Low bone mineral density at axial and appendicular sites in amenorrheic athletes

Dion H. Zappe, Clarke G. Tankersley, Todd G. Meister, William Lawrence Kenney, Jr.

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The purpose of this study was to test the hypothesis that changes in exercise intensity dominate the PV response to cycle exercise in the heat independent of the initial plasma volume (PV) and total circulating protein (TCP) content. The two . experimental treatments (counterbalanced design) were performed by nine trained male cyclists (age = 23 ± 1 yr, VO2peak = 63 ± 4 ml • kg-1vmin-1) in both a euhydrated (EU) and hypohydrated (HP, 24-h fluid restriction) state. Blood volume was measured (carbon monoxide dilution) 30 min prior to each test and subsequent changes in PV were calculated from serial venous blood samples using hematocrit and hemoglobin concentration. Following 20 min of seated rest in a warm environment (Tdb = 30°C, 50-60% RH), each subject cycled in a semi-reclining posture for 60 min at three successive intensities (60, 120, and 180 W for 20 min each, representing ˜ 22, 37, and 53% VO2peak). Fluid restriction reduced (P < 0.05) body weight by 1.4 ± 0.3 kg (1.8 ± 0.4%), PV by 353 ± 73 ml (8 ± 2%), TCP by 20 ± 7 g (7 ± 2%), and elevated serum osmolality by 6 ± 2 mOsm-kg-1 (2 ± 1 %). After 20 min of passive heat exposure (prior to exercise), TCP content remained lower (P < 0.05) in HP (17 ± 5 g) compared with EU as PV increased (P < 0.05) in EU (222 ± 27 ml) but not (P > 0.05) in HP (122 ± 35 ml). During exercise, TCP decreased (P < 0.05) in HP by 14 ± 3 g, which further increased the difference (P < 0.05) between EU and HP. However, during exercise the overall loss of PV was similar between EU (472 ± 54 ml; 10.7 ± 1%) and HP (470 ± 43 ml; 11.2 ± 1%), respectively. These data support the hypothesis that in trained subjects, despite differences in TCP content between hydration states, hypohydration induced by 24-h fluid restriction does not affect the subsequent rate of PV loss during cycle exercise in a warm environment. This implies that, during cycle exercise, hydrostatic forces (rather than oncotic forces) drive PV exchanges.

Original languageEnglish (US)
Pages (from-to)1225-1230
Number of pages6
JournalMedicine and Science in Sports and Exercise
Volume25
Issue number11
StatePublished - Jan 1 1993

Fingerprint

Plasma Volume
Athletes
Bone Density
Exercise
Proteins
Plasma Exchange
Carbon Monoxide
Blood Volume
Posture
Hematocrit
Hemoglobins
Hot Temperature

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Zappe, Dion H. ; Tankersley, Clarke G. ; Meister, Todd G. ; Kenney, Jr., William Lawrence. / Low bone mineral density at axial and appendicular sites in amenorrheic athletes. In: Medicine and Science in Sports and Exercise. 1993 ; Vol. 25, No. 11. pp. 1225-1230.
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abstract = "The purpose of this study was to test the hypothesis that changes in exercise intensity dominate the PV response to cycle exercise in the heat independent of the initial plasma volume (PV) and total circulating protein (TCP) content. The two . experimental treatments (counterbalanced design) were performed by nine trained male cyclists (age = 23 ± 1 yr, VO2peak = 63 ± 4 ml • kg-1vmin-1) in both a euhydrated (EU) and hypohydrated (HP, 24-h fluid restriction) state. Blood volume was measured (carbon monoxide dilution) 30 min prior to each test and subsequent changes in PV were calculated from serial venous blood samples using hematocrit and hemoglobin concentration. Following 20 min of seated rest in a warm environment (Tdb = 30°C, 50-60{\%} RH), each subject cycled in a semi-reclining posture for 60 min at three successive intensities (60, 120, and 180 W for 20 min each, representing ˜ 22, 37, and 53{\%} VO2peak). Fluid restriction reduced (P < 0.05) body weight by 1.4 ± 0.3 kg (1.8 ± 0.4{\%}), PV by 353 ± 73 ml (8 ± 2{\%}), TCP by 20 ± 7 g (7 ± 2{\%}), and elevated serum osmolality by 6 ± 2 mOsm-kg-1 (2 ± 1 {\%}). After 20 min of passive heat exposure (prior to exercise), TCP content remained lower (P < 0.05) in HP (17 ± 5 g) compared with EU as PV increased (P < 0.05) in EU (222 ± 27 ml) but not (P > 0.05) in HP (122 ± 35 ml). During exercise, TCP decreased (P < 0.05) in HP by 14 ± 3 g, which further increased the difference (P < 0.05) between EU and HP. However, during exercise the overall loss of PV was similar between EU (472 ± 54 ml; 10.7 ± 1{\%}) and HP (470 ± 43 ml; 11.2 ± 1{\%}), respectively. These data support the hypothesis that in trained subjects, despite differences in TCP content between hydration states, hypohydration induced by 24-h fluid restriction does not affect the subsequent rate of PV loss during cycle exercise in a warm environment. This implies that, during cycle exercise, hydrostatic forces (rather than oncotic forces) drive PV exchanges.",
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Low bone mineral density at axial and appendicular sites in amenorrheic athletes. / Zappe, Dion H.; Tankersley, Clarke G.; Meister, Todd G.; Kenney, Jr., William Lawrence.

In: Medicine and Science in Sports and Exercise, Vol. 25, No. 11, 01.01.1993, p. 1225-1230.

Research output: Contribution to journalArticle

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N2 - The purpose of this study was to test the hypothesis that changes in exercise intensity dominate the PV response to cycle exercise in the heat independent of the initial plasma volume (PV) and total circulating protein (TCP) content. The two . experimental treatments (counterbalanced design) were performed by nine trained male cyclists (age = 23 ± 1 yr, VO2peak = 63 ± 4 ml • kg-1vmin-1) in both a euhydrated (EU) and hypohydrated (HP, 24-h fluid restriction) state. Blood volume was measured (carbon monoxide dilution) 30 min prior to each test and subsequent changes in PV were calculated from serial venous blood samples using hematocrit and hemoglobin concentration. Following 20 min of seated rest in a warm environment (Tdb = 30°C, 50-60% RH), each subject cycled in a semi-reclining posture for 60 min at three successive intensities (60, 120, and 180 W for 20 min each, representing ˜ 22, 37, and 53% VO2peak). Fluid restriction reduced (P < 0.05) body weight by 1.4 ± 0.3 kg (1.8 ± 0.4%), PV by 353 ± 73 ml (8 ± 2%), TCP by 20 ± 7 g (7 ± 2%), and elevated serum osmolality by 6 ± 2 mOsm-kg-1 (2 ± 1 %). After 20 min of passive heat exposure (prior to exercise), TCP content remained lower (P < 0.05) in HP (17 ± 5 g) compared with EU as PV increased (P < 0.05) in EU (222 ± 27 ml) but not (P > 0.05) in HP (122 ± 35 ml). During exercise, TCP decreased (P < 0.05) in HP by 14 ± 3 g, which further increased the difference (P < 0.05) between EU and HP. However, during exercise the overall loss of PV was similar between EU (472 ± 54 ml; 10.7 ± 1%) and HP (470 ± 43 ml; 11.2 ± 1%), respectively. These data support the hypothesis that in trained subjects, despite differences in TCP content between hydration states, hypohydration induced by 24-h fluid restriction does not affect the subsequent rate of PV loss during cycle exercise in a warm environment. This implies that, during cycle exercise, hydrostatic forces (rather than oncotic forces) drive PV exchanges.

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