MUSCLE FATIGUE: PHYSIOLOGICAL AND BIOCHEMICAL STUDIES (EXERCISE, SPRINT, ENDURANCE)
The purpose of this study was to examine the etiology of muscle fatigue in fast and slow skeletal muscles giving particular interest to the relationship of H+ ion and muscle contractile properties. A further objective was to evaluate to what extent endurance and sprint exercise training protects against the development of fatigue. Endurance exercise involved running 1.2 mph at a 15% grade 2 hours per day, 5 days per week for 10 weeks. The sprint training program consisted of 6 sprints of 4.5 minute duration at 40 m.min -1 and 15% slope with 2.5 minute rest intervals performed 5 days per week for six weeks. Muscle fatigue was produced in the predominantly type I Soleus, the type IIA and IIB extensor digitorum longus and the type IIB superficial region of the vastus lateralis by electrical stimulation in vitro at 22 C. Muscles were stimulated at 45 trains.min-1 for 1, 5 or 10 minutes. In both training modalities, train tension decreased faster in controls compared to the exercise trained group. This suggested that exercise training leads to a delay in the development of fatigue being most pronounced following a regimen of sprint training. This training adaptation can be explained in part by an improved oxidative and glycolytic capacity of the working musculature as evidenced by an improvement in citrate synthase and PFK activity. Examination of contractile properties following exercise training revealed a reduced contraction time and one-half relaxation time in the slow twitch muscles following endurance training. Similar adaptations in the fast twitch muscles were observed only in sprint trained groups. Shortened velocity improved in slow twitch fibers only with endurance training and in slow and fast twitch fibers following sprint training. These changes suggest an alteration in excitation-contraction coupling, crossbridge activation or in Ca++ reuptake and relaxation. Additional findings also help to explain the observed delay in fatigue development. Lactic acid accumulates following high intensity activity and is accompanied by a similar increase in H+ ion concentration. Training resulted in lower values following intense muscular activity. This may be a result of the muscles' capacity to buffer the accumulation of acid thus allowing work to continue for longer periods. Depletion of glycogen, ATP and CP cannot be considered primary causative agents of fatigue. The avoidance of fatigue development is a result of an improvement in regulation of the H+ ion. (Abstract shortened with permission of author.)
JOHN PATRICK TROUP,
"MUSCLE FATIGUE: PHYSIOLOGICAL AND BIOCHEMICAL STUDIES (EXERCISE, SPRINT, ENDURANCE)"
(January 1, 1985).
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