Effects of type 1 diabetes, sprint training and sex on skeletal muscle sarcoplasmic reticulum Ca2+ uptake and Ca2+‐ATPase activity
Key points Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important during exercise, it has not been investigated in human diabetes or compared between sexes. We show that Ca2+‐ATPase activity and...
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| Published in | The Journal of physiology Vol. 592; no. 3; pp. 523 - 535 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Wiley Subscription Services, Inc
01.02.2014
Blackwell Publishing Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3751 1469-7793 1469-7793 |
| DOI | 10.1113/jphysiol.2013.261172 |
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| Abstract | Key points
Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important during exercise, it has not been investigated in human diabetes or compared between sexes.
We show that Ca2+‐ATPase activity and Ca2+ uptake are higher among people with type 1 diabetes (T1D) compared with matched non‐diabetic controls (CON), but that performance during intense exercise was similar; Ca2+‐ATPase activity and Ca2+ uptake are also higher among men than women.
We show that Ca2+‐ATPase activity is reduced during intense exercise in men but not women, and is reduced by high‐intensity exercise training (HIET) in T1D and CON.
Fatigue is commonly reported by people with diabetes, but our data show that muscle calcium resequestration and performance during intense exercise and after HIET is not impaired in T1D, and hence other physiological or psychological mechanisms for fatigue in diabetes must be sought.
Sex influences muscle calcium regulation.
Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high‐intensity exercise. Ca2+ handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high‐intensity exercise and sprint training on skeletal muscle Ca2+ regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non‐diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca2+ regulation. Subjects undertook 7 weeks of three times‐weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high‐intensity exercise. In T1D, higher Ca2+‐ATPase activity (+28%) and Ca2+ uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca2+‐ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca2+‐ATPase activity, but not Ca2+ uptake, was lower (−24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca2+‐ATPase activity in T1D or CON. However, sex differences were evident: Ca2+‐ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca2+‐ATPase (−8%, P < 0.05), but not Ca2+ uptake, in T1D and CON. In summary, skeletal muscle Ca2+ resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca2+‐ATPase in T1D and CON. Sex differences in Ca2+‐ATPase activity were evident and may be linked with fibre type proportion differences. |
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| AbstractList | Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca(2+) handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca(2+) regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca(2+) regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca(2+)-ATPase activity (+28%) and Ca(2+) uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca(2+)-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca(2+)-ATPase activity, but not Ca(2+) uptake, was lower (-24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca(2+)-ATPase activity in T1D or CON. However, sex differences were evident: Ca(2+)-ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca(2+)-ATPase (-8%, P < 0.05), but not Ca(2+) uptake, in T1D and CON. In summary, skeletal muscle Ca(2+) resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca(2+)-ATPase in T1D and CON. Sex differences in Ca(2+)-ATPase activity were evident and may be linked with fibre type proportion differences. Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca2+ handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca2+ regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca2+ regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca2+-ATPase activity (+28%) and Ca2+ uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca2+-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca2+-ATPase activity, but not Ca2+ uptake, was lower (−24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca2+-ATPase activity in T1D or CON. However, sex differences were evident: Ca2+-ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca2+-ATPase (−8%, P < 0.05), but not Ca2+ uptake, in T1D and CON. In summary, skeletal muscle Ca2+ resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca2+-ATPase in T1D and CON. Sex differences in Ca2+-ATPase activity were evident and may be linked with fibre type proportion differences. Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important during exercise, it has not been investigated in human diabetes or compared between sexes.We show that Ca2+-ATPase activity and Ca2+ uptake are higher among people with type 1 diabetes (T1D) compared with matched non-diabetic controls (CON), but that performance during intense exercise was similar; Ca2+-ATPase activity and Ca2+ uptake are also higher among men than women.We show that Ca2+-ATPase activity is reduced during intense exercise in men but not women, and is reduced by high-intensity exercise training (HIET) in T1D and CON.Fatigue is commonly reported by people with diabetes, but our data show that muscle calcium resequestration and performance during intense exercise and after HIET is not impaired in T1D, and hence other physiological or psychological mechanisms for fatigue in diabetes must be sought.Sex influences muscle calcium regulation. Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca2+ handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca2+ regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca2+ regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca2+-ATPase activity (+28%) and Ca2+ uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca2+-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca2+-ATPase activity, but not Ca2+ uptake, was lower (-24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca2+-ATPase activity in T1D or CON. However, sex differences were evident: Ca2+-ATPase was reduced with exercise among men but increased among women across both days (time sex interaction, P < 0.05). Sprint training reduced Ca2+-ATPase (-8%, P < 0.05), but not Ca2+ uptake, in T1D and CON. In summary, skeletal muscle Ca2+ resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca2+-ATPase in T1D and CON. Sex differences in Ca2+-ATPase activity were evident and may be linked with fibre type proportion differences. Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca(2+) handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca(2+) regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca(2+) regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca(2+)-ATPase activity (+28%) and Ca(2+) uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca(2+)-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca(2+)-ATPase activity, but not Ca(2+) uptake, was lower (-24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca(2+)-ATPase activity in T1D or CON. However, sex differences were evident: Ca(2+)-ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca(2+)-ATPase (-8%, P < 0.05), but not Ca(2+) uptake, in T1D and CON. In summary, skeletal muscle Ca(2+) resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca(2+)-ATPase in T1D and CON. Sex differences in Ca(2+)-ATPase activity were evident and may be linked with fibre type proportion differences.Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca(2+) handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca(2+) regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca(2+) regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca(2+)-ATPase activity (+28%) and Ca(2+) uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca(2+)-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca(2+)-ATPase activity, but not Ca(2+) uptake, was lower (-24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca(2+)-ATPase activity in T1D or CON. However, sex differences were evident: Ca(2+)-ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca(2+)-ATPase (-8%, P < 0.05), but not Ca(2+) uptake, in T1D and CON. In summary, skeletal muscle Ca(2+) resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca(2+)-ATPase in T1D and CON. Sex differences in Ca(2+)-ATPase activity were evident and may be linked with fibre type proportion differences. Key points Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important during exercise, it has not been investigated in human diabetes or compared between sexes. We show that Ca2+‐ATPase activity and Ca2+ uptake are higher among people with type 1 diabetes (T1D) compared with matched non‐diabetic controls (CON), but that performance during intense exercise was similar; Ca2+‐ATPase activity and Ca2+ uptake are also higher among men than women. We show that Ca2+‐ATPase activity is reduced during intense exercise in men but not women, and is reduced by high‐intensity exercise training (HIET) in T1D and CON. Fatigue is commonly reported by people with diabetes, but our data show that muscle calcium resequestration and performance during intense exercise and after HIET is not impaired in T1D, and hence other physiological or psychological mechanisms for fatigue in diabetes must be sought. Sex influences muscle calcium regulation. Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high‐intensity exercise. Ca2+ handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high‐intensity exercise and sprint training on skeletal muscle Ca2+ regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non‐diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca2+ regulation. Subjects undertook 7 weeks of three times‐weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high‐intensity exercise. In T1D, higher Ca2+‐ATPase activity (+28%) and Ca2+ uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca2+‐ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca2+‐ATPase activity, but not Ca2+ uptake, was lower (−24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca2+‐ATPase activity in T1D or CON. However, sex differences were evident: Ca2+‐ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca2+‐ATPase (−8%, P < 0.05), but not Ca2+ uptake, in T1D and CON. In summary, skeletal muscle Ca2+ resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca2+‐ATPase in T1D and CON. Sex differences in Ca2+‐ATPase activity were evident and may be linked with fibre type proportion differences. Key points Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important during exercise, it has not been investigated in human diabetes or compared between sexes. We show that Ca2+-ATPase activity and Ca2+ uptake are higher among people with type 1 diabetes (T1D) compared with matched non-diabetic controls (CON), but that performance during intense exercise was similar; Ca2+-ATPase activity and Ca2+ uptake are also higher among men than women. We show that Ca2+-ATPase activity is reduced during intense exercise in men but not women, and is reduced by high-intensity exercise training (HIET) in T1D and CON. Fatigue is commonly reported by people with diabetes, but our data show that muscle calcium resequestration and performance during intense exercise and after HIET is not impaired in T1D, and hence other physiological or psychological mechanisms for fatigue in diabetes must be sought. Sex influences muscle calcium regulation. Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca2+ handling is altered by diabetes mellitus, but has not previously been investigated in human skeletal muscle. We investigated effects of high-intensity exercise and sprint training on skeletal muscle Ca2+ regulation among men and women with type 1 diabetes (T1D, n = 8, 3F, 5M) and matched non-diabetic controls (CON, n = 8, 3F, 5M). Secondarily, we examined sex differences in Ca2+ regulation. Subjects undertook 7 weeks of three times-weekly cycle sprint training. Before and after training, performance was measured, and blood and muscle were sampled at rest and after high-intensity exercise. In T1D, higher Ca2+-ATPase activity (+28%) and Ca2+ uptake (+21%) than in CON were evident across both times and days (P < 0.05), but performance was similar. In T1D, resting Ca2+-ATPase activity correlated with work performed until exhaustion (r = 0.7, P < 0.01). Ca2+-ATPase activity, but not Ca2+ uptake, was lower (-24%, P < 0.05) among the women across both times and days. Intense exercise did not alter Ca2+-ATPase activity in T1D or CON. However, sex differences were evident: Ca2+-ATPase was reduced with exercise among men but increased among women across both days (time × sex interaction, P < 0.05). Sprint training reduced Ca2+-ATPase (-8%, P < 0.05), but not Ca2+ uptake, in T1D and CON. In summary, skeletal muscle Ca2+ resequestration capacity was increased in T1D, but performance was not greater than CON. Sprint training reduced Ca2+-ATPase in T1D and CON. Sex differences in Ca2+-ATPase activity were evident and may be linked with fibre type proportion differences. [PUBLICATION ABSTRACT] |
| Author | McKenna, M. J. Hunter, S. K. Thom, J. M. Ruell, P. A. Harmer, A. R. Chisholm, D. J. Flack, J. R. |
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Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration... Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca(2+) handling is altered by... Key points Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration... Skeletal muscle calcium resequestration and performance is increased in male rats with induced diabetes; and whilst muscle calcium resequestration is important... Calcium cycling is integral to muscle performance during the rapid muscle contraction and relaxation of high-intensity exercise. Ca2+ handling is altered by... |
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| SubjectTerms | Adult Calcium - metabolism Calcium-Transporting ATPases - metabolism Case-Control Studies Diabetes Mellitus, Type 1 - metabolism Exercise Female Humans Male Muscle, Skeletal - metabolism Muscle, Skeletal - physiology Sarcoplasmic Reticulum - metabolism Sex Factors Skeletal Muscle and Exercise |
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| Title | Effects of type 1 diabetes, sprint training and sex on skeletal muscle sarcoplasmic reticulum Ca2+ uptake and Ca2+‐ATPase activity |
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