Influence of body heat content on hand function during prolonged cold exposures.

We examined the influence of 1) prior increase [preheating (PHT)], 2) increase throughout [heating (HT)], and 3) no increase [control (Con)] of body heat content (H(b)) on neuromuscular function and manual dexterity of the hands during a 130-min exposure to -20 degrees C (coldEx). Ten volunteers randomly underwent three passive coldEx, incorporating a 10-min moderate-exercise period at the 65th min while wearing a liquid conditioning garment (LCG) and military arctic clothing. In PHT, 50 degrees C water was circulated in the LCG before coldEx until core temperature was increased by 0.5 degrees C. In HT, participants regulated the inlet LCG water temperature throughout coldEx to subjective comfort, while the LCG was not operating in Con. Thermal comfort, rectal temperature, mean skin temperature, mean finger temperature (T(fing)), change in H(b) (DeltaH(b)), rate of body heat storage, Purdue pegboard test, finger tapping, handgrip, maximum voluntary contraction, and evoked twitch force of the first dorsal interosseus muscle were recorded. Results demonstrated that, unlike in HT and PHT, thermal comfort, rectal temperature, mean skin temperature, twitch force, maximum voluntary contraction, and finger tapping declined significantly in Con. In contrast, T(fing) and Purdue pegboard test remained constant only in HT. Generalized estimating equations demonstrated that DeltaH(b) and T(fing) were associated over time with hand function, whereas no significant association was detected for rate of body heat storage. It is concluded that increasing H(b) not only throughout but also before a coldEx is effective in maintaining hand function. In addition, we found that the best indicator of hand function is DeltaH(b) followed by T(fing).

Malleability of human skeletal muscle Na(+)-K(+)-ATPase pump with short-term training.

To investigate the hypothesis that short-term submaximal training would result in changes in Na(+)-K(+)-ATPase content, activity, and isoform distribution in skeletal muscle, seven healthy, untrained men [peak aerobic power (peak oxygen consumption; Vo(2 peak)) = 45.6 ml x kg(-1) x min(-1) (SE 5.4)] cycled for 2 h/day at 60-65% Vo(2 peak) for 6 days. Muscle tissue, sampled from the vastus lateralis before training (0 days) and after 3 and 6 days of training and analyzed for Na(+)-K(+)-ATPase content, as assessed by the vanadate facilitated [(3)H]ouabain-binding technique, was increased (P < 0.05) at 3 days (294 +/- 8.6 pmol/g wet wt) and 6 days (308 +/- 15 pmol/g wet wt) of training compared with 0 days (272 +/- 9.7 pmol/g wet wt). Maximal Na(+)-K(+)-ATPase activity as evaluated by the 3-O-methylfluorescein phosphatase assay was increased (P < 0.05) by 6 days (53.4 +/- 5.9 nmol x h(-1) x mg protein(-1)) but not by 3 days (35.9 +/- 4.5 nmol x h(-1) x mg protein(-1)) compared with 0 days (37.8 +/- 3.7 nmol x h(-1) x mg protein(-1)) of training. Relative isoform distribution, measured by Western blot techniques, indicated increases (P < 0.05) in alpha(2)-content by 3 days and beta(1)-content by 6 days of training. These results indicate that prolonged aerobic exercise represents a potent stimulus for the rapid adaptation of Na(+)-K(+)-ATPase content, isoform, and activity characteristics.

Effects of prolonged exercise and recovery on sarcoplasmic reticulum Ca2+ cycling properties in rat muscle homogenates.

AIM: To examine the effects of exercise and exercise plus active and passive recovery on sarcoplasmic reticulum (SR) Ca2+-handling properties. METHODS: Crude muscle homogenates were prepared from adult rat gastrocnemius muscle from two experiments. In one experiment, the muscle was extracted immediately after prolonged treadmill running (RUN), after a 45 min period of reduced exercise intensity (RUN+) following RUN and compared with controls (CON). In the second experiment, muscle was extracted during passive recovery following the same run protocol at 10 min (REC10), 25 min (REC25) and 45 min (REC45) and compared with CON. RESULTS: Sarcoplasmic reticulum Ca2+-uptake was 31% higher (P < 0.05) in RUN+ compared with CON and RUN. Higher values (P < 0.05) were also found in REC25 (48%) and REC45 (50%) compared with CON. Maximal Ca2+-ATPase was increased by 23% (P < 0.05) in RUN+ compared with CON and RUN and by 65-68% (P < 0.05) in REC25 and REC45 compared with CON. A higher (P < 0.05) Hill coefficient for Ca2+-ATPase activity was observed in RUN+ (2.3 +/- 0.2) compared with CON (1.7 +/- 0.2) or RUN (1.6 +/- 0.2), but not for any REC conditions. In addition, the coupling ratio (Ca2+-uptake/Ca2+-ATPase activity) was higher (P < 0.05) in RUN+ (2.2 +/- 0.10) compared with CON (1.9 +/- 0.05) and RUN (1.9 +/- 0.08). CONCLUSIONS: It is concluded that in crude homogenates, SR Ca2+-uptake and Ca2+-ATPase activity are elevated in recovery following prolonged running and that the elevation in these properties is more pronounced during passive compared with active recovery.

Na+-K+-ATPase in rat skeletal muscle: content, isoform, and activity characteristics.

The purpose of this study was to investigate the hypothesis that muscle Na+-K+-ATPase activity is directly related to Na+-K+-ATPase content and the content of the alpha2-catalytic isoform in muscles of different fiber-type composition. To investigate this hypothesis, tissue was sampled from soleus (Sol), red gastrocnemius (RG), white gastrocnemius (WG), and extensor digitorum longus (EDL) muscles at rest from 38 male Wistar rats weighing 413 +/- 6.0 g (mean +/- SE). Na+-K+-ATPase activity was determined in homogenates (Hom) and isolated crude membranes (CM) by the regenerating ouabain-inhibitable hydrolytic activity assay (ATPase) and the 3-O-methylfluorescein K+-stimulated phosphatase (3-O-MFPase) assay in vitro. In addition, Na+-K+-ATPase content (Bmax) and the distribution of alpha1-, alpha2-, beta1-, and beta2-isoforms were determined by [3H]ouabain binding and Western blot, respectively. For the ATPase assay, differences (P < 0.05) in enzyme activity between muscles were observed in Hom (EDL > WG) and in CM (Sol > EDL = WG). For the 3-O-MFPase assay, differences (P < 0.05) were also found for Hom (Sol > RG = EDL > WG) and CM (Sol = WG > RG). For Bmax, differences in the order of RG = EDL > Sol = WG (P < 0.05) were observed. Isoform distribution was similar between Hom and CM and indicated in CM, a greater density (P < 0.05) of alpha1 in Sol than WG and EDL (P < 0.05), but more equal distribution of alpha2 between muscles. The beta1 was greater (P < 0.05) in Sol and RG, and the beta2 was greater in EDL and WG (P < 0.05). Over all muscles, the correlation (r) between Hom 3-O-MFPase and Bmax was 0.45 (P < 0.05) and between Hom alpha2 and Bmax, 0.59 (P < 0.05). The alpha1 distribution correlated to Hom 3-O-MFPase (r = 0.79, P < 0.05) CM ATPase (r = 0.69, P < 0.005) and CM 3-O-MFPase activity (r = 0.32, P < 0.05). The alpha2 distribution was not correlated with any of the Na+-K+-ATPase activity measurements. The results indicate generally poor relationships between activity and total pump content and alpha2 isoform content of the Na+-K+-ATPase. Several factors, including the type of preparation and the type of assay, appear important in this regard.

Coexistence of potentiation and low-frequency fatigue during voluntary exercise in human skeletal muscle.

The role of muscle potentiation in overcoming low-frequency fatigue (LFF) as it developed during submaximal voluntary exercise was investigated in eight males (age 26.4 +/- 0.7 years, mean +/- SE) performing isometric leg extension at approximately 30% of maximal voluntary contraction for 60 min using a 0.5-duty cycle (1 s contraction, 1 s rest). At 5, 20, 40, and 60 min, exercise was interrupted for 3 min, and the maximum positive rate of force development (+dF/dtmax) and maximal twitch force (Pt) were measured in maximal twitch contractions at 0, 1, 2, and 3 min of rest (R0, R1, R2, R3); they were also measured at 15 min of recovery following the entire 60-min exercise period. These measures were compared with pre-exercise (PRE) as an indicator of potentiation. Force at low frequency (10 Hz) was also measured at R0, R1, R2, and R3, and at 15 min of recovery, while force at high frequency (100 Hz) was measured only at R0 and R3 and in recovery. Voluntary exercise increased twitch +dF/dtmax at R0 following 5, 20, 40, and 60 min of exercise, from 2553 +/- 150 N/s at PRE to 39%, 41%, 42%, and 36% above PRE, respectively (P<0.005). Twitch +dF/dtmax decayed at brief rest (R3) following 20, 40, and 60 min of exercise (P<0.05). Pt at R0 following 5 and 20 min of exercise was above that at PRE (P<0.05), indicating that during the early phase of moderate-intensity repetitive exercise, potentiation occurs in the relative absence of LFF. At 40 and 60 min of exercise, Pt at R0 was unchanged from PRE. The LFF (10 Hz) induced by the protocol was evident at 40 and 60 min (R0-R3; P<0.05) and at 15 min following exercise (P<0.05). High-frequency force was not significantly compromised by the protocol. Since twitch force was maintained, these results suggest that as exercise progresses, LFF develops, which can be compensated for by potentiation.

Reduced activity of muscle Na(+)-K(+)-ATPase after prolonged running in rats.

The purpose of this study was to investigate the hypothesis that Na(+)-K(+)-ATPase activity is reduced in muscle of different fiber composition after a single session of aerobic exercise in rats. In one experiment, untrained female Sprague-Dawley rats (weight 275 +/- 21 g; means +/- SE; n = 30) were run (Run) on a treadmill at 21 m/min and 8% grade until fatigue, or to a maximum of 2 h, which served as control (Con), or performed an additional 45 min of low-intensity exercise at 10 m/min (Run+). In a second experiment, utilizing rats of similar characteristics (weight 258 +/- 18 g; n = 32), Run was followed by passive recovery (Rec). Directly after exercise, rats were anesthetized, and tissue was extracted from Soleus (Sol), red vastus lateralis (RV), white vastus lateralis (WV), and extensor digitorum longus (EDL) and frozen for later analysis. 3-O-methylfluorescein phosphatase activity (3-O-MFPase) was determined as an indicator of Na(+)-K(+)-ATPase activity, and glycogen depletion identified recruitment of each muscle during exercise. 3-O-MFPase was decreased (P < 0.05) at Run+ by an average of 12% from Con in all muscles (P < 0.05). No difference was found between Con and Run. Glycogen was lower (P < 0.05) by 65, 57, 44, and 33% (Sol, EDL, RV, and WV, respectively) at Run, and there was no further depletion during the continued low-intensity exercise period. No differences in Na(+)-K(+)-ATPase activity was observed between Con and Rec. The results of this study indicate that inactivation of Na(+)-K(+)-ATPase can be induced by aerobic exercise in a volume-dependent manner and that the inactivation that occurs is not specific to muscles of different fiber-type composition. Inactivation of Na(+)-K(+)-ATPase suggests intrinsic structural modifications by mechanisms that are unclear.

Human neuromuscular fatigue is associated with altered Na+-K+-ATPase activity following isometric exercise.

The purpose of this study was to investigate the hypothesis that reductions in Na+-K+- ATPase activity are associated with neuromuscular fatigue following isometric exercise. In control (Con) and exercised (Ex) legs, force and electromyogram were measured in 14 volunteers [age, 23.4 +/- 0.7 (SE) yr] before and immediately after (PST0), 1 h after (PST1), and 4 h after (PST4) isometric, single-leg extension exercise at ~60% of maximal voluntary contraction for 30 min using a 0.5 duty cycle (5-s contraction, 5-s rest). Tissue was obtained from vastus lateralis muscle before exercise in Con and after exercise in both the Con (PST0) and Ex legs (PST0, PST1, PST4), for the measurements of Na+-K+-ATPase activity, as determined by the 3-O-methylfluorescein phosphatase (3-O-MFPase) assay. Voluntary (maximal voluntary contraction) and elicited (10, 20, 50, 100 Hz) force was reduced 30-55% (P < 0.05) at PST0 and did not recover by PST4. Muscle action potential (M-wave) amplitude and area (measured in the vastus medialis) and 3-O-MFPase activity at PST0-Ex were less than that at PST0-Con (P < 0.05) by 37, 25, and 38%, respectively. M-wave area at PST1-Ex was also less than that at PST1-Con (P < 0.05). Changes in 3-O-MFPase activity correlated to changes in M-wave area across all time points (r = 0.38, P < 0.05, n = 45). These results demonstrate that Na+-K+- ATPase activity is reduced by sustained isometric exercise in humans from that in a matched Con leg and that this reduction in Na+-K+-ATPase activity is associated with loss of excitability as indicated by M-wave alterations.

The effects of acute passive stretch on muscle protein synthesis in humans.

We examined the effect of an isolated bout of maximal tolerated passive stretch on fractional muscle protein synthetic rate in human soleus muscle. Eight healthy males performed two separate trials with the same leg: one session of passive stretch and one of intermittent active isometric contraction at a force equivalent to that which occurred during the passive stretch trial. This force was approximately 40% of maximum voluntary contraction force and produced volitional fatigue in approximately 27 min. Intermittent passive stretch, for the same duration, elicited a 6.1 degrees increase in joint angle (P<.0005) with silent electromyography. Fractional protein synthetic rate from experimental and control soleus in each trial was assessed from biopsy samples over the period 10-22 hr postexercise by the incorporation rate of L-[1-13C] leucine into muscle. Protein synthesis was elevated in the soleus of the exercised leg following the active contraction trial by 49% (P<.05) but not following the passive stretch trial. Results indicate that a single bout of maximal passive stretch does not significantly elevate fractional muscle protein synthetic rate in humans and thus suggests that muscle stretch per se is not the stimulus for the muscle hypertrophy that occurs with resistance training.

Macronutrient intake and whole body protein metabolism following resistance exercise.

UNLABELLED: The provision of carbohydrate (CHO) supplements following resistance exercise attenuated muscle protein (PRO) degradation (Roy et al. J. Appl. Physiol. 82:1882-1888, 1997). The addition of PRO may have a synergistic effect upon whole body protein balance by increasing synthesis (Biolo et al. Am. J. Physiol. 273:E122-E129, 1997). PURPOSE: To determine if the macronutrient composition of a postexercise beverage would alter muscle anabolism and/or catabolism following resistance exercise. METHODS: We provided isoenergetic CHO (1 g x kg(-1)) and CHO/PRO/FAT supplements and placebo (PL) immediately (t = 0 h) and 1 h (t = + 1 h) following resistance exercise (9 exercises/3 sets/80% 1 RM) to 10 young, healthy, resistance-trained males. Whole body leucine turnover was determined from L-[1-13C]leucine kinetics at approximately 4 h postexercise. RESULTS: No differences were observed for urinary 3-methylhistidine or urea nitrogen excretion between the trials. Leucine flux was significantly elevated at approximately 4 h postexercise for both CHO/PRO/FAT (177.59+/-12.68 micromol x kg(-1) x h(-1)) and CHO (156.18+/-7.77 micromol x kg(-1) x h(-1)) versus PL (126.32+/-10.51 micromol x kg(-1) x h(-1)) (P < 0.01). Whole body leucine oxidation was elevated at approximately 4 h for CHO/PRO/FAT (29.50+/-3.34 micromol x kg(-1) h(-1)) versus CHO (16.32+/-2.33 micromol x kg(-1) x h(-1)) (P < 0.01) and PL (21.29+/-2.54 micromol x kg(-1) x h(-1)) (P < 0.05). Nonoxidative leucine disposal (NOLD) was significantly elevated at approximately 4 h for both CHO/PRO/FAT (148.09+/-10.37 micromol x kg(-1) x h(-1)) and CHO (139.86+/-7.02 micromol x kg(-1) x h(-1)) versus PL (105.03+/-8.97 micromol x kg(-1) x h(-1)) (P < 0.01). CONCLUSIONS: These results suggest that consumption of either CHO or CHO/PRO/FAT immediately and 1 h following a resistance training bout increased NOLD as compared with a placebo.

Reduced strength after passive stretch of the human plantarflexors.

The purpose of this study was to assess strength performance after an acute bout of maximally tolerable passive stretch (PS(max)) in human subjects. Ten young adults (6 men and 4 women) underwent 30 min of cyclical PS(max) (13 stretches of 135 s each over 33 min) and a similar control period (Con) of no stretch of the ankle plantarflexors. Measures of isometric strength (maximal voluntary contraction), with twitch interpolation and electromyography, and twitch characteristics were assessed before (Pre), immediately after (Post), and at 5, 15, 30, 45, and 60 min after PS(max) or Con. Compared with Pre, maximal voluntary contraction was decreased at Post (28%) and at 5 (21%), 15 (13%), 30 (12%), 45 (10%), and 60 (9%) min after PS(max) (P < 0.05). Motor unit activation and electromyogram were significantly depressed after PS(max) but had recovered by 15 min. An additional testing trial confirmed that the torque-joint angle relation may have been temporarily altered, but at Post only. These data indicate that prolonged stretching of a single muscle decreases voluntary strength for up to 1 h after the stretch as a result of impaired activation and contractile force in the early phase of deficit and by impaired contractile force throughout the entire period of deficit.