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Context: Ergogenic effects of caffeine on aerobic or endurance exercise are well documented. Conversely, the ergogenic value of caffeine on high-intensity, primarily anaerobic performance is not well understood even though the proposed mechanisms of action for caffeine permit a strong theoretical basis for application to this type of exercise. Purpose: This study examined effects of caffeine (Ca) on number repetitions (reps), ratings of perceived exertion (RPE), and peak heart rate (PHR) during resistance-training exercise with reps performed to volitional failure. Methods: Subjects (N = 17) were tested for 10-rep maximum in bench press (BP) and leg press (LP). In sessions 2 and 3, Ca (~6 mg/kg) or placebo (Pl) was ingested 1 hr beforehand in a double-blind manner and counterbalanced order. Subjects performed 3 sets to failure (BP and LP) with reps, PHR, and RPE recorded each set. Repeated-measures ANOVAs, 2 (trial) × 3 (set), were used to analyze dependent measures with the Tukey honestly significant difference used when necessary as the post hoc test. Results: In BP, no significant differences (Ca vs Pl) were observed (reps, RPE, PHR). During set 3 of LP training, Ca was associated with significantly higher reps (12.5 ± 4.2 vs 9.9 ± 2.6) and PHR (158.5 ± 11.9 vs 151.8 ± 13.2). No significant RPE differences were found during LP. Conclusions: The findings of similar RPE concurrent with higher reps suggest that caffeine can blunt pain responses, possibly delaying fatigue in high-intensity resistance training. Ergogenic effects might be limited to the later sets in a resistance-training session. Further research is warranted regarding ergogenic effects of caffeine during resistance training and potential mechanisms of action.Caffeine can enhance endurance-based exercise performance with ergogenic properties attributed to mechanisms such as enhanced free-fatty-acid mobilization 1,2

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.

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Based on these findings, interventions can be developed for the varied needs of a diverse student population as it pertains to PA participation.

INT and REC independently showed moderate correspondence for RPE-[La] and RPE-HR. However, tighter overall coupling of HR with RPE (vs [La] with RPE) and a dissociation between RPE-[La] suggest RPE during intervals of intense cycling were more sensitive to acute metabolic demand (evidenced by HR) versus [La].

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.

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.