Purpose: We investigated the consequence of varying hypoxia severity during an initial set of repeated cycling sprints on performance, neuromuscular fatigability, and exercise-related sensations during a subsequent set of repeated sprints in normoxia.
Methods: Nine active males performed ten 4-s sprints (recovery = 30 s) at sea level (SL; FiO ~ 0.21), moderate (MH; FiO ~ 0.
Purposes: We manipulated the inspired oxygen fraction (FiO) to examine the effects of physiological perturbations on exercise-related sensations and the neural drive of the quadriceps during repeated, brief, maximal cycle sprints.
Methods: Nine active males completed a repeated sprint cycle protocol (10 × 4-s maximal sprints with 30 s of passive recovery) in normoxia (NM; FiO 0.21) and severe normobaric hypoxia (HY; FiO 0.
Central motor drive to active muscles is believed to be reduced during numerous exercise tasks to prevent excessive peripheral fatigue development. The purpose of the present study was to use hypoxia to exacerbate physiological perturbations during a novel, intermittent exercise task and to explore the time-course and interplay between central and peripheral neuromuscular adjustments. On separate days, 14 healthy men performed four sets of 6 × 5 maximal-intensity, isokinetic leg extensions (1 repetition lasting ∼7 s) at 300°/s (15 and 100 s of passive rest between repetitions and sets, respectively) under normoxia (NM, fraction of inspired O2 0.
View Article and Find Full Text PDFPurpose: We explored the effects of the sense of effort and accompanying perceptions of peripheral discomfort on self-selected cycle power output under two different inspired O2 fractions.
Methods: On separate days, eight trained males cycled for 5 min at a constant subjective effort (sense of effort of '3' on a modified Borg CR10 scale), immediately followed by five 4-s progressive submaximal (sense of effort of "4, 5, 6, 7, and 8"; 40 s between bouts) and two 4-s maximal (sense of effort of "10"; 3 min between bouts) bouts under normoxia (NM: fraction of inspired O2 [FiO2] 0.21) and hypoxia (HY: [FiO2] 0.
Objectives: To determine whether an individualised hydration regimen reduces thermal, physiological and perceptual strain during match-play tennis in the heat, and minimises alterations in neuromuscular function and physical performance postmatch and into recovery.
Methods: 10 men undertook two matches for an effective playing time (ball in play) of 20 min (∼113 min) in ∼37°C and ∼33% RH conditions. Participants consumed fluids ad libitum during the first match (HOT) and followed a hydration regimen (HYD) in the second match based on undertaking play euhydrated, standardising sodium intake and minimising body mass losses.
Objectives: To assess the time course of changes in physical performance in response to match-play tennis under heat stress.
Methods: Two matches consisting of 20 min of effective playing time (2×10 min segments) were played in COOL (∼102 min; ∼22°C and 70% relative humidity (RH)) and HOT (∼119 min; ∼36°C and 35% RH) environments. Repeated-sprint ability (3×15 m, 15 s rest), 15 m sprint time with a direction change (180°), vertical jump height (squat and countermovement jumps) and leg stiffness (multirebound jumps) were assessed in 12 competitive male players prematch, midmatch and postmatch, and 24 and 48 h after match completion.
Objectives: This study compared the thermal, physiological and perceptual responses associated with match-play tennis in HOT (∼34°C wet-bulb-globe temperature (WBGT)) and COOL (∼19°C WBGT) conditions, along with the accompanying alterations in match characteristics.
Methods: 12 male tennis players undertook two matches for an effective playing time (ie, ball in play) of 20 min, corresponding to ∼119 and ∼102 min of play in HOT and COOL conditions, respectively. Rectal and skin temperatures, heart rate, subjective ratings of thermal comfort, thermal sensation and perceived exertion were recorded, along with match characteristics.
This study examined whether central fatigue was exacerbated by an increase in muscle contractile speed caused by passive hyperthermia (PaH) and whether exercise-induced hyperthermia (ExH) combined with related peripheral fatigue influenced this response. The ExH was induced by cycling at 60% of maximal oxygen uptake in 38°C conditions and the PaH by sitting in a 48°C climate chamber. Ten men performed brief (≈ 5 s) and sustained (30 s) maximal voluntary isometric contractions (MVCs) of the knee extensors at baseline (CON, ∼37.
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