Creatine supplementation attenuates hemodynamic and arterial stiffness responses following an acute bout of isokinetic exercise


Journal Title (Medline/Pubmed accepted abbreviation): Eur J Appl Physiol
Year: 2011
Volume: 111
Number:
Page number: 1965-1971
doi : 10.1007/s00421-011-1832-4

Summary of background and research design:

Background: Acute exercise induces increased heart rate (HR) and blood pressure (BP) during and after exercise. These increases are likely due, in part, to metaboreceptor stimulation in the active muscle and corresponding sympathetic nervous system activation. Central arterial tonicity (stiffness) is associated with increased systolic BP (SBP), hemodynamic stress, and higher myocardial oxygen demand, both normally during exercise and pathologically in acute cardiovascular events. Creatine supplementation improves anaerobic performance, reduces accumulation of muscle stress metabolites, and attenuates exercise-associated increases in HR. Reduction of muscle metabolites after exercise may reduce post-exercise indicators of aortic stiffness (pulse wave velocity; PWV), and hemodynamic response (HR and BP).

Hypothesis/purpose of study: Creatine supplementation may attenuate HR, BP, and PWV responses in male volunteers after acute exercise.

Subjects: Sixteen healthy, young (22.6 ± 0.6 y), sedentary or moderately active (≤ 3 hr/wk), males participated in the study. All participants were normotensive (SBP < 140 mmHg and diastolic BP [DBP] < 90 mmHg).

Experimental design: Double blind, placebo-controlled

Treatments Protocol: After familiarization, fasted (> 4 hr) participants underwent resting baseline data acquisition consisting of electrocardiogram (ECG), BP, and PWV assessment. Participants were randomized to receive creatine monohydrate (2 × 5 g/day) or maltodextrin placebo (2 × 5 g/day) for 3 weeks. Exercise consisted of 2 sets of 50 repetitions of maximal (100% peak torque) single-leg knee extensions at an angular velocity of 180°/second for the left leg with a passive 1-second eccentric phase in an isokinetic dynamometer. Rate pressure product (RPP; the product of SBP and HR divided by 100) was collected twice at each time point and averaged. Muscle endurance was assessed using the isokinetic fatigue index (FI) calculated as the difference between work performed during the last and first 10 repetitions, divided by total work during first 10 reps and multiplied times 100. Cardiovascular measurements were assessed before exercise and at 5 and 15 minutes post-exercise (PE5 and PE15) while participants were in the supine recovery position.


Summary of research findings:
  • Resting cardiovascular and isokinetic measurements were similar between groups before and after supplementation.
  • After supplementation, HR, SBP, RPP, and brachial ankle (ba)PWV had significant treatment-by-time interaction from rest to PE5 and PE15 in the placebo group, but not in the creatine group (P < .05).
    • HR increased significantly from rest to PE5 and PE15 in both treatment groups (P < .01).
    • SBP increased significantly at PE5 in both groups (P ≤ .05) and at PE15 in the placebo group only (P < .01).
    • RPP increased significantly in both groups at both time points (P < .01 for all measurements).
    • baPWV increased significantly from rest in the placebo group at both time points (P <.01); however, no change was observed in the creatine group.
  • Exercised leg PWV was reduced in both groups at PE5 compared with rest (placebo, –1.1 m/sec; creatine –0.9 m/sec; P < .01)
    • This change returned to normal by PE15 in both groups.
    • No change was observed in the non-exercised leg.

Interpretation of findings/Key practice applications:

Compared with those who received placebo, men who received creatine supplementation for 3 weeks had attenuated post-exercise increases in HR, SBP, RPP, and brachial arterial stiffness following acute isokinetic exercise. No changes in at-rest cardiovascular measures were observed. A novel finding was that increased SBP post-exercise was attenuated at PE5 and completely suppressed at PE15 by creatine supplementation. Additionally, the authors state that reduction in post-exercise RPP after creatine supplementation may occur through reduced left ventricular afterload following exercise. The authors conclude that creatine supplementation in healthy young men reduces hemodynamic response and arterial stiffness following acute exercise without affecting cardiovascular function at rest. Study limitations included small sample size, no assessment of creatine concentration, no assessment of aortic PWV for arterial stiffness, and no assessment of hemodynamic responses before supplementation (may have identified attenuated responses prior to study).

 
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