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INFLUENCE OF PROLONGED BED REST ON THE EXERCISE PRESSOR RESPONSE Alan Kacin 1,2, Igor B Mekjavic 1,2, Samuel Rodman 3, Roger Kölegard and Ola Eiken Swedish.

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Presentation on theme: "INFLUENCE OF PROLONGED BED REST ON THE EXERCISE PRESSOR RESPONSE Alan Kacin 1,2, Igor B Mekjavic 1,2, Samuel Rodman 3, Roger Kölegard and Ola Eiken Swedish."— Presentation transcript:

1 INFLUENCE OF PROLONGED BED REST ON THE EXERCISE PRESSOR RESPONSE Alan Kacin 1,2, Igor B Mekjavic 1,2, Samuel Rodman 3, Roger Kölegard and Ola Eiken Swedish Defence Research Agency, Karolinska Institutet, Stockholm, Sweden 1 Institute of Biomedical and Biomolecular Sciences, Department of Sports and Exercise Science, University of Portsmouth, Portsmouth, United Kingdom 2 Department of Automation, Biocybernetics and Robotics, Institute Jozef Stefan & 3 Faculty of Mechanical Engineering, University of Ljubljana, Ljubljana, Slovenia RESULTS Active recovery increased (p<.01) MVC by 25%, from 50.0±4.3 to 62.6±9.2 kp (Student’s t Test). The relative increases in mean arterial pressure ( MAP) and heart rate ( HR) before and after active recovery were similar before and after recovery (Fig. 2. and Fig. 3.). BACKGROUND and PURPOSE Prolonged bed rest has been shown to attenuate the magnitude of the pressor response to sustained submaximal hand grip contraction conducted at identical levels relative to maximum voluntary contractions (Spaak et al., 2001). The present study investigated the effects of active recovery, following 35 days of horizontal bed rest, on the magnitude and response time of the pressor and heart rate responses to isometric contraction of knee extensors. METHODS Subjects: 10 healthy males. Protocol: 4 weeks of active recovery (cycle ergometry and resistance training 3 times weekly) following 35 days of horizontal bed rest. Trials: Maximal voluntary contraction (MVC) of knee extensor muscles post bed rest (Post BR) and after active recovery (Recovery). Sustained 90 second unilateral isometric knee extension conducted post bed rest and after active recovery. The maintained force in both conditions was 30% of post bed rest MVC (ie. the absolute force was identical). Measurements: Arterial blood pressure and heart rate were measured using the volume-clamp technique (Fig. 1) during the sustained contractions. MEAN ARTERIAL PRESSURE (n=10) Figure 2 HEART RATE (n=9) Figure 3 CONCLUSIONS That the arterial pressure response remained almost identical in the face of a 25% increase in muscle strength may, in line with the suggestions of Spaak et al. (2001), be interpreted as a bed rest-induced attenuation of the exercise pressor response. Exponential regression curves for the  MAP and  HR responses were derived for each subject using the Levenberg-Marquardt algorithm. The time course of individual pressor and heart rate responses during the 90 seconds of sustained isometric contraction were derived from these regression curves. For each individual, baseline MAP and HR values were average values prior to the onset of contraction. Asymptotic MAP and HR values were defined as the average of ten highest values prior to cessation of the contraction. Figure 2. The average magnitude of  MAP response was similar post bed rest (Post BR, orange line) and after recovery (Recovery, green line), whereas the average  MAP response time was slightly faster (p<.05) after recovery. References Spaak J, Sundblad P, Linnarsson D. Impaired pressor response after space flight and bed rest: evidence for cardiovascular dysfunction. Eur J Appl Physiol 2001; 85: 49-55. Figure 1: Experimental arrangement, showing the subject seated,and in preparation for a sustained isometric contraction of the right knee extensors. The volume-clamp device (Portapres, TNO, The Netherlands) is positioned on his left hand. Figure 3. Both the average magnitude and response time for  HR were similar before (Post BR, orange line) and after recovery (Recovery, green line). Acknowledgements The authors are indebted to the personnel at the Valdoltra Orthopaedic Hospital in Ankaran (Slovenia).


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