Browsing Research from April 2016 by Publisher "American Physiological Society"
Now showing items 1-3 of 3
Downhill running and exercise in hot environments increase leukocyte Hsp72 (HSPA1A) and Hsp90 (HSPC1) gene transcriptsStressors within humans and other species activate Hsp72 and Hsp90 mRNA transcription, although it is unclear which environmental temperature or treadmill gradient induces the largest increase. To determine the optimal stressor for priming the Hsp system, physically active but not heat-acclimated participants (19.8 1.9 and 20.9 3.6 yr) exercised at lactate threshold in either temperate (20°C, 50% relative humidity; RH) or hot (30°C, 50% RH) environmental conditions. Within each condition, participants completed a flat running (temperate flat or hot flat) and a downhill running (temperate downhill or hot downhill) experimental trial in a randomized counterbalanced order separated by at least 7 days. Venous blood samples were taken immediately before (basal), immediately after exercise, and 3 and 24 h postexercise. RNA was extracted from leukocytes and RT-quantitative PCR conducted to determine Hsp72 and Hsp90 mRNA relative expression. Leukocyte Hsp72 mRNA was increased immediately after exercise following downhill running (1.9 0.9-fold) compared with flat running (1.3 0.4-fold; P 0.001) and in hot (1.9 0.6-fold) compared with temperate conditions (1.1 0.5-fold; P 0.003). Leukocyte Hsp90 mRNA increased immediately after exercise following downhill running (1.4 0.8-fold) compared with flat running (0.9 0.6-fold; P 0.002) and in hot (1.6 1.0-fold) compared with temperate conditions (0.9 0.6-fold; P 0.003). Downhill running and exercise in hot conditions induced the largest stimuli for leukocyte Hsp72 and Hsp90 mRNA increases.
Heat acclimation attenuates physiological strain and the HSP72, but not HSP90α, mRNA response to acute normobaric hypoxiaHeat acclimation (HA) attenuates physiological strain in hot conditions via phenotypic and cellular adaptation. The aim of this study was to determine whether HA reduced physiological strain, and heat shock protein (HSP) 72 and HSP90α mRNA responses in acute normobaric hypoxia. Sixteen male participants completed ten 90-min sessions of isothermic HA (40°C/40% relative humidity) or exercise training [control (CON); 20°C/40% relative humidity]. HA or CON were preceded (HYP1) and proceeded (HYP2) by a 30-min normobaric hypoxic exposure [inspired O2 fraction = 0.12; 10-min rest, 10-min cycling at 40% peak O2 uptake (V̇o2 peak), 10-min cycling at 65% V̇o2 peak]. HA induced greater rectal temperatures, sweat rate, and heart rates (HR) than CON during the training sessions. HA, but not CON, reduced resting rectal temperatures and resting HR and increased sweat rate and plasma volume. Hemoglobin mass did not change following HA nor CON. HSP72 and HSP90α mRNA increased in response to each HA session, but did not change with CON. HR during HYP2 was lower and O2 saturation higher at 65% V̇o2 peak following HA, but not CON. O2 uptake/HR was greater at rest and 65% V̇o2 peak in HYP2 following HA, but was unchanged after CON. At rest, the respiratory exchange ratio was reduced during HYP2 following HA, but not CON. The increase in HSP72 mRNA during HYP1 did not occur in HYP2 following HA. In CON, HSP72 mRNA expression was unchanged during HYP1 and HYP2. In HA and CON, increases in HSP90α mRNA during HYP1 were maintained in HYP2. HA reduces physiological strain, and the transcription of HSP72, but not HSP90α mRNA in acute normobaric hypoxia.
β-alanine supplementation enhances human skeletal muscle relaxation speed but not force production capacityPURPOSE: β-alanine (BA) supplementation improves human exercise performance. One possible explanation for this is an enhancement of muscle contractile properties, occurring via elevated intramuscular carnosine resulting in improved calcium sensitivity and handling. This study investigated the effect of BA supplementation on in vivo contractile properties and voluntary neuromuscular performance. METHODS: Twenty-three men completed two experimental sessions, pre- and post-28 days supplementation with 6.4 g·d-1 39 of BA (n = 12) or placebo (PLA; n = 11). During each session, force was recorded during a series of knee extensor contractions: resting and potentiated twitches and octet (8 pulses, 300 Hz) contractions elicited via femoral nerve stimulation; tetanic contractions (1 s, 1 – 100 Hz) via superficial muscle stimulation; and maximum and explosive voluntary contractions. RESULTS: BA supplementation had no effect on the force-frequency relationship, or the force responses (force at 25 ms and 50 ms from onset, peak force) of resting or potentiated twitches, and octet contractions (P > 0.05). Resting and potentiated twitch electromechanical delay and time-to-peak tension were unaffected by BA supplementation (P > 0.05), although half-relaxation time declined by 7-12% (P < 0.05). Maximum and explosive voluntary forces were unchanged after BA supplementation. CONCLUSION: BA supplementation had no effect on evoked force responses, implying that altered calcium sensitivity and/or release are not the mechanisms by which BA supplementation influences exercise performance. The reduced half-relaxation time with BA supplementation might, however, be explained by enhanced reuptake of calcium, which has implications for the efficiency of muscle contraction following BA supplementation.