M. Ball-Burnett

Regulation of fiber size, oxidative potential, and capillarization in human muscle by resistance exercise

To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 +/- 2.3 ml. kg-1. min-1; mean +/- SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions (P < 0.05) in type IIB fibers (15.1 +/- 2.1% vs. 7.2 +/- 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase (P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 ± 2.3 ml ⋅ kg-1 ⋅ min-1; mean ± SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions ( P < 0.05) in type IIB fibers (15.1 ± 2.1% vs. 7.2 ± 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase ( P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.

Energy metabolism in human slow and fast twitch fibres during prolonged cycle exercise.

1. The effects of prolonged exercise on energy metabolism in type I and type II muscle fibres in the vastus lateralis muscle were investigated in six male subjects (20.0 +/‐ 0.5 years, mean +/‐ S.E.M.) who performed one‐legged cycling at 61% of maximum O2 consumption (VO2,max; determined with one leg) until fatigue or for a maximum of 2 h. 2. Analysis of pools of freeze‐dried fibres obtained by needle biopsy and separated into specific types by the myofibrillar ATPase histochemical procedure indicated higher (P less than 0.05) lactate concentrations in type II fibres compared to type I fibres at 15 min (43.9 +/‐ 9.7 and 51.2 +/‐ 9.8 mmol (kg dry wt)‐1) and at 60 min (18.2 +/‐ 4.7 and 25.9 +/‐ 6.5 mmol (kg dry wt)‐1). No differences existed in lactate concentration between fibre types for pre‐exercise (10.0 +/‐ 1.6 and 13.3 +/‐ 2.8 mmol (kg dry wt)‐1) or post‐exercise. 3. Glycogen degradation was most pronounced in type I fibres. By the end of exercise, glycogen concentration was 82.4 +/‐ 45 mmol glucosyl units (kg dry wt)‐1 in type I fibres and 175 +/‐ 62 mmol glucosyl units (kg dry wt)‐1 in type II fibres. 4. No significant changes in ATP and creatine phosphate (CrP) were found in either fibre type with exercise. 5. It is concluded that, at least for lactate and glycogen, fibre‐specific differences are evident in prolonged submaximal exercise. The cause of the difference probably relates both to the unique energy metabolic characteristics of each fibre type and to the manner in which they are utilized during the exercise. 6. The failure to find a reduction in ATP concentration in either fibre type during prolonged exercise in the face of a progressive increase in the number of fibres showing little or no glycogen concentration suggests that protective mechanisms exist that prevent an energy crisis. The nature of these protective mechanisms remains to be elucidated.

High-resistance training and muscle metabolism during prolonged exercise

To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance training (HRT), active but untrained males (age 20 ± 0.7 yr; mean ± SE) performed lower-limb weight training 3 days/wk for 12 wk using three sets of 6-8 repetitions maximal (RM)/day. Muscle metabolism was examined at different stages of training (4, 7, and 12 wk) using a two-stage continuous cycle test performed at the same absolute power output and duration (56.4 ± 2.9 min) and representing 57 and 72% of pretraining peak aerobic power (V˙o 2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher ( P < 0.05) phosphocreatine (PCr; 27.4 ± 6.7 vs. 38.0 ± 1.9 mmol/kg dry wt), a lower lactate (38.9 ± 8.5 vs. 24.4 ± 6.1 mmol/kg dry wt), and a higher ( P < 0.05) glycogen content (132 ± 11 vs. 181 ± 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72%V˙o 2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found onV˙o 2 peak with training (41.2 ± 2.9 vs. 41.0 ± 2.1 ml ⋅ kg-1 ⋅ min-1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy.To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance training (HRT), active but untrained males (age 20 +/- 0.7 yr; mean +/- SE) performed lower-limb weight training 3 days/wk for 12 wk using three sets of 6-8 repetitions maximal (RM)/day. Muscle metabolism was examined at different stages of training (4, 7, and 12 wk) using a two-stage continuous cycle test performed at the same absolute power output and duration (56.4 +/- 2.9 min) and representing 57 and 72% of pretraining peak aerobic power (VO2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher (P < 0.05) phosphocreatine (PCr; 27.4 +/- 6. 7 vs. 38.0 +/- 1.9 mmol/kg dry wt), a lower lactate (38.9 +/- 8.5 vs. 24.4 +/- 6.1 mmol/kg dry wt), and a higher (P < 0.05) glycogen content (132 +/- 11 vs. 181 +/- 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72% VO2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found on VO2 peak with training (41.2 +/- 2.9 vs. 41.0 +/- 2.1 ml. kg-1. min-1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy.