ABSTRACT
The aims of the present study were to verify the contributions of the energy systems during repeated sprints with a short recovery time and the associations of the time- and power-performance of repeated sprints with energetic contributions and aerobic and anaerobic variables. 13 healthy men performed the running-based anaerobic sprint test (RAST) followed by an incremental protocol for lactate minimum intensity determination. During the RAST, the net energy system was estimated using the oxygen consumption and the blood lactate responses. The relative contributions of oxidative phosphorylation, glycolytic, and phosphagen pathways were 38, 34, and 28%, respectively. The contribution of the oxidative pathway increased significantly during RAST especially from the third sprint, at the same time that power- and time-performances decreases significantly. The phosphagen pathway was associated with power-performance (peak power=432±107 W, r=0.65; mean power=325±80 W, r=0.65; minimum power=241±77 W, r=0.57; force impulse=1 846±478 N·s, r=0.74; p<0.05). The time-performance (total time=37.9±2.5 s; best time=5.7±0.4 s; mean time=6.3±0.4 s; worst time=7.0±0.6 s) was significantly correlated with the oxidative phosphorylation pathway (0.57
Subject(s)
Energy Metabolism , Metabolic Networks and Pathways , Running/physiology , Adult , Anaerobic Threshold/physiology , Athletic Performance/physiology , Exercise Test , Humans , Lactic Acid/blood , Male , Oxygen Consumption/physiology , Physical Endurance/physiology , Rest , Time Factors , Young AdultABSTRACT
The assessment of aerobic endurance is important for training prescription in soccer, and is usually measured by straight running without the ball on a track or treadmill. Due to the ball control and technical demands during a specific soccer test, the running speeds are likely to be lower compared to a continuous incremental test. The aim of the present study was to compare the heart rate (HR), rating of perceived exertion (RPE) and speeds corresponding to 2.0 mmolâL(-1), 3.5 mmolâL(-1), lactate threshold (Dmax method) and peak lactate determined in the laboratory and in the Hoff circuit soccer-specific test. Sixteen soccer players (16±1 years) underwent two incremental tests (laboratory and Hoff circuit tests). The speeds were significantly higher in the treadmill test than on the Hoff circuit (2.0 mmolâL(-1): 9.5±1.2 and 8.1±1.0 kmâh(-1); 3.5 mmolâL(-1): 12.0±1.2 and 10.2±1.1 kmâh(-1); Dmax: 11.4±1.4 and 9.3±0.4 kmâh(-1); peak lactate: 14.9±1.6 and 10.9±0.8 kmâh(-1)). The HR corresponding to 3.5 mmolâL-1 was significantly higher on the Hoff circuit compared to the laboratory test (187.5±18.0 and 178.2±17.6 bpm, respectively; P <0.001), while the RPE at the last incremental stage was lower on the Hoff circuit (P < 0.01). The speeds during the Hoff specific soccer test and the HR corresponding to 2.0 mmolâL(-1), 3.5 mmolâL(-1) and Dmax/threshold were different compared with the laboratory test. The present study shows that it is possible to assess submaximal endurance related variables specifically in soccer players.
Subject(s)
Anti-Bacterial Agents/adverse effects , Enterocolitis/chemically induced , Nafcillin/adverse effects , Neutropenia/chemically induced , Osteomyelitis/drug therapy , Prosthesis-Related Infections/drug therapy , Rifampin/adverse effects , Adult , Appendicitis/complications , Drug Therapy, Combination , Enterocolitis/complications , Humans , Male , Neutropenia/complications , Osteomyelitis/complications , Osteomyelitis/etiology , Prosthesis-Related Infections/complications , Prosthesis-Related Infections/microbiology , Staphylococcal Infections/complications , Staphylococcal Infections/drug therapy , Staphylococcal Infections/etiology , Tibial Fractures/complications , Tibial Fractures/surgerySubject(s)
Carpal Bones/injuries , Carpal Bones/surgery , Fractures, Bone/surgery , Joint Dislocations/surgery , Wrist Injuries/surgery , Adult , Carpal Bones/diagnostic imaging , Fractures, Bone/diagnostic imaging , Humans , Joint Dislocations/diagnostic imaging , Male , Radiography , Wrist Injuries/diagnostic imagingABSTRACT
Osteomyelitis involving the tubular bones of the hand is a rare and potentially devastating disease. An early and accurate diagnosis combined with aggressive surgical debridement and appropriate antibiotics remains the cornerstone of treatment. This article reviews current principles involving the etiology, pathophysiology, diagnosis, and treatment of osteomyelitis of the hand.
Subject(s)
Hand , Osteomyelitis/therapy , Amputation, Surgical , Anti-Bacterial Agents/therapeutic use , Debridement , Fractures, Bone/therapy , Hand Injuries/therapy , Humans , Osteomyelitis/diagnosis , Osteomyelitis/physiopathologyABSTRACT
Carpal tunnel release is the most common hand operation performed in this country. In the absence of specific systemic diseases, the etiology and persistence of pain and dysfunction even after surgical decompression is poorly understood. The focus of this investigation was to investigate the biological factors present within the patients serum that may lead to increased sensitivity to pain. Tissue was collected from patients during surgery. The tissue was homogenized and the homogenate analyzed for the presence of IL-1, IL-6, prostaglandin E series (PGE2). The levels were compared with volunteers that had no evidence of carpal tunnel syndrome or pain. The results showed similar levels of IL-1 (range 42-26 ng/ml) in tissue homogenates, and a significant increase in levels of IL-6 and malionaldehyde bis-(diethyl acetal) in CTS patients in comparison to control tissues. This increase may be associated with oxidative changes occurring as a result of ischemia and reperfusion. Tissue homogenates were also evaluated for PGE2. The CTS tissues showed a five fold elevation in PGE2 compared to control tissues. Levels of PGE2 in CTS tissues were statistically different using a two-tailed student T-test. Increased levels of PGE2 can enhance vascular permeability at the site of injury, and can play an important role in activating adenylate cyclase which increases intracellular cyclic adenosine monophosphate (cAMP). This increase in cAMP levels can inhibit functional responses to other inflammatory stimuli. Increases in PGE2 can also cause sensitization of the nerve endings so that a normal stimulus that would not necessarily cause pain will now be experienced as painful. The results of this study demonstrate that arachidonic acid metabolites PGE2 may be responsible for both the pathological changes and clinical symptomatology in carpal tunnel syndrome.