סקירה מקיפה זו מגלה שבעוד שפעילות גופנית מתונה קבועה מספקת יתרונות קרדיווסקולריים עצומים—הפחתת סיכון להתקף לב ב-50%, הארכת תוחלת החיים ב-3 שנים, ושיפור מדדי בריאות רבים—אימון אתלטי אינטנסיבי יכול לעיתים להוביל לשינויים לבביים מדאיגים. המאמר בוחן את תופעת "לב הספורטאי" שבה ספורטאים עליתיים מפתחים חדרי לב מורחבים ושינויים חשמליים שיכולים לחקות מצבי לב חמורים, דן כיצד פעילות סיבולת קיצונית עלולה במקרים נדירים לגרום לנזק לבבי באנשים בריאים קודם לכן, ובודק את ההשפעות הלבביות המסוכנות של תרופות לשיפור ביצועים המשמשות חלק מהספורטאים.
פעילות גופנית וליבך: היתרונות המדהימים, הסיכונים הפוטנציאליים והסכנות הנסתרות
תוכן עניינים
- מבוא: מדוע פעילות גופנית חשובה לבריאות הלב
- הטוב: יתרונות יוצאי דופן של פעילות גופנית סדירה
- לב הספורטאי: הבנת ההסתגלויות התקינות
- שינויים באק"ג אצל ספורטאים: מה תקין ומה לא
- מימדי הלב אצל ספורטאים: מתי גדול מדי?
- הבחנה בין לב ספורטאי למצבי לב חמורים
- מוות לבבי פתאומי אצל ספורטאים: נדיר אך טרגי
- האם פעילות גופנית יכולה לפגוע בלב בריא? העדויות המתגלות
- פרפור פרוזדורים ובעיות קצב לב אצל ספורטאים
- עיצוב מחדש שלילי של הלב והפרעות קצב חדריות
- חומרים משפרי ביצועים: הצד המכוער של הספורט
- המלצות למטופלים והנחיות מעשיות
- מגבלות המחקר ושיקולים חשובים
- מידע מקור
מבוא: מדוע פעילות גופנית חשובה לבריאות הלב
היתרונות של פעילות גופנית סדירה לבריאות הלב וכלי הדם הם בלתי ניתנים לערעור ונתמכים היטב בעדויות מדעיות. סקירה מקיפה זו בוחנת הן את היתרונות העצומים של פעילות גופנית והן את הסיכונים הפוטנציאליים שעלולים להופיע בקצוות הקיצוניים של אימונים אתלטיים.
בעוד שפעילות גופנית מתונה מספקת הגנה עמוקה מפני מחלות לב, ספורטאים תחרותיים הדוחפים מעבר לרמות הפעילות המומלצות מדגימים הסתגלויות לב ייחודיות שלעיתים יכולות לחפוף עם מצבים רפואיים חמורים. הבנת הבחנות אלה חיונית עבור ספורטאים, אנשים פעילים ונותני שירותי בריאות כאחד.
המאמר מארגן יחסים מורכבים אלה לשלוש קטגוריות: הטוב (יתרונות מוכחים של פעילות גופנית), הרע (תופעות לוואי פוטנציאליות של פעילות גופנית קיצונית) והמכוער (השלכות מסוכנות של חומרים משפרי ביצועים). מסגרת זו מסייעת למטופלים להבין את התמונה המלאה של כיצד פעילות גופנית משפיעה על בריאות הלב ברמות עצימות ואוכלוסיות שונות.
הטוב: יתרונות יוצאי דופן של פעילות גופנית סדירה
פעילות גופנית סדירה מספקת הגנה קרדיווסקולרית מקיפה שהיא גם חזקה וגם מתועדת היטב. אנשים העוסקים בפעילות גופנית עקבית מפתחים פרופיל סיכון קרדיווסקולרי חיובי המפחית משמעותית את הסבירות שלהם לפתח מחלת עורקים כליליים.
היתרון הבולט ביותר הוא הירידה של 50% בסיכון לאוטם שריר הלב (התקף לב) שנצפתה אצל אנשים פעילים בהשוואה לעמיתיהם היושבניים. הגנה מדהימה זו תועדה לראשונה בשנות ה-1950 כאשר חוקרים גילו שלעובדי אוטובוסים ודואר פעילים היו חצי משיעורי האירועים הכליליים של נהגי אוטובוסים ועובדים משרדיים פחות פעילים.
מחקר עדכני יותר שכלל מעל 44,000 גברים מקצועיים עם תקופת מעקב של 475,755 שנות-אדם אישר שפעילות גופנית סדירה מפחיתה את שיעורי האירועים הכליליים בהיקף דומה. כמות הפעילות הגופנית הנדרשת להשגת יתרונות אלה היא צנועה יחסית - רק שעתיים בשבוע בעוצמה של 6-10 MET (שווה ערך מטבולי) המחולקות לשלושה מפגשי אימון.
דוגמאות לעוצמה זו כוללות:
- הליכה נמרצת בקצב שמגביר באופן מורגש את הנשימה ודופק הלב
- ריצה קלה במהירות 6.4-8 קמ"ש
- רכיבה על אופניים במהירות 15-20 קמ"ש
אפילו עוצמות נמוכות יותר של פעילות גופנית מספקות יתרונות משמעותיים בהשוואה לחוסר פעילות מוחלט. מחקרים מראים שעל כל MET של פעילות גופנית שהושגה, יש ירידה של 12-20% בתמותה קרדיווסקולרית. זה אומר שכל תנועה טובה יותר מאף תנועה, ופעילות אינטנסיבית יותר מספקת הגנה הולכת וגדלה.
עבור מטופלים עם מחלת עורקים כליליים מבוססת, לפעילות גופנית יש תפקיד טיפולי קריטי. סקירה שיטתית ומטה-אנליזה של 34 ניסויים אקראיים מבוקרים הדגימו כי שיקום לב מבוסס פעילות גופנית לאחר אוטם שריר הלב מפחית משמעותית את הסיכון ל:
- אוטם חוזר (התקפי לב נוספים)
- תמותה לבבית (מוות מסיבות לב)
- תמותה מכל סיבה
יתרונות אלה נובעים מיכולתה של הפעילות הגופנית לווסת מסלולי איתות המעורבים בעיצוב מחדש של הלב תוך שיפור בו-זמנית של גורמי סיכון קונבנציונליים לטרשת עורקים כלילית. בחולי אי-ספיקת לב, פעילות גופנית סדירה משפרת את היכולת התפקודית ומפחיתה במעט את שיעורי האשפוז והתמותה הכללית.
מעבר ליתרונות הקרדיווסקולריים, פעילות גופנית מספקת הגנה מפני מצבי בריאות רבים נוספים:
- מפחיתה סיכון לסרטן הערמונית והשד בכ-12%
- מונעת אוסטאופורוזיס ושומרת על צפיפות העצם
- עשויה לעכב הופעת דמנציה וירידה קוגניטיבית
- משפרת סיבולת ומקדמת ביטחון עצמי
- פועלת כנוגד דיכאון טבעי עבור רבים
אולי המרשים ביותר, אנשים העוסקים בפעילות גופנית סדירה חיים לפחות 3 שנים יותר מעמיתיהם היושבניים. יתרון אריכות חיים זה, המשולב עם ההגנות הבריאותיות הרחבות, הופך את הפעילות הגופנית לאחת התרפיות היעילות, הנגישות והזולות ביותר שרופאים יכולים להמליץ עליהן.
לב הספורטאי: הבנת ההסתגלויות התקינות
בעוד שההנחיות האירופיות והאמריקאיות הנוכחיות ממליצות על מינימום של 150 דקות של פעילות גופנית בעצימות בינונית לשבוע למבוגרים, ספורטאים תחרותיים מבצעים הרבה מעבר להמלצות אלה. רבים עוסקים באופן קבוע בלמעלה מ-20 שעות של פעילות גופנית אינטנסיבית (העולה על 15 MET) בשבוע.
רמות פעילות קיצוניות אלה דורשות עלייה מתמשכת של פי 5-6 בתפוקת הלב למשך תקופות ממושכות. הלב עומד בדרישות יוצאות דופן אלה באמצעות הסתגלויות חשמליות, מבניות ותפקודיות ייחודיות המכונות collectively "לב הספורטאי".
הסתגלויות אלה מייצגות תגובות פיזיולוגיות נורמליות לאימונים אינטנסיביים ולא תהליכי מחלה. הלב הופך ליעיל יותר בשאיבת דם, כאשר כל החדרים מתרחבים באופן סימטרי כדי להתמודד עם נפח דם מוגבר ודרישות שאיבה.
ספורטאים בדרך כלל מראים עלייה של 10-20% בעובי דופן החדר השמאלי ועלייה של 10-15% בגודל חלל החדר השמאלי והימני בהשוואה לאנשים יושבניים בגיל וגודל דומים. שינויים אלה מאפשרים ללב להתמלא יותר במהלך הדיאסטולה (שלב המנוחה), להגביר את נפח הפעימה גם בדופק לב גבוה מאוד, ולספק יותר חמצן לשרירים הפועלים.
גם שרירי השלד של ספורטאים מסתגלים על ידי פיתוח יכולת חמצון מוגברת והולכה נימית, מה שמביא לצריכת חמצן שיא גבוהה יותר במהלך פעילות גופנית. הסתגלות קרדיווסקולרית ושרירית מקיפה זו מאפשרת את הביצועים האתלטיים יוצאי הדופן שאנו עדים להם אצל מתחרים עלית.
שינויים באק"ג אצל ספורטאים: מה תקין ומה לא
הביטויים החשמליים של אימון אתלטי נופלים לשתי קטגוריות רחבות: אלה הנובעים מטונוס וגאלי גבוה (הפעלת מערכת העצבים הפאראסימפתטית) ואלה המשקפים גודל חלל לב מוגבר. הבנת וריאציות נורמליות אלה מסייעת להבחין בין הסתגלויות פיזיולוגיות לבין אנומליות מדאיגות.
דפוסי אק"ג נורמליים נפוצים אצל ספורטאים כוללים:
- ברדיקרדיה סינוסית (דופק לב איטי) - לעתים קרובות נמוך עד 30-40 פעימות לדקה במנוחה
- אריתמיה סינוסית (וריאציה נורמלית בדופק הלב עם נשימה)
- הרמת נקודת J עם מקטעי ST עולים (דפוס רפולריזציה מוקדמת)
- חסימת AV מדרגה ראשונה (עיכוב קל בהולכה חשמלית)
- קריטריוני מתח להיפרטרופיה של החדר השמאלי והימני (אותות חשמליים מוגברים עקב שריר לב גדול יותר)
- חסימה לא מלאה של צרור היסימן הימני (עיכוב הולכה קל)
כמה ספורטאים מדגימים קצב צומתי או חסימת AV מדרגה שנייה מסוג Mobitz במנוחה שנפתרת עם מאמץ קל. דפוסים אלה משקפים טונוס וגאלי גבוה ובדרך כלל נחשבים וריאציות נורמליות אצל ספורטאים מאומנים.
ספקטרום השינויים הנורמליים באק"ג של ספורטאי מושפע מכמה גורמים:
- גיל: ספורטאים מתבגרים מתחת לגיל 14 מראים לעתים קרובות דפוס אק"ג נערי עם היפוך גל T בעופרות V1–V4
- מין: נשים מראות שינויים דומים לגברים אך במידה כמותית פחותה
- מוצא אתני: ספורטאים ממוצא אפריקאי ואפרו-קריבי מדגימים שינויים רפולריזציה בולטים יותר
- סוג ספורט: ספורטאי סיבולת מציגים את השכיחות הגבוהה ביותר של דפוסים חשמליים של לב הספורטאי
ספורטאים שחורים מראים דפוסים ייחודיים במיוחד שנחשבו חריגים באוכלוסיות אחרות. הרמת מקטע ST שכיחה פי 6 אצל ספורטאים שחורים בהשוואה לספורטאים לבנים. היפוך גל T - שהיה מעורר דאגה ברוב הספורטאים הקווקזיים - מופיע עד 25% מהספורטאים השחורים.
הדפוס הנפוץ ביותר אצל ספורטאים שחורים הוא היפוך גל T אסימטרי עמוק שלפניו הרמת מקטע ST קמורה בעופרות V1–V4. מחקר לא הראה שדפוס זה מתואם עם פתולוגיה לבבית או תוצאות שליליות. המשמעות של היפוך גל T בעופרות התחתונות נותרה לא ידועה אך כנראה וריאציה נורמלית אצל ספורטאים שחורים.
סטיית ציר וקריטריוני מתח להרחבת פרוזדור נחשבים וריאציות נורמליות כאשר הם מופיעים בבידוד ואינם מצדיקים בירור נוסף בהיעדר תסמינים, בדיקה גופנית תקינה, או היסטוריה משפחתית רלוונטית.
מימדי הלב אצל ספורטאים: מתי גדול מדי?
העומס המוקדם והמאוחר המוגבר של הלב הקשור לפעילות גופנית אינטנסיבית כרונית גורם להרחבה סימטרית של כל חדרי הלב. הבנת הגבולות העליונים של הסתגלות נורמלית מסייעת להבחין בין שינויים פיזיולוגיים למצבים פתולוגיים.
מחקרים מראים שעד 50% מהספורטאים הגברים יש מימדי חלל חדר שמאלי וימני העולים על הגבולות העליונים החזויים עבור אנשים יושבניים. מחקר של מעל 1,300 ספורטאים אולימפיים איטלקיים לבנים מצא ש-45% היו עם גודל חלל חדר שמאלי העולה על הגבולות העליונים החזויים, ו-14% היו עם חלל גדול מ-60 מ"מ - מימדים שיכולים להיות עקביים עם קרדיומיופתיה מורחבת.
מחקר עדכני יותר של כמעט 700 ספורטאים מדורגים לאומיים שחורים ולבנים חשף שכמעט 40% מהספורטאים הגברים הציגו הרחבה של החדר הימני הדומה לזו שנצפתה בחולים עם קרדיומיופתיה חדרית ימנית אריתמוגנית (ARVC).
הגבולות העליונים למימדי הלב משתנים לפי אוכלוסייה:
- לא ספורטאים: קוטר סוף דיאסטולי של חדר שמאל (LVEDD) עד 59 מ"מ בגברים, 53 מ"מ בנשים
- ספורטאים קווקזיים: LVEDD עד 63 מ"מ בגברים, 56 מ"מ בנשים; עובי דופן חדר שמאלי עד 12 מ"מ בגברים, 11 מ"מ בנשים
- ספורטאים שחורים: LVEDD עד 62 מ"מ בגברים, 56 מ"מ בנשים; עובי דופן חדר שמאלי עד 15 מ"מ בגברים, 12 מ"מ בנשים
הסתגלויות אלו בדרך כלל קטנות יותר בספורטאים מתבגרים אשר פחות בוגרים פיזית ומתאמנים במשך תקופות קצרות יותר. הממדים הלבביים הגדולים ביותר מופיעים בדרך כלל בספורטאי סיבולת גברים עם שטחי גוף גדולים, במיוחד חותרים ורוכבי אופניים למרחקים ארוכים.
במונחים מוחלטים, עובי דופן החדר השמאלי בספורטאים בדרך כלל נשאר בטווחים הנורמליים המקובלים באוכלוסייה היושבנית (12-8 מ"מ). רק 2% מהספורטאים הקווקזיים מראים עובי דופן חדר שמאלי העולה על 12 מ"מ, וממדים כאלה מוגבלים לספורטאים גברים.
לעומת זאת, היפרטרופיה של החדר השמאלי העולה על 12 מ"מ נפוצה יחסית בספורטאים גברים שחורים. עד 13% מהגברים השחורים ו-3% מהספורטאיות השחורות מראים עובי דופן חדר שמאלי העולה על 12 מ"מ. ללא קשר למוצא אתני, עובי דופן חדר שמאלי העולה על 16 מ"מ הוא נדיר ביותר ויש להעלות חשד להיפרטרופיה פתולוגית.
ספורטאים גם מראים קוטר שורש אבי העורקים מוגדל במעט בהשוואה לאנשים יושבניים, אך שורש אבי העורקים הגדול מ-40 מ"מ הוא נדיר ויש לראות בו חריג.
הבחנה בין לב ספורטאי למצבי לב חמורים
השינויים החשמליים והמבניים בספורטאים נחשבים בדרך כלל שפירים והפיכים לאחר הפסקת אימונים. עם זאת, שילוב של היפרטרופיה של החדר השמאלי עם שינויים ברפולריזציה או גודל חלל חדרי מוגדל עם שבר פליטה נמוך גבולי עשוי לחפוף לקרדיומיופתיה.
אתגר אבחוני זה רלוונטי במיוחד עבור ספורטאים שחורים, שלהם שכיחות גבוהה יותר של היפרטרופיה של החדר השמאלי ושינויים ברפולריזציה, וספורטאי סיבולת, אשר לרוב מציגים חללים חדריים גדולים מאוד עם שברי פליטה נמוכים גבוליים.
בנסיבות אלו, ההערכה צריכה להתבצע על ידי מומחים מכיוון שאבחנה שגויה של קרדיומיופתיה עלולה לגרום לפסילה לא必要ית מספורט. לעומת זאת, אבחון שגוי של לב ספורטאי אצל מישהו עם קרדיומיופתיה ממשית עלול לסכן חיים צעירים.
הבחנה בין פיזיולוגיה לפתולוגיה דורשת מספר אמצעי בדיקה:
- ניתוח מפורט של אק"ג
- אקוקרדיוגרפיה מקיפה
- בדיקת מאמץ קרדיו-ריאתית עם אקוקרדיוגרפיה במאמץ
- דימות תהודה מגנטית של הלב (Cardiac Magnetic Resonance Imaging - CMRI)
- ניטור אק"ג 24 שעות (הולטר)
- בדיקה גנטית כאשר מתאים
תסמינים נלווים והיסטוריה משפחתית רלוונטית של קרדיומיופתיה תומכים בפתולוגיה לבבית. ממצאים מדאיגים ספציפיים כוללים:
- דיכאון מקטע ST בכל ליד
- היפוך גל T בלידים הצדדיים
- גלי Q פתולוגיים (יחס Q/R גדול מ-0.25)
- חסימה של צרור היס באק"ג
- מדדים לא תקינים של תפקוד דיאסטולי
- תפקוד סיסטולי אורכי מופחת
- הפרעות תנועה אזוריות של הדופן
- עדות להעצמה מאוחרת של גדוליניום (Late Gadolinium Enhancement - LGE) ב-CMRI
- הפרעות קצב המושרות במאמץ
- הפרעות קצב חדריות מורכבות בניטור הולטר
- צריכת חמצן מרבית נמוכה (פחות מ-50 מ"ל/דקה/ק"ג או פחות מ-120% מהצפוי)
בספורטאים עם היפרטרופיה של החדר השמאלי במידה של 16-13 מ"מ, חלל חדר שמאלי יחסית קטן (פחות מ-50 מ"מ) וחסימה דינמית של מוצא החדר השמאלי במהלך מאמץ יתאימו לקרדיומיופתיה היפרטרופית.
בספורטאים עם חדר שמאלי מורחב ושבר פליטה נמוך גבולי, כישלון בשיפור תפקוד החדר השמאלי או צריכת חמצן מרבית מתחת ל-50 מ"ל/דקה/ק"ג (או מתחת ל-120% מהצפוי) יתמכו בקרדיומיופתיה מורחבת.
בספורטאי עם חדר ימין מורחב, הממצאים הבאים מצביעים על קרדיומיופתיה חדרית ימנית אריתמוגנית:
- הפרעות תנועה אזוריות של הדופן או מקטעים אקינטיים
- היפוך גל T בלידים V1–V3
- מקטעי ST איזואלקטריים מקדימים או דיכאון מקטע ST
- גלי אפסילון
- מתחמי QRS משרעת נמוכה בלידים הגפיים
- פוטנציאלים מאוחרים באק"ג ממוצע אות
- יותר מ-1000 פעימות לב נוספות (פעימות אקטופיות)
אי-התכנסות של החדר השמאלי (Left Ventricular Non-Compaction - LVNC) מציבה אתגר אבחוני נוסף. הפרעה מיוקרדיאלית זו מתאפיינת בטרבקולציה מוגברת של החדר השמאלי, תפקוד סיסטולי לקוי ונטייה להפרעות קצב קטלניות. כ-20% מהספורטאים הצעירים מראים טרבקולציה מוגברת של החדר השמאלי, ו-8% עומדים בקריטריונים האבחוניים ל-LVNC.
בספורטאים העומדים בקריטריונים האקוקרדיוגרפיים ל-LVNC, יש לשקול אבחנה פתולוגית רק כאשר היא מלווה ב:
- תפקוד חדר שמאלי מופחת
- היפוך גל T צדדי באק"ג
- צריכת חמצן מרבית נמוכה
- הפרעות קצב חדריות בבדיקת מאמץ או ניטור הולטר
- נוכחות פיברוזיס בדימות תהודה מגנטית של הלב
כאשר הדילמה האבחונית נותרת ללא פתרון למרות בדיקה מקיפה, ניתן להמליץ על תקופת הפסקת אימונים של 8-6 שבועות כדי לבדוק נסיגה של האנומליות החשמליות והמבניות. עם זאת, שכנוע ספורטאים תחרותיים להפסיק אימונים הוא קשה מכיוון שהוא פוגע בכושר ובבחירת הנבחרת.
מוות לבבי פתאומי בספורטאים: נדיר אך טרגי
לעיתים, ספורטאי עלול למות באופן פתאומי במהלך או מיד לאחר תחרות. אסונות אלו נדירים אך הרסניים, פוגעים בספורטאים צעירים עם קרדיומיופתיות בסיסיות, מחלת עורקים כליליים, מסלולים נוספים, או הפרעות בתעלות יונים, ובספורטאים בגיל הביניים עם טרשת עורקים כלילית מתקדמת.
שכיחות המוות הלבבי הפתאומי משתנה לפי שיטות איסוף הנתונים, אך הנתונים האמינים ביותר מצביעים על שכיחות של כ-1 ל-50,000 בספורטאים תחרותיים צעירים ו-1 במשתתפי מרתון בגיל הביניים. תשעים אחוז מהקורבנות הם גברים.
למרות שמוות בספורטאים תחרותיים מקבל תשומת לב תקשורתית ניכרת, מעל 90% מכלל מקרי המוות הלבביים הפתאומיים הקשורים למאמץ מתרחשים בספורטאים חובבנים. סיקור קרדיווסקולרי לזיהוי ספורטאים המועדים למוות לבבי פתאומי הקשור למאמץ נותר שנוי במחלוקת לאור שיעורי האירועים הנמוכים.
נתונים ממחקר פרוספקטיבי איטלקי גדול מצביעים על כך שהערכת ספורטאים צעירים עם אק"ג 12-לידים יעילה בהפחתת הסיכון למוות לבבי פתאומי. הצלחת תוכנית זו יוחסה ליכולת האק"ג לזהות מחלת תעלות יונים ומסלולים נוספים, מכיוון שרוב החולים עם קרדיומיופתיה ראשונית מציגים אק"ג לא תקין.
לעומת זאת, רוב הספורטאים בגיל הביניים מתים ממחלת עורקים כליליים, אשר נדיר שהיא מתגלה באק"ג משטח. ההמלצות הנוכחיות לזיהוי ספורטאים בגיל הביניים בסיכון הגבוה ביותר למוות לבבי פתאומי מסתמכות על בדיקת מאמץ. עם זאת, רוב בדיקות המאמץ הלא תקינות בספורטאים בגיל הביניים ללא תסמינים מייצגות תוצאות חיוביות שגויות ובעלות דיוק ניבוי נמוך.
נתונים נוכחיים מצביעים על כך שהחייאה קרדיו-ריאתית על ידי עוברי אורח ויישום מוקדם של דפיברילטור חיצוני אוטומטי הם השיטות היעילות ביותר למניעת מוות לבבי פתאומי בקבוצה זו. ברוב המקרים של מוות לבבי פתאומי בספורט, מאמץ נחשב כגורם מעורר לאריתמוגנזה באנשים מועדים ולא כגורם ישיר למצע הפתולוגי.
האם מאמץ יכול לפגוע בלב בריא? הראיות העולות
שני העשורים האחרונים היו עדים לגל השתתפות באירועי סיבולת מפרכים כמו תחרויות רכיבה על אופניים, מרתונים, טריאתלונים ותחרויות Ironman. במקביל למגמה זו, מחקרים רבים הדגימו ריכוזים מוגברים בדם של סמני נזק לבבי בספורטאים רבים כאלה.
המנגנון וההשלכות של סמנים לבביים מוגברים לאחר מאמץ נותרו שנויים במחלוקת. עם זאת, עלו שאלות האם פרצי מאמץ חוזרים של אימוני סיבולת לאורך חיים עלולים ליצור מצע אריתמוגני through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through through 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עדויות חדשות מצביעות על כך שלעיתים להפרעות קצב חדריות בספורטאים בריאים יש פרוגנוזה חמורה יותר ממה שהיה מוכר בעבר. חוקרים צפו בשכיחות גבוהה של אירועים קצביים משמעותיים, כולל מוות לבבי פתאומי (20%), ב-46 ספורטאים צעירים שהציגו פעימות חדריות מוקדמות תכופות או טכיקרדיה חדרית לא מתמשכת במהלך תקופת מעקב של 5 שנים.
שמונים אחוז מההפרעות הקצביות החדריות הללו מקורן בחדר הימני. מחקרים עוקבים מאותה קבוצת מחקר מצביעים על כך שאימון סיבולת כרוני מקדם שינוי מבני שלילי בחדר הימני.
מחקרים פולשניים במהלך פעילות גופנית מגלים כי לחצים בעורק הריאתי יכולים להגיע עד 80 מ"מ כספית, ויוצרים עומס אחר גבוה על החדר הימני. חוקרים בחנו 40 ספורטאים בריאים בתחילת המחקר ולאחר מרוץ סיבולת, וגילו הגדלה זמנית של החדר הימני המלווה בפגיעה בתפקוד החדר הימני באקוקרדיוגרפיה.
טרופונין לבבי ופפטידים נטריורטיים מסוג B היו מוגברים לאחר המירוץ ותאמו למשך הפעילות הגופנית ולעוצמת הירידה בתפקוד החדר הימני. החוקרים שיערו כי עומס חוזר על החדר הימני בעקבות פעילות סיבולת ממושכת עלול לקדם שינוי מבני שלילי עם נטייה להפרעות קצב קטלניות – מושג הידוע בשם קרדיומיופתיה חדרית ימנית אריתמוגנית המושרית על ידי פעילות גופנית.
מינון הפעילות הגופנית הנדרש להשפעה זו הוא כנראה יותר מ-20 שעות בשבוע במשך יותר מ-20 שנים. בעוד שדיווחים הולכים ומצטברים מצביעים על כך שהשתתפות סדירה בפעילות גופנית אינטנסיבית ביותר עלולה לגרום למצעים אריתמוגניים לבביים בחלק מהספורטאים, מסקנות אלו נותרות ספקולטיביות ומבוססות בעיקר על מחקרים תצפיתיים הכוללים קבוצות קטנות ונבחרות של ספורטאים סימפטומטיים הפונים לטיפול רפואי.
אם מקרים כאלו ייצגו את השכיחות האמיתית של ספורטאים הנושאים מצעים אריתמוגניים המושרים על ידי פעילות גופנית, האחוז הנפגע יהיה זעיר בהתחשב בכ-10 מיליון משתתפים במרתונים, טריאתלונים ואירועי Ironman ברחבי העולם מדי שנה.
מחקר פרוספקטיבי של 114 ספורטאי סיבולת אולימפיים שהתחרו ב-2–5 משחקים אולימפיים רצופים לא הראה הידרדרות בתפקוד הלבבי או סיכון מוגבר להפרעות קצב. פעילות גופנית גם מפחיתה ירידות קשורות לגיל בגמישות ובאלסטיות שעלולות לגרום לתחלואה קרדיווסקולרית בהמשך החיים.
יתרה מכך, מחקרים רבים גילו כי ספורטאים העוסקים באירועי הסיבולת המפרכים ביותר, כולל הטור דה פראנס, חיים זמן רב יותר מאנשים לא פעילים. היתרון באריכות החיים עשוי להיות מיוחס לאורח חיים בריא יותר באופן כללי או לעליונות גנטית, אך אין בכך כדי להפחית מהעובדה ששנים של פעילות גופנית אינטנסיבית לא היו קשורות בסיכון מוגבר לתחלואה לבבית באוכלוסיות אלו.
עדויות עדכניות מצביעות על כך שרק מספר קטן של ספורטאים עלול להיות בסיכון לנזק לבבי מפעילות גופנית אינטנסיבית ממושכת, ואין להתעלם מהאופוריה המתווכת על ידי אנדורפינים הקשורה בפרקטיקה כזו ברוב האנשים.
חומרים משפרי ביצועים: הצד המכוער של הספורט
בעידן הנוכחי של ספורטאים מפורסמים וחוזי ספורט רווחיים, מספר ספורטאים נכנעו לשימוש בחומרים משפרי ביצועים המזיקים profoundly לבריאות הלב. חומרים אלו מייצגים את ההיבט "המכוער" של קרדיולוגיית הספורט, ומספקים שיפור ביצועים מלאכותי במחיר של נזק קרדיווסקולרי.
חומרים משפרי ביצועים שונים משפיעים על הלב באמצעות מנגנונים שונים:
- אנדרוגנים אנבוליים: גורמים ליתר לחץ דם, הפרעות קצב, היפרטרופיה של החדר השמאלי, מחלת עורקים כליליים, אוטם בשריר הלב, אי ספיקת לב ומוות לבבי פתאומי
- גונדוטרופין כוריוני אנושי: קשור ביתר לחץ דם, הפרעות קצב והיפרטרופיה של החדר השמאלי
- אריתרופויאטין: מגביר את הסיכון ליתר לחץ דם ועשוי לתרום להיווצרות קרישי דם
- אגוניסטים לבטא-2: עלולים לגרום להפרעות קצב, היפרטרופיה של החדר השמאלי ואוטם בשריר הלב
- משתנים: עלולים לגרום לחוסר איזון אלקטרוליטי המשפיע על קצב הלב
- אמפטמינים: קשורים ביתר לחץ דם, הפרעות קצב, היפרטרופיה של החדר השמאלי, מחלת עורקים כליליים ואוטם בשריר הלב
- קוקאין: גורם ליתר לחץ דם, הפרעות קצב, היפרטרופיה של החדר השמאלי, מחלת עורקים כליליים, אוטם בשריר הלב, אי ספיקת לב ומוות לבבי פתאומי
- אפדרין: סיכונים קרדיווסקולריים דומים לאמפטמינים
- נרקוטיקה וקנבינואידים: עלולים לגרום להפרעות קצב וסיבוכים קרדיווסקולריים אחרים
- גלוקוקורטיקואידים ואלכוהול: תורמים ליתר לחץ דם, היפרטרופיה של החדר השמאלי ובעיות לבביות אחרות
החתירה למצוינות אתלטית באמצעים פרמקולוגיים מגיעה במחיר