RPE drift during cycling in 18 degrees C vs 30 degrees C wet bulb globe temperature.

AIM: The potential influence of a hotter vs cooler environment on ratings of perceived exertion (RPE) estimations during longer duration exercise is not well-understood. This study compared overall and differentiated RPEs during cycling in 18 degrees C vs 30 degrees C wet bulb globe temperature (WBGT). METHODS: Male volunteers (n=16) completed a maximal cycling trial (60 rev . min(-1), 25 Watts . min(-1)) to determine VO(2) max and ventilatory threshold (VT) before completing 2 (counterbalanced) longer duration cycling trials. At 30 degrees C WBGT (30C) and 18 degrees C WBGT (18C), subjects cycled 60 min (60 rev . min(-1), 90% individualized VT). Heart rate (HR, b . min(-1)) and rectal temperature (Tre, degrees C) were recorded every 5 min with corresponding RPE-overall (RPE-O), RPE-legs (RPE-L) and RPE-chest (RPE-C) estimations. RESULTS: HR was not significantly different at 5 min but was greater (P<0.05) for 30C at all other time points. During 30C, Tre was significantly greater (25, 30, 35, 40, 45, 50, 55 and 60 min), RPE-O was significantly greater (5, 40, 45, 50, 55 and 60 min), RPE-L was significantly greater (55 and 60 min) and RPE-C was significantly greater (35, 40, 45, 50, 55 and 60 min). CONCLUSIONS: Greater cardiovascular (HR) and thermal (Tre) strain partially explain greater perceptual ratings during 30C. Discernible RPE differences resulted mid-way through 60 min cycling with minimal differences initially. Results suggest RPEs are magnified in a 30 degrees C (vs 18 degrees C) environment beyond 30 min duration. Additionally, a 30 degrees C environment resulted in a less pronounced impact on RPE-L (vs RPE-C and RPE-O).

Influence of aerobic fitness on ratings of perceived exertion during graded and extended duration cycling.

AIM: Ratings of perceived exertion (RPE) have been shown similar across subjects of varying fitness when estimations are made at relative physiological criteria. Because few studies have investigated the influence of fitness during longer duration bouts, the current investigation compared overall exertion (RPE-O), leg exertion (RPE-L) and breathing/chest exertion (RPE-C) between aerobically fit and unfit subjects. METHODS: Aerobically fit (61.6+/-2.5 mL . kg . min(-1)) (n=7) and unfit (41.8+/-6.3 mL . kg . min(-1)) (n=6) males completed a maximal bike test and then cycled for 60 min at approximately 90% of individualized ventilatory threshold (VT) (V(E)/VO(2) vs V(E)/VCO(2)). Heart rate (HR, b . min(-1)), rectal temperature (Tre, degrees C) and RPE estimations were collected during graded testing every 2 min and every 10 min during 60 min bouts. RESULTS: During graded testing, RPE estimations at VT were not significantly different between groups. During 60 min cycling, HR and Tre were not significantly different between groups. Also, there were no significant differences for HR increase (HR 60 min HR 5 min) or Tre increase (Tre 60 min Tre 5 min). Interactions between groups were; RPE-O (P=0.09), RPE-L (P=0.06) and RPE-C (P=0.19). Analyses suggest groups experienced similar relative cardiovascular (HR) and thermal (Tre) strain. CONCLUSIONS: Although RPE responses between groups were similar at 10, 20 and 30 min, RPE drift was magnified in aerobically unfit subjects (vs aerobically fit subjects) beyond the 30 min point. Contrary to previous studies suggesting aerobic fitness does not influence RPE, current results show lower aerobic fitness magnifies RPE at individualized relative intensities when cycling extends beyond 30 min.

RPE-lactate dissociation during extended cycling.

This study examined the association of blood lactate concentration [La] and heart rate (HR) with ratings of perceived exertion (RPE) during 60 min of steady workload cycling. Physically active college-aged subjects (n = 14) completed an exhaustive cycling test to determine VO(2) (peak) and lactate threshold (2.5 mmol l(-1)). Subjects then cycled for 60 min at the power output associated with 2.5 mmol l(-1) [LA]. HR, [LA], RPE-overall, RPE-legs and RPE-chest were recorded at 5, 10, 20, 30, 40, 50 and 60 min. The 60-min trials were below maximal lactate steady state, with peak lactate concentration occurring at 20 min after which [LA] declined. The 20-min point was therefore considered pivotal, and data at other points were compared to this time point. Repeated measures ANOVA with simple contrasts (alpha = 0.05) showed (a) [LA] at 40, 50 and 60 min was significantly lower than at 20 min, (b) RPE-O and RPE-L were significantly greater at 30, 40, 50 and 60 min than at 20 min, (c) RPE-C was significantly greater at 40, 50 and 60 min than at 20 min, and (d) HR was significantly greater at 30, 40, 50 and 60 min than at 20 min. Significant (P < 0.05) positive correlations were found between HR and RPE-O (r = 0.43), RPE-L (r = 0.48) and RPE-C (r = 0.41) while correlations for [LA]-HR (r = 0.13) and [LA]-RPE (RPE-O: r = -0.11, RPE-L: r = 0.01, RPE-C: r = -0.06) were weak and non-significant. There is a dissociation of RPE and [LA] owing to RPE drift and lactate kinetics in longer duration sub-maximal exercise. Apparently, [LA] is not a strong RPE mediator during extended cycling.

Sweat lactate response during cycling at 30 degrees C and 18 degrees C WBGT.

Sweat lactate reflects eccrine gland metabolism. However, the metabolic tendencies of eccrine glands in a hot versus thermoneutral environment are not well understood. Sixteen male volunteers completed a maximal cycling trial and two 60-min cycling trials [30 degrees C = 30 +/- 1 degrees C and 18 degrees C = 18 +/- 1 degrees C wet bulb globe temperature (WBGT)]. The participants were requested to maintain a cadence of 60 rev min(-1) with the intensity individualized at approximately 90% of the ventilatory threshold. Sweat samples at 10, 20, 30, 40, 50 and 60 min were analysed for lactate concentration. Sweat rate at 30 degrees C (1380 +/- 325 ml x h(-1)) was significantly greater (P < 0.05) than at 18 degrees C (632 +/- 311 ml x h(-1)). Sweat lactate concentration was significantly greater (P < 0.05) at each time point during the 18 degrees C trial, with values between trials tending to converge across time. During the 30 degrees C trial, both heart rate (20, 30, 40, 50 and 60 min) and rectal temperature (30, 40, 50 and 60 min) were significantly higher than in the 18 degrees C trial. Higher sweat lactate concentrations coupled with lower sweat rates may indicate a greater relative contribution of oxygen-independent metabolism within eccrine glands during exercise at 18 degrees C. Decreases in sweat lactate concentration across time suggest either greater dilution due to greater sweat volume or increased reliance on aerobic metabolism within eccrine glands. The convergence of lactate concentrations between trials may indicate that time-dependent modifications in sweat gland metabolism occur at different rates contingent partially on environmental conditions.

Sweat lactate response between males with high and low aerobic fitness.

Sweat lactate indirectly reflects eccrine gland metabolism. However the potential influence of aerobic fitness on sweat lactate is not well-understood. Six males with high aerobic fitness [peak oxygen consumption ( VO(2)peak): 61.6 (2.5) ml.kg(-1).min(-1)] and seven males with low aerobic fitness [ VO(2)peak: 41.8 (6.4) ml.kg(-1).min(-1)] completed a maximal exertion cycling trial followed on a different day by 60 min of cycling (60 rev.min(-1)) in a 30 degrees C wet bulb globe temperature environment. Intensity was individualized at 90% of the ventilatory threshold ( V(E)/ VO(2) increase with no concurrent V(E)/ VCO(2) increase). Sweat samples were collected from the lumbar region every 10 min and analyzed for lactate concentration. Sweat rate (SR) was significantly greater ( p<0.05) for subjects with a high [1445 (254) ml.h(-1)] versus a low [1056 (261) ml.h(-1)] fitness level. Also, estimated total lactate excretion (SRxmean sweat lactate concentration) was marginally greater ( p=0.2) in highly fit males. However, repeated measures ANOVA showed no significant differences ( p>0.05) between groups for sweat lactate concentration at any time point. Current results show highly fit (vs. low fitness level) males have a greater sweat rate which is consistent with previous literature. However aerobic fitness and subsequent variations in SR do not appear to influence sweat lactate concentrations in males.

The effects of creatine supplementation on repeated upper- and lower-body Wingate performance.

Nineteen physically active men supplemented their diet with 20 g per day creatine monohydrate (Cr group) or placebo (PI group) for 6 days. Before and after supplementation, subjects performed 3 arm Wingates (AW1, AW2, and AW3) and 3 leg Wingates (LW1, LW2, and LW3) on consecutive days. Wingates were separated by 2 minutes each. Mean power (MP), peak power (PP), and percent decrease (%D) were compared between and within groups. MP did not change significantly for arms or legs. PP did not change significantly for legs. PP increased significantly in the Cr group (AW1) and for the P1 group (AW1 and AW3). MP and PP were not significantly different between groups. The %D increased significantly in the P1 group (AW1, AW3, and LW3). For the Cr group, %D decreased significantly (pre vs. post) and was significantly lower than for the P1 group (LW2-post). Results suggest that short-term Cr supplementation does not enhance MP and PP during repeated upper- and lower-body Wingate tests when not accompanied by an increase in body weight. However, changes in %D suggest possible ergogenic effects.

Effects of high and low blood lactate concentrations on sweat lactate response.

Sweat lactate results from eccrine gland metabolism, however, the possible clearance of blood lactate through sweat has not been resolved. On separate days in an environmental chamber (32 +/- 1 C) 12 subjects completed a constant load (CON) (30 min at 40% VO2 max) and an interval cycling trial (INT) (15 one-min intervals at 80% VO2 max, each separated by one min rest) each designed to elicit different blood lactate responses. Each 30 min cycling trial was preceded by 15 min warm-up (30 watts) and followed by 15 min passive rest. Sweat and blood were analyzed for lactate concentration at 15, 25, 35, 45, and 60 min during CON and INT. Total body water loss was used to calculate sweat rate (ml/hr). Blood lactate was significantly greater (p < or = 0.05) at 25, 35, 45, and 60 min during INT compared to CON (approximately 5 mmol/L vs 1.5 mmol/L). Sweat lactate was not significantly different (p>0.05) between trials at any time (approximately 10 mmol/L). Sweat rates (approximately 600ml/hr) and estimated total lactate secretion were not significantly different (CON vs. INT) (p > 0.05). Elevated blood lactate was not associated with changes in sweat lactate concentration. Sweat lactate seems to originate in eccrine glands independent of blood lactate.

Muscle contraction and fatigue. The role of adenosine 5'-diphosphate and inorganic phosphate.

Though many explanations are offered for the fatigue process in contracting skeletal muscle (both central and peripheral factors), none completely explain the decline in force production capability because fatigue is specific to the activity being performed. However, one needs to look no further than the muscle contraction crossbridge cycle itself in order to explain a major contributor to the fatigue process in exercise of any duration. The byproducts of adenosine 5'-triphosphate (ATP) hydrolysis, adenosine 5'-diphosphate (ADP) and inorganic phosphate (Pi) are released during the crossbridge cycle and can be implicated in the fatigue process due to the requirement of their release for proper crossbridge activity. Pi release is coupled to the powerstroke of the crossbridge cycle. The accumulation of Pi during exercise would lead to a reversal of its release step, therefore causing a decrement in force production capability. Due to the release of Pi with both the immediate (phosphagen) energy system and the hydrolysis of ATP, Pi accumulation is probably the largest contributor to the fatigue process in exercise of any duration. ADP release occurs near the end of the crossbridge cycle and therefore controls the velocity of crossbridge detachment. Therefore, ADP accumulation, which occurs during exercise of extended duration (or in ischaemic conditions), causes a slowing of the rate constants (and therefore a decrease in the maximal velocity of shortening). in the crossbridge cycle and a reduced oscillatory power output. The combined effects of these accumulated hydrolysis byproducts accounts for a large amount of the fatigue process in exercise of any intensity or duration.