Carol D. Rodgers
Michigan State University
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Featured researches published by Carol D. Rodgers.
Medicine and Science in Sports and Exercise | 1995
Carol D. Rodgers; Jaci L. VanHeest; Candice L. Schachter
This study was designed to determine whether Exerstriding, a modified form of walking using walking sticks (Exerstriders), resulted in an augmented cardiorespiratory response and a greater energy expenditure than when walking without Exerstriders. Female subjects (23.6 +/- 4.0 yr; 58.5 +/- 5.5 kg) completed two randomly assigned trials of treadmill walking (6.7 km.h-1; 0% grade; 30 min.) with (Exerstrider (E)) and without Exerstriders (Control (C)). Mean oxygen consumption (E = 20.5 +/- 1.2 ml.min-1.kg-1; C = 18.3 +/- 2.5 ml.min-1.kg-1), heart rate (E = 132.5 +/- 19.2 beats.min-1; C = 121.5 +/- 21.2 beats.min-1) and respiratory exchange ratio (E = .82 +/- .03; C = .78 +/- .04) were significantly greater (P < or = 0.05) while walking with Exerstriders. Total caloric expenditure was also significantly greater during the Exerstrider condition (E = 173.7 +/- 20.9 kcal; C = 140.7 +/- 27.2 kcal.). In contrast, the rating of perceived exertion did not differ significantly between the two conditions. These data suggest that Exerstriding provides a means to increase caloric expenditure during submaximal walking, a factor that may be of critical importance in enhancing health benefits--such as improved body composition and aerobic capacity--typically associated with walking programs.
Medicine and Science in Sports and Exercise | 2014
Jaci L. VanHeest; Carol D. Rodgers; Carrie E. Mahoney; Mary Jane De Souza
INTRODUCTION Competitive female athletes restrict energy intake and increase exercise energy expenditure frequently resulting in ovarian suppression. The purpose of this study was to determine the impact of ovarian suppression and energy deficit on swimming performance (400-m swim velocity). METHODS Menstrual status was determined by circulating estradiol (E2) and progesterone (P4) in ten junior elite female swimmers (15-17 yr). The athletes were categorized as cyclic (CYC) or ovarian-suppressed (OVS). They were evaluated every 2 wk for metabolic hormones, bioenergetic parameters, and sport performance during the 12-wk season. RESULTS CYC and OVS athletes were similar (P > 0.05) in age (CYC = 16.2 ± 1.8 yr, OVS = 17 ± 1.7 yr), body mass index (CYC = 21 ± 0.4 kg·m, OVS = 25 ± 0.8 kg·m), and gynecological age (CYC = 2.6 ± 1.1 yr, OVS = 2.8 ± 1.5 yr). OVS had suppressed P4 (P < 0.001) and E2 (P = 0.002) across the season. Total triiodothyronine (TT3) and insulin-like growth factor (IGF-1) were lower in OVS (TT3: CYC = 1.6 ± 0.2 nmol·L, OVS = 1.4 ± 0.1 nmol·L, P < 0.001; IGF-1: CYC = 243 ± 1 μg·mL, OVS = 214 ± 3 μg·mL P < 0.001) than CYC at week 12. Energy intake (P < 0.001) and energy availability (P < 0.001) were significantly lower in OVS versus CYC. OVS exhibited a 9.8% decline in Δ400-m swim velocity compared with an 8.2% improvement in CYC at week 12. CONCLUSIONS Ovarian steroids (P4 and E2), metabolic hormones (TT3 and IGF-1), and energy status markers (EA and EI) were highly correlated with sport performance. This study illustrates that when exercise training occurs in the presence of ovarian suppression with evidence for energy conservation (i.e., reduced TT3), it is associated with poor sport performance. These data from junior elite female athletes support the need for dietary periodization to help optimize energy intake for appropriate training adaptation and maximal sport performance.
Cell Stress & Chaperones | 2005
Eva Najemnikova; Carol D. Rodgers; Marius Locke
Abstract The heat shock response involves activation of heat shock transcription factor 1 (Hsf1) followed by the rapid synthesis of the protective heat shock proteins (Hsps). To determine if the stress experienced during streptozotocin (STZ)-induced diabetes altered the heat shock response, male Sprague-Dawley rats (n = 33; 280–300 g) were assigned to 4 groups: (1) control, (2) diabetic (30 days after 55 mg/kg STZ i.v.), (3) heat stressed (42°C for 15 minutes), and (4) diabetic heat-stressed group (heat stressed 42°C for 15 minutes, 30 days after 55 mg/kg STZ i.v.). The content of Hsp72, Hsp25, and Hsf1 in skeletal muscles, heart, kidney, and liver was assessed by Western blotting, while electrophoretic mobility shift gel analysis was used to assess Hsf activation. Without heat stress, the constitutive expression of Hsp25, Hsp72, and Hsf1 in tissues from diabetic animals and controls was similar. However, 24 hours following heat stress, the heart, kidney, and liver from diabetic animals showed an increased Hsp72 and Hsp25 content compared to the same tissues from heat-stressed nondiabetic animals (P < 0.05). The white gastrocnemius and plantaris muscles from heat-stressed animals (diabetic and nondiabetic) both showed significant and similar elevations in Hsp72 content. Interestingly, while all muscles from nondiabetic animals showed significant (P < 0.05) increase in Hsp25 content after heat stress, no increase in Hsp25 content was detected in muscles from heat-stressed diabetic animals. As expected, Hsf activation was undetectable in all tissues from non–heat-stressed animals but was detectable in tissues from both diabetic and nondiabetic animals following heat stress with the exception of diabetic skeletal muscle, where it was attenuated. Hsf1 content was unaltered in all tissues examined except in the white gastrocnemius muscles from heat-stressed diabetic animals. where it was undetectable. These results suggest that when tissues from STZ-induced diabetic animals are heat stressed, the Hsp/stress response is altered in a tissue-specific manner. This impaired ability to activate the stress response may explain, at least in part, the selective atrophy of certain muscles or muscle fiber types during diabetes.
American Journal of Physiology-endocrinology and Metabolism | 1997
Jaci L. VanHeest; Carol D. Rodgers
This study was designed to evaluate the effects of chronic endurance training on glucose and lipid homeostasis in diabetic mothers and their offspring. Female Sprague-Dawley rats were rendered diabetic (>20 mmol/l glucose) by streptozotocin and subdivided into three treatments (n = 10/group): exercise (20 m/min; 0% grade; 1 h/day; 5 days/wk) before and during gestation (EE), exercise before gestation with cessation on conception (ES), and sedentary before and during gestation (SS). Response of dams to a preconception and third trimester glucose tolerance test, litter number (EE = ES = SS = 3), and average litter size (EE = 9.7 +/- 1.5; ES = 9.0 +/- 1.5; SS = 8.3 +/- 0.3) did not differ among groups. Number of offspring remaining viable was significantly different among groups (EE = 17; ES = 0; SS = 14). Response to a glucose challenge and fasting glucose and insulin were different between the EE and SS pups. Exercise before and during gestation did not reduce the viability of offspring. Cessation of exercise during early pregnancy negatively affected offspring viability.This study was designed to evaluate the effects of chronic endurance training on glucose and lipid homeostasis in diabetic mothers and their offspring. Female Sprague-Dawley rats were rendered diabetic (>20 mmol/l glucose) by streptozotocin and subdivided into three treatments ( n = 10/group): exercise (20 m/min; 0% grade; 1 h/day; 5 days/wk) before and during gestation (EE), exercise before gestation with cessation on conception (ES), and sedentary before and during gestation (SS). Response of dams to a preconception and third trimester glucose tolerance test, litter number (EE = ES = SS = 3), and average litter size (EE = 9.7 ± 1.5; ES = 9.0 ± 1.5; SS = 8.3 ± 0.3) did not differ among groups. Number of offspring remaining viable was significantly different among groups (EE = 17; ES = 0; SS = 14). Response to a glucose challenge and fasting glucose and insulin were different between the EE and SS pups. Exercise before and during gestation did not reduce the viability of offspring. Cessation of exercise during early pregnancy negatively affected offspring viability.
Journal of Strength and Conditioning Research | 2003
Mary Barth Noel; Jaci L. VanHeest; Phil Zaneteas; Carol D. Rodgers
Obesity Research | 1997
Michael J. Carella; Carol D. Rodgers; David Anderson; Ved V. Gossain
The Endocrine System in Sports and Exercise | 2008
Jaci L. VanHeest; Carrie E. Mahoney; Carol D. Rodgers
Journal of Strength and Conditioning Research | 2000
Carol D. Rodgers; Ray T. Hermiston
Archive | 2007
Carol D. Rodgers; Pam E. Burch; Jaci L. VanHeest; K. Suzuki; Chantal T. Bussiere; A Rachel
Medicine and Science in Sports and Exercise | 2003
Jaci L. VanHeest; Carrie E. Mahoney; J M. Cappaert; K W. Hill; M. J. De Souza; Carol D. Rodgers