Joke Kokkonen’s research while affiliated with Brigham Young University–Hawaii 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.

Since strength and muscular strength endurance are linked, it is possible that the inhibitory influence that prior stretching has on strength can also extend to the reduction of muscle strength endurance. To date, however, studies measuring muscle strength endurance poststretching have been criticized because of problems with their reliability. The purpose of this study was twofold: both the muscle strength endurance performance after acute static stretching exercises and the repeatability of those differences were measured. Two separate experiments were conducted. In experiment 1, the knee-flexion muscle strength endurance exercise was measured by exercise performed at 60 and 40% of body weight following either a no-stretching or stretching regimen. In experiment 2, using a test-retest protocol, a knee-flexion muscle strength endurance exercise was performed at 50% body weight on 4 different days, with 2 tests following a no-stretching regimen (RNS) and 2 tests following a stretching regimen (RST). For experiment 1, when exercise was performed at 60% of body weight, stretching significantly (p < 0.05) reduced muscle strength endurance by 24%, and at 40% of body weight, it was reduced by 9%. For experiment 2, reliability was high (RNS, intraclass correlation = 0.94; RST, intraclass correlation = 0.97). Stretching also significantly (p < 0.05) reduced muscle strength endurance by 28%. Therefore, it is recommended that heavy static stretching exercises of a muscle group be avoided prior to any performances requiring maximal muscle strength endurance.

Recent research has shown that a regimen of stretching provides an acute inhibition of maximal force production by the stretched muscle group. To further characterize this phenomenon, the effect of an acute stretching regimen on maximal isokinetic knee-extension torque at 5 specific movement velocities (1.05, 1.57, 2.62, 3.67, and 4.71 rad x s(-1)) was examined in 10 men and 5 women (22-28 years). Each person's 5 baseline maximal isokinetic knee-extension torques (dominant leg) were measured on a Cybex NORM dynamometer. Following the baseline torque measurements, the participants stretched the dominant quadriceps for 15 minutes using 1 active and 3 passive stretching exercises. Once the stretching exercises were completed, the maximal torque measurements were repeated. Poststretch maximal torque at 1.05 rad x s(-1) was significantly reduced (p < 0.05) from 218 +/- 47 Nm (mean +/- SD) to 199 +/- 49 Nm (7.2% decrease). At 1.57 rad x s(-1), a similar decrease (p < 0.05) was also seen (204 +/- 48 Nm vs. 195 +/- 47 Nm; 4.5% decrease), but at the other velocities (2.62, 3.67, and 4.71 rad x s(-1)), poststretch maximal torque was unaltered (p > 0.05). It appears, therefore, that the deleterious impact of stretching activities on maximal torque production might be limited to movements performed at relatively slow velocities.

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.