expression of some important proteins, such as the ‘master switch’ peroxisome proliferator-activated receptor (PPAR)-γ-coactivator-1α (PGC-1α) and heat shock proteins (HSPs), both of which are severely downregulated in the muscles of diabetic patients; and (ii) the restoration or attenuation of the low UCP3 expression in skeletal muscle mitochondria of diabetic patients, which is suggested to play a pivotal role in mitochondrial dysfunction.There is evidence that chronic exercise and lifestyle interventions reverse impairments in mitochondrial density and size, in the activity of respiratory chain complexes and in cardiolipin content; however, the mechanisms by which chronic exercise alters mitochondrial respiratory parameters, mitochondrial antioxidant systems and other specific proteins involved in mitochondrial metabolism in the muscles of diabetic patients remain to be elucidated.

Exercise as a beneficial adjunct therapy during Doxorubicin treatment—Role of mitochondria in cardioprotection

One of the mostly used chemotherapeutic drugs is the highly effective anthracycline Doxorubicin. However, its clinical use is limited by the dose-related and cumulative cardiotoxicity and consequent dysfunction. It has been proposed that the etiology of this toxicity is related to mitochondrial dysfunction. The present review aimed to analyze the promising results regarding the effect of several types of physical exercise in cardiac tolerance of animals treated with acute and sub-chronic doses of Doxorubicin (DOX), highlighting the importance of cardiac mitochondrial-related mechanisms in the process. Physical exercise positively modulates some important cardiac defense systems to antagonize the toxic effects caused by DOX treatment, including antioxidant capacity, the overexpression of heat shock proteins and other anti-apoptotic proteins. An important role in this protective phenotype afforded by exercise should be attributed to mitochondrial plasticity, as related adaptations could be translated into improved cardiac function in the setting of the DOX cardiomyopathy.

PHYSICAL EXERCISE IMPROVES BRAIN CORTEX AND CEREBELLUM MITOCHONDRIAL BIOENERGETICS AND ALTERS APOPTOTIC, DYNAMIC AND AUTO(MITO)PHAGY MARKERS

We here investigate the effects of two exercise modalities (endurance treadmill training-TM and voluntary free-wheel activity-FW) on the brain cortex and cerebellum mitochondrial bioenergetics, permeability transition pore (mPTP), oxidative stress, as well as on proteins involved in mitochondrial biogenesis, apoptosis, and quality control. Eighteen male rats were assigned to sedentary-SED, TM and FW groups. Behavioral alterations and ex vivo brain mitochondrial function endpoints were assessed. Proteins involved in oxidative phosphorylation (OXPHOS, including the adenine nucleotide translocator), oxidative stress markers and regulatory proteins (SIRT3, p66shc, UCP2, carbonyls, MDA, -SH, aconitase, Mn-SOD), as well as proteins involved in mitochondrial biogenesis (PGC1α, TFAM) were evaluated. Apoptotic signaling was measured through quantifying caspase 3, 8 and 9-like activities, Bax, Bcl2, CypD, and cofilin expression. Mitochondrial dynamics (Mfn1/2, OPA1 and DRP1) and auto(mito)phagy (LC3II, Beclin1, Pink1, Parkin, p62)-related proteins were also measured by Western blotting. Only the TM exercise group showed increased spontaneous alternation and exploratory activity. Both exercise regimens improved mitochondrial respiratory activity, increased OXPHOS complexes I, III and V subunits in both brain subareas and decreased oxidative stress markers. Increased resistance to mPTP and decreased apoptotic signaling were observed in the brain cortex from TM and in the cerebellum from TM and FW groups. Also, exercise increased the expression of proteins involved in mitochondrial biogenesis, autophagy and fusion, simultaneous with decreased expression of mitochondrial fission-related protein DRP1. In conclusion, physical exercise improves brain cortex and cerebellum mitochondrial function, decreasing oxidative stress and apoptotic related markers. It is also possible that favorable alterations in mitochondrial biogenesis, dynamics and autophagy signaling induced by exercise contributed to increased mitochondrial plasticity leading to a more robust phenotype.

Physical exercise prior and during treatment reduces sub-chronic doxorubicin-induced mitochondrial toxicity and oxidative stress

Doxorubicin (DOX) is an anti-cancer agent whose clinical usage results in a cumulative and dose-dependent cardiotoxicity. We have previously shown that exercise performed prior to DOX treatment reduces the resulting cardiac(mito) toxicity. We sought to determine the effects on cardiac mitochondrial toxicity of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free-wheel activity-FW) when used prior and during DOX treatment. Male-young Sprague-Dawley rats were divided into six groups (n=6 per group): SAL+SED (saline sedentary), SAL+TM (12-weeks TM), SAL+FW (12-weeks FW), DOX+SED (7-weeks of chronic DOX treatment 2mg/kg per week), DOX+TM and DOX+FW. DOX administration started 5weeks after the beginning of the exercise protocol. Heart mitochondrial ultrastructural alterations, mitochondrial function (oxygen consumption and membrane potential), semi-quantification of oxidative phosphorylation (OXPHOS) proteins and their in-gel activity, as well as proteins involved in mitochondrial oxidative stress (SIRT3, p66shc and UCP2), biogenesis (PGC1α and TFAM), acetylation and markers for oxidative damage (carbonyl groups, MDA,SH, aconitase, Mn-SOD activity) were evaluated. DOX treatment resulted in ultrastructural and functional alterations and decreased OXPHOS. Moreover, DOX decreased complex I activity and content, mitochondrial biogenesis (TFAM), increased acetylation and oxidative stress. TM and FW prevented DOX-induced alteration in OXPHOS, the increase in oxidative stress, the decrease in complex V activity and in complex I activity and content. DOX-induced decreases in TFAM and SIRT3 content were prevented by TM only. Both chronic models of physical exercise performed before and during the course of sub-chronic DOX treatment translated into an improved mitochondrial bioenergetic fitness, which may result in part from the prevention of mitochondrial oxidative stress and damage.