The sections in this article are: Motor Unit Fibers per Motor Unit Contractile Properties Biochemical Basis for Differences in Twitch Properties Histochemical Differentiation of Muscle Fibers Ultrastructural Basis for Skeletal Muscle Fiber Typing Maximal Contractile Force Speed of Contraction Fatigue Characteristics Metabolic Characteristics Ionic Composition of Skeletal Muscle Summary Muscle Fiber Composition in Human Skeletal Muscle Motor‐Unit Recruitment Adaptive Response in Skeletal Muscle Muscle Size Metabolic Capacity Connective Tissue Capillaries Methodology Anatomy Capillary Density Capillary Length and Diameter Use and Disuse Regulation Significance of Adaptation Muscular Size Substrate Stores Enzyme Activities Summary

SUMMARY1. Glycogen depletion pattern in human skeletal muscle fibres was studied after bicycle exercise of varying intensity performed at different pedalling rates. Work intensities studied were equivalent to 30-150 % of 70o, max. with pedalling rates of 30-120 rev/mi.2. Glycogen depletion increased dramatically with increasing exercise intensity; depletion was 2-7 and 7-4 times greater respectively at workloads demanding 64 and 84 % ro2 max. than at workloads calling for 31 % 1702 max. Even greater rates of glycogen utilization occurred at supramaximal loads.3. Slow twitch, high oxidative (ST) fibres were the first to lose glycogen (reduced PAS staining) at all workloads below T°2 max. Progressive glycogen depletion occurred in fast twitch (FT) fibres as work continued. Large quantities of glycogen remained in the muscle after 3 hr of exercise at low exercise intensity. This was almost exclusively found in FT fibres. At workloads exceeding maximal aerobic power, there was an initial depletion of glycogen in both fibre types. Varying the pedalling rate and, thus, the total force exerted in each pedal thrust had no effect on the pattern of glycogen depletion in the fibres. 4. Results point to primary reliance upon ST fibres during submaximal endurance exercise, FT fibres being recruited after ST fibres are depleted of glycogen. During exertion requiring energy expenditure greater than the maximal aerobic power, both fibre types appeared to be continuously involved in carrying out the exercise.

13 male subjects were studied and placed in 3 groups. Each group exercised one leg with sprint (S), or endurance (E) training and the other leg oppositely or not at all (NT). Oxygen uptake (Vo2), heart rate and blood lactate were measured for each leg separately and for both legs together during submaximal and maximal bicycle work before and after 4 weeks of training with 4-5 sessions per week. Muscle samples were obtained from the quadriceps muscle and assayed for succinate dehydrogenase (SDH) activity, and stained for myofibrillar ATPase. In addition, eight of the subjects performed after the training two-legged exercise at 70% Vo2 max for one hour. The measurements included muscle glycogen and lactate concentrations of the two legs as well as the blood flow and the a-v difference for O2, glucose and lactate.

Horses were exercised at 40, 65, and 90% of their maximum O2 uptake (VO2max) until moderately fatigued (approximately 38, 15, and 9 min, respectively) to assess heat loss through different routes. Approximately 4,232, 3,195, and 2,333 kcal of heat were generated in response to exercise at these intensities. Of this, approximately 7, 16, and 20% remained as stored heat 30 min postexercise. Respiratory heat loss, estimated from the temperature difference between blood in the pulmonary and carotid arteries and the cardiac output, was estimated to be 30, 19, and 23% of the heat produced during exercise at the three intensities. The kinetics of the increases in muscle and blood temperature were similar, with the greatest change in temperature occurring in muscle (+3.8, 5.2, and 6.1 degrees C after exercise at 40, 65, and 90% of VO2max, respectively). The temperature of blood in the superficial thoracic vein was approximately 2 degrees C below that of arterial blood at rest. This difference had increased to approximately 3 degrees C during the last minute of exercise. The rate of sweating at sites on the back and neck increased with exercise intensity to a common peak of approximately 40 ml.m-2.min-1. If complete evaporation had occurred, water loss in response to exercise (estimated to be 12, 10, and 7.7 liters for the different intensities of exercise) greatly surpassed that required for dissipation of the metabolic heat load.

The effect of training on the skeletal muscle metabolism of 11‐to 13‐year‐old boys was examined. In one experiment changes in blood lactate, and muscle lactate, CP, ATP, and glycogen were determined at rest and following exercise before and after 4 months of training. The concentrations of glycogen, CP and ATP at rest were higher (P<0.01) following training. Blood and muscle lactate were 23 and 56 % higher after maximal work following training. A greater reduction in muscle glycogen occurred during maximal work after training but the pattern for ATP and CP depletion was unchanged. In a second experiment boys trained by pedalling a bicycle ergometer an average of 30 min 3 times a week for 6 weeks. Biopsy samples of the vastus lateralis were examined for oxidative (succinate dehydrogenase) and anaerobic (phosphofructokinase) capacity before and after training. The fiber composition and relative oxidative capacity in the fibers was determined histochemically. Succinate dehydrogenase and phosphofructokinase activities increased 30 and 83 %, respectively, following training. Fiber distribution was unchanged by training but the oxidative capacity of both fiber types appeared to increase.

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A theoretical model is proposed to explain how the increase in mitochondrial protein concentration, and therefore of the oxidative enzymes, that occurs with endurance training could operate to alter the choice of substrate during submaximal exercise in a manner such that the oxidation of fatty acids increases, glycogen depletion and lactate production are reduced, and work capacity is enhanced. The model is based on the control of enzyme activities both by enzyme and substrate concentrations. The effect of altering enzyme concentration on reaction velocities is presented on the basis of standard Henri-Michaelis-Menten kinetics. It is shown that the reaction velocity at a given substrate concentration is a function of total enzyme concentration. With an increase in total enzyme concentration there is a parallel increase in reaction velocity at the same substrate level. This would have its greatest impact at substrate levels below the Km of the enzyme. It would have an effect of enhancing fatty acid flux through the oxidative pathways while inhibiting the Embden-Meyerhof pathway. The model, as proposed, is consistent with known alterations in metabolism as they occur in man during submaximal exercise following endurance training.

The effect of muscular enlargement produced by surgical ablation of a synergist and the combination of synergist ablation and exercise on the number of fibers in the soleus (S), plantaris (P), and extensor digitorum longus (EDL) muscles of the rat was studied. The number of fibers per muscle was determined by direct counts of individual fibers dissected from HNO3-treated muscles. Ablation of a synergist produced average enlargements of about 25, 45, and 29% for the S, P, and EDL muscles, respectively. Exercise and synergist ablation produced increases in wet weight to about 44 and 88% for the S and P muscles, respectively, whereas no further increases were observed in the EDL muscles. Intra-animal comparisons revealed that no differences existed for total fiber number or the incidence of fibers with bifurcations between the enlarged and contralateral control muscles. The difference in dry weight of fibers from the enlarged as compared with control muscles was closely correlated to differences in total muscle wet weight. These data demonstrate that hypertrophy rather than hyperplasia was responsible for increases from 10 to over 100% in the weight of skeletal muscles.