Randy Day’s research while affiliated with Louisiana State University and other places

Recently, it was shown that glycogen supercompensation tended (P = 0.06) to be greater if creatine and glycogen were loaded simultaneously. Because the authors suggested that creatine loading increased cell volumes and, therefore, enhanced glycogen supercompensation, we decided to determine whether an enhanced glycogen supercompensation could be realized if the glycogen loading protocol was preceded by a 5-d creatine load. Twelve men (19-28 yr) performed two standard glycogen loading protocols interspersed with a standard creatine load of 20 g.d(-1) for 5 d. The vastus lateralis muscle was biopsied before and after each loading protocol. The initial glycogen loading protocol showed a significant 4% increase (P < 0.05) in muscle glycogen (Delta upward arrow 164 +/- 87 mmol.kg(-1) d.m.), and no change (P > 0.05) in total muscle creatine. Biopsies pre- and post-creatine loading showed significant increases in total muscle creatine levels in both the left leg (Delta upward arrow 41.1 +/- 31.1 mmol.kg(-1) d.m.) and the right leg (Delta upward arrow 36.6 +/- 19.8 mmol.kg(-1) d.m.), with no change in either leg's muscle glycogen content. After the final glycogen loading, a significant 53% increase in muscle glycogen (Delta upward arrow 241 +/- 150 mmol.kg-1 d.m.) was detected. Finally, the postcreatine load total glycogen content (694 +/- 156 mmol.kg(-1) d.m.) was significantly (P < 0.05) greater than the precreatine load total glycogen content (597 +/- 142 mmol.kg(-1) d.m.). It is suggested that a muscle's glycogen loading capacity is influenced by its initial levels of creatine and the accompanying alterations in cell volume.

To determine the effects of creatine supplementation on cardiorespiratory responses during a graded exercise test (GXT) 36 trained adults (20 male, 16 female; 21–27 years old) performed two maximal GXTs on a cycle ergometer. The first GXT was done in a non-supplemented condition, and the second GXT was done following 7 days of ingesting either 5 g creatine monohydrate, encased in gelatin capsules, four times daily (CS, 13 male, 6 female), or the same number of glucose capsules (PL, 7 male, 10 female). CS significantly (P < 0.05) improved total test time [pre-CS=1217 (240) s, mean (std. dev.) versus post-CS=1289 (215) s], while PL administration had no effect (P > 0.05) on total test time [pre-PL=1037 (181) s versus post-PL=1047 (172) s]. In addition, both oxygen consumption (V˙ O2) and heart rate at the end of each of the first five GXT stages were significantly lower after CS, but were unchanged after PL. Moreover, the ventilatory threshold occurred at a significantly greater V˙ O2 for CS [pre-CS=2.2 (0.4) l · min−1 or 66% of peak V˙ O2 versus post-CS=2.6 (0.5) l · min−1 or 78% of peak V˙ O2; pre-PL=2.6 (0.9) l · min−1 or 70% peak V˙ O2 versus post-PL=2.6 (1.1) l · min−1 or 68% of peak V˙ O2]. Neither CS nor PL had an effect on peak V˙ O2 [pre-CS=3.4 (0.7) l · min−1 versus post-CS=3.3 (0.7) l · min−1; pre-PL=3.7 (1.1) l · min−1 versus post-PL=3.7 (1.1) l · min−1]. Apparently, CS can alter the contributions of the different metabolic systems during the initial stages of a GXT. Thus, the body is able to perform the sub-maximal workloads at a lower oxygen cost with a concomitant reduction in the work performed by the cardiovascular system.

To determine the thermoregulatory response of humans to heat following an ingestion of capsaicin. The thermoregulatory responses of 7 men (aged 22-28 years) to a 2-hour exposure to 38 degrees C (50% relative humidity) were compared following ingestion of either placebo or capsaicin. The capsaicin dose (2 mg x kg(-1)) was ingested 1 hour prior to the heat exposure, and all subjects were encouraged to overhydrate for 48 hours prior to each trial. Core temperature, mean skin temperature, cardiac output, and oxygen consumption were measured every 30 minutes. In addition, the changes (pre-exposure vs postexposure) in body mass and plasma volume were calculated. As expected, core temperature, cardiac output, and oxygen consumption all increased significantly (P < .05) with exposure time. There were also significant decreases over time in body mass and plasma volume. These aforementioned changes, however, were not significantly different (P > .05) between the placebo and capsaicin trials, except for mean skin temperature. The treatment effect for mean skin temperature was significant (P = .013), with the capsaicin response (34.7 degrees C) registering lower than the placebo measurement (35.1 degrees C). It appears that humans respond differently than animals to capsaicin ingestion. For humans, ingesting a 2-mg x kg(-1) dose of capsaicin 1 hour prior to heat exposure does not alter a person's ability to thermoregulate in the heat.

Animals respond to acute local or systemic administration of capsaicin with strong nociceptive reactions. The present investigation examined the thermal sensation in males who were given capsaicin (CAP, 2 mg x kg(-1) body weight) vs a placebo (PL, a maltodextrin capsule) before immersion in cold water. Seven Caucasian males ages 20-28 years were immersed in 18 degrees C and 22 degrees C twice (PL vs CAP) for 120 minutes. The following were examined: metabolism (VO2; L x min(-1)), rectal temperature (Tre; degrees C), and thermal sensation (TS). For VO2 there were no significant differences between treatments (PL vs CAP) when the variables were pooled jointly over the two immersion temperatures (18 degrees C and 22 degrees C) and across time. However, for Tre there were significant differences detected across time (p = 0.01) when Tre was pooled jointly across two treatments and two immersion temperatures. Postanalysis of variance revealed specific significant differences between 5 minutes (mean +/- SE; 37.2 +/- 0.07) and 120 minutes (36.0 +/- 0.09). For TS, there was a trend (p = 0.0699) which demonstrated differences between immersion temperatures only when TS was pooled jointly over the two treatments and across time, whereby TS was lower in 18 degrees C (6.2 +/- 0.5) than in 22 degrees C (3.7 +/- 0.6). From these data it appears that although Tre differed across time and temperature, respectively, a CAP feeding did not affect differentially the TS and metabolic response of males during acute cold water immersion.