Abstract
Little is presently known about the effects of acute high-intensity exercise or training on release and uptake of Ca2+ by the sarcoplasmic reticulum (SR). The aims here were to characterize this regulation in highly trained athletes following (1) repeated bouts of high-intensity exercise and (2) a period of endurance training including high-intensity sessions. Eleven cross-country skiers (25 ± 4 years, 65 ± 4 mL O2⋅kg−1⋅min–1) performed four self-paced sprint time-trials (STT 1-4) lasting ≈ 4 min each (STT 1–4) and separated by 45 min of recovery; while 19 triathletes and road cyclists (25 ± 4 years, 65 ± 5 mL O2⋅kg−1⋅min–1) completed 4 weeks of endurance training in combination with three sessions of high-intensity interval cycling per week. Release (μmol⋅g–1 prot⋅min–1) and uptake [tau (s)] of Ca2+ by SR vesicles isolated from m. triceps brachii and m. vastus lateralis were determined before and after STT 1 and 4 in the skiers and in m. vastus lateralis before and after the 4 weeks of training in the endurance athletes. The Ca2+ release rate was reduced by 17–18% in both limbs already after STT 1 (arms: 2.52 ± 0.74 to 2.08 ± 0.60; legs: 2.41 ± 0.45 to 1.98 ± 0.51, P < 0.0001) and attenuated further following STT 4 (arms: 2.24 ± 0.67 to 1.95 ± 0.45; legs: 2.13 ± 0.51 to 1.83 ± 0.36, P < 0.0001). Also, there was a tendency toward an impairment in the SR Ca2+ uptake from pre STT1 to post STT4 in both arms and legs (arms: from 22.0 ± 3.7 s to 25.3 ± 6.0 s; legs: from 22.5 ± 4.7 s to 25.5 ± 7.7 s, P = 0.05). Endurance training combined with high-intensity exercise increased the Ca2+ release rate by 9% (1.76 ± 0.38 to 1.91 ± 0.44, P = 0.009), without altering the Ca2+ uptake (29.6 ± 7.0 to 29.1 ± 8.7 s; P = 0.98). In conclusion, the Ca2+ release and uptake rates by SR in exercising limbs of highly trained athletes declines gradually by repetitive bouts of high-intensity exercise. We also demonstrate, for the first time, that the SR Ca2+ release rate can be enhanced by a specific program of training in highly trained athletes, which may have important implications for performance parameters.
Highlights
The functional capacity of skeletal muscles relies partly on intrinsic metabolic and mechanic properties and by repetitive contractions these may be disrupted leading to a reduction in skeletal muscle function and performance, i.e., fatigue (Allen et al, 2008)
The simulated sprint cross-country skiing competition, consisting of 4 × 4 min of high-intensity exercise interspersed with 45 min recovery periods, lead to significant fluctuations in the sarcoplasmic reticulum (SR) Ca2+ handling in both arms and legs (Figures 3, 4)
During the fourth bout of high-intensity exercise (i.e., sprint time-trials (STTs) 4), the SR Ca2+ release rate were further reduced by 13–14% (Figures 3A,B)
Summary
The functional capacity of skeletal muscles relies partly on intrinsic metabolic and mechanic properties and by repetitive contractions these may be disrupted leading to a reduction in skeletal muscle function and performance, i.e., fatigue (Allen et al, 2008). Studies in intact single fibers of rodent and human skeletal muscle have repeatedly revealed that steps in the E-C coupling involving myofibrillar Ca2+ regulation are an important part of the decrease in force production following repeated contractions, with the underlying cellular mechanisms being, (i) an impaired SR Ca2+ release, (ii) a reduced myofibrillar Ca2+ sensitivity or (iii) a reduced maximal Ca2+ activated force production, with the importance of each depending on muscle activation pattern and duration (Allen et al, 2008). These studies have revealed decreases in muscle fiber relaxation rate and rates of myofibrillar Ca2+ decline
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