Effect of caffeine on metabolism, exercise endurance, and catecholamine responses after withdrawal.
ABSTRACT In this study the effects of acute caffeine ingestion on exercise performance, hormonal (epinephrine, norepinephrine, insulin), and metabolic (free fatty acids, glycerol, glucose, lactate, expired gases) parameters during short-term withdrawal from dietary caffeine were investigated. Recreational athletes who were habitual caffeine users (n = 6) (maximum oxygen uptake 54.5 +/- 3.3 ml x kg-1 x min-1 and daily caffeine intake 761.3 +/- 11.8 mg/day) were tested under conditions of no withdrawal and 2-day and 4-day withdrawal from dietary caffeine. There were seven trials in total with a minimum of 10 days between trials. On the day of the exercise trial, subjects ingested either dextrose placebo or 6 mg/kg caffeine in capsule form 1 h before cycle ergometry to exhaustion at 80-85% of maximum oxygen uptake. Test substances were assigned in a random, double-blind manner. A final placebo control trial completed the experiment. There was no significant difference in any measured parameters among days of withdrawal after ingestion of placebo. At exhaustion in the 2- and 4-day withdrawal trials, there were significant increases in plasma norepinephrine in response to caffeine ingestion. Caffeine-induced increases in serum free fatty acids occurred after 4 days and only at rest. Subjects responded to caffeine with increases in plasma epinephrine (P < 0.05) at exhaustion and prolonged exercise time in all caffeine trials compared with placebo, regardless of withdrawal from caffeine. It is concluded that increased endurance is unrelated to hormonal or metabolic changes and that it is not related to prior caffeine habituation in recreational athletes.
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ABSTRACT: To investigate whether caffeine ingestion counteracts the morning reduction in neuromuscular performance associated with the circadian rhythm pattern. Twelve highly resistance-trained men underwent a battery of neuromuscular tests under three different conditions; i) morning (10:00 a.m.) with caffeine ingestion (i.e., 3 mg kg(-1); AM(CAFF) trial); ii) morning (10:00 a.m.) with placebo ingestion (AM(PLAC) trial); and iii) afternoon (18:00 p.m.) with placebo ingestion (PM(PLAC) trial). A randomized, double-blind, crossover, placebo controlled experimental design was used, with all subjects serving as their own controls. The neuromuscular test battery consisted in the measurement of bar displacement velocity during free-weight full-squat (SQ) and bench press (BP) exercises against loads that elicit maximum strength (75% 1RM load) and muscle power adaptations (1 m s(-1) load). Isometric maximum voluntary contraction (MVC(LEG)) and isometric electrically evoked strength of the right knee (EVOK(LEG)) were measured to identify caffeine's action mechanisms. Steroid hormone levels (serum testosterone, cortisol and growth hormone) were evaluated at the beginning of each trial (PRE). In addition, plasma norepinephrine (NE) and epinephrine were measured PRE and at the end of each trial following a standardized intense (85% 1RM) 6 repetitions bout of SQ (POST). In the PM(PLAC) trial, dynamic muscle strength and power output were significantly enhanced compared with AM(PLAC) treatment (3.0%-7.5%; p≤0.05). During AM(CAFF) trial, muscle strength and power output increased above AM(PLAC) levels (4.6%-5.7%; p≤0.05) except for BP velocity with 1 m s(-1) load (p = 0.06). During AM(CAFF), EVOK(LEG) and NE (a surrogate of maximal muscle sympathetic nerve activation) were increased above AM(PLAC) trial (14.6% and 96.8% respectively; p≤0.05). These results indicate that caffeine ingestion reverses the morning neuromuscular declines in highly resistance-trained men, raising performance to the levels of the afternoon trial. Our electrical stimulation data, along with the NE values, suggest that caffeine increases neuromuscular performance having a direct effect in the muscle.PLoS ONE 01/2012; 7(4):e33807. · 3.73 Impact Factor
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ABSTRACT: Treatment of p53(-/-) mice orally with caffeine, voluntary exercise or their combination for 2 weeks prior to a single irradiation with UVB (i) decreased the weight of the epididymal fat pads by 22, 40 and 56%, (ii) decreased the thickness of the dermal fat layer by 10, 26 and 42%, (iii) increased the number of apoptotic sunburn cells by 29, 100 and 489%, (iv) increased the number of caspase-3-positive cells by 33, 117 and 667% and (v) increased the number of mitotic cells with cyclin B1-positive staining by 40, 210 and 510%, respectively. Pearson's correlation coefficient indicated a statistically significant inverse relationship between the level of tissue fat and the number of mitotic cells with cyclin B1 in p53(-/-) mice but not in p53(+/+) littermates. Western blot analysis indicated that treatment of p53(-/-) mice with caffeine together with exercise increased the level of cyclin B1 significantly more than in p53(+/+) mice. p53(-/-) mice, but not p53(+/+) mice, treated with caffeine during exercise exhibited a dramatic decrease in the level of survivin. Our results suggest that voluntary exercise in combination with oral caffeine may exert a synergistic increase in UVB-induced apoptosis and that tissue fat may be a more important modulator of apoptosis and carcinogenesis in p53-deficient mice than in p53-normal mice. The stimulatory effects on apoptosis in p53(-/-) mice by the combination treatment might be associated with increased levels of cyclin B1 and decreased levels of survivin.Carcinogenesis 11/2009; 31(4):671-8. · 5.64 Impact Factor
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ABSTRACT: It is not known if ergogenic effects of caffeine ingestion in athletic groups occur in the sedentary. To investigate this, we used a counterbalanced, double-blind, crossover design to examine the effects of caffeine ingestion (6 mg · kg⁻¹ body-mass) on exercise performance, substrate utilisation and perceived exertion during 30 minutes of self-paced stationary cycling in sedentary men. Participants performed two trials, one week apart, after ingestion of either caffeine or placebo one hour before exercise. Participants were instructed to cycle as quickly as they could during each trial. External work (J · kg⁻¹) after caffeine ingestion was greater than after placebo (P = 0.001, effect size [ES] = 0.3). Further, heart rate, oxygen uptake and energy expenditure during exercise were greater after caffeine ingestion (P = 0.031, ES = 0.4; P = 0.009, ES = 0.3 and P = 0.018, ES = 0.3; respectively), whereas ratings of perceived exertion and respiratory exchange ratio values did not differ between trials (P = 0.877, ES = 0.1; P = 0.760, ES = 0.1; respectively). The ability to do more exercise after caffeine ingestion, without an accompanying increase in effort sensation, could motivate sedentary men to participate in exercise more often and so reduce adverse effects of inactivity on health.Journal of Sports Sciences 05/2012; 30(12):1235-40. · 2.08 Impact Factor