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It is unclear if the exaggerated exercise pressor reflex observed in peripheral arterial disease (PAD) patients facilitates Oxygen (O2) transport during presymptomatic exercise. Accordingly, this study compared O2 transport between PAD patients and healthy controls during graded presymptomatic work. Seven PAD patients and seven healthy controls performed dynamic plantar flexion in the bore of a 3T MRI scanner. Perfusion, T2* (an index of relative tissue oxygenation), and SvO2 (a measure of venous oxygen saturation) were collected from the medial gastrocnemius (MG) during the final 10 seconds of each stage. Blood pressure was also collected during the final minute of each stage. As expected, the pressor response to presymptomatic work (4 kg) was exaggerated in PAD patients compared to controls (+14 mmHg ± 4 and +7 mmHg ± 2, P ≤ 0.034). When normalized to changes in free water content (S0), T2* was lower at 2 kg in PAD patients compared to controls (−0.91 Δms/ΔAU ± 0.3 and 0.57 Δms/ΔAU ± 0.3, P ≤ 0.008); followed by a greater increase in perfusion at 4 kg in the PAD group (+18.8 mL/min/100g ± 6.2 vs. −0.21 mL/min/100g ± 3.2 in PAD and controls, P ≤ 0.026). Lastly, SvO2 decreased at 4 kg in both groups (−13% ± 4 and −2% ± 4 in PAD and controls, P ≤ 0.049), suggesting an increase in O2 extraction in the PAD group. Based on these findings, O2 transport appears to be augmented during graded presymptomatic work in PAD patients, and this may be partially mediated by an exaggerated pressor response.

We determined if interval exercise plus a low‐calorie diet (LCD + INT) increases endothelial function more than an energy‐matched LCD. Obese women (47.2 ± 2.6y, 37.5 ± 1.3kg/m2) were randomized to 13 days of a LCD (n = 12; mixed meals of ~ 1200kcal/d) or LCD + INT (n = 13; 12 supervised 60‐min INT bouts of 3 min at 90% and 50% HRpeak). LCD + INT subjects received 350kcal postexercise to equate energy availability with LCD. Fitness (VO2peak) and body composition (BodPod) were determined and a 120 min, 75 g oral glucose tolerance test was performed to examine fasting and postprandial flow‐mediated dilation (FMD, endothelial function), respiratory exchange ratio (RER) via indirect calorimetry as well as glucose and insulin incremental area under the curve (iAUC120min). LCD + INT increased VO2peak (P = 0.02) compared with LCD, and both treatments decreased fat mass (P 50%; LCD n = 5, LCD + INT n = 7), LCD + INT increased fasted (P = 0.005) and decreased iAUC120min (P = 0.003) FMD compared with LCD. Enhanced fitness correlated with increased fasting FMD (r = 0.43, P = 0.03) and diminished FMD iAUC120min (r = −0.44, P = 0.03). Decreased FMD iAUC120min correlated with reduced glucose iAUC120min (r = 0.64, P = 0.001) as well as increased 60‐min RER (r = −0.42, P = 0.04). Low baseline fasting and iAUC120min FMD was also linked to enhanced fasting and iAUC120min FMD post‐treatment (r = −0.71, P

Obesity has been associated with a slowing of V˙O2 dynamics in children and adolescents, but this problem has not been studied in adults. Cardiovascular mechanisms underlying this effect are not clear. In this study, 48 adults (18 males, 30 females) grouped according to body mass index (BMI) (lean

Beta‐adrenoreceptor antagonists (β blockers) reduce systemic O2 delivery and blood pressure (BP) during exercise, but the subsequent effects on O2 extraction within the active limb muscles are unknown. In this study, we examined the effects of the fast‐acting, β 1 selective blocker esmolol on systemic hemodynamics and leg muscle O2 saturation (near infrared spectroscopy, NIRS) during submaximal leg ergometry. Our main hypothesis was that esmolol would augment exercise‐induced reductions in leg muscle O2 saturation. Eight healthy adults (6 men, 2 women; 23–67 year) performed light and moderate intensity bouts of recumbent leg cycling before (PRE), during (β 1‐blocked), and 45 min following (POST) intravenous infusion of esmolol. Oxygen uptake, heart rate (HR), BP, and O2 saturation (SmO2) of the vastus lateralis (VL) and medial gastrocnemius (MG) muscles were measured continuously. Esmolol attenuated the increases in HR and systolic BP during light (−12 ± 9 bpm and −26 ± 12 mmHg vs. PRE) and moderate intensity (−20 ± 10 bpm and −40 ± 18 mmHg vs. PRE) cycling (all P

Dietary nitrate ( NO 3 − ) is converted to nitrite ( NO 2 − ) and can be further reduced to the vasodilator nitric oxide (NO) amid a low O 2 environment. Accordingly, dietary NO 3 − increases hind limb blood flow in rats during treadmill exercise; however, the evidence of such an effect in humans is unclear. We tested the hypothesis that acute dietary NO 3 − (via beetroot [BR] juice) increases forearm blood flow (FBF) via local vasodilation during handgrip exercise in young adults ( n = 11; 25 ± 2 years). FBF (Doppler ultrasound) and blood pressure (Finapres) were measured at rest and during graded handgrip exercise at 5%, 15%, and 25% maximal voluntary contraction (MVC) lasting 4 min each. At the highest workload (25% MVC), systemic hypoxia (80% SaO 2 ) was induced and exercise continued for three additional minutes. Subjects ingested concentrated BR (12.6 mmol nitrate ( n = 5) or 16.8 mmol nitrate ( n = 6) and repeated the exercise bout either 2 (12.6 mmol) or 3 h (16.8 mmol) postconsumption. Compared to control, BR significantly increased FBF at 15% MVC (184 ± 15 vs. 164 ± 15 mL/min), 25% MVC (323 ± 27 vs. 286 ± 28 mL/min), and 25% + hypoxia (373 ± 39 vs. 343 ± 32 mL/min) and this was due to increases in vascular conductance (i.e., vasodilation). The effect of BR on hemodynamics was not different between the two doses of BR ingested. Forearm VO 2 was also elevated during exercise at 15% and 25% MVC. We conclude that acute increases in circulating NO 3 − and NO 2 − via BR increases muscle blood flow during moderate‐ to high‐intensity handgrip exercise via local vasodilation. These findings may have important implications for aging and diseased populations that demonstrate impaired muscle perfusion and exercise intolerance.

Sestrins (1, 2, 3) are a family of stress‐inducible proteins capable of attenuating oxidative stress, regulating metabolism, and stimulating autophagy. Sequestosome1 (p62) is also a stress‐inducible multifunctional protein acting as a signaling hub for oxidative stress and selective autophagy. It is unclear whether Sestrin and p62Ser403 are regulated acutely or chronically by resistance exercise (RE) or training (RT) in human skeletal muscle. Therefore, the acute and chronic effects of RE on Sestrin and p62 in human skeletal muscle were examined through two studies. In Study 1, nine active men (22.1 ± 2.2 years) performed a bout of single‐leg strength exercises and muscle biopsies were collected before, 2, 24, and 48 h after exercise. In Study 2, 10 active men (21.3 ± 1.9 years) strength trained for 12 weeks (2 days per week) and biopsies were collected pre‐ and post‐training. Acutely, 2 h postexercise, phosphorylation of p62Ser403 was downregulated, while there was a mobility shift of Sestrin2, indicative of increased phosphorylation. Forty‐eight hours postexercise, the protein expression of both Sestrin1 and total p62 increased. Chronic exercise had no impact on the gene or protein expression of Sestrin2/3 or p62, but Sestrin1 protein was upregulated. These findings demonstrated an inverse relationship between Sestrin2 and p62 phosphorylation after a single bout of RE, indicating they are transiently regulated. Contrarily, 12 weeks of RT increased protein expression of Sestrin1, suggesting that despite the strong sequence homology of the Sestrin family, they are differentially regulated in response to acute RE and chronic RT.

The objective of this study is to test the hypothesis that increased muscle mass has positive effects on cardiovascular function. Specifically, we tested the hypothesis that increases in lean body mass caused by deletion of myostatin improves cardiac performance and vascular function. Echocardiography was used to quantify left ventricular function at baseline and after acute administration of propranolol and isoproterenol to assess β ‐adrenergic reactivity. Additionally, resistance vessels in several beds were removed, cannulated, pressurized to 60 mmHg and reactivity to vasoactive stimuli was assessed. Hemodynamics were measured using in vivo radiotelemetry. Myostatin deletion results in increased fractional shortening at baseline. Additionally, arterioles in the coronary and muscular microcirculations are more sensitive to endothelial‐dependent dilation while nonmuscular beds or the aorta were unaffected. β ‐adrenergic dilation was increased in both coronary and conduit arteries, suggesting a systemic effect of increased muscle mass on vascular function. Overall hemodynamics and physical characteristics (heart weight and size) remained unchanged. Myostatin deletion mimics in part the effects of exercise on cardiovascular function. It significantly increases lean muscle mass and results in muscle‐specific increases in endothelium‐dependent vasodilation. This suggests that increases in muscle mass may serve as a buffer against pathological states that specifically target cardiac function (heart failure), the β ‐adrenergic system (age), and nitric oxide bio‐availability (atherosclerosis). Taken together, pharmacological inhibition of the myostatin pathway could prove an excellent mechanism by which the benefits of exercise can be conferred in patients that are unable to exercise.

It was evaluated whether upper‐body compared to lower‐body musculature exhibits a different phenotype in relation to capacity for handling reactive oxygen species (ROS), H + , La − , Na + , K + and also whether it differs in adaptive potential to exercise training. Eighty‐three sedentary premenopausal women aged 45 ± 6 years (mean ± SD) were randomized into a high‐intensity intermittent swimming group (HIS, n = 21), a moderate‐intensity swimming group (MOS, n = 21), a soccer group (SOC, n = 21), or a control group (CON, n = 20). Intervention groups completed three weekly training sessions for 15 weeks, and pre‐ and postintervention biopsies were obtained from deltoideus and vastus lateralis muscle. Before training, monocarboxylate transporter 4 (MCT4), Na + /K + pump α 2 , and superoxide dismutase 2 (SOD2) expressions were lower ( P 0.05) in m . deltoideus than in m . vastus lateralis, whereas deltoid had higher ( P 0.05) Na + /H + exchanger 1 (NHE1) expression. As a result of training, Na + /K + pump α 2 isoform expression was elevated only in deltoideus muscle, while upregulation ( P 0.05) of the α 1 and β 1 subunits, phospholemman (FXYD1), NHE1, and superoxide dismutase 1 expression occurred exclusively in vastus lateralis muscle. The increased ( P 0.05) expression of MCT4 and SOD2 in deltoid muscle after HIS and vastus lateralis muscle after SOC were similar. In conclusion, arm musculature displays lower basal ROS, La − , K + handling capability but higher Na + ‐dependent H + extrusion capacity than leg musculature. Training‐induced changes in the ion‐transporting and antioxidant proteins clearly differed between muscle groups.

The predominating β‐adrenergic receptor subtype expressed on human alveolar tissue is the β 2 AR. The homozygous arginine (Arg16Arg) single‐nucleotide polymorphism (SNP) at codon 16 of the β 2 AR gene has been associated with abnormal β 2 AR function accompanied by decreased resting alveolar‐capillary membrane gas‐transfer in certain healthy adults. Although not previously studied in the context of the β 2 AR gene, pulmonary gas‐transfer is also influenced by alveolar volume (V A) and with it the availability of alveolar surface area, particularly during exercise. Small V A implies less alveolar surface area available for O2 transport. We tested the following hypothesis in healthy adults during exercise: compared with Gly16Gly and Arg16Gly β2AR genotypes, Arg16Arg will demonstrate reduced V A and ventilation (V̇ A) relative to V̇ E and oxidative metabolic demand. Age‐ BMI‐ and gender‐matched groups of Arg16Arg (N = 16), Gly16Gly (N = 31), and Arg16Gly (N = 17) performed consecutive low (9‐min, 40%‐peak workload) and moderate (9‐min, 75%‐peak workload) intensity exercise. We derived V A and V̇ A using “ideal” alveolar equations via arterialized gases combined with breath‐by‐breath ventilation and gas‐exchange measurements; whereas steady‐state V̇O2 was used in metabolic equations to derive exercise economy (EC = workload÷V̇O2). Variables at rest did not differ across β 2 AR genotype. Strongest β 2 AR genotype effects occurred during moderate exercise. Accordingly, while V̇ E did not differ across genotype (P > 0.05), decreased in Arg16Arg versus Arg16Gly and Gly16Gly were V̇O2 (1110 ± 263, 1269 ± 221, 1300 ± 319 mL/(min·m2), respectively, both P 0.05) (1.81 ± 0.23, 1.99 ± 0.30, and 1.94 ± 0.26 kcal/(L·m2), respectively). Compared with Gly16Gly and Arg16Gly genotypes, these data suggest the Arg16Arg β 2 AR genotype plays a role in the loss of oxidative metabolic efficiency coupled with an inadaptive V A and, hence, smaller alveolar surface area available for O2 transport during submaximal exercise in healthy adults.

An impaired amino acid sensing is associated with age‐related loss of skeletal muscle mass. We tested whether light‐load resistance exercise (LL‐RE) affects postprandial amino acid transporter (AAT) expression in aging skeletal muscle. Untrained, healthy men (age: +65 years) were subjected to 13 h of supine rest. After 2 1/2 h of rest, unilateral LL‐RE was conducted (leg extensions, 10 sets of 36 repetitions) at 16% 1RM. Thereafter, the subjects were randomized into groups that orally ingested 40 g of whey protein either as hourly drinks (4 g per drink) (PULSE, N = 10) or two boluses (28 g at 0 h and 12 g at 7 h) (BOLUS, N = 10), or hourly isocaloric maltodextrin drinks (placebo, N = 10). Quadriceps muscle biopsies were taken at 0, 3, 7, and 10 h postexercise from both the resting and exercised leg, from which the membrane protein and mRNA expression of select AATs were analyzed by Western Blot and RT‐PCR, respectively. LAT1 and PAT1 protein expression increased in response to LL‐RE in the PULSE group, and SNAT2 and PAT1 protein expression increased in the BOLUS group when plasma BCAA concentration was low. In all three groups, LL‐RE increased LAT1 mRNA expression, whereas a time course decrease in SNAT2 mRNA expression was observed. LL‐RE increased membrane‐associated AAT protein expression and mRNA expression. Altered AAT protein expression was only seen in groups that ingested whey protein, with the greatest effect observed after hourly feeding. This points toward an importance of AATs in the anabolic response following LL‐RE and protein intake.

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔT re ) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m 2 ; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m 2 ], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm −2 ·min −1 ·°C −1 ). The maximum potential for evaporation (E max ) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO 2max , (2) a heat production (H prod ) of 520 W, (3) H prod relative to mass (6 W·kg −1 ), and (4) H prod relative to mass above E max (3 W·kg −1 >E max ). E max was similar between LG (347 ± 39 W, 154 ± 15 W·m −2 ) and SM (313 ± 63 W, 176 ± 34 W·m −2 , P > 0.12). ΔT re was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P 0.001) and at 50% of VO 2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P 0.001). However, ΔT re was similar between groups when H prod was either 6 W·kg −1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P = 0.98) and 3 W·kg −1 >E max (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P = 0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm −2 ·min −1 , P = 0.50). In conclusion, systematic differences in ΔT re and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed H prod in W·kg −1 or W·kg −1 >E max .

We evaluated the association between aerobic power (defined by peak oxygen consumption; V O 2peak ) and the contribution of nitric oxide synthase (NOS) to the sweating response in young and older individuals during exercise in the heat. Data from 44 young (24 ± 1 years) and 48 older (61 ± 2 years) males with mean VO 2peak of 47.8 ± 2.4 (range, 28.0–62.3) and 39.1 ± 2.3 (range, 26.4–55.7) mLO 2 kg −1 min −1 , respectively, were compiled from our prior studies. Participants performed two 15‐ to 30‐min bouts of exercise at a fixed rate of metabolic heat production of 400 or 500 W, each separated by 15–20 min recovery in the heat (35°C, relative humidity of 20%). Forearm sweat rate (ventilated capsule technique) was measured at two skin sites that were continuously and simultaneously administered with lactated Ringers solution (Control) or 10 mmol/L N G ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME, nonselective NOS inhibitor) via intradermal microdialysis. Sweat rate during the final 5 min of each exercise bout was lower with L ‐NAME compared to the Control in both groups (all P 0.05). The magnitude of the attenuation in sweat rate induced by L ‐NAME compared to the Control was not correlated with V O 2peak (all P ≥ 0.46) while this attenuation was negatively correlated with the sweat rate at the Control in both groups and in both exercise bouts (all P 0.01, R ≤ −0.43). These results suggest that NOS‐dependent sweating is not associated with aerobic power per se , while it becomes evident in individuals who produce larger sweat rates during exercise irrespective of age.

This study examined the use of carbohydrates by men and women during lift/carry exercise. Effects of menstrual cycle variation were examined in women. Twenty‐five subjects (15 M, 10 F) were studied; age 25 ± 2y M, 26 ± 3y F, weight 85 ± 3 kg* M, 63 ± 3 kg F, and height 181 ± 2 cm* M, 161 ± 2 cm F (* P

We evaluated cold sensation at rest and in response to exercise‐induced changes in core and skin temperatures in cold‐sensitive exercise trained females. Fifty‐eight trained young females were screened by a questionnaire, selecting cold‐sensitive (Cold‐sensitive, n = 7) and non‐cold‐sensitive (Control, n = 7) individuals. Participants rested in a room at 29.5°C for ~100 min after which ambient temperature was reduced to 23.5°C where they remained resting for 60 min. Participants then performed 30‐min of moderate intensity cycling (50% peak oxygen uptake) followed by a 60‐min recovery. Core and mean skin temperatures and cold sensation over the whole‐body and extremities (fingers and toes) were assessed throughout. Resting core temperature was lower in the Cold‐sensitive relative to Control group (36.4 ± 0.3 vs. 36.7 ± 0.2°C). Core temperature increased to similar levels at end‐exercise (~37.2°C) and gradually returned to near preexercise rest levels at the end of recovery (>36.6°C). Whole‐body cold sensation was greater in the Cold‐sensitive relative to Control group during resting at a room temperature of 23.5°C only without a difference in mean skin temperature between groups. In contrast, cold sensation of the extremities was greater in the Cold‐sensitive group prior to, during and following exercise albeit this was not paralleled by differences in mean extremity skin temperature. We show that young trained females who are sensitive to cold exhibit augmented whole‐body cold sensation during rest under temperate ambient conditions. However, this response is diminished during and following exercise. In contrast, cold sensation of extremities is augmented during resting that persists during and following exercise.

We tested the hypothesis during the combined challenges of altered inspired O 2 fraction (F I O 2 ) and posture changes at lower power output regardless of body position that the vascular conductance (VC) recruitment to the exercising muscle would not limit muscle perfusion and estimated O 2 delivery (DO 2 est ). However, in head‐down tilt at the higher power output exercise in hypoxia, the recruitment of VC would have a functional limitation which would restrict muscle blood flow (MBF) leading to a limitation in DO 2 est with consequent increases in metabolic stress. Ten healthy volunteers repeated plantar flexion contractions at 20% (low power output = LPO) and 30% (higher power output = HPO) of their maximal voluntary contraction in horizontal (HOR), 35° head‐down‐tilt (HDT) and 45° head‐up‐tilt (HUT). Popliteal diameter and muscle blood flow velocity were measured by ultrasound determining MBF. VC was estimated by dividing MBF flow by MPP, and DO 2 est was estimated by MBF times saturation. LPO HUT in hypoxia was associated with no changes in VC and MBF leading to reduced DO 2 est . In LPO HDT under hypoxia, despite no apparent functional limitation in the VC recruitment, rise in MBF to maintain DO 2 est was associated with marked increase in muscle electromyographic activity, indicating greater metabolic stress. In HPO HDT under hypoxia, a functional limitation for the recruitment of VC constrained MBF and DO 2 est . Elevated muscle electromyographic signal in HPO HDT under hypoxia was consistent with challenged aerobic metabolisms which contributed to a greater increase in the relative stress of the exercise challenge and advance the onset of muscle fatigue.

Progressive metabolic complications accompanied by oxidative stress are the hallmarks of type 2 diabetes. The precise molecular mechanisms of the disease complications, however, remain elusive. Exercise‐induced nontherapeutic management of type 2 diabetes is the first line of choice to control hyperglycemia and diabetes associated complications. In this study, using 11‐month‐old type 2 Goto‐Kakizaki (GK) rats, we have investigated the effects of exercise on mitochondrial metabolic and oxidative stress in the pancreas. Our results showed an increase in the NADPH oxidase enzyme activity and reactive oxygen species (ROS) production in GK rats, which was inhibited after exercise. Increased lipid peroxidation and protein carbonylation and SOD activity were also inhibited after exercise. Interestingly, glutathione (GSH) level was markedly high in the pancreas of GK diabetic rats even after exercise. However, GSH‐peroxidase and GSH‐reductase activities were significantly reduced. Exercise also induced energy metabolism as observed by increased hexokinase and glutamate dehydrogenase activities. A significant decrease in the activities of mitochondrial Complexes II/III and IV were observed in the GK rats. Exercise improved only Complex IV activity suggesting increased utilization of oxygen. We also observed increased activities of cytochrome P450s in the pancreas of GK rats which was reduced significantly after exercise. SDS‐PAGE results have shown a decreased expression of NF‐κB, Glut‐2, and PPAR‐ϒ in GK rats which was markedly increased after exercise. These results suggest differential oxidative stress and antioxidant defense responses after exercise. Our results also suggest improved mitochondrial function and energy utilization in the pancreas of exercising GK rats.

Recent evidence suggests that exercise stimulates the degradation of cellular components in skeletal muscle through activation of autophagy, but the time course of the autophagy response during recovery from exercise has not been determined. Furthermore, the regulatory mechanisms behind exercise‐induced autophagy remain unclear, although the muscle oxidative phenotype has been linked with basal autophagy levels. Therefore, the aim of this study was to investigate the role of the key regulator of muscle oxidative capacity, PGC‐1 α , in exercise‐induced autophagy at several time points during recovery. Mice with transgenic muscle‐specific overexpression (TG) or knockout (MKO) of PGC‐1 α and their respective littermate controls were subjected to a single 1 h bout of treadmill running and euthanized immediately (0 h), 2, 6, and 10 h after exercise. In the PGC‐1 α MKO strain, quadriceps protein content of the autophagy marker LC3II was increased from 2 h into recovery in lox/lox control, but not in MKO mice. In the PGC‐1 α TG strain, quadriceps protein content of LC3II was increased from 2 h after exercise in TG, but not in WT. Although AMPK and ACC phosphorylation was increased immediately following exercise, the observed exercise‐induced autophagy response was not associated with phosphorylation of the AMPK‐target ULK1. However, lower protein carbonyl content was observed in lox/lox and TG mice after exercise coinciding with the increased LC3 lipidation. In conclusion, the present results suggest a role of skeletal muscle PGC‐1 α in coordinating several exercise‐induced adaptive responses including autophagic removal of damaged cellular components.

Exercise increases skeletal muscle glucose uptake, but the underlying mechanisms are only partially understood. The atypical protein kinase C (PKC) isoforms λ and ζ (PKC‐ λ / ζ ) have been shown to be necessary for insulin‐, AICAR‐, and metformin‐stimulated glucose uptake in skeletal muscle, but not for treadmill exercise‐stimulated muscle glucose uptake. To investigate if PKC‐ λ / ζ activity is required for contraction‐stimulated muscle glucose uptake, we used mice with tibialis anterior muscle‐specific overexpression of an empty vector (WT), wild‐type PKC‐ ζ (PKC‐ ζ WT), or an enzymatically inactive T410A‐PKC‐ ζ mutant (PKC‐ ζ T410A). We also studied skeletal muscle‐specific PKC‐ λ knockout (M λ KO) mice. Basal glucose uptake was similar between WT, PKC‐ ζ WT, and PKC‐ ζ T410A tibialis anterior muscles. In contrast, in situ contraction‐stimulated glucose uptake was increased in PKC‐ ζ T410A tibialis anterior muscles compared to WT or PKC‐ ζ WT tibialis anterior muscles. Furthermore, in vitro contraction‐stimulated glucose uptake was greater in soleus muscles of M λ KO mice than WT controls. Thus, loss of PKC‐ λ / ζ activity increases contraction‐stimulated muscle glucose uptake. These data clearly demonstrate that PKC‐ λ  ζ activity is not necessary for contraction‐stimulated glucose uptake.